Austrian Karl Landsteiner(1901) discovered – Human blood possess different antigenic and immune properties Blood clumping was an immunological reaction. Nobel Prize in Physiology and Medicine in 1930. Adriano Sturli and Alfred von Decastello who were working under Landsteiner discovered type AB a year later in 1902. Janský is credited with the first classification of blood into the four types (A, B, AB, O)in 1907, which remains in use today

1. Blood Groups
Blood Transfusion
Blood Banking
Dr.Ranadhi Das
MD PGT
IMS and SUM Hospital

2. Austrian Karl Landsteiner(1901) discovered –
•Human blood possess different antigenic and immune properties
•Blood clumping was an immunological reaction.
•Nobel Prize in Physiology and Medicine in 1930.
•Adriano Sturli and Alfred von Decastello who were working under
Landsteiner discovered type AB a year later in 1902.
•Janský is credited with the first classification of blood into the four types
(A, B, AB, O)in 1907, which remains in use today.
Introduction

3. They are group specific substrate on the surface of RBC and enable the different
individual to be identified from each other just like fingerprints.
CLASSIFICATION-
Major blood group system- ABO system, Rh system, MNS system
Minor blood group system- Kell, Duffy, Lutheran, Lewis, Deigo, kidd Etc.
Thirty-five major blood group systems were recognized by the International Society
of Blood Transfusion (ISBT) in October 2012.
Blood Group System

4. I. Discovery
II. Antigen and Antibodies
III. Inheritance
ABO Blood Group System

5. • Karl Landsteiner(1901) classified human blood into A,B,O groups.
• Von Decastello and Sturli (1902) discovered AB blood group.
• Von Dungern and Hirszfeld(1911) divided group A into 2 subgroups A1 and A2.
Discovery

6. • Appear in the sixth week of fetal life.
• Present on red cell membrane and in other tissues like salivary glands, pancreas, kidney,
liver, lung, semen, testes, amniotic fluid.( EXCEPT CNS)
• Antibodies formed in children after few months of birth.
Antigens

7. Glucose
Galactose
N-acetylglucosamine
Galactose
RBC
Fucose N-acetylgalactosamine
N-acetyl-galactosaminyl Transferase (product of A gene- GENES at 9q34.1)
Formation of the A antigen

8. Formation of the B antigen
Glucose
Galactose
N-acetylglucosamine
Galactose
RBC
Fucose Galactose
D-galactosyl Transferase(product of B gene- GENES at 19 q13.2)

9. • Mostly IgM type.
• Produced by bone marrow and lymph gland cells .
• Known as cold antibodies.
Anti-A and Anti-B agglutinins

10. ABO
Group
Antigen
(agglutinogen)
Present
Antigen
Missing
Antibody
(agglutinin)
Present
A A B Anti-B
B B A Anti-A
O None A and B Anti-A&B
AB A and B None None
Antigen and Antibody
Present in ABO Blood Group

11. LANDSTEINER’s LAW-
1.If an agglutinogen (antigen) is present on red blood cell membrane ,the corresponding
agglutinin (antibody) must be absent in the plasma.
2.If an agglutinogen (antigen) is absent on red blood cell membrane, then corresponding
agglutinin (antibody) must be present in the plasma.
2nd law doesnot hold good for Rh factor (Rh factor absent anti D absent)

12. Inheritance of ABO blood group
Follows Mendelian Law.
In 1924, Felix Bernstein
proposed presently accepted theory.
Heterozygous: AO or BO
Homozygous: AA or BB
Mom Dad Offspring
Blood Group
AA BB 100% AB
BO OO 50% each of
B or O
OO OO 100% O
OO AO 50% each of
A or O

13. If baby is Parents must
have
Mother blood
group
Father
would not
be
O O+O No matter which AB
AB A+B No matter which O
A A+O
A+A
B or O B or O
B B+O
B+B
A or O A or O
PaternityDispute

14. The Rhesus Blood Group System
I. Discovery of Rh system
II. Antigen and antibodies
III. Inheritance
IV. Haemolytic disease of newborn

15. •History of the Rh System
• Levine and Stetson(1939) described a hemolytic transfusion reaction in an
obstetric patient following delivery of stillborn infant.
• An antibody was isolated from the mother’s serum. It was postulated that the fetus and the
father possessed a common factor that the mother lacked.
•While the mother carry the fetus, the mother was exposed to this factor and developed
antibody against the transfused red cells from the father and resulted in transfusion reaction.
•At that time ,the responsible antibody was not named.

16. • Landsteiner and Wiener(1940) injected RBC’s of rhesus monkeys in rabbits
developed antibodies.
• The antibody was named as anti-Rh.
• When resulting antiserum was mixed with human RBC’s, then agglutination occurred.
•The RBC antigen responsible for this reaction was called as Rh factor.
•The antibody discovered by Levin and Stetson in the mother was subsequently re-
examined and found identical in activity as the anti-Rh antibody found by Landsteiner
and Weiner.
•So this work led to discovery of Rh system.

17. •Anti-rhesus formed by the animals was renamed anti-LW (Landsteiner and Wiener).
•Fisher and Race(1943 and 1944) discovered C, E, c, e Ag and their corresponding antibodies
anti-C , anti -E ,anti- c ,anti -e.

18. Rh Antigens
• Rh system involves 6 Rh
antigens D,d,C,c,E,e
Rh positive
Presence of rh D
85% occurrence
Rh negative
Absence of rhD
15% Occurrence
•Integral membrane proteins with an active phoshpholipid component.
•Present on red blood cells.
•D antigen is commonest and most immunogenic.

19. • IgG type.
• Known as warm antibodies.
• Produced by exposure to foreign Rh antigen .
Rh Antibodies

20. • D Ag is inherited as a dominant gene D.
• Genotype of individual may be:
DD
Dd
dd
Inheritance

21. Examples-
Heterozygous Rh +
Homozygous Rh-
50% hetrozygous rh+
50% homozygous rh-

22. • ABO Incompatibility- immediate reaction as antibodies are naturally present.
• Rh Incompatibility-
First exposure-
Primary response
Immunological memory
Second exposure-
Immediate and severe response.
Incompatibility

23. • Transfusion reactions are the adverse reactions in the body, which occur due
to transfusion error that involves transfusion of incompatible (mismatched)
blood.
• The reactions may be mild causing only fever and hives (skin disorder
characterized by itching) or may be severe leading to renal failure, shock and
death.
Transfusion Reactions Due To ABO Incompatibility

24. • 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 red blood
cells.
 In most instances of erythroblastosis fetalis, the mother is Rh negative and
the father 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.
• In turn, the mother’s agglutinins diffuse through the placenta into the fetus
and cause red blood cell agglutination.

25. I.Erythroblastosis fetalis-
• Erythroblastosis
Mechanism- Rapid production of red blood cells by haematopoeitic tissues of baby in order
to replace haemolysed RBC’s.
• Anaemia
• Hydrops fetalis- Grossly edemataous, Intra uterine fetal death usually occurs.
II.Icterus gravis neonatorum-
1. Infant born at term
2. Jaundice within 24 hrs
3. No anemia ( compensated by normoblastic response in bone marrow)
4. Nucleated RBC in circulation
5. Severely damaged liver
6. splenomegaly
7. Kernicterus- unconjugated bilirubin is deposited in basal ganglia
Manifestations

26. HYDROPS FETALIS
ERYTHROBLASTOSIS
FETALIS
ICTERUS GRAVIS
NEONATORUM
KERNICTERUS

27. I. Anti-D Prophylaxis –
• Based on principle antibody mediated immunosuppression.
• Inject anti-D antibody in mother soon after child birth within 72 hrs.
• RhoGAM –Ɣ glodulin rich in anti D
• Fetal Rh typing by amniocentesis or chorionic villi sampling, then give
Rh immunoglobulin to expectant mother between 28 to 30 weeks.
II. Exchange transfusion –
About 400 ml of Rh – ve blood is transfused over a period of 1.5 hr or
more while the neonates taking out the Rh +ve blood.
III. Phototherapy –
Any new-born with a total serum bilirubin greater than 18mg/dL
should receive phototherapy.
Prevention And Treatment

28. • THE Ii SYSTEM-
Weiner et al (1956)
2 antigens –I and i
Difference-
• At birth , RBC’s are rich in i Ag ,not I Ag.
• In first second years of life, gradual changeover from i to I.
• THE DUFFY SYSTEM
Cutbush , Mollison and Parkin(1950).
System has 3 blood groups-Fya ,Fyb and Fyab.
Fyab blood groups are resistant to plasmodium vivax whereas Fya and Fyb are susceptible to
vivax malaria.
Other Blood Group Systems

29. • KELL SYSTEM-
Coombs ,Mourant , Race(1946).
Antigen - K
Rare In India(.3 To .7%)
• MN SYSTEM -
Landsteiner and Levine(1927).
Required for-
• Paternity tests
• Anthropological and genetic studies.
• Bombay Blood Group-
Dr.Y.M. Bhenda(1952)
Also known as HH blood group. They do not express H antigen, as a result they cannot form A Ag
or B Ag on their RBC.
They can donate blood to anybody but can receive blood only from Bombay blood group people.

30. I. In blood transfusion.
II. In preventing Hemolytic Diseases of Newborn due to Rh Incompatibility.
III. In paternity disputes.
IV. In medicolegal cases.
V. Anthropological study
VI. In knowing susceptibility to diseases.
A group- Gastric cancer, Pancreatic cancer, Diabetes mallitus
B group- Gastrointestinal disorder
O group- Peptic ulcer, Rheumatic fever
Clinical Implications

31. I. Indications
II. Donor and Recepeints
III. Precautions
IV. Hazards
Blood Transfusion

32.  Richard Lower pioneered the first blood transfusion from animal
to human in 1665 at the Royal Society( Banned in 1668).
 Proper transfusion done by Landsteiner and Weiner
 In 1840 Dr. Blundell, performed the first successful whole blood
transfusion to treat haemophilia.
 In 1914 Lewisham brought the concept of transfusion during
1st world war
Introduction

33. I. Blood loss ( Hemorrhage, Surgery)
II. For quick restoration of Hb.
III. Exchange transfusion ( erythroblastosis fetalis)
IV. Bone marrow failure (aplastic anaemia, leukaemia )
V. To correct clotting factor deficiency-hemophilia, purpurae,clotting defects.
VI. Restore plasma volume- Burn
VII. Acute poisoning (carbon monoxide)
VIII. Acute infections or fever when gamma globulin is needed.
IX. Shock
X. To improve oxygen transport to tissue- severe anemia
Indications

34. • Donor selection-
I. Healthy and age between 18 to 60 years.
II. Hemoglobin > 12 gm%
III. Weight more than 45 kg.
IV. Females should not be Pregnant, lactating and menstruating.
V. No diseases like AIDS, Viral Hepatitis ,Malaria, Syphilis.
VI. No past H/O jaundice , HTN,TB, and cardiac diseases.
 Jehovah Witnesses (1870,Pittsburgh,Pennsylvania,USA)- Christian community which
refuses blood transfusion.
Donor And Recepient

35. Blood transfusion-who can receive
blood from whom?
Blood
Group
Antigens Antibodies Can give
blood to
Can
receive
blood from
AB
(universal
recipient)
A and B None AB AB, A, B, O
A
A B A and AB A and O
B B A B and AB B and O
O
(universal
donor)
None A and B AB, A, B, O O

36. • For safe and compatible blood transfusion-
• ABO and Rh typing
• Cross matching
• Antibody screening
Investigations

37. • Processing and Testing of Blood
 Donated blood is usually subjected to processing after it is collected, to make it suitable for use in
specific patient populations.
 Collected blood is then separated into blood components by centrifugation:
red blood cells, plasma, platelets, albumin protein, clotting factor
concentrates, cryoprecipitate, fibrinogen concentrate and immunoglobulins (antibodies)
 All donated blood is tested for infections like HIVs, Hepatitis B, Hepatitis C, Syphilis
 All donated blood is also tested for ABO and Rh groups, along with the presence of any red blood cell
antibodies.
 Pathogen Reduction treatment done.

38. Determination Of Blood Group
Blood Typing

39. Under Microscope
Human RBC before (left) and after (right) adding serum containing antibodies.
No agglutination Agglutination

40. II. Cross Matching-
Major cross matching -Donor’s RBCs are mixed with recepient’s plasma.
Minor cross matching- Recepient’s RBC’s are mixed with donor’s plasma.
When no agglutination then only donors blood can be transfused.
Cross Matching

41. III. Antibody Screening –
Antibody Screening

42. IV. Rh positive blood should never be transfused to Rh negative blood.
V. Check blood bag for correct label.
VI. Transfuse blood at slow rate(not >20 drops/min) under proper aseptic measures.
VII. Careful watch on recipient's condition.
VIII. Stop transfusion if reaction occurs.

43. Transfusion reactions
• Hemolysis- Massive destruction of RBC of donor release of Hb in blood
hemolytic jaundice.
• Renal vasoconstriction- Due to release of toxic substances from hemolysed RBC.
• Circulatory Shock- Loss of RBC and release of toxins from hemolytic RBC lead to
fall of BP. Decrease renal blood flow oliguria
• Hemoglobinuria- Free Hb binds with haptoglobin present in plasma pass through
glomerular membrane and passed through urine.
• Renal tubular damage- Free Hb precipitate in tubules as acid hematin.
• Anuria- Absence of urine due to vasoconstriction, shock, hypotension, renal tubular
damage.
• Uremia- increased nitrogenous substances and K⁺  renal failure coma death.
• Transmission of blood borne diseases- AIDS, Hepatitis, Malaria, Syphilis
• Fever, Chill, Rigor
• Hyperkalemia
• Hypocalcemia
• Tightness of chest

44. • Replacement of more than 50% of circulating blood volume in less than 3 hrs
Or, transfusion @ >150ml/min Or, > 10 units of blood within 24 hrs.
• Blood loss-
• < 20% of total blood volume - well tolerated by the body
• 20%-40% of total blood volume - changes in vital signs
• > 40% of total blood volume - Hemorrhagic shock
Massive Blood Transfusion

45. • Plasma, normal saline
• Hydroxy ethyle starch
• Low molecular weight dextran (Lomodex)
• Synthetic Blood-
• Fluosol-DA (colorless, Oxygen carrying capacity 7 days, dev in Japan)
• Coconut water
Recent advances-
Synthetic bio-molecule blood substitutes-
• Perflurocarbon based- Oxycyte, NVX-108
• Hemoglobin based oxygen carrier- Hemopure,
Hemospan.
• Hyperbranched Polymer protected porphyrine-
Polyheme
Blood Substitutes

46. • Safely given- 1:1:1 protocol- ‘O’ negative packed cell : FFP : Random donor
platelet.
• Advance trauma centre equipped with – Thromboelastography (gives idea
about the amount of blood loss and efficiency of blood coagulation).
Blood loss-Unknown amount

47. • It is a centre where blood gathered as a result of blood donation, stored and
preserved for later use in blood transfusion.
• Equipped with proper testing for blood and blood
products.
• 1unit = 450 ml of CPD mixed blood.
• Stored at 4°C with 63 ml of anticoagulants.
• CPD – Citrate(anticoagulant by chelating calcium),
Phosphate(synthesize ATP),
Dextrose(nutrition).
• Blood can be kept 21 days at 4°C in blood bank.
• Blood donation-
 Weight- 45-55 kg  350ml/ 49 ml anticoagulant
 Weight- > 55 kg  450ml/ 63 ml anticoagulant
Blood Bank

48. • RBC- with CPD 35 days,
with SAGM (saline, adenine, glucose, manitol) 42 days
• Platelet- 5 days
• Plasma- 1 year
• Clotting factors Cryoprecipitate- 1 year
 Drawback in old blood- (Lesion of storage)
• Na+K+ ATPase pump stops working leading to
Hyperkalemia
• Fall in serum Calcium level  swelling of the RBC
• Build up of lactic acids
• Decrease in glucose consumption
• Decrease in ATP level
• Decrease in pH.
• Diminish activity of 2,3 DPG reduce the ability to deliver oxygen
• Decrease platelet.
Storage