Awareness of treatment of maternal and child blood group incompatibility

  I Overview.
  Pregnant women and fetuses with blood group incompatibility, the mother’s antibodies combined with antigens on the fetal red blood cells, causing the destruction of fetal red blood cells, resulting in hemolysis and anemia, is called maternal-child blood group incompatibility hemolytic disease. The first is the ABO blood group disorder, the second is the Rh blood group disorder, there are also some rare blood group system hemolysis.
  Causes.
  Under normal circumstances, the blood of the mother and the fetus are separated by a membrane in the placenta, through which substances are exchanged to ensure the entry and exit of nutrients and metabolic substances of the fetus, and the blood of the mother and the fetus are not the same. However, for some reason, the natural barrier of the placenta is damaged and a small amount of fetal blood flows into the mother, which is equivalent to a transfusion of blood from the fetus to the mother, and because the mother and child have different blood types, the fetal blood stimulates the mother to produce antibodies. The antibodies produced by the mother are brought to the fetus through the placenta, which then interacts with the fetal red blood cells, especially when more antibodies enter the fetus, which will destroy the fetal red blood cells, resulting in fetal hemolysis or neonatal hemolytic disease.
  Third, the harm caused by mother-child blood group incompatibility
  The discovery of mother-child blood group incompatibility can cause miscarriage, premature birth, stillbirth, fetal edema, neonatal hemolytic jaundice, anemia and death of the newborn; among them, jaundice, anemia and edema are more frequent;
  1, anemia.
  The degree varies, with cord blood Hb>140 g/L in mild hemolysis; cord blood Hb<110 g/L in moderate hemolysis; in severe cases, cord blood Hb<80 g/L, and often accompanied by fetal edema, and the hemolysis continues to worsen after birth, and the anemia is further aggravated than at birth. Some children with hemolytic disease caused by Rh blood group incompatibility may develop significant anemia (Hb<80 g/L) 2-6 weeks after birth, which is called late anemia.
  2. Fetal edema.
  Mostly seen in severe cases, the infant has generalized swelling, pallor, skin petechiae, pleural effusion,, ascites, low heart sounds, rapid heart rate, respiratory distress, and hepatosplenomegaly. Most of the children with edema are born prematurely and often die shortly after birth if they are not treated promptly. Many children with edema have died in utero, and the occurrence of edema is mostly related to low plasma protein disorder.
  3. Jaundice.
  Fetal bilirubin produced by hemolysis are handled by the mother’s liver on behalf of the newborn, so the umbilical cord blood is generally not jaundiced, and in severe cases there can be 0.3 mg of bilirubin. After birth, all bilirubin processing is done by the newborn, and because of the incompetence of liver detoxification, jaundice can be seen 4-5 hours after birth and rapidly deepens, reaching a peak in 3-4 days after birth, and it is not uncommon to see more than 20mg/dl. Bilirubin is predominantly unspliced bilirubin.
  Jaundice begins on the face, and if bilirubin rises, jaundice also appears on the limbs and trunk, and eventually spreads to the palms and soles of the feet. jaundice in children with Rh hemolysis appears early and rises quickly compared to children with ABO hemolysis, and most jaundice appears within 24 hours, while in ABO hemolysis it is mostly 2 to 3 days after birth. If the jaundice continues to increase, not only does the skin and sclera become jaundiced, but the jaundice also enters the brain to form nuclear jaundice, causing damage to the brain tissue, affecting the baby’s intelligence, and also causing hearing impairment or motor impairment, or even death in severe cases.
  IV. Prenatal examination for maternal and child blood group incompatibility.
  1.Medical history.
  This disease should be considered in all cases where the medical history has been a history of poor maternity, such as excessive amniotic fluid, a previous birth of an edematous child, a giant placenta, stillbirth, miscarriage, preterm birth, early neonatal death or early onset jaundice within 24 hours of birth.
  Rh(-) women with a history of blood transfusion, ectopic pregnancy or miscarriage before their first intrauterine pregnancy.
  2. Blood group test: For suspected mother-child blood group incompatibility, blood group test can be performed on the pregnant woman and her husband in early pregnancy
  A ABO blood group incompatibility, the mother O, the father A sex, B, AB may occur;
  B Rh blood group incompatibility, mother D (negative), father D (positive), if D antigen incompatibility and a high clinical suspicion, should be further examined Rh system other antigens.
  3. Antigen screening.
  If a pregnant woman has a positive serological test and has been sensitized, the antibody potency should be measured regularly; it can be checked once every 1-2 months in the early and middle stages of pregnancy; it should be measured every 2 weeks from 28 to 32 weeks of pregnancy, and once a week after 32 weeks of pregnancy; if the antibody potency of ABO blood group incompatibility gradually rises above 1:512, and the potency of Rh blood group incompatibility rises above 1:32, it indicates a more serious condition.
  4.Ultrasound examination: observe whether the fetus has edema, hepatosplenomegaly and ascites, and perform cordocentesis if necessary (hospitalization is required for examination).
  5. Fetal heart monitoring: there may be a sine curve or a graph of fetal hypoxia.
  V. Prevention and control measures for maternal and child blood group incompatibility
  (i) Treatment during pregnancy.
  1. Take Chinese herbal medicine according to the doctor’s prescription, including Artemisia Inchi Tang with addition and some drugs to activate blood circulation and remove blood stasis and regulate qi can inhibit the production of immune antibodies in blood.
  Specific types and sources.
  2.Improve fetal resistance: 10 days of comprehensive treatment at 24 weeks 30 weeks and 33 weeks of gestation each, with intravenous injection of 25% glucose 40ml daily, plus vitamin c 500mg, and oral vitamin E 30mg twice a day; intermittent oxygen intake 3 times a day for 20 minutes each time;
  3.Plasma replacement can be done when the antibody potency is high: plasma replacement should be done when the mother’s serum specific antibody rises 2 times, and monitor the antibody titer, and plasma replacement can be repeated when it rises again.
  4. Combined Chinese and Western medicine treatment.
  5. Indications for termination of pregnancy.
  A If the antibody potency reaches 1:512 for ABO and 1:32 for Rh, or if the effect of treatment is not good if it rises 2 times or more, cesarean section should be considered.
  B Although the antibody potency does not meet the above criteria, but there is a history of miscarriage, stillbirth, severe neonatal hemolysis, and it is estimated that the fetus will be viable after delivery. 35 weeks should be used to promote lung maturation.
  C The pregnancy has reached 37 weeks.
  (B) Neonatal treatment: See the contents of Pediatrics
  1.Medication (including phenobarbital, adrenal corticosteroids, etc.) ;
  2.Light therapy;
  3.Blood exchange therapy;
  4.Human albumin or plasma therapy;
  5.Treatment of anemia;