NE20A Parent Child Nursing

Antenatal Care ABO Blood Groups Rhesus (Rh) Blood Types

Brenda Lois Scarlett Miller November 2008

Learning Outcomes Explain the ABO and Rh Concepts Describe the Clinical Application Explain the importance of Anti-Rho(D) immune globulin (RhoGAM) Blood Groups The ABO blood groups. May years ago it was found that there might be present in the blood of any human a factor called A, or another factor called B or both or neither. There are therefore four groups of people: I. II. III. IV. A B AB O with factor A only in their blood with factor B only with both factors with neither factor

The relative frequency of these four groups varies with race and country. For transfusion purposes, remember, Dont give anybody anything they havent already got. Because if you do, the foreign factor will excite the production in the recipient of antibodies e.g. anti-A bodies (=A antibodies) if group A blood is given to someone from Group O. This can cause a transfusion reaction with one or more of pyrexia, rigors, lumbar (renal0 pain, headache, dyspnoea, shock, bloody urine, oliguria and jaundice. A second incompatible transfusion can be fatal. If you make a 16 square and write the groups along the top as donors and along the side as recipients, you can easily work out whose blood can safely be given to whom () and which bloods are incompatible (x). Group O blood containing O (= nothing) can be given to any group: therefore the owner is a universal donor. Group AB blood can receive blood from anyone: whatever they have, he already has: therefore the owner is a universal recipient.

DONOR AB R E C I P I E N T AB A B O X X X A X X B X X O

In practice, therefore, before transfusion the ABO groups of recipient and of donor must be ascertained and found to be compatible. As a further precaution, their compatibility is checked by mixing the bloods on a glass slide cross matching. But even after precautions became the rule, transfusion reactions still occasionally occurred. Some were due to the donor blood being too old, or too cold, or too hot, or infected. But others were suspected of being due to blood factors other then A and B. Other factors were sought and found, but all were unimportant in relation to blood transfusion, until in 1040 the Rhesus (Rh) factor was discovered. The Rh factor. This factor is present in the blood of most people; they are called Rh-positive. It is absent in the minority; they are Rh-negative. In transfusion the same law as before applies: Dont give anybody anything they havent already got. So you do not give Rh-positive blood to an Rh-negative person: if you do, the latter will produce Rh antibodies. You can give Rh-negative blood to an Rhpositive as you would be giving nothing. Now, therefore, before transfusion both ABO and Rh groups of recipient and donor must be ascertained and found compatible and the compatibility checked by crossmatching. The Rh Factor in Pregnancy If an Rh-negative woman is pregnant and the foetus in her uterus is Rh-positive, then if some foetal red cells enter her circulation, the Rh factor in them, being foreign to her, will excite the production of Rh antibodies. This process is called Rhisoimmunisation. These Rh antibodies in the mothers blood cannot harm her because they are antiRh and she has no Rh factor. But the antibodies may cross the placenta to the foetus and attack the foetal Rh-positive red cells, causing agglutination (clumping) and haemolysis (breakdown) of these red cells. The haemolysis causes anaemia and a high level of pigment in the foetal blood, and so one of the degrees of haemolytic Disease of the Newborn (HDN) (also called erythroblastosis fetalis) detailed below. Thus an Rh-negative woman may have Rh antibodies in her blood either: a) Because at some time she was, wrongly, transfused with Rh-positive blood, in which case even her first Rh-positive baby can be affected; or, more commonly.

b) Because during pregnancy with an Rh-positive foetus a breach in the placental barrier allowed a transplacental haemorrhage (TPH) of foetal red cells into her circulation. This TPH usually occurs during labour, especially if there has been antepartum haemorrhage or interference such as Caesarian section or manual removal of the placenta; therefore the first Rh-positive foetus of an Rh-negative mother usually escapes HDN because it is already born before there is time for antibodies to form in the mothers blood and cross to the foetus. This fact is the basis of a procedure to prevent sensitization to the Rh factor and HDN. Note carefully that if the mother is Rh-positive, HDN due to the Rh factor cannot occur as the foetus cannot give her anything she hasnt already got. But other factors present in the foetal but not the maternal blood can similarly through the foetal but not the maternal blood can similarly through TPH cause antibody formation and HDN. Fro example, if the mother is group O and the foetus group A, A antibodies may be produced and cause HDN. But HDN due to factors may be produced and cause HDN. But HDN due to factors other than Rh is seldom severe. Nevertheless, if a neonate develops jaundice, HDN due to any factor must be excluded. Inheritance of Rh Group. The Rh group is not a single entity but a combination of six of several possible components. One of these, D, is the cause of over 90% of cases of HDN. The Rh group is inherited from both parents equally: the Rh-negative person is doubly negative; the Rh positive person may be doubly positive HOMOZYGOUS, or half positive and half negative HETEROZYGOUS. Rh antibodies, once formed, persist through every future pregnancy, even with an Rh-negative foetus. So the presence of antibodies does not mean the foetus of the particular pregnancy must be affected whether it is Rh-negative or Rh-positive depends on the fathers Rh status: if he is HOMOZYGOUS Rh-positive, all his sperm are Rh-positive and so he can father only Rh-positive babies, which, with a sensitized Rh-negative mother, are liable to HDN; if he is HETEROZYGOUS, half of his sperm are Rh-positive and half Rhnegative, so there is a 50% chance that any baby he fathers on a sensitized Rh-negative woman will be Rh-negative and incapable of developing HDN. The husbands detailed blood group is therefore determined if a woman with an affected baby wants to know their chances for a subsequent baby. Rh antibodies are of two types: complete (saline agglutinin) and incomplete (albumin Agglutinin). The latter is much more serious as a cause of HDN.

Clinical Application Knowledge of the above leads the Midwife to their clinical application in Ten Rh Commandments. (1) Have the ABO and Rh group of every pregnant woman determined: (a0 in her own interest in case she should need a transfusion; and (b) in the interests of her baby to exclude it being affected by HDN. (2) If she is Rh-positive, HDN is unlikely. (3) If she is Rh-negative, test her blood at first visit and subsequently as ordered by the Doctor but at least at the 28th 30th week for Rh antibodies. Therefore it is important to remember that blood group and Rhesus factor status must be ascertained on all pregnant woman at their antenatal booking visit. (4) Give every pregnant Rh-negative woman a simple printed explanation of her blood group. (5) If antibodies are present, the baby may (not will) be affected by HDN. Therefore book the woman for delivery in an institution where the baby can be tested at birth and, if necessary, treated. (6) The Doctor will decide whether and when to induce premature labour on the basis of the previous history and of various test results including the titre (amount) of antibody, and especially the amount of bilirubin (pigment) found in liquor drawn off by abdominal puncture of the uterus (amniocentesis) at the 28th-32nd week or earlier if a previous baby has been severely affected. Amniocentesis is repeated by the Doctor as necessary. Where the history and findings suggest a foetus very seriously affected before the 32nd week, the doctor may attempt intrauterine transfusion of the baby through a cannula passed through the mothers abdominal wall and uterus into the babys peritoneal cavity. (7) At delivery, tie the cord as early as possible to prevent the transfer of any further antibodies from mother to baby. Leaving the cord 10-12 cm. long has been abandoned as the doctor usually transfuses through the umbilical vein at skin level. (8) Collect blood from the cut placental end of the cord for four tests: a. COOMBS test: a positive result means the baby is affected by antibodies; b. Haemoglobin level and red cell count to assess the degree of anaemia; c. Serum bilirubin to assess the level of pigment in the blood because a high indirect bilirubin level brings a danger of KERNICTERUS; and d. Blood group and Rh factor. (9) According to the results of these tests, the Doctor decides whether to perform a transfusion. An exchange transfusion is given if the serum bilirubin is high or rising and the haemoglobin low or falling, because in this way pigment and antibodies are withdrawn at the same time as replacement blood is given. Transfusion of 175 ml/kg. (80 ml/lb). effects an 80-90% exchange. Concerns about exchange transfusion are related to the use of blood products, which include the potential for HIV and hepatitis infection. A simple transfusion is given for simple anaemia. The haemoglobin and bilirubin tests are repeated at least daily to see if transfusion needs to be repeated.

Note: the baby is Rh-positive but the blood transfused is Rh-negative - a loan of compatible fresh blood which cannot be affected by any remaining antibodies, and which is of the same ABO group as the babys. (10) The baby after leaving hospital is followed up at the paediatric clinic to make sure that there is no anaemia or liver or other damage. Clinical Types of Haemolytic Disease of the Newborn (HDN) There are four degrees of HDN: Simple anaemia is the least degree. The Coombs test is positive. The haemoglobin is a little low but above 110%. The serum bilirubin is usually so low that there is no jaundice. The doctor will watch but may give a simple transfusion, or in mild jaundice prescribe phenobarbitone or order phototherapy to reduce the bilirubin level or prevent it rising. Phototherapy breaks down the bilirubin in the blood and is secreted in sweat, urine and feces. Icterus gravis. The liquor [/liquor/ (liker) (likwor)] may be yellow. The baby becomes jaundiced within hours of birth and the spleen and liver may be enlarged. The Coombs test is positive. The haemoglobin is below 100% and the serum bilirubin is high or rising. The doctor performs exchange transfusion, repeated if necessary or followed later by a topping-up simple transfusion. Hydrops fetalis is a gross degree of HDN. There may be hydramnios and toxaemia. The baby is grossly edematous as is the placenta. The baby is stillborn or dies at birth, but vary rarely it survives after exchange transfusion. Intrauterine death. In the most severe degree, the foetus dies in utero, usually after the 28th week. If it is not delivered within three weeks of death, the mother may develop impaired blood clotting. The Prevention of HDN The chances of Rh-isoimmunisation and consequent HDN can be reduced to 1% by the intramuscular injection of anti-D, 100mcg. every time an Rh-negative woman has delivered an Rh-positive baby and 50 mcg. every time an Rh-negative woman has had an abortion completed surgically, unless the patient is to be sterilized. Blood is taken from the mother for a KLEIHAUER TEST which identified foetal red cells, so that the dose of anti-D can be increased if indicated by the size of the TPH. Anti-D given within 60-72 hours destroys the foetal red cells before they can stimulate the mother to produce Rh antibodies. So in other words, it inactivates the foetal Rh antigens and prevents the formation of antibodies by the mother. This Anti-D is a specific type of antibody also called anti-Rho(D) immune globulin (RhoGAM). Anti-D must not be given to the baby.

Kernicterus Kernicterus is damage of the brain due to staining by excessive blood pigment (bilirubin). It used to be seen occasionally in icterus gravis before watch was kept on serum bilirubin levels and exchange transfusions freely made. But it can also occur: (a) in very premature babies whose immature liver cannot deal with even a normal amount of pigment; (b) after the administration of certain drugs or of large doses of vitamin K which is why the maximum dose of vitamin K is now 1 mg. In kernisterus in addition to jaundice there are signs of cerebral irritation such as head retraction, high-pitched cry, convulsions, twitching, muscular rigidity and rolling of the eyes. Of the survives it may show permanent brain damage. PREVENTION is based on a avoiding causative drugs and in watching carefully the serum bilirubin level in jaundiced babies. The critical level for kernicterus is a serum bilirubin of 20 mg or 342 mols/dl. TREATMENT is by exchange transfusion, repeated as necessary. To convert mg to mols/dl x 17.1 To convert mols/dl to mg 17.1