A or B or AB Immune (7S) Usually positive Usually positive Moderately low Variably elevated Spherocytes
Rh same as infant group O only
3. Elevated indirect bilirubin level*
4. Demonstration of incompatible blood group a. Group O mother may have an infant who is group A or B.
b. Rarely, mother may be A and baby B or AB or mother may be B and baby A or AB.
5. Direct Coombs' test on infant's red cells usually positive
6. Demonstration of antibody in infant's serum a. When free anti-A is present in a group A infant or anti-B is present in a group B infant, ABO hemolytic disease may be presumed. These antibodies can be demonstrated by the indirect Coombs' test in the infant's serum using adult erythrocytes possessing the corresponding A or B antigen. This is proof that the antibody has crossed from the mother's to the baby's circulation.
b. Antibody can be eluted from the infant's red cells and identified.
7. Demonstration of antibodies in maternal serum. When an infant has signs of hemolytic disease, the mother's serum may show the presence of immune
*In the era of early discharge of newborns, the use of the critical bilirubin level of 4 mg/dL at the sixth hour of life will predict significant hyperbilirubinemia and 6 mg/dL at the sixth hour will predict severe hemolytic disease of the newborn. The reticulocyte count, a positive Coombs' test, and a sibling with neonatal jaundice are additional predictors of significant hyperbilirubinemia and reason for careful surveillance of the newborn.
agglutinins persisting after neutralization with A and B substance and hemolysins.
In ABO hemolytic disease, unlike Rh disease, antenatal management or premature delivery is not required. After delivery, management of an infant with ABO hemolytic disease is directed toward controlling the hyperbilirubinemia by frequent determination of unconjugated bilirubin levels, with a view to the need for phototherapy or exchange transfusion. The principles and methods are the same as those described for Rh hemolytic disease. Group O blood of the same Rh type as that of the infant should be used. Whole blood is used to permit maximum bilirubin removal by albumin.
Infants not requiring an exchange transfusion for hyperbilirubinemia following immune hemolytic anemia may develop significant anemia during the first 6 weeks of life because of persistent maternal IgG antibodies hemolyzing the infant's red blood cells associated with a reticulocytopenia (antibodies destroy the reticulocytes as well as the red blood cells). For this reason, follow-up hemoglobin levels weekly for 4-6 weeks should be done in those infants.
Nonimmune Hemolytic Anemia
The causes of nonimmune hemolytic anemia are listed in Table 2-1. Vitamin E Deficiency
Vitamin E is one of several free-radical scavengers that serve as antioxidants to protect cellular components against peroxidative damage. Serum levels of 1.5 mg/dL are adequate; levels greater than 3.0 mg/dL should be avoided because they may be associated with serious morbidity and mortality.
Vitamin E protects double bonds of lipids in the membranes of all tissues, including blood cells. Vitamin E requirements increase with exposure to oxidant stress and increase as dietary polyunsaturated fatty acid (PUFA) content increases. Vitamin E is now supplemented in infant formulas in proportion to their PUFA content in a ratio of E:PUFA > 0.6. The lipoproteins that transport and bind vitamin E are low in neonates.
Hemolytic anemia and reticulocytosis Thrombocytosis Acanthocytosis Peripheral edema Neurologic signs: Cerebellar degeneration Ataxia
Hemolytic anemia develops under the following conditions:
Diets high in PUFA supplemented with iron, which is a powerful oxidant Prematurity
Oxygen administration, a powerful oxidant.
Peroxide hemolysis test: Red cells are incubated with small amounts of hydrogen peroxide, and the amount of hemolysis is measured.
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