Rh-Blood TYPES

Rh-Blood groups:

    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-femaleshaving ^(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-type	Agglutinogen 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.

(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  &   no antibody-D  in 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, transfusion reaction results & clumping (agglutination) 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 RBC & 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^-)

                                    &      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^-

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.

                                                                                                         In the later pregnancies, a problem can arise because the mother has been sensitized (i.e. formed antibody-D) against antigen D.

When  the mother becomes pregnant again with another Rh+ fetus she had produced 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 (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  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. & low hemoglobin concentration .

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.

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 more common than 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.