Rh-Blood TYPES

Rh-Blood groups: Rh-Blood groups: The Rh-factor named for the rhesus monkey because it was first studied using the blood of this animal. The Rh-factor named for the rhesus monkey because it was first studied using the blood of this animal. Rh-agglutinogens (antigens): there are six common types of Rh-antigens each of which is called Rh-factor. These types are C, D, E, c, d, & e.The type D (Rh)-antigen is more antigenic. The major difference between ABO system and Rh system is that agglutinins causing transfusion reactions in ABO developed spontaneously, where in the Rh system spontaneous agglutinins NEVER occur,unless the Rh - person exposed first to Rh+ blood by transfusion.,Or if the Rh-females having (Rh+) child, anti-D antibodies developed in her blood slowly reaching maximum concentration about 2-4 months later.Exposure to another Rh+ blood, transfusion reaction occurs. The major difference between ABO system and Rh system is that agglutinins causing transfusion reactions in ABO developed spontaneously, where in the Rh system spontaneous agglutinins NEVER occur,unless the Rh - person exposed first to Rh+ blood by transfusion.,Or if the Rh-females having (Rh+) child, anti-D antibodies developed in her blood slowly reaching maximum concentration about 2-4 months later.Exposure to another Rh+ blood, transfusion reaction occurs.

anyone who has antigen D on RBC membrane is said to be Rh-positive (Rh+) or D-positive (D+) about 85% of population are Rh+, while persons who does not have antigen D on their RBC is said to be Rh-negative (Rh-) or D- & about 15% are D - (Rh - Rh+ is dominant while Rh- is recessive. Rh-agglutinins: The Rh+ individual has no antibody in their plasma. The Rh- person has also no antibody D in the plasma, but Rh- individual forms the antibody D when transfused with D + (Rh + ) cells. Antibodies against Rh-antigen do not develop unless an Rh- person is exposed to Rh+ blood. This can occur through a transfusion or entrance of fetal blood into the maternal circulation across the placenta.

Table: Rh –type, agglutiongen, agglutinin, and % of each Rh -group Rh-typeAgglutinogen on RBC Agglutinins in plasma % Rh + D-85 Rh - No D antigen- Unless exposed to Rh+ blood 15

The ABO blood type & the Rh -blood type usually are designated together. The ABO blood type & the Rh -blood type usually are designated together. (ABO system) (Rh system) For example a person designated as A positive (A+) is blood group A in the ABO- system and Rh+ in the Rh blood group. This person has antigens A & D on RBC & antibody-B& in no antibody-D the plasma.

Rh –Transfusion Reaction: is the reaction between antigen -D in Rh+ blood of donor & antibody D in Rh- blood of recipient. When an Rh- receives a first transfusion of Rh+ blood, the recipient becomes sensitized to the Rh+ antigen & produces antibodies D. If the same person receive a second transfusion of Rh+ blood, reactions results & clumping of RBC’s occurs.

Hemolytic disease of newborn (HDN) or erythroblastosis fetalis:  HDN: is a disease of the fetus & neonate. characterized by agglutination of RBCs of the fetus due to reaction between antigen D in the fetus & antibody D produce by the mother. Fetus may develop hemolytic anemia in two major ways as a consequence of developing antibodies.  1. Rh- incompatibility. 2. ABO- incompatibility. 1.HDN due to Rh-incompatibility.

Mother Rh- (Rh- Rh - ) X father+ (Rh+ Rh-) Fetus 50% Rh+ (Rh+ Rh - ) Fetus 50% Rh+ (Rh+ Rh - ) & 50% Rh - (Rh - Rh - ) A 100% chance of producing an Rh+ fetus if the father is homozygous (Rh+ Rh+). & 50% Rh - (Rh - Rh - ) A 100% chance of producing an Rh+ fetus if the father is homozygous (Rh+ Rh+). Mother (Rh- Rh-) X father (Rh+ Rh+) Fetus 100% Rh+ Rh - Fetus 100% Rh+ Rh -

At the time of delivery small amount of fetal blood which contain antigen D leak into the maternal circulation & some of them develop antibody D during postpartum period. In the woman’s first pregnancy there is no problem. The leakage of fetal blood which contain antigen D is usually the result of a tear in the placenta that takes place during delivery. Thus there is no enough time for the mother to produce enough D- antibodies to harm the fetus. In the later pregnancies, a problem can arise because the mother has been sensitized (i.e. forming antibody-D) against antigen D. When the mother becomes pregnant again with another Rh+ fetus, and if there is any leakage of fetal blood into the mother’s blood through the placenta she rapidly produce large amounts of Rh- antibodies & HDN develops in the fetus. The term erythroblastosis fetalis is also used to describe HDN since blood smears from these babies show the presence of many immature red blood cells or erythroblasts.

Prevalence of disease: About 3% of second Rh –positive babies exhibit some signs of HDN; 17% of the third babies exhibit the disease; and the incidence rises progressively with subsequent pregnancies. About 50% of Rh negative individuals are sensitized (develop an anti-Rh titer) by transfusion of Rh + blood.

Symptoms of disease: 1.Hemolysis,&severe jaundice 2. edema (hydrops fetalis). 3.Kernicterus due to deposition of bilirubin in the basal ganglia which result in brain damage & mental retardation. 4. Splenomegaly & hepatomegaly (i.e. enlargement of spleen & liver). Laboratory findings of HDN: Presence of erythroblasts and reticulocytosis in the blood smear. Low PCV. Level of unconjugated bilirubin will be high (more than 10 mg/dl).

Treatment of HDN 1.Treatment of mother: The Rh- woman should be given an injection of single dose of anti-D antibodies within 72 hours during the postpartum period or during pregnancy or immediately after each abortion. The injection contains anti-D against antigen-D.The injected antibodies will bind to Rh – antigens of fetus erythrocytes that may have entered the mother's blood and destroy the antigen D on fetal RBC before the immune system of the mother is activated. In other words, the fetal RBCs will be destroyed before the mother is able to develop her own antibodies against these erythrocytes. Hence she will be able to conceive another Rh+ child without any complication.

2.Treatment of erythroblastic neonate: 1. By exchange transfusion i.e. slowly removing the newborn’s blood & replacing it with Rh—blood to reduces the level of maternal antibody-D, which thereby decreases the level of fetal RBC hemolysis. 2. Exposure of newborn to fluorescent light to breakdown the large amount of bilirubin formed as a result of erythrocyte destruction. High levels of bilirubin are toxic to the nervous system and can damage brain tissues.3.In addition fetal Rh-typing with obtained material by amniocentesis or choronic villus sampling is now possible.

HDN due to ABO-incompatibility: when a mother of type O blood becomes pregnant & the fetus has type A or B antigens on RBC this may result in anemia known as HDN. The ABO-HDN is the more common that Rh-HDN. Approximately 23% of all pregnancies involve incompatible ABO system. HDN due to ABO-incompatibility: when a mother of type O blood becomes pregnant & the fetus has type A or B antigens on RBC this may result in anemia known as HDN. The ABO-HDN is the more common that Rh-HDN. Approximately 23% of all pregnancies involve incompatible ABO system.

 1- Blood Typing : blood typing and blood matching is done by mixing the blood with saline. Then it is mixed with anti-A,anti-B & anti-D after several minutes,look for agglutination.  2- Cross Matching : RBCs of the donor mixed with the serum of the recipient and look for agglutination.If it is +ve the blood is incompatible,if there is no agglutination the blood of the donor and recipient is compatible.

Acute kidney Shutdown There are three causes: 1-Toxic substances from hemolyzing blood due to antigen-antibody reaction cause renal vasoconstriction. 2- circulatory shock due to loss of RBCs,the blood pressure decreases renal blood flow and urine out put decreases. 3-Excess hemoglobin of haptoglobin leak into kidney tubule and precipitate into tubule and block them. ALL OF THE ABOVE 3 CAUSES ACUTE RENAL SHUT DOWN AND DEATH WITHIN AWEEK.