RED CELL ANTIBODIES

RED CELL ANTIBODIES

1. Blood group and antibodies tested at booking and at 28/40. Common antibodies include...

   • D (positive)
   • C
   • c
   • e
   • K

2. RHESUS ISOIMMUNISATION

   • The fetus inherits a gene from each parent and as rhesus D is a dominant gene if one or two genes are inherited then the baby will be rhesus positive (Rh +ve).
     • Only if the baby inherits two recessive d genes will the blood group be rhesus negative (Rh -ve).
       • If the mother is Rh -ve and the baby is Rh +ve, haemolysis of fetal red cells may occur.
         • This rarely affects the first baby as there are no spontaneous anti-D antibodies present in the woman's blood prior to her first pregnancy.
           • This may happen if fetal red blood cells cross the placental barrier during that pregnancy or if she has been transfused accidentally with Rh +ve blood.
             • During pregnancy and labour there is usually no mixing of maternal and fetal circulations.
               • When the placenta separates, the chorionic villi tear and there is a risk of fetomaternal haemorrhage (FMH): usually between 0.5ml and 5ml of fetal blood enters the maternal circulation If the fetus is Rh +ve the production of antibodies will be stimulated and memory cells will mount a secondary response should the mother become pregnant with a second Rh +ve baby. This process is called isoimmunisation.
                 • Stables and Rankin (2011)

3. FETOMATERNAL HAEMORRHAGE AND ANTIBODY FORMATION

   • Fetomaternal hemorrhage (FMH) refers to the entry of fetal blood into the maternal circulation before or during delivery.
   • Spontaneous or therapeutic abortion, amniocentesis, antepartum haemorrhage or external cephalic version may lead to an FMH and antibody formation.
     • The problem arises in subsequent pregnancies because anti-D antibodies cross the placenta and haemolyse fetal red cells.
       • Some protection occurs if the mother and fetus are ABO incompatible, as the naturally occurring anti-A or anti-B will destroy fetal red cells before the maternal immune system can respond to the rhesus factor.
         • Stables and Rankin (2011)

4. PREVENTION OF MATERNAL ISOIMMUNISATION

   • In the past haemolytic disease of the newborn led to fetal or neonatal death from rhesus haemolytic disease but this is now largely preventable if three conditions are met:
     • 1) Rhesus-positive blood should never be transfused if a woman’s blood group is unknown.
       • 2) Unnecessary risk of FMH should be avoided, for example by placental localisation prior to amniocentesis. Abdominal palpation of women with an antepartum haemorrhage should be kept to a minimum.
         • 3) If there has been a risk of FMH, anti-D immunoglobulin (rhesus D antibodies) must be administered to the mother within 72 h; this confers passive immunity for about 3 months. The antibodies will coat and destroy any fetal red cells in the maternal circulation.
   • Stables and Rankin (2011)
   • The dose of anti-D immunoglobulin (Ig) is normally 250 IU (international units) before 20 weeks of preg- nancy and 500 IU after 20 weeks
     • Occasionally the FMH is so large that one dose of anti-D is insufficient to prevent isoimmunisation. The number of fetal red cells in maternal blood is estimated by means of a Kleihauer test and, if a second dose is needed, the laboratory will inform the doctor.

5. NICE 2008 GUIDELINES FOR "Routine antenatal anti-D prophylaxis for women who are rhesus D negative"

   • Routine antenatal anti-D prophylaxis is recommended as a treatment option for all pregnant women who are RhD negative and who are not known to be 'sensitised'.
   • RAADP can be given as two doses of anti-D immunoglobulin of 500 IU (one at 28 weeks and one at 34 weeks gestation), as two doses of anti-D immunoglobulin of 1000–1650 IU (one at 28 weeks and one at 34 weeks gestation), or as a single dose of 1500 IU either at 28 weeks or between 28 and 30 weeks gestation.
     • RAADP is not used uniformly throughout the NHS. In 2005, a survey of obstetric units reported that 75% offered RAADP, and of these 81% used one of the two-dose regimens. RAADP is usually administered by community midwives or at antenatal clinics.

6. ANTENATAL MANAGEMENT: ANTI-D PROPHYLAXIS

   • Every pregnant woman has her blood tested for ABO and rhesus types early in pregnancy. Any rhesus-negative women will be screened for RhD antibodies. If the test is negative further screening will be carried out.
     • It is now recommended that all non-sensitised women should receive anti-D prophylaxis of at least 500 IU, usually at 28 and 34 weeks of pregnancy. Because some fetomaternal bleeds are undetected in pregnancy, some authorities recommend the use of antepartum RhD Ig prophylaxis ( NICE 2007 ).
       • Failure to adhere to protocols of anti-D Ig administration means there are still incidences of women becoming sensitised and their babies developing haemolytic disease of the newborn
         • Failings include...
           • Not testing the size of an FMH to ensure an appropriate dose of anti-D Ig was given.
           • Some women do not receive anti-D Ig, including those who attend accident and emergency departments with bleeding in early pregnancy.
           • Not administering anti-D Ig for abdominal trauma in 80% of cases.
           • Using an inadequate dose of anti-D Ig following antepartum haemorrhage.
           • Not managing sensitising events occurring after 20 weeks gestation.
           • Not understanding Kleihauer test results, with a negative result interpreted as a reason not to give anti-D Ig.
           • Postnatal omissions resulting because of confusion with women who had recently received antenatal treatment with anti-D Ig.

7. CARE AT DELIVERY

   • When a mother is rhesus negative, the umbilical cord is clamped immediately to minimise the amount of placental blood with possible maternal antibodies entering the baby’s circulation
     • Cord blood is taken for testing by using a syringe and needle directly into a placental vein to avoid the risk of contamination by maternal blood and Wharton’s jelly which would make interpretation of the results difficult. The needle is removed prior to transferring the blood into a bottle to avoid haemolysis.
       • Cord blood is tested for ABO and rhesus type, direct Coombs test looking for maternal antibodies on direct Coombs test looking for maternal antibodies on fetal red cells, and a haemoglobin estimate to check for haemolysis. If the mother has rhesus antibodies, the cord blood is also tested for serum bilirubin level.

8. MANAGEMENT IF RHESUS ANTIBODIES ARE PRESENT DURING PREGNANCY

   • If antibodies are detected, the titre is checked. Although titre does not relate directly to the fetal condition, it indicates a necessity to carry out an amniotic fluid test.
     • The amount of bilirubin excreted from red cell haemolysis can be measured by optical density to allow judgements for further management. it is best to avoid amnicentesis until after 26 weeks when the fetus is considered viable.
       • The fetus is monitored for oedema and hepato-splenomegaly (enlarged liver and spleen) by ultrasound.
         • Intravenous immunoglobulin may maintain the fetus until fetal transfusion of O-negative packed cells can be given. If the fetus is considered mature enough to survive and it is considered dangerous to continue the pregnancy, the baby is delivered when all facilities, including pathology laboratory, are available.

9. RHESUS HAEMOLYTIC DISEASE

   • All babies whose mothers have rhesus antibodies should be transferred to a neonatal intensive care unit until the results of the cord blood tests are known. Depending on the percentage of red blood cells destroyed this disease varies in severity.......
     • 1) Congenital haemolytic anaemia
       • occurs if haemolysis is minimal. Hepatosplenomegaly will be present but jaundice will not be severe. If the baby’s haemoglobin (Hb) level is low a transfusion of packed cells can be given.
       • 2) In ictarus gravis neonatorum (severe jaundice of the newborn)
         • there has been fetal haemolysis and the baby’s haemoglobin is low. Because the placenta transfers bilirubin to the mother for excretion, the baby is not usually jaundiced at birth. After delivery when the baby’s liver has to cope with excessive bilirubin, jaundice rapidly develops. Treatment includes restoring the Hb level, reducing the bilirubin level and removing maternal antibodies.
         • In hydrops fetalis
           • severe intrauterine anaemia results in congestive cardiac failure. The baby and placenta are pale and oedematous and the baby may be stillborn. If the baby is alive an immediate transfusion of packed cells will allow tissue oxygenation. Bilirubin and maternal antibodies are removed by an exchange transfusion via an umbilical catheter.

10. PRINCIPLES OF EXCHANGE TRANFUSION

    • Umbilical vein catheterisation should only be carried out in a specialist unit by an experienced doctor who should be aware of the correct direction and position for the catheter.
      • 1) Blood is drawn out into a syringe via an umbilical vein catheter ( Fig. 14.3 ). 2) This blood is discarded into a waste container. 3) Blood, warmed to body temperature, is drawn into this syringe. The blood is cross-matched for compat- ibility with blood from the baby’s mother. 4) This blood is injected slowly. The process is repeated until twice the baby’s blood volume has been exchanged.

11. ABO INCOMPATIBILITY

    • In this condition the mother is blood group O and the baby either group AO or BO. Maternal blood contains unprovoked anti-A and anti-B antibodies even in the first pregnancy and these cross over the placenta to haemolyse fetal red cells. The first child can be affected but jaundice which appears in the first 24 h is usually mild. Treatment will depend on the rate of bilirubin rise in the neonate’s blood.

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