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Blood Transfusion

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BLOOD TRANSFUSION
By Dr.Amith
1st yr PG
OMFS
RRDCH
CONTENTS
Introduction
 Components of blood
 Functions of blood
 History of blood transfusion
 ABO blood groups
 Rh blood group
 Other common significant blood groups
 General indications for blood transfusion
 Pre-transfusion testing
 Principles of blood transfusion
 Precautions to be taken while blood transfusion
 Blood products
 Complications of blood transfusion
 Newer modalities

INTRODUCTION
Blood is a connective tissue in liquid form . It is
considered to be the fluid of life as it supplies oxygen
to various parts of the body.
 Blood transfusion can be defined as the transfusion
of the whole blood or its components from one person
to the other.
(Or)
 Transfusion is simply the transplantation of a tissue
consisting of a suspension of cells in a serum
It involves the collection of blood from the donor and
administration of the blood to the patient

FUNCTIONS OF BLOOD
COMPOSITION OF BLOOD
Blood
Cells (45%)
Erythrocytes
[5
million/cumm]
Leucocytes
[4000 – 11000/
cumm]
Agranulocytes
Plasma(55%)
Thrombocytes
[1.5-4 lakhs]
Granulocytes
91% Water
9% solids
1% inorganic
8% organic
HISTORY OF BLOOD TRANSFUSION
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As early as the 17th century, blood has been
used as a therapy for a variety of ailments..
Here is a look at some of the bigger
milestones related to blood transfusion over
the years.
1665 – First recorded blood transfusion in
England , R Lower revived a dog by
transfusing blood from another dog via a tied
artery
1818 James Blundell performs the first
successful blood transfusion of human blood
to treat postpartum hemorrhage.
1840 The first whole blood transfusion to
treat hemophilia is successfully completed.
1900 Karl Landsteiner discovers the first
three human blood groups, A, B and O.
1902 Landsteiner’s colleagues, Alfred
Decastello and Adriano Sturli, add a fourth
blood type, AB.
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1907 Blood typing and cross matching
between donors and patients is
attempted to improve the safety of
transfusions. The universality of the O
blood group is identified.
1914 Adolf Hustin discovers that
sodium citrate can anticoagulate blood
for transfusion, allowing it to be stored
and later transfused safely to patients
on the battlefield
1940 The Rh blood group is discovered
when RBCs of monkeys were injected
into rabbits .
1961 Platelet concentrates are
recognized to reduce mortality from
hemorrhaging in cancer patients.
1972 The process of apheresis is
discovered, allowing the extraction of
one component of blood, returning the
rest to the donor.
1985 The first HIV blood-screening test
is licensed and implemented by blood
banks.
ABO BLOOD GROUPS
The ABO antigens (agglutinogen) are carbohydrate
structures carried on large oligosaccharide molecules,
which are attached to glycoproteins and glycolipids
in the RBC membrane
 The RBC membranes have over 2 million ABO
antigens

Surface of RBC
when viewed under
Electron
microscope
LANDSTEINER'S LAW
Based on his observations Karl
Landsteiner in 1900 framed a law
called Landsteiner's Law
It has 2 major components , they are :
 If an agglutinogen is present in the
RBCs of an individual , the
corresponding agglutinin must be
absent from the plasma
 If the agglutinogen is absent in the
individual RBCs , the corresponding
agglutinin must be present in the
plasma

The agglutinins are gamma
globulins as are other antibodies .
Most of them are IgM molecules
RHESUS BLOOD GROUP
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The Rh system, which includes the D, C, c, E, and e
antigens, differs from the ABO system in several ways
It is second only to the ABO system in importance in
transfusion medicine.
The Rh antigens are highly immunogenic, especially the D
antigen since these antigens are membrane-spanning
proteins, in contrast to polysaccharide moieties.
In the Rh system the antibodies are of IgG type and
antigen –antibody reaction occurs best at body
temperature .[warm antibodies]
In Rh negative individuals , anti – D antibodies are not
naturally present in the plasma
In Rh negative individuals the anti – D antibodies
might be evoked by :
a) Transfusion with Rh positive blood i.e. D positive
RBCs
b) Entrance of the D positive RBCs from the Rh
positive fetus into the maternal circulation of Rh
negative mother
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HEMOLYTIC DISEASE OR ERYTHROBLASTOSIS
FETALIS
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Erythroblastosis fetalis is a disease of the fetus and new born infant
characterised by the progressive agglutination and subsequent
phagocytosis of the RBCs
If the mother is Rh negative and fetus is Rh positive serious
complications may occur.
RBCs containing D antigen may cross the placenta from the fetus to
the mother, either during pregnancy or a small amount of fetal
blood leaks into the maternal circulation at the time of the delivery.
The mother reacts by forming anti D which returns to the fetal
circulation and tends to destroy the fetal RBCs
CLINICAL PICTURE OF ERYTHROBLASTOSIS
FETALIS
Treatment of erythroblastosis fetalis
Transfusion of Rh –ve blood is done i.e. 400ml for 1.5 hrs
or more
It is repeated several times for the first few weeks of life
This is done so as to keep the blirubin levels low
Prevention of the Rh hemolytic disease
a. Destruction of Rh positive fetal cells in the maternal
blood can be brought about by administering a single
dose of anti Rh antibodies in the form of Rh
immunoglobulins soon after child birth
b. This prevents the formation of active antibodies by
the mother
OTHER COMMON SIGNIFICANT BLOOD
GROUPS
There are 34 other known blood groups systems
with more than 300 known variants . These are
all classified by the antigens found on the surface
of our red blood cells.
 The “MNS blood group antigens” were discovered
in the 1920s by Karl Landsteiner.It’s common to
find antibodies to the M blood group in the
plasma of patients, as these are sometimes
formed after infection, and testing is required to
ensure the patient’s anti-M antibodies do not
destroy donated red blood cells.

Another blood group, the “S/s variants”, are
named after Sydney, where the blood group was
discovered. This blood group is signified by a
particular type of molecule on the red blood cells
that is a target of the malaria parasite.
 A blood group known as Duffy is also associated
with infection by malaria .When this protein is
absent from the red blood cells, the cells are
resistant to infection by the malaria parasite. This
protein is absent from the blood cells of 90% of
sub-Saharan Africans, conferring malaria
resistance on this population. Antibodies to the
Duffy antigens are commonly found in a patient’s
plasma and are a cause of transfusion reactions if
carefully matched antigen negative blood is not
given.

The K antigen was first detected in the 1940s as a
result of a woman without the K antigen on her
red blood cells being pregnant with a
baby with the K antigen on the red blood cells.
While almost all women post-partum have
antibodies to some antigens found on the baby’s
white blood cells, red cell antibodies are less
common.
 Another blood group, Kidd ( Jk) was named after
the patient in whom it was discovered. The Kidd
proteins are related to proteins in the kidney that
help get rid of waste from the body. For the Kidd
blood group it’s very important to avoid damaging
reactions, and therefore carefully matched antigen
negative blood is given.

BOMBAY BLOOD GROUP[OH GROUP]
Rare individuals also lack the H antigen and
are designated as the “Bombay” phenotype (group
Oh). They make potent anti-H in addition to antiA and anti-B and must be transfused blood only
from other individuals with the Bombay
phenotype.
o
It is observed to occur in 1 out
of every 250,000 people
It was discovered by Y.M
Bhende
RBC compatibility
Plasma compatibility
ANTICOAGULANTS
1916 - First anticoagulant preservative was
discovered by Rous and turner – Citrate glucose
 1943 – Acid citrate dextrose was introduced by
Loutit and Mollison
 1957 - Gibson et al developed citrate phosphate
dextrose (CPD)
 1978 – citrate phosphate with adenine (CPDA-1)
 15ml o ACD or 14 ml of CPD/CPDA-1 is used in
preserving 100 ml o blood
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PURPOSE: a. To prevent coagulation.
b. To preserve the life and survival of RBCs so as to
have the maximum post transfusion survival.
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DONOR SELECTION
Donor history and risk factor assessment
 Infectious disease testing
 ABO and Rh typing
 Cross matching
 Noting post donation information
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DONOR HISTORY
GENERAL PHYSICAL EXAMINATION :
 General Appearance : should appear to be in good
health.
 Age : between 18 and 65 years.
Weight : 45-55 Kg - 350 ml blood
55 Kg & above - 450 ml.
 Temperature : should not exceed 37.5 C / 99.5 F
 Pulse : 60 to 100 beats/min & regular pulse
 Blood Pressure : SBP : b/w 100 and 160 mm of Hg
DBP : b/w 60-90 mm of Hg
 Skin : free of any skin lesion or infections
MEDICAL HISTORY :
 History of malaria : accepted after 3 months.
 History of jaundice : deferred up to 1 year.
 History of being HIV, HBsAg / HCV antibody
positive : permanently deferred.

Intimate contact with HIV, HBsAg / HCV
antibody positive individual : deferred for 1 year.
 History of measles/mumps/chickenpox : deferred
for 8 weeks
 History of influenza : deferred till 1 week after
treatment
 Having history of diarrhoea in preceding week
particularly if associated with fever should be
deferred
HISTORY OF VACCINATION
 vaccination against TAB/TT/ Cholera/Hepatitis-A :
accepted if free of symptoms.
 Hepatitis B vaccination : accepted after 7 days of
vaccination.
 Yellow fever/measles/polio : deferred for 2 weeks
 Rabies vaccination : deferred for 1 year.
 Those bitten by any animal : deferred for one year.
 Hepatitis B Immunoglobulin : should be deferred
for 1 year
PREGNANCY
 not be accepted during period of pregnancy and till
12 months after full term delivery and also during
lactation.
ASPIRIN INGESTION
Ingestion of Aspirin or any related medicine within 3
days prior to donation should preclude use of donor
as a source of platelet preparation.
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SURGICAL PROCEDURES
Major : one year after the recovery
Minor : 6months
LABORATORY EXAMINATION :
 Haemoglobin : not less than 12.0 gm/dl
 Hematocrit : not less than 36%
DONOR INFECTIOUS DISEASE TESTING
Hepatitis B, HbsAg and anti-core antibody
 •Hepatitis C antibody
 •HIV 1 and 2 antibodies
 •HTLV [Human T-cell lymphotropic virus] 1 and
2 antibodies
 •Serologic Test for Syphilis
 •Nucleic Acid Testing (NAT) for HIV, HCV
 •Detection of Bacteria in platelet products
 •CMV [Cytomegalo virus] antibody for select
recipients
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CROSS MATCHING
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Blood matching between a patient and a donor is a direct
compatibility test
RBCs and plasma are crossmatched through major and
minor crossmatching process
“Major” crossmatch is comparing donor erythrocytes to
recipient serum where as the “minor” crossmatch is
designed to test opposite compatibility which is the donor's
serum/plasma with the recipient's red cells.
Minor cross match has almost been eliminated in most
blood banks, because the donor samples are screened before
hand for antibodies
GENERAL INDICATIONS OF BLOOD
TRANSFUSION
1. External bleeding
2. Internal bleeding (i) non-traumatic
(ii) traumatic
3. RBC lysis : e.g. malaria, HIV
4. Anaemia
5. Bleeding disorders
6. Burns
6. Anticipated need for blood
PHLEBOTOMY
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The maximum volume of blood that may be collected is 10.5
mL/kg of body weight
About 350- 450 ml is taken each time
The withdrawal of blood takes 10-15 mins
APHERESIS
•Apheresis refers to the process of separating
the cellular and soluble components of blood
using a machine.
• Apheresis is often done on donors where whole
blood is centrifuged to obtain individual
components ( RBCs, platelets, plasma based on
specific gravity) to use for transfusion in
different patients.
•Here the required component is collected and
the rest is returned to the donor
•Selective collection of RBCs/WBCs/platelets is
called cytapheresis
•Selective collection of plasma is called
plasmapheresis
•Here the anticoagulants such as citrate and
heparin is used
BLOOD PRODUCTS
BANKED WHOLE BLOOD
No components have been removed
 Contains RBCs ,WBCs ,platelets and Plasma
 Can be stored for 5 weeks
 Transfusions of whole blood are rarely required
 They might be necessary in cases of acute blood
loss in major surgeries > 15% blood loss
 It is a poor source of platelets and clotting factor
5 and 8
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PACKED RED CELLS
Red cells from a donor unit diluted with plasma ,
to a hematocrit of 75%
 Volume is about 200ml
 Storing red cells just above freezing allows
survival for about 42 days
 It is the product of choice for most clinical
situations
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INDICATIONS FOR PACKED RED CELLS
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In the field of orofacial surgery, a red blood cell
transfusion (RBCT) is occasionally required during
double jaw and oral cancer surgery
In the field of orofacial surgery, transfusion is
performed for the purpose of oxygen transfer to
hypoxic tissues and plasma volume expansion when
there is bleeding.
RBCT can be a life-saving procedure for most
patients with acute anemia caused by perioperative
bleeding
RBCT is the fastest way to increase the oxygen
carrying capacity of blood
A unit of RBCT will increase the Hct by 3% and Hb by
1-1.5 gm/dl
TRANSFUSION STRATEGY & TRIGGER
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a)
b)
The indications and triggers for RBCT are on-going
issues. There have been many studies and there are
still on-going studies in search of an answer. Based on
studies to date, there are two strategies :
In 1988, the “10/30 Rule”( liberal strategy) was
presented at the National Institutes of Health
Consensus Development Conference, which
presented the level of RBCT during perioperative
period to be less than Hb 10 g/dL and Hct 30% and
transfusions were performed based on those values
Recently, the restrictive strategy (Hb level below 7
g/dL) has become more accepted due to the
accumulation of evidence regarding the negative
impact on prognoses following RBCT per the liberal
strategy as well as the complications and costs
associated with RBCT
FROZEN RED CELLS
Concentrations of red blood
cells preserved frozen at -80ºC.
 It reduces the risk of transfusing antigens or
foreign bodies that the body might regard as
potentially dangerous in previously sensitized
patients
 Not available for use in emergency situations
 RBC viability is improved
 ADP and 2,3 DPG(2,3-diphosphoglycerate) is
maintained
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PLATELET CONCENTRATES
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a)
b)
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Composed of platelets and 50 ml plasma
Contains cellular components that help in the clotting
process
Platelets can be stored up to 5 days in room
temperature
Indicated in :
Platelet disorders
When massive blood loss has occurred
One unit will usually raise the count to 5-10k / micro
liter
FRESH FROZEN PLASMA
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Obtained from freshly donated blood
Source of vit k dependent clotting factors
Only source of factor 5
Indicated for coagulopathy and different clotting factors
1 unit FPP = 3% increase in CF
CRYOPRECIPITATED ANTIHAEMOPHYLIC FACTOR
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Its an antihaemophyllic concentrate, Cryoprecipitate
which is produced by allowing FFP to thaw slowly at
1–6°C
It is prepared from plasma and rich in clotting factors
It is used in people with haemophyllia and Von
willebrand disease or other major abnormalities to
control bleeding
Its contents are major portion of factor 8 and
fibronectin which is present in freshly drawn and
separated plasma
Indications for transfusion of cryoprecipitate include
repletion of fibrinogen levels activation of platelets;
emergent replacement of factor VIII, vWF, or factor
XIII when recombinant factors are unavailable; and
as part of a massive transfusion protocol
PRINCIPLES OF BLOOD TRANSFUSION
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1. Transfusion is only one part of the
patient’s management.
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2. Blood loss should be minimized to reduce
the patient’s need for transfusion.
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3. Acute blood loss should be given effective
resuscitation while the need for transfusion is
being assessed.
4. The patient’s haemoglobin value, although
important, should not be the sole deciding
factor for transfusion.
5. The clinician should be aware of the risks
of transfusion- transmissible infections
PRECAUTIONS TO BE TAKEN DURING
BLOOD TRANSFUSION
1. Use of Sterile Apparatus.
2. Blood bag should be checked
3. Temperature of blood to be
transfused must be same as body
temperature.
4. Transfusion rate must be slow
in order to prevent increase load
on heart.
5. Care full watch on the
recipients condition for 10 mins
DONATION INTERVAL
The interval b/w 2 donations : at least 12 weeks.
 At least 48 hours must elapse after
plasmapheresis or cytapheresis before whole blood
is collected from a donor.
 Apheresis should be done only after 90 days of
whole blood collection or in an event when red cells
are not returned at the end of apheresis.
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PREVENTION IS BETTER THAN CURE
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Even though blood can supply a range
of products useful in a variety of
situations
Perioperative blood loss and
anaemia is best dealt with by
reducing the amount of blood lost
at surgery through minimizing
trauma, improving mechanical
haemostasis
Limiting phlebotomy to essential
diagnostic tests, using microsample
laboratory techniques; and giving
antifibrinolytics, such as EACA or
tranexamic acid (or, for high-risk
procedures, aprotinin)
Erythropoietin can also help where
blood has been lost but the
replacement of blood by transfusion
can be essential after severe
haemorrhage and in some other
circumstances
BLOOD SALVAGE
COMPLICATIONS OF BLOOD TRANSFUSION
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a.
b.
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1.
2.
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a.
b.
A carefully prepared and supervised blood transfusion is
quite safe
However 5-6% of transfusions , untoward complications
occur, some of which are minor while others are more
serious and at times fatal
Adverse reactions of blood transfusion can be classified
into :
Immunological complications
Non immunological complications
Based on duration taken for the symptoms to occur they
can be classified as:
Acute
Delayed
They can also be classified as
Non infectious complications
Infectious complications
NON INFECTIOUS COMPLICATIONS
Reactions associated with high morbidity
i.
Transfusion related acute lung injury
ii.
Transfusion associated circulatory overload
iii. Hemolytic reactions
iv. Anaphylaxis
v.
Transfusion associated graft vs. host disease
vi. Post transfusion purpura
Reactions associated with low morbidity
i.
Febrile non hemolytic transfusion reactions
ii.
Mild allergic reactions
iii. Acute hypotensive transfusion reactions
TRANSFUSION RELATED ACUTE LUNG
INJURY [TRALI]
Transfusion-related acute lung injury (TRALI)
was first recognized in 1926 and was previously
known as pulmonary hypersensitivity reaction
Pathophysiology :
 TRALI’s pathogenesis revolves around the
transfusion of antibodies and/ or other non
immunologic mediators to a susceptible patient
 The most frequently implicated antibodies are
human leukocyte antigen (HLA) class I, HLA
class II, and human neutrophil antibodies
(HNA)5,7; these antibodies activate the
leukocytes, which bind to the endothelium in the
lungs, causing endothelial injury and edema

TREATMENT OF TRALI
As with all transfusion reactions, immediate
cessation of the transfusion and stabilization of
the patient are critical.
 Respiratory support may range from
supplemental oxygen to intubation. Steroids have
not been proven to be beneficial.
 TRALI reactions usually resolve over the course
of a few days with only supportive measures
being needed

TRANSFUSION ASSOCIATED CIRCULATORY
OVERLOAD[TACO]
Transfusion-associated circulatory overload (TACO) is
generally the most common high-morbidity
transfusion reaction encountered in clinical practice
 Certain patient characteristics are known to increase
the risk of TACO, including older age, renal disease,
cardiac disease, positive fluid balance, and critically
ill status
Pathophysiology : Unlike the majority of transfusion
reactions, which are immunologically mediated,
TACO’s pathophysiology invokes simple physics—too
much fluid is added to the system too quickly (or in
volumes that cannot be tolerated) for the transfusion
recipient.
 Because the circulatory system cannot cope with the
additional volume of the transfused products,
pulmonary edema and respiratory distress result as
fluid “backs up” into the lungs

DIFFERENCE BETWEEN TRALI AND TACO
TREATMENT OF TACO
If the transfusion is still running, it should be
stopped immediately
 In some cases, the patient will improve with
simply stopping the infusion
 patients will require some form of respiratory
support, at least temporarily
 Diuretics are useful in the treatment of TACO;
the decrease in circulatory volume relieves
cardiovascular stress, improving the pulmonary
edema
 TACO can be prevented ,patients at risk of fluid
overload at increased risk of TACO and should be
transfused at a slow rate

HEMOLYTIC REACTIONS
Transfusions leading to RBC
hemolysis can be among the
most devastating and feared
complications of blood product
administration
 They represent a spectrum of
signs and symptoms and,
depending on the clinical
scenario, may be acute or
delayed, intra- or extra
vascular, attributable to ABO
or non-ABO antibodies, and
in some circumstances, may
even be caused by mechanical
forms of hemolysis due to
improper infusion techniques

INTRAVASCULAR HEMOLYSIS
Pathophysiology : Once the complement cascade
has been fixed and activated on the incompatible
cells, the resulting membrane attack complex
punches holes in the red cell, resulting in its lysis and
destruction
 IgM class antibodies are most efficient at fixing
complement and, therefore, acute intravascular
hemolysis is strongly associated with
incompatibilities within ABO antibodies (which are
most likely to be IgM in nature)
 Generation of free RBC membranes in the
intravascular space can cause concomitant activation
of the coagulation system, resulting in the
development of disseminated intravascular
coagulation (DIC)

Complement generation and RBC release of
hemoglobin can induce acute kidney injury and
renal failure, a particularly feared complication of
hemolysis.
 Complement activation can also cause smooth
muscle constriction, increased small vessel
permeability, and leukocyte activation, contributing
to the shock like symptom often seen in
intravascular hemolytic reactions.
 Acute hemolytic transfusion incidence estimated at
about 1 in 76,000 transfusions
 Prevention : Rigorous identification of patient blood
group during , before and after testing has to be
performed

EXTRAVASCULAR HAEMOLYSIS
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Pathophysiology : In contrast to intravascular
hemolysis, which is typically acute and thunderous at
onset, extravascular hemolysis is generally associated
with a more subdued, slower RBC clearance
For this type of hemolytic reaction, RBC clearance
occurs because incompatible cells are coated by IgG
class antibodies, with antibody-coated cells
subsequently phagocytosed
As such, most extravascular reactions are mediated by
non-ABO antibodies (e.g., anti-Jk, anti-K, and anti-E
Because of the slower, extravascular nature of these
reactions the likelihood of end organ damage and a
shock like symptom is markedly reduced, particularly
when compared with intravascular hemolysis
TREATMENT OF HEMOLYTIC DISEASES
Approaches to managing these reactions typically
include assessing their severity, providing
supportive transfusions to overcome the acute
anemia (and coagulation disorders, if they exist),
and steps to preserve renal function.
 New unit(s) are to be administered which are fully
compatible with the patient using the posttransfusion reaction specimen
 In urgent situations and gravely ill patients , O
negative blood can be given until the cause of
hemolysis is rectified.
 Renal function must be closely monitored both
clinically and via laboratory assays such as
creatinine

ANAPHYLAXIS
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Anaphylactic transfusion reactions represent the
most severe and extreme reactions in the spectrum of
allergic reactions
Pathophysiology : Most anaphylactic reactions are
associated with platelets or plasma but they can occur
with the transfusion of any blood product
It is caused by complement, mast cell, and basophil
activation in response to a specific antigen/allergen
Anaphylactic reactions are characterized by rapid
onset of respiratory distress, laryngeal edema,
hypotension, and/or gastrointestinal symptoms, often
within minutes of starting a transfusion
Other allergic symptoms such as rashes and urticaria
may occur in conjunction with these more severe
symptoms
Diagnostic criteria : These symptoms must appear
within 4 h of a transfusion to meet the criteria for an
allergic transfusion reaction
TREATMENT OF ANAPHYLAXIS
Blood transfusion must be stopped immediately,
and the patient must be stabilized as necessary.
 Respiratory support is vital, and intubation may
be required
 Epinephrine, intravenous diphenhydramine, and
volume resuscitation are often helpful
 Patients who have anaphylactic reactions to
blood products may require washed products in
the future
 Any future transfusions in a patient with a
history of anaphylactic transfusion reactions
should be considered with great caution, and the
patient must be closely monitored.

TRANSFUSION-ASSOCIATED GRAFTVERSUS-HOST DISEASE
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Transfusion-associated graft-versus-host disease is a rare
but serious complication of blood transfusion.
People at risk include those who have:
received blood transfusions from HLA-matched donors,
including family members
had a stem-cell transplant
inherited immune defects
acquired immune defects, such as Hodgkin disease been
treated with purine analogues, such as fludarabine,
cladribine or deoxycoformycin.
Transfusion-associated graft-versus-host disease results
from transfused leukocytes; gamma irradiation of the
transfused blood will obviate the reaction
Patients should be pre-warned and should carry a
warning card themselves
POST-TRANSFUSION PURPURA
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Post transfusion purpura is a relatively
uncommon complication of blood
transfusion
Pathophysiology : It can be thought of a
delayed transfusion reaction involving
platelets
Here there is an immunological response
to a previously encountered foreign
platelet that leads to an increase in the
production of antiplatelet antibodies by
the recipient
Treatment :The current treatment of
choice is intravenous immunoglobulin
(IVIG), along with consideration of
corticosteroids
REACTIONS ASSOCIATED WITH LOW MORBIDITY
1. Mild allergic reactions



Allergic reactions are the most
common adverse events associated
with transfusion
The main factor in allergic
transfusion reactions appears to
be the transfer of either antigen or
antibodies to the recipient via
donor plasma
Usually treatment is not
necessary, but in some cases
Diphenhydramine is the
treatment of choice; some patients
may also receive famotidine if
diphenhydramine is not effective
2. Febrile non-hemolytic transfusion reactions
common transfusion reaction identified
 Etiology is not known
 Diagnostic criteria : to qualify as an FNHTR the
fever or chills/rigors must occur within 4 h of
completion of the transfusion
 Treatment : transfusion should be stopped as soon
as reaction is suspected

3. Acute hypertensive transfusion reaction
Characterized by sudden increase in the systolic
blood pressure
 Attributable to the increase in bradykinin
 Treatment :Once the transfusion is stopped, the
hypotension resolves nearly immediately

Hyperkalemia associated with blood transfusions




Transfusion-associated hyperkalemic cardiac arrest is a serious
complication in patients receiving packed red blood cell (PRBC)
transfusions.
Mortality from hyperkalemia increases with large volumes of
PRBC transfusion, increased rate of transfusion, and the use of
stored PRBCs
The supernatant of stored RBCs usually contains more than 60
mEq/L of potassium .
Potassium in stored blood increases due to decrease in ATP
production and leakage of potassium into the supernatant. The
initial high levels of potassium in stored blood predispose to
post-transfusion hyperkalemia.
•Pre-washing of RBCs is an
essential practice for reducing
potassium load in irradiated
PRBC
HYPOKALEMIA
Hypokalemia is more common than the
hyperkalemia after transfusion because donor
red cells re- accumulate the ion intracellularly
 Citrate metabolism causes further movement of
potassium into the cells. Catecholamine release
and aldosterone urinary loss can also trigger
hypokalemia in the setting of massive
transfusion.
 No treatment or preventive strategy is usually
necessary

Flat prolonged t waves
Inverted t
wave
HYPOTHERMIA
It may be caused by transfusion of large volume
of cold blood products.
 It can cause cardiac arrhythmia and also
interferes with platelet function, clotting factor
interaction and bleeding time.
 Blood warmers may be used to prevent
hypothermia

INFECTIOUS COMPLICATIONS
Based on the etiology , the infectious
complications can be broadly classified into
complications caused by :
 Viruses
 Bacteria
 Parasites
 Prions

NEW CONCEPTS IN TRANSFUSION
MEDICINE
Development of in vitro/ex vivo blood cells
 Laboratory-derived platelets
 Red blood cells in the setting of
hemoglobinopathies
 Extending platelets’ shelf lives
 New testing approaches

DEVELOPMENT OF IN VITRO BLOOD CELLS
LABORATORY DERIVED PLATELETS
REFERENCES
Clinical principles of blood transfusion – 1st Ed –
Robert W Maitta
 Clinical laboratory blood banking and
transfusion medicine
 Essential Pathology -4th Ed – Harsh Mohan
 Human physiology –fourth Ed –A K Jain
 Perioperative red blood cell transfusion – NCBI
 Medical problems in dentistry -7th Ed - Scully
 Oral & maxillofacial surgery Vol-1 – Laskin D M
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