BLOOD TRANSFUSION

DR SHARAD JOHRI
READER
PG DEPARTMENT OF KAYACHIKITSA
STATE AYURVEDIC COLLEGE
LUCKNOW
Blood group system
&
Pre­
transfusion
testing
 ABO blood group system

•1st system discovered in 1900 by Karl Landsteiner

•Gene on chromosome 9p and inherited in Mendelian
co-dominant manner
Blood Antigen Antibody
Group on RBC in plasma

0 None Anti A and

Anti B
A A Anti B
B B Anti A
AB AB None

•What is “Bombay” blood group ?

The Rh blood group system
•2nd most important system
•Gene on chromosome 1
•The presence of D antigen confers
Rh positivity
•15% lack this antigen
•Exposure of Rh­- recipients to Rh+
cells results in production of anti­D
antibodies
Other blood group systems
•More than 100 systems recognised,
composed of more than 500 antigens

•CIinicaIIy significant systems are

1.Kelly, Kidd & Duffy system
2.MNS system
3.Lewis & P system
4.I / i system
Pre-tranfusion testing
Two stages - “type & screen”

1. Forward type
° Determine ABO & Rh phenotype of recipient
RBC
° Antisera against A, B & D antigens used

2. Reverse type
° Determine the antibodies: anti-A, anti-B &
anti-D in patient’s serum
° Should correlate with ABO phenotype
Čont...
1. Antibody screen
° Determine antibodies in patient’s serum directed
against other RBC antigens.

° Type O RBC (containing major antibodies of most

blood groups) is mixed with patient’s serum.

2. Cross-matching
° Performed after antibody screen, when the
antibodies in patient’s serum are recognised.

° Blood selected for cross matching should be ABO

compatible and lack the antigens for which patient
has antibodies
Blood Components
 Whole blood
•450 ml donor blood collected as “whole blood” into 63
ml CPDA-1 (citrate phosphate dextrose adenine) as
anticoagulant preservative.

•Hematocrit is 30-40%

•Stored at 4°C

•At this temperature, platelets lose viability, granulocytes

disintegrate and labile coagulation factors decline.

•Indication: acute hemorrhage with >25% blood loss.

•Provide both oxygen carrying capacity & volume expansion

Blood Component Separation
Blood Components
Packed red blood cells
•VoIume is 180-200 ml
•SheIf life of 35 days at 4°C
•Hematocrit is 65-75%
•1 unit PRBC raises Hb by 1 g/dL or Hct by J%
•Increases oxygen carrying capacity in
anemic patients but without volume
expansion
•Transfusion threshold is 7 g/dl in
normovolumic patients without cardiac disease
and comorbid conditions
•In critical patients, Hb target is 10 g/dl
 Platelets
Random Donor platelets(RDP)/Pooled
platelets: Prepared from whole blood by
centrifugation.
Single Donor platelets(SDP)/ Jumbo
platelets: Prepared by plasma apheresis
machine.
Volume of RDP IS 50-70 ml and SDP is
200- 400 ml
Shelf life of 5 days at 22 ° c.
 Platelets cont...
•1 unit of SDP = 6 units of RDP
•1 RDP increases platelet count by 5000-10000,
in unsensitised patient without increased
platelet consumption (DIC, splenomegaly,
fever)
•ThreshoId for prophylactic platelet transfusion
is 10000
•If patient is without fever or infection (eg ITP),
a threshold of 5000 is sufficient
•For invasive procedures & surgeries, platelet
target is 50000
 Fresh frozen Plasma
•FFP contains coagulation factors & plasma
proteins - albumin, fibrinogen, anti- thrombin,
protein C & S.
•VoIume is 200-250 ml.
•SheIf life of 1 year at -30°C, if thawed can be
stored for 24 hr at 4°C
•Indications are coagulation disorders like DIC,
liver diseases, congenital bleeding disorders &
reversal of warfarin therapy
•Doze is 10-15 ml/kg body weight
•1 unit FFP raises coagulation factors by 7%
•Transfusion monitored by PT/INR, stopped
when INR <1.5
 Cryoprecipitate
•It contains fibrinogen, factor VIII & von Willebrand

•1 unit cryoprecipitate contains 80 units of factor

VIII
•VoIume is 10-15 ml
•SheIf life of 1 year at -30°C
•Indications are DIC (serum fibrinogen<100mg/dl),
hemophilia A ( poor countries), and von Willebrand
disease.
 Granulocytes

Harvested from donors by apheresis after

stimulation by G-CSF (Granulocytes-colony
stimulation factor) and dexamethsone.
Indicated in febrile neutropenia(ANC<500
cells/mm3).
 Plasma derivatives

Specific proteins concentrates including

albumin, intravenous immunoglobulins, anti-
thrombin and coagulation factors.
Hyper immune globulins such as anti-D, anti
sera to hepatitis B virus(HBV), varicella-zoster
virus, CMV and other infectious agents.
 Artificial Blood
Two main categories of oxygen
carrying blood substitutes
1. Hemoglobin based oxygen
carriers( HBOCs).
2. Perfluorocarbon based oxygen
carriers.

•In trial stage

Complication of blood
transfusion
 Adverse reactions to blood
transfusion
1. Immune-mediated reactions are due to
preformed donor or recipient antibody,
however cellular components of stored blood
may also cause immune reactions
2. Non-immune reactions are due to the chemical
and physical properties of stored blood
components and its additives like anticoagulant.
It include infections complications.
Risk of transfusion com
ications
IMMUNE­MEDIATED
REACTIONS
 Acute hemolytic
Transfusion Reactions
Mechanism: The recipient has preformed
antibodies that lyse donor RBC
The ABO alloantibodies are responsible
for the majority, however, alloantibodies
against other RBC antigens, Rh, Kell, and
Duffy are associated with more fatal
reactions
Presentation: Hypotension, tachypnea,
tachycardia, fever, chills, hemoglobinuria,
chest pain, flank pain, and discomfort at
the infusion site
AHTR Cont...
Management:
•When suspected, stop transfusion immediately.
•Direct Coombs test detects the antibody bound to
RBC
•HemoIysis studies including serum
haptoglobin, lactate dehydrogenase, and indirect
bilirubin levels
•HemoIysis causes renal dysfunction. Give
intravenous fluids to induce diuresis
•Tissue factor released from lysed erythrocytes
may initiate DIC. Coagulation studies including PT,
aPTT, fibrinogen, and platelet count
 Delayed hemolytic
Transfusion Reactions
Mechanism: These patients are previously
sensitized to RBC antigens, but have low
antibody levels and negative antibody
screen. When re-transfused with the
same antigen, memory response results in
early production of antibody (1—2 weeks
after transfusion)
The transfused, antibody-coated RBC
are removedby the reticuloendothelial
system
Presentation: Mild reaction
Management: No specific therapy is
usually required
 Febrile Non-hemolytic
Transfusion Reaction
The most frequent blood transfusion
reaction
Mechanism: Antibodies directed against
donor WBC, and Cytokines released from
cells within stored blood components
Presentation : Fever with chills and rigors
Management: Use leukocyte-reduced blood
products
 Graft -versus-Host disease
Mechanism : Donor T lymphocytes recognize
recipient’s HLA antigens as foreign and mount an
immune response.
Presentation: Fever ,cutanious eruptions,
diarrhoea and liver function abnormalities.
Management: Resistant to immunosuppessive
therapies, clinical manifestations appear at 8-10 days
and death occurs at 3-4 weeks.
Prevention: Irradiation of cellular components
before transfusion.
 Allergic Reactions

Mechanism :Allergy to plasma proteins in

transfused components.
Presentation: Urticaria , pruritus ,
anaplylaxis
Management : stop transfusion, temporarily
and administer anti histamines ,corticosteroids
if severe.
Prevention: Cellular components washing to
remove residual plasma.
Transfusion-related acute lung injury

TRALI is the most common cause of

transfusion related fatalities
Definition: TRALI is defined as an acute lung
injury (PaO2/FiO2 <300 mmHg) that is
temporally related to a blood transfusion;
specifically, it occurs within the first six hours
following a transfusion
Mechanism: The donor anti-HLA class II
antibodies bind recipient neutrophils, these
neutrophils aggregate in pulmonary
vasculature and release inflammatory
mediators that increase capillary permeability
TRALI Cont...
Risk factors: Smoking, chronic alcohol use, shock,
liver surgery, mechanical ventilation and positive
fluid balance

Presentation: Symptoms of hypoxia (PaO2/FiO2

<300 mmHg) and signs of non- cardiogenic
pulmonary edema, including bilateral interstitial
infiltrates on chest x-ray
Management: Supportive
Chest X­ray of
TRALI

Bilateral interstitial
infiltrates
 Post-transfusion Purpura

Mechanism: Anti-platelet antibodies are

produced that react to both donor and
recipient platelets
Presentation: Delayed thrombocytopenia 7
—10 days after platelet transfusion
Management: Intravenous
immunoglobulin to neutralize the
antibodies, or plasma exchange to remove
the antibodies
NON IMMUNOLOGIC
REACTION
 Fluid overload

• BIood components are excellent volume expanders,

and transfusion may quickly lead to transfusion
associated circulatory overload (TACO)
•Dyspnea with SpaO2 <90%, bilateral on chest x-ray, and
systolic hypertension are found with TACO
•Monitoring the rate and volume of transfusion and using
a diuretic can minimize this problem
 Hypothermia

•Refrigerated (4°C) or frozen (—18°C or below)

blood components when rapidly infused

•Cardiac dysrhythmias on exposure of the SA

node to cold fluid

•An in-line warmer will prevent this complication

 Electrolyte Toxicity
Hyperkalemia:
•RBC leakage during storage increases the potassium
concentration in blood unit
•Prevented by using fresh or washed RBCs in high
risk patients like renal failure

Hyeocalcemia:
•Citrate, used as anticoagulant, chelates calcium and
inhibits coagulation
•HypocaIcemia manifest by circumoral numbness
and tingling sensation of fingers and toes.
 Iron Overload
•Each unit of RBCs contains 200-250 mg of iron
•Symptoms and signs appears after 100 units of
RBC transfusion (total-body iron load of 20 g)
•Prevent by using alternative therapies (eg
erythropoietin in CKD) and judicious transfusion
•CheIating agents, such as deferoxamine and
deferasirox, used but response is often suboptimal
 Immunomodulation
• •Transfusion of allogeneic blood is immunosuppressive.

• Transfusion-related immunomoduation is thought to be

mediated by transfused leukocytes.
.

•Leukocyte-depleted cellular products may cause less

immunosuppression
INFECTIOUS COMPLICATIONS
National blood safety policy
Testing for every unit of blood is mandatory for
1. HIV
2. Hepatitis B
3. Hepatitis C
4. Malaria
5. Syphilis
 Viral contamination
1. Hepatitis C (HCV): antibodies to HCV and HCV
RNA.
2. Human immunodeficiency virus (HIV):
antibodies to HIV, p24 antigen and HIV RNA
3. Hepatitis B (HBV): HbsAg antigen
4. Other Hepatitis viruses
5. West Nile virus
6. Cytomegalovirus (CMV)
7. Human T lymphotropic virus (HTLV) type 1
8. Parvovirus B19
Bacterial Contamination
•Most bacteria don’t grow well at cold temperatures,
hence not common with PRBC and FFP. However,
some gram-negative bacteria can grow at 1—6°C, eg
Yersinia, Pseudomonas, Serratia, Acinetobacter and
Escherichia species.

•PIateIet, stored at room temperature are more likely

to contain skin contaminants eg. Coagulase –negative
staphylococci.
•Presentation: Fever and chills, which can progress
to septic shock and DIC.

•Treatment: stop transfusion immediately if suspected,

manage shock and give broad-spectrum antibiotics.

•Sent blood component bag for culture and Gram stain

 Other Infectious Agents

Various parasites,including those causing

malaria, babesiosis and Chagas’ disease and
syphilis can be transmitted by blood
transfusion.
Massive Blood
Transfusion
Massive Blood Transfusion
Definition
The replacement of one blood volume (equivalent to
10 units of blood) in any 24 hour period,

or

Half of the blood volume (5 units of blood) in four

hour period in an adult
Massive transfusion indications
Severe trauma
Ruptured aortic aneurysm
Vascular/aortic surgeries
Obstetric compalications
Massive Transfusion Protocol

These parameters should be measured frequently (every

30-60 minutes, or after transfusion of blood component).
Temperature
Acid-base status
Ionised calcium (Ca)
Haemoglobin
Platelets (PLt)
PT/APTT (activated partial thromboplastin time)
Fibrinogen
 Mortality

Mortality is high in massive transfusion

Its etiology includes hypotension, acidosis,
coagulopathy, shock and underlying condition
of the patient
The lethal triad of acidosis, hypothermia and
coagulopathy have the highest mortality rate
It is often the underlying cause and
consequences of major hemorrhage that
result in complications, rather than the
transfusion itself.