L 5 ABO Blood group -blood transfusion copy.pdf

5 ABO BLOOD TYPES-RH SYSTEM BLOOD TRANSFUSION ILOs By the end of this lecture, students will be able to 1. Describe ABO blood grouping system, Rh system 2. List the various types of blood groups 3. Explain why a person having a particular blood group, cannot have antibody of the same type in the pla...

5 ABO BLOOD TYPES-RH SYSTEM BLOOD TRANSFUSION ILOs By the end of this lecture, students will be able to 1. Describe ABO blood grouping system, Rh system 2. List the various types of blood groups 3. Explain why a person having a particular blood group, cannot have antibody of the same type in the plasma. 4. Define Rh incompatibility 5. Understand how Rh may complicate the pregnancy 6. Describe the hemolytic disease of the newborn 7. Understand the indications for blood transfusion 8. Relate the importance of blood typing and crossmatching tests to incompatible blood transfusion reactions 9. Discuss the complications of mismatched blood transfusion in relation to their pathophysiology At least 30 commonly occurring antigens and hundreds of other rare antigens, have been found on the surfaces of the cell membranes of human blood cells. Most of the antigens are weak.Two particular types of antigen systems are much more likely than the others to cause blood transfusion reactions. They are the O-A-B system of antigens and the Rh system. ABO antigen System AGGLUTINOGENS Two antigens—type A and type B—occur on the surfaces of the RBCs in a large proportion of people (also called agglutinogens because they often cause RBC agglutination). The blood is normally classified into four major O-A-B blood types, depending on the presence or absence of the two agglutinogens, the A and B agglutinogens. Table-1: ABO blood groups When neither A nor B agglutinogen is present, the blood is type O. When only type A agglutinogen is present, the blood is type A. When only type B agglutinogen is present, the blood is type B. When both A and B agglutinogens are present, the blood is type AB. (Table1) Page 1 of 6 AGGLUTININS Antibodies against erythrocyte antigens are present in human plasma. Accordingly, the plasma of type A blood contains anti-B antibodies, type B blood contains anti-A antibodies, no antibodies related to the ABO system are present in type AB blood, and both anti-A and anti-B antibodies are present in type O blood. UNIVERSAL BLOOD DONORS AND RECIPIENTS Because type O individuals have no A or B antigens, their erythrocytes will not be attacked by either anti-A or anti-B antibodies, so they are considered universal donors. Their blood can be transfused into people of any blood type. However, type O individuals can receive only type O blood because the anti-A and anti-B anti- bodies in their plasma will attack either A or B antigens in incoming blood. In contrast, type AB individuals are called universal recipients. Lacking both anti-A and anti-B antibodies, they can accept donor blood of any type, although they can donate blood only to other AB people. Because their erythrocytes have both A and B antigens, their cells would be attacked if transfused into individuals with antibodies against either of these antigens. Origin of Agglutinins in Plasma. The agglutinins are gamma globulins, as are almost all antibodies, and they are produced by the same bone marrow and lymph gland cells that produce antibodies to any other antigens. Most of them are IgM and IgG immunoglobulin molecules. Rh antigen system In addition to the ABO system, many other erythrocyte antigens and plasma antibodies can cause transfusion reactions, the most important is the Rh factor. People who have the Rh factor (an erythrocyte antigen first observed in rhesus monkeys, hence the designation Rh) are said to have Rh-positive blood, whereas those lacking the Rh factor are considered Rh-negative. In contrast to the ABO system, no naturally occurring antibodies develop against the Rh factor. Instead, the person must first be massively exposed to an Rh antigen such as by transfusion of blood containing the Rh antigen before enough agglutinins to cause a significant transfusion reaction will develop. Rh Antigens—Rh-Positive and Rh-Negative. There are six common types of Rh antigens, each of which is called an Rh factor. These types are designated C, D, E, c, d, and e. The type D antigen is widely prevalent in the population and is considerably more antigenic than the other Rh antigens. Anyone who has this type of antigen is said to be Rh positive, whereas a person who does not have type D antigen is said to be Rh negative. About 85% of all whites are Rh positive, and 15% are Rh negative. (Fig. 2) Rh IMMUNE RESPONSE Formation of Anti-Rh Agglutinins. When RBCs containing Rh factor are injected into a person whose blood does not contain the Rh factor (Rh- negative person), anti-Rh agglutinins develop Page 2 of 6 slowly, reaching a maximum concentration of agglutinins about 2 to 4 months later (delayed transfusion reaction). This immune response occurs to a much greater extent in some people than in others. With multiple exposures to the Rh factor, an Rh-negative person eventually becomes strongly sensitized to Rh factor, the transfusion reaction is greatly enhanced and can be immediate and as severe as a transfusion reaction caused by mismatched type A or B blood. Erythroblastosis Fetalis (Hemolytic Disease of the Newborn) Erythroblastosis fetalis is a disease of the fetus and newborn child characterized by agglutination and phagocytosis of the fetus’s RBCs. In erythroblastosis fetalis, the mother is Rh negative and the father is Rh positive. The baby has inherited the Rh-positive antigen from the father, and the mother develops anti-Rh agglutinins from exposure to the fetus’s Rh antigen during birth. In turn, the mother’s agglutinins diffuse through the placenta into the next fetus and cause RBC agglutination. An Rh-negative mother having her first Rh-positive child usually does not develop sufficient anti-Rh agglutinins to cause any harm. However, about 3% of second Rh-positive babies exhibit some signs of erythroblastosis fetalis, about 10% of third babies exhibit the disease, and the incidence rises progressively with subsequent pregnancies. (Fig.3) Effect of Mother’s Antibodies on the Fetus. After anti- Rh antibodies have formed in the mother, they diffuse slowly through the placental membrane into the fetus’s blood. There they cause agglutination of the fetus’s blood. The agglutinated RBCs subsequently hemolyze, releasing hemoglobin into the blood. The fetus’s macrophages then convert the hemoglobin into bilirubin. The antibodies can also attack and damage other cells of the body. Clinical Picture of Erythroblastosis. 1. Erythroblastotic newborn baby is usually anemic at birth, and the anti-Rh agglutinins from the mother usually circulate in the infant’s blood for another 1 to 2 months after birth, destroying more and more RBCs. 2. The hematopoietic tissues of the infant try to replace the hemolyzed RBCs. The liver and spleen become greatly enlarged and produce more RBCs. Because of the rapid production of RBCs, many early forms of RBCs, including many nucleated blastic forms, are passed from the baby’s bone marrow into the circulatory system, and it is because of the presence of these nucleated blastic RBCs that the disease is called erythroblastosis fetalis. 3. Hemolysis of the RBCs with increased concentration of bilirubin may cause Jaundice. In some cases, there is precipitation of bilirubin in the neuronal cells, causing the destruction of many of these cells with permanent mental impairment or damage to motor areas of the brain; this condition called kernicterus. (Fig.4) Page 3 of 6 Fig.3: Hemolytic diseases of newborn Fig.4: Manifestations of Hemolytic diseases of newborn Prevention of Erythroblastosis Fetalis. By administration of Rh immunoglobulin globin, (an anti- D antibody) to the expectant mother starting at 28 to 30 weeks of gestation or within 72 hours of delivery. The anti-D antibody is also administered to Rh-negative women who deliver Rh-positive babies to prevent sensitization of the mothers to the D antigen. This step greatly reduces the risk of developing large amounts of D antibodies during the second pregnancy. The anti-D antibody inhibits the antibody production in the expectant mother. The administered anti-D antibody also attaches to D antigen sites on Rh-positive fetal RBCs that may cross the placenta and enter the circulation of the expectant mother, thereby interfering with the immune response to the D antigen. Treatment of Neonates with Erythroblastosis Fetalis. One treatment for erythroblastosis fetalis is to replace the neonate’s blood with Rh-negative blood. The Rh-negative blood is infused over a period of 1.5 or more hours while the neonate’s own Rh-positive blood is being removed. This procedure may be repeated several times during the first few weeks of life, mainly to keep the bilirubin level low and thereby prevent kernicterus. By the time these transfused Rh-negative cells are replaced with the infant’s own Rh-positive cells, a process that requires 6 weeks or more, the anti-Rh agglutinins that had come from the mother are destroyed. Page 4 of 6 Indication of blood transfusion Transfusion of whole blood: indicated in cases of; Acute blood loss and shock Transfusion of Packed red blood cells: indicated in cases of Chronic severe anaemia or leukaemia Transfusion of Platelets concentrate indicated in cases of Thrombocytopenia and bleeding due to platelets dysfunctions Transfusion Reaction If a person is given blood of an incompatible type, two different antigen–antibody interactions take place. The more serious consequences arise from the effect of the antibodies in the recipient’s plasma on the incoming donor erythrocytes. The effect of the donor’s antibodies on the recipient’s erythrocyte-bound antigens is less important unless a large amount of blood is transfused, because the donor’s antibodies are so diluted by the recipient’s plasma that little red blood cell damage takes place in the recipient. Antibody interaction with erythrocyte-bound antigen may result in agglutination (clumping) or hemolysis (rupture) of the attacked red blood cells. Agglutination and hemolysis of donor red blood cells by antibodies in the recipient’s plasma can lead to a transfusion reaction. Typically, one would expect antibody production against A or B antigen to be induced only if blood containing the antigen were injected into the body. However, high levels of these antibodies are found in the plasma of people who have never been exposed to a different type of blood. Consequently, these were considered naturally occurring antibodies, that is, produced without any known exposure to the antigen. Therefore, before giving a blood transfusion to a person, it is necessary to determine the blood type of the recipient and donor blood so that the bloods can be appropriately matched. This process is called blood typing and crossmatching. Blood typing is the first step. It focuses on the antigens on the surface of the red cell. This test finds out the blood type A, AB, B, or O. Also, to find out if the blood Rh type is negative or positive. Blood typing is performed in the following way. The RBCs are first separated from the plasma and diluted with saline solution. One portion is then mixed with anti-A agglutinin and another portion is mixed with anti-B agglutinin. After several minutes, the mixtures are observed under a microscope. If the RBCs have become clumped—that is, agglutinated—then an antibody-antigen reaction has resulted. (Fig.5) Crossmatching: It focuses on antibodies in the plasma. In a crossmatch, donor red cells are mixed with the plasma of the recipient. If antibodies exist in the recipient plasma to antigens on the red cells of the donor, transfusion reactions can occur. Agglutination of RBCS: When bloods are mismatched so that anti-A or anti-B plasma agglutinins are mixed with RBCs that contain A or B agglutinogens, respectively, the RBCs agglutinate as a result of the agglutinins attaching themselves to the RBCs. Because the agglutinins have two binding sites Page 5 of 6 (IgG type) or ten binding sites (IgM type), a single agglutinin can attach to two or more RBCs at the same time, thereby causing the cells to be bound together by the agglutinin. This binding causes the cells to clump, which is the process of agglutination. Then these clumps plug small blood vessels throughout the circulatory system. During the ensuing hours to days, physical distortion of the cells or attack by phagocytic white blood cells destroys the membranes of the agglutinated cells, releasing hemoglobin into the plasma, called hemolysis of the RBCs. Manifestations of transfusion reaction ▪ ▪ ▪ ▪ ▪ Allergic reaction Circulatory overload Febrile reaction Transfusion transmitted infection Hemolytic reaction: All transfusion reactions eventually cause immediate hemolysis. Hemoglobin released from the RBCs is then converted by the phagocytes into bilirubin and then excreted in the bile by the liver, The concentration of bilirubin in the body fluids often rises high enough to cause jaundice, the person’s internal tissues and skin become colored with yellow bile pigment. However, if liver function is normal, the bile pigment will be excreted into the intestines by way of the liver bile, so jaundice usually does not appear in an adult unless more than 400 milliliters of blood are hemolyzed in less than a day. Acute Kidney Failure After Transfusion Reactions. One of the most lethal effects of transfusion reactions is kidney failure, which can begin within a few minutes to a few hours and continue until the person dies of acute renal failure. The kidney shutdown seems to have three causes: 1. The antigen-antibody reaction of the transfusion reaction releases toxic substances from the hemolyzing blood that cause powerful renal vasoconstriction. 2. Loss of circulating RBCs in the recipient, along with production of toxic substances from the hemolyzed cells and the immune reaction, often cause circulatory shock. The arterial blood pressure falls very low, and renal blood flow and urine output decrease. 3. If the total amount of free hemoglobin released into the circulating blood is greater than the quantity that can bind with haptoglobin (a plasma protein that binds small amounts of hemoglobin), much of the excess leaks through the glomerular membranes into the kidney tubules. If the hemoglobin concentration rises so high in the kidney tubules, the hemoglobin precipitates, and blocks many of the kidney tubules. Leads to, renal vasoconstriction, and renal tubular blockage together cause acute renal shutdown. Page 6 of 6