ABO Hemolytic Disease And General Management And Prophylaxis Of Hemolytic Disease Of Newborn
Hemolytic Disease Of New Born
In 15-20% of pregnancies ABO incompatibility occurs between the mother and fetus. IgG antibodies against fetal red cells are produced in the mother. Group O mothers produce antibodies more readily than A or B group mothers. The ABO hemolytic disease of the newborn is mild compared to Rh hemolytic disease. Further differences are:
- The first pregnancy may be affected as frequently as subsequent pregnancies, and
- Even if one pregnancy is affected, the subsequent one may escape.
The clinical features are milder compared to Rh hemolytic disease and they may subside spontaneously. Phototherapy and exchange transfusion may be required at times.
Investigation in a suspected case of Rh isoimmunisation
The mother’s blood shows the presence of antibodies by the indirect Coomb’s test. Titers above 1/64 or rising titers are indicative of risk to the fetus. Further adjuncts to diagnosis are amniocentesis and analysis of bile pigments in amniotic fluid.
Unlike normal amniotic fluid which is colourless, in Rh hemolytic disease, the amniotic fluid is bright yellow and this can be quantified spectroscopically.
The baby’s blood shows positive direct Coomb’s test, elevated serum bilirubin, reticulocytosis, anemia and presence of large number of erythroblasts (over 10% of nucleated cells).
Erythroblastosis fetalis » Symptoms
Immunization Is Very Important
Rh immunization is a preventable disease by proper Rh typing during the prenatal check up.
- When the mother is not immunized or the Rh antibody titer is low and static, the pregnancy is allowed to continue.
- If the risk of hydrops fetalis or stillbirth is high, induction of labour between 34 and 38 weeks is indicated.
- If there is risk of hydrops fetalis or still birth before 34 weeks, the baby is treated with intrauterine intraperitoneal transfusions to carry the pregnancy till 34 weeks and then labour is induced. Test for pulmonary maturity is carried out by estimating the lecithin sphingomyelin (L/S) ration of the amniotic fluid. If the L/S ratio is above 2/1, the pulmonary surfactant will be normal and so there is no risk of acute respiratory distress syndrome in the newborn.
The principles of management include the correction of anemia, acidosis, hypoglycemia and hyperbilirubinemia. When the serum level of unconjugated bilirubin is above 20 mg/dl in term babies or 15 mg/dl in preterm babies, exchange transfusion with Rh negative group O blood is indicated. By this procedure, antibody coated erythrocytes and excess bilirubin are removed and anemia is corrected. Hemoglobin level below 14g/dl and serum bilirubin above 3 mg/dl in cord blood are also indications for immediate exchange transfusion. Usually 150 ml/Kg body weight of compatible blood is used for each exchange.
Other forms of therapy: Mild or even moderate cases can be controlled by phototherapy and phenobarbitone. Natural sunlight and fluorescent ligh oxidize bilirubin to biliverdin and then to nontoxic watersoluble products. Phototherapy reduces indirect bilirubin level and helps to reduce the need for exchange transfusion. Phenobarbitone induces liver enzymes to conjugate bilirubin and favour their excretion.
Immunisation of susceptible Rh negative mothers can be prevented by the administration of 300 ug of anti-D gammaglobulin (Rhogam) within 72 hours of delivery or abortion, amniocentesis or rupture of ectopic gestation.
© 2014 Funom Theophilus Makama