Lecture on Blood Groups,Transfusion, Rh Incompatibility by Dr. Roomi

BLOOD PHYSIOLOGYGuyton chapter = 35

Blood Types; Transfusion; Tissue and Organ Transplantation

ByDr. Mudassar Ali Roomi (MBBS, M. Phil.)

Assistant Professor Physiology

Blood group antigens are present on the surface of RBCs

O-A-B Blood Types• A and B Antigens—Agglutinogens:– Two antigens—type A and type B.– occur on the surfaces of the red blood cells

• 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.

Agglutinins/antibodies When type A agglutinogen is not present in a

person’s red blood cells, antibodies known as anti-A agglutinins develop in the plasma.

Also, when type B agglutinogen is not present in the red blood cells, antibodies known as anti-B agglutinins develop in the plasma.

Average titers of anti-A and anti-B agglutinins in the plasma of people with different blood types.

• The agglutinins are gamma globulins (antibodies) and they are produced by plasma cells

• Most of them are IgM and IgG immunoglobulin molecules.

• agglutinin formation occurs almost entirely after birth when type A and/or B antigens enter the body in food, in bacteria, and in other ways.

Landsteiner’s law

• The reciprocal relationship between antigens on the red blood cells and antibodies in the serum is known as Landsteiner’s law

• It states that:– If an agglutinogen is present in the red cells of a blood, the

corresponding agglutinin must be absent from the plasma.– If an agglutinogen is absent in the red cells of a blood, the

corresponding agglutinin must be present in the plasma

Relative Frequencies of the Different Blood Types in western population

Rh Antigens-“Rh-Positive” and “Rh-Negative” People.

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

A person who has a C antigen does not have the c antigen, but the person missing the C antigen always has the c antigen. The same is true for the D-d and E-e antigens.

D Ag: 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.

85 % people are Rh +ve

Rh Antigens-“Rh-Positive” and “Rh-Negative” People.

Importance of Blood Grouping

1.Blood Transfusion: – it is on the basis of presence or absence of antigens

on red cells– blood is grouped for purpose of transfusion

2. Medicolegal Importance: - Blood spot on weapon, clothing or some other site - To solve the issue of Disputed paternity and maternity

3. Relation with Disease: - Peptic ulcer is common in blood group O - Carcinoma stomach is more common in blood group A

Antisera for blood grouping

• These are prepared in the body of a horse.

• Stored in fridge at 4 degree C.

For blood transfusion we consider

• Donor’s antigen on RBCs• Recipient’s antibody in serum• Donor’s antibodies are diluted in the plasma

of recipient, that’s why are not considered.

Who can donate and who can receive blood?

Pre-requisites of blood transfusion

• Blood grouping/typing of donor and recipient• Cross matching• Screening for infections e.g. hepatitis B,

hepatitis C, HIV/AIDS

Cross matching of blood

• cross matching is done after Blood typing• Cross matching is Performed prior to blood

transfusion and it serves as the last guard to ensure a safe transfusion

• We mix recipients serum and donor’s RBCs to check the full compatibility of donor’s blood with that of recipient.

• Significance: It is to rule out the incompatibility of other minor antigens b/w donor and recipients.

Erythroblastosis Fetalis (“Hemolytic Disease of the Newborn/HDN)

• Why called so?– Because blasts are seen in blood

circulation.

• Erythroblastosis fetalis is a disease of the fetus and newborn child characterized by agglutination and phagocytosis of the fetus’s red blood cells

• The mother is Rh-negative, the father is Rh- positive and the baby is Rh-positive

Erythroblastosis Fetalis (“Hemolytic Disease of the Newborn/HDN)

Effect of the Mother’s Antibodies on the Fetus

After Ig-G 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 RBCs followed by their lysis.

Incidence of the Disease1st pregnancy…No Agglutinins in mother

2nd Pregnancy…3 per cent of second Rh-positive babies exhibit some signs

10 per cent of third Rh +ve babies exhibit disease

Clinical Features of Erythroblastosis Fetalis (“Hemolytic Disease of the Newborn/HDN)

• Jaundice• Kernicterus (deposition of unconjugated bilirubin in the

brain) can occur. It can lead to mental retardation and cerebral palsy

• Hemolytic Anemia• Nucleated Erythroblast are present in the peripheral

blood • Hydrops fetalis (fetus is swollen)• Abortion may occur• Enlarged spleen and liver

Treatment of the Erythroblastotic Neonate.

1. Exchange Transfusion with O negative blood

2. Phototherapy

1. Exchange blood transfusion

• 400 ml Rh+ blood of the baby is removed and same quantity of Rh- blood is transfused.

• This procedure is repeated several times till the mother’s antibodies are cleared from the plasma of baby.

2. phototherapy

• UV-rays convert unconjugated bilirubin (lipid soluble) into water soluble form which is excreted in urine.

Prevention of Erythroblastosis Fetalis

an anti-D antibody that is administered to the expectant Rh –ve mother starting at 28 to 30 weeks of gestation.

Give inj of Anti D antibodies within 24 – 48 hours of delivery & these neutralize RBCs of baby in mother’s circulation. This prevents the mother’s sensitization by baby’s RBCs.

Prevention of Erythroblastosis Fetalis

Rh+ Blood transfusion to an Rh- person?(e.g. A+ transfusion to A- person)

• In contrast to ABO system, in Rh system Anti Rh antibodies are not present naturally. These are produced when an Rh- person is transfused with Rh+ blood

• Such transfusion can be done one time. Not more than once!

• Such first Rh+ transfusion sensitizes the Rh- Person. Second Rh+ transfusion will cause hemolysis

ABO incompatibility b/w mother and fetus(e.g. mother is B+ and Fetus is A+)

• It is very less common than Rh incompatibility• Reason: The antibodies in ABO system are of

Ig M type, which being five times larger than Ig G antibodies, cannot cross the placenta.

Acute complications of blood transfusion1. Acute haemolytic transfusion reaction due to mismatch of donor’s

and recipient’s blood groups2. Septic/infective shock due to bacteria3. Transfusion related acute lung injury (TRALI)4. Fluid overload and lung edema in case of multiple transfusion over a

short period of time5. Non-haemolytic febrile reactions (fever, chills)6. Severe generalized allergic reaction or anaphylaxis7. Hyperkalemia (inc. K+) due to lysis of RBCs8. Hypocalcemia (dec. Ca++): as Ca++ binds with citrate in the

transfusion bags 9. Air embolism (air can enter in the blood vessels)

Delayed complications of blood transfusion

1. Delayed haemolysis of transfused RBCs2. Development of antibodies that react with

antigens of WBCs or platelets3. Post-transfusion purpura (pin point hemorrhage)

due to decrease in number of platelets.4. Iron overload due to frequent transfusions e.g. in

thalassemia5. Transmission of Infection e.g. Hepatitis B, Hep. C

and HIV.

Acute Transfusion Reactions Resulting from Mismatched Blood Types

• Red blood cells of the donor blood are agglutinated.

• The plasma portion of the donor blood immediately becomes diluted by all the plasma of the recipient

• Hb bilirubin jaundice

Mismatched/Hemolytic transfusion reactions

• These are the result of antibodies in the recipient's plasma directed against antigens on the donor's RBCs.

• This results in rapid intravascular hemolysis of the donor RBCs.

• ABO incompatibility due to clerical error is the most frequent cause.

• immunoglobulin M (IgM) typically result in severe, potentially fatal complement-mediated intravascular hemolysis

1. Fever2. Chills3. Flushing4. Nausea5. Burning at the intravenous (IV) line site6. Chest tightness7. Restlessness and Apprehension8. Back pain9. Difficulty in breathing, increase in heart rate, fall in B.P.,

circulatory Shock10. No urine production (oliguria) due to acute renal shut

down

CLINICAL FEATURES OF HEMOLYTIC TRANSFUSION REACTIONS

Acute Kidney Shutdown After mis-matched Transfusion

One of the most lethal effects of transfusion reactions is kidney failure.

The kidney shutdown seems to result from three causes:

1. Renal vasoconstriction2. Circulatory shock3. Obstruction of renal

tubules

Acute

Renal

Shutdow

n

1. Renal Vaso

constriction

2.Circulatory

Shock3.Renal Tubular

Blockage

1

1. Renal vasoconstriction

antigen-antibod

y reaction

releases toxic

substances from blood cells

powerful renal vaso-

constriction

2. Circulatory shock

• ↓ BP • ↓ Renal blood flow • ↓ urine formation

(oliguria)Toxic Subs , Loss

of RBCs

Circulatory Shock, ↓ BP Oligur

ia

3. Obstruction of renal tubules

• Haptoglobin can bind up to 10 % free Hb.

• Excess Hb precipitates and blocks many of the kidney tubules.

Excess Hb

is filtere

d

Blocks

renal tubul

es

Other blood group systems

• Thirty-three major blood group systems (including the AB and Rh systems) have been recognised

• a few other systems are :MNS system, Kell system, Lewis system.