Blood transfusion involves transfusing whole blood or blood components from a donor to a recipient. The main components are packed red blood cells, plasma, platelets, and cryoprecipitate. Blood is typed by antigens including A, B, and Rh factors to avoid incompatible transfusions. Transfusions are given to treat anemia or bleeding. Risks include allergic reactions, infections, and complications affecting the lungs, circulation or immune system. Careful donor screening and compatibility testing are vital for safe blood transfusions.

1. Blood Transfusion
Presented by:
Dr. Dhritiman Chakrabarti

2.  An adult human has about 4–6 liters of blood
circulating in the body. Among other
things, the primary function of blood is to
transport oxygen to various parts of the body.
 Blood consists of several types of cells
floating around in a fluid called Plasma.

3. The Red Blood Cells contain Hemoglobin, a
protein that binds oxygen. Red blood cells
transport oxygen to, and remove carbon
dioxide from, the body tissues.
The White Blood Cells are the cells primarily
responsible for immunity.
The Platelets help in hemostasis.
The Plasma contains ions and various kinds
of proteins serving diverse functions.

4. Definitions
A Blood Transfusion is the infusion of whole
blood or a blood component such as
plasma, red blood cells, or platelets into the
patient’s venous circulation.
A blood transfusion is given because of red
blood cell loss, such as with hemorrage or
when the body is not adequately producing
cells such as platelets. The person receiving
the blood is the Recipient. The person giving
the blood is the Donor.

5. Blood Groups
An Individual’s blood is commonly classified
into one of the four main groups
(A, B, AB, and O). The surface of an
individual’s red blood cells contains a number
of proteins known as Antigens that are unique
for each person. Many blood antigens have
been identified, but the antigens A, B, and Rh
are the most important in determining blood
group or type. Because antigens promote
agglutination or clumping of blood cells, they
also known as Agglutinogens.

6. The A antigen or agglutinogen is present on the
RBCs of people with blood group A , the B
antigen is present in people with blood group
B, and both A and B antigens are found on the
RBC surface in people with group AB blood.
Neither antigen is present in people with group
O blood .

7. Preformed antibodies to RBC antigens are
present in the plasma; these antibodies are
often called Agglutinins. People with blood
group A have B antibodies (Agglutinins ), A
antibodies are present in people with blood
group B , and people with blood group O have
antibodies to both A and B antigens . People
with group AB blood do not have antibodies
to either A or B antigens .

8. If a person with type O blood is transfused
with blood from a person with either group A
or group B blood, there would be destruction
of the recipient’s red blood cells because his
or her anti-A or anti-B agglutinins would react
with the A or B antigens in the donor’s red
blood cells.

9. This example shows why individuals with type
AB blood are often called Universal
Recipients (because people in this blood
group have no agglutinins for either A or B
antigens) and group O people are often called
Universal Donors (because they have neither
A nor B antigens).

12. Rhesus (RH) Factor
The Rh factor is an inherited antigen in human
blood.
Blood that contains the Rh factor is known as
Rh-positive, when it is not present the blood is
said to be Rh-negative. Rh blood does not
naturally contain Rh antibodies. If Rh-positive
blood is injected into an Rh-negative
person, the recipient develops Rh antibodies.
Subsequent transfusion with Rh-positive blood
may cause serious reactions with clumping and
hemolysis of red blood cells.

14. Other Blood Groups
 In addition to the ABO antigens and Rh
antigens, many other antigens are expressed on the
RBC surface membrane.
 The International Society of Blood Transfusion
currently recognizes 30 blood-group systems
(including the ABO and Rh systems).
 For Eg. MNS, Kell, Kidd, Duffy, Lewis etc.
 These are mostly involved in Delayed Hemolytic
Transfusion reactions.

15. Typing and Cross Matching
Before any blood can be given to a patient, it
must be determined that the blood of the donor
is compatible with the patient. The laboratory
examination to determine a person’s blood
group and Rh factor is called Blood Typing.

16. The process of determining compatibility
between blood specimens is Crossmatching.
RBCs from the donor blood are mixed with
serum from the recipient, a reagent (Coombs’
serum) is added, and the mixture is examined
for visible agglutination. If no antibodies to
the donated RBCs are present in the
recipient’s serum, agglutination does not occur
and the risk of transfusion reaction is small.

17. Selection of Blood Donors
Blood donors must be selected with care. Not only
must the donor’s blood be accurately typed, but it
is also important to determine that the donor is free
from diseases.
The primary tests recommended by WHO are the
following:
1. Surface antigen for hepatitis B( HbsAg)
2. Antibody to Hepatitis C
3. HIV antibody (Subtypes 1 & 2)
4. Serology tests for Syphilis

18.  Other tests carried out depending on local need :
1. Prion diseases – Creutzfeldt Jacob Disease
2. Cytomegalovirus
3. HIV Nucleic acid test (p24)
Also mandatory that the donor should be free from
fever a fortnight before donating blood.
Also should be free from parasitic diseases like
Malaria and Filariasis.

19. Transfusion of blood and blood
products

20. Blood Conservative Strategies
 Preoperative Autologous Donation
– Effectiveness is limited because of less vigorous
erythropoietic response and the process simply
results in anemia at time of surgery.
– Benefits are the elimination of disease
transmission, allergic and incompatible reactions.
– But, more expensive, sometimes wasted.
– Usage has declined.

21.  Acute Normovolemic Hemodilution
– Patient is bled immediately before surgery.
– Down to haematocrit 25-30% with CVP monitoring
– Strategy is that intraoperatively the patient will lose blood
of low hematocrit value and reduce total red blood cell loss.
– Collected blood is transfused back after surgery.
– Less frequently used.

22.  Intraoperative blood salvage
– Blood is salvaged intraoperatively from sites
where fresh blood has collected before the surgery
– Only applicable to clean operative sites without
bacterial, bowel or tumor cell contamination.
– Contemporary cell salvage devices anticoagulate
the blood, separate the RBCs from the blood, wash
the RBCs extensively in saline and reinfused to the
patient in aliquots of 125 – 225ml with Hematocrit
of 45 – 65%.

23.  Transfusion of Whole blood has been largely
replaced by FFP and specific component
therapy depending on nature of deficiency.

24.  Whole blood
– Haematocrit of 35%-45%
– 300 ml of 4:1 mixture of donor plasma and a nutrient
citrate anticoagulant solution
– Stored at 2-6 deg C (maximum for 35 days)
– Deterioration is rapid when kept out of refrigerator or
transport box
– Transfusion should be completed within 4 hrs
– Warmer is used if large volume has to be transfused in a
short time
– Not suitable for symptomatic or critical anemia

26.  Packed Red Blood Cells
– Obtained from single donor
– Contains Red cells in CPDA solution
(citrate, phosphate, dextrose and adenine) with Hct of 70-
75% and a total volume of 250-275ml.
– Has a shelf life of 35 days at storage temp. of 1-6 deg C.
– In case Additive solution solution is added, the infusate is
of Hct 60%, Total volume 250-350ml., less citrate, longer
shelf life of 42 days at storage temp. of 1-6 deg C.
– Improves tissue oxygenation after hemorrhage and in
anemic patient
– One unit of PRBCs typically will raise the hematocrit by 3-
4% and the blood hemoglobin concentration by 1 g/dl.

27. Additive Solutions
Three additive solutions are available
1. Adsol ( AS-1 ) [Baxter Laboratories]
2. Nutricel (AS-3) [Medsep Corporation]
3. Optisol (AS-5) [Terumo Corporation]

28. Red Blood Cell Transfusion Guidelines
Acute and Perioperative Blood Loss
1. Estimate blood loss
If > 30-40% of rapid blood loss: transfuse RBCs and use
volume expanders
If < 30-40% of rapid blood loss: RBCs not usually needed in
otherwise healthy person
2. Monitor vital signs; Tachycardia and hypotension not corrected
with volume expanders: RBCs needed
3. Measure haemoglobin
If Hb > 10 g/dL: RBCs rarely needed
If Hb < 7 g/dL: RBCs usually needed
If Hb 7-10 g/dL: RBCs may be needed, determined by
additional clinical conditions
4. Hematocrit trigger point for transfusion is <21%.
5. For cardiac disease patients, threshold goes up to Hb <10gm%
and hematocrit <30%.

29.  Chronic Anaemia
1. Transfuse only to decrease symptoms and to
minimize risk (generally at Hb of less than 7 g
/dL). Do not transfuse above 7g/dL Hb unless
patient is symptomatic.
2. Treat nutritional and mild blood loss anemia
with specific therapeutic agents as indicated
(iron, folic acid, B12).

30. Guidelines for Paediatric Transfusion
 If Hb is < 4 g/dL, transfuse.
 If Hb is > 4 g/dL and < 5 g/dL, transfuse when signs of
respiratory distress or cardiac failure are present. If
patient is clinically stable, monitor closely and treat the
cause of the anaemia.
 If Hb is > 5 g/dL, transfusion is usually not necessary.
Consider transfusion in cases of shock or severe burns.
Otherwise, treat the cause of the underlying anaemia.
 Transfuse with 10 to 15 ml/kg of PRBCs or 20 ml/kg of
whole blood.
 In the presence of profound anaemia or very high
malaria parasitaemia, a higher amount may be needed.

32.  Platelets
– Available as concentrates from single or multiple donors
– Manual Thrombapheresis is done either by ‘soft spin’
centrifugation or re-centrifugation of buffy coat layer.
– Can also be prepared from single donor by an Automated
Apheresis machine
– Platelets have very short shelf life, typically five days & are
stored under constant agitation at 20-24 deg C.
– No effective preservative solutions, lose potency very
quickly, best when fresh, thus very short turnover time.
– One unit has about 3 10^11 platelets

33. Indications for platelet transfusion
 Indicated when platelets count fall 50,000/cumm
1. Chemotherapy, Radiotherapy for leukemia, multiple
myeloma
2. Aplastic anemia
3. AIDS
4. Hypersplenism
5. ITP
6. Sepsis
7. Bone marrow transplant, organ transplant or surgeries such
as cardiopulmonary bypass.
Avoided in those with heparin-induced thrombocytopenia
(HIT) or disseminated intravascular coagulation (DIC) or
Thrombotic thrombocytopenic purpura(TTP).

34. Expected Platelet Counts After Infusion
 Platelet count increase as well as platelet survival after
transfusion is related to the dose of platelets infused and to the
patient's body surface area (BSA). Usually these values are
less than what would be expected.
 Expected platelet increase (per μL) = # platelets infused x CCI
/ BSA (m2)
 The theoretical value of the CCI is 20,000/μL but
clinically, the value is closer to 10,000/μL. If the CCI is less
than 5,000/μL, patients are said to have "refractoriness" to
platelet transfusion.
(Corrected platelet count increment (CCI) = platelet increment at
one hr x BSA (m2) / # platelets infused x 10^11 )

35.  Fresh-frozen plasma
– Produced from a Single donation
– 200-300 ml of plasma with 40-60 ml of citrate
anticoagulant nutrient mixture
– Stored at -30 deg C (shelf life of 12 months)
– Thawed rapidly at 37 deg C
– Infused intravenously through a standard blood set with on-
line filter
– ABO group must be compatible
– Infusion of 1 unit should be complete within 4 hr of
thawing

36.  Indication for FFP transfusion
– To correct isolated plasma protein deficiencies
– To reverse oral warfarin anticoagulation
– In patient with liver disease, major hepatic
resection and severe liver injuries
– DIC
– Bleeding diathesis after large volume blood
transfusion
– TTP

37.  Cryoprecipitate
– Concentrate of factor VIII, VonWillebrand’s
factor, fibrinogen and factor XIII
– Each 15 mL unit typically contains 100 IU of
factor VIII, and 250 mg of fibrinogen.
– The product is manufactured by slowly thawing a
unit of FFP at temperatures just above freezing (1-
6 C) and then centrifuged to remove the majority
of the plasma, and the precipitate is resuspended in
the remaining plasma or in sterile saline
– Stored at -30 deg C (shelf life 12 month).
– Also thawed at 37 deg C.
– Transfusion should be completed within 4 hrs.

38.  Indication of Cryoprecipitate transfusion
– Fibrinogen deficiency and dysfibrinogenaemia
– Uraemic bleeding
– VonWillebrand’s disease

39.  Special blood components
– Irradiated components:-
It is the only effective means of preventing Graft
vs. Host Disease while transfusing blood
components to immuno-compromised patients.
– Leuco-reduced cellular component:-
Benefits are
1. Decreased alloimmunization/platelet refractoriness in
multiply transfused leukemics.
2. Prevention of febrile reactions to RBC/platelet
transfusions in multiply transfused patients.
3. Reduction of CMV transmission.
4. Reduction in inflammatory mediator accumulation during
storage – preventive strategy for TRALI.

40. Adverse effect of transfusion of
blood and blood products
 Acute
– Allergic
– Anaphylaxis
– Hemolytic
– Metabolic
– Transfusion related acute lung injury
– Circulatory overload
– Non-hemolytic febrile transfusion reactions
– Haemostatic: dilution of clotting factors and
thrombocytopenia
– Infective Risks

41.  Late
– Delayed hemolytic transfusion reactions
– Sensitization/Alloimunization
– Transfusion Related Immune Modulation
– Graft-vs-Host disease
– Transfusion iron overload (haemosiderosis)

42.  Non hemolytic Febrile Transfusion
Reactions
– Result of alloimmunization to leucocyte and
platelet antigens ( HLA antigens)
– Symptoms: Rigor followed by Fever usually
within the start of 30-60 min of transfusion
– Managed by cessation or slowing of the
transfusion and administration of an antipyretic
– Pretreated with antipyretic in repeated transfusions
and patient who has history
– If above measure fail, leucocyte-depleted cell
components are given.

43.  Allergic reaction
– Symptoms: Urticarial rash and itch within minutes
– Treatment:
 Antihistamines
 and reduction of transfusion rate

44.  Anaphylaxis
– Rare, fatal, caused by antibodies to IgA in patients
who have extremely low levels of this
immunoglobulin in plasma (Hereditary IgA
Deficiency), who have been sensitized to IgA in
previous transfusions.
– Treatment: Termination of blood transfusion, IV
crystalloids, Maintenance of
airway, Oxygen, Adrenalin, IV antihistamine and
salbutamol

45.  Acute haemolytic reaction
– Result of ABO incompatibility
– Serious complication
– Mortality is high when more than 200 ml has been
transfused
– Clinical feature
 Pain at the infusion site and along the vein
 Facial burning
 Chest and back pain
 Fever, rigor and vomiting
 Restlessness, breathlessness, flushing and
hypotension
 Bleeding from vascular access sites and wound

46. Management
 Immediate recognition
 Cessation of transfusion
 Replacement of the blood transfusion set
 Adequate hydration
 Forced diuresis
 Vasopressor/ Inotrope support might be required
 Further investigations
– Re-cross matching and serological testing
– Blood unit for culture
– Blood sample for clinical chemistry
– Coagulation screen

47.  Transfusion Related Acute Lung Injury
– Occurs when mediators (anti HLA antibodies and anti-
granulocyte antibodies) present in the donor plasma
activate leucocytes in the host.
– Pulmonary microvascular occlusion by platelets, leucocytes
and fibrin
– Clinical feature (within 6 hrs of transfusion)
 Fever
 Breathlessness
 Non-productive cough
 Hypoxia
– Chest X-ray shows typical features of ARDS
– Transfusion related circulatory overload should be ruled
out.
– Multiparous female donors have been identified as most
common source in TRALI fatalities.

48.  Treatment of TRALI
1. Treatment is largely supportive.
2. Monitor Oxygen saturation, Provide
supplemental oxygen to maintain saturation
above 92%
3. Hypoxemia severe enough to require
Endotracheal Intubation and PPV occurs in
70-75% of patients.
4. No evidence supports the routine use of
Corticosteroids.

49.  Metabolic complications
– In patients with massive blood transfusion( 1
ml/kg/min or 1 unit of blood per 5 minutes).
– Metabolic consequences include
1. Hypothermia (prevented by transfusing blood
through blood warmer)
2. Acidosis
3. Increased affinity of oxyhaemoglobin for oxygen(
due to transfusion of 2,3 DPG depleted blood)
4. Citrate intoxication( causes temporary reductions in
ionised calcium levels – If symptomatic treated by
administering calcium gluconate)
5. Hyperkalemia

50. Haemostatic complications
1. Dilutional Coagulopathy
– Stored blood is deficient in platelets and labile clotting
factor (factor V and VIII)
– Massive transfusion induces dilution of
Fibrinogen, Clotting factor – II, V and VIII in addition to
moderate Thrombocytopenia.
– Treated by administering FFP or platelets as decided on
basis of laboratory evidence of coagulopathy or by clinical
suspicion due to rapid ongoing blood loss.
2. Post Transfusion Purpura
– Platelet-specific alloantibodies may cause post-transfusion
purpura
– It is initially treated with high dose corticosteroids and
intravenous immunoglobulin
– If platelets needed , have to be compatible with patient
alloantibodies

51.  Circulatory overload
1. Encountered when blood is administered too
rapidly or in large volumes
2. Pulmonary edema is common
3. Must be differentiated from ARDS
4. Diuretics may be used – Furosemide administered
at incremental dosage of 20-40 mg depending on
response 6-8 hrly until desired diuresis occurs.

52.  Transfusion haemosiderosis
– Iron overload in monocyte-macrophage system
– Especially a problem in childhood anemias (e.g.
thalassemia) and in patients with chronic refractory
anemia
– Iron chelation therapy with desferrioxamine

53.  Graft-versus-host disease
– Rare, but fatal complication
– Occurs mainly in immunodeficient patients
– Caused by the T-lymphocytes from donor blood
get engrafted into the immunodeficient host’s
marrow and launch an immune response against
the host.
– Starts 3-30 days after the transfusion
– Patient develops high fever, diffuse erythematous
skin rash, desquamation, GI symptoms, severe
hepatic dysfunction and pancytopenia
– Prevented by administering gamma-irradiated
cellular components

54.  Delayed Hemolytic Transfusion Reactions
1. Result of Anamnestic Response to Donor RBC antigen to
which a recipient has been previously exposed.
2. Commonly involve antibodies against Kell, Kidd and
Rhesus antigens.
3. Occur within first or second week following transfusion
4. Symptoms include low grade fever, increased indirect
bilirubin or unexpected reduction in Hb concentrations.
5. It is typically mild and self limiting.
6. Treatment is supportive including Hb monitoring, hydration
and provision of compatible blood if necessary.

55.  Transfusion Related Immunomodulation
1. There are changes in immunity related processes
such as T-lymphocyte Helper/Suppressor
ratio, function of T Killer cells, Lymphocyte
responsiveness and Delayed Hypersensitivity.
2. Adverse effects on immunocompetence such as
accelerated reccurences of malignancy, increased
rates of infection and more rapid progression of
HIV/AIDS.
3. Cause Unknown.

56.  Infective risks
1. Hepatitis B, C and G
2. HIV 1 and 2
3. HTLV 1 and 2
4. Cytomegalovirus
5. Parasitic diseases – Malaria, Filariasis and Chaga’s
disease.
6. Prion related Diseases ( CJD)

57. 7. Bacterial Contamination:
 More common with platelet transfusions.
 Risk is less in single donor apheresis derived units.
 Gram negative Yersinia enterocolitica is the most common
cause of fatal sepsis.
 Symptoms –
Fever, Chills, Tachycardia, Dyspnea, Shock, DIC and Acute
Renal Failure.
 Needs to be distinguished from other common transfusion
reactions.
 Treatment:
1. Transfusion stopped immediately
2. Blood cultures obtained
3. Broad spectrum Antibiotics
4. Supportive care as required.
5. Notification of blood bank.

58. Thanks