Blood transfusion in OMFS

BLOOD TRANSFUSION
By Dr Rayan M
Moderator Dr (Col) Suresh Menon

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
 Autotransfusion
 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

BLOOD
Plasma (55%)
Cells (45%)
RBC
WBC
90% Water 10% Solids Platelets
Organic Inorganic
Plasma protein Ions
Clotting factors

HISTORY OF BLOOD TRANSFUSION
As early as the 17th century, blood has been
used as a therapy for a variety of ailments.
1665 – First recorded blood transfusion in
England , Richard 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.
 1870 The first whole blood transfusion to
treat hemophilia is successfully completed.
 1901 Karl Landsteiner discovers the first
three human blood groups, A, B andO.
 1902 Landsteiner’s colleagues, Alfred
Decastello and Adriano Sturli, add a
fourth blood type, AB.

 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.
 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.
 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 1901 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
 The Rh system, which includes the C D E & c d 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

HEMOLYTIC DISEASE OR ERYTHROBLASTOSIS FETALIS
 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 27 other known blood groups systems with more
than 300 known antigens . These are all classified by the
antigens found on the surface of our red blood cells.
 The “MN blood group antigens” were discovered in the
1920s by Karl Landsteiner.
 In this there are 3 groups, M N & MN.
 It hold importance in paternity testing.

 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 Kid blood group it’s very important to avoid damaging
reactions, and therefore carefully matched antigen negative
blood is given.

BOMBAY BLOOD GROUP [OH GROUP]
o Rare individuals also lack the H antigen and are
designated as the “Bombay” phenotype (group
Oh). They make potent anti-H in addition to anti-A
and anti-B and must be transfused blood only from
other individuals with the Bombay group
It is observed to occur in 1
out of every 250,000 people
It was discovered by Y.M
Bhende

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)
 Acid Citrate Dextrose (ACD)
 Citrate Phosphate Dextrose (CPD)
 Citrate Phosphate Dextrose Adenine (CPDA-1)
 15 ml of ACD, 14ml of CPD or CPDA is used for preserving
100ml of blood

 PURPOSE:
A Toprevent coagulation.
B To preserve the life and survival of RBCs so as to
have the maximum post transfusion survival.
• CITRATE: Acts by chelating Calcium.
• DEXTROSE: Necessary for the metabolism of stored RBCs.
• It passes from plasma into the red cells and is utilized for
energy production.
• CITRIC ACID: Prevents carmalization of glucose in citrate
dextrose solution during autoclaving.
• ADENINE: Improves the viability of red cells.

COMPOSITIONS OF
PRESERVATIVES/ANTICOAGULANTS

DONOR SELECTION
 Donor history and risk factor assessment
 Infectious disease testing
 ABO and Rh typing
 Cross matching
 Noting post donation information

DONOR HISTORY & EXAMINATION
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.
 SURGICAL PROCEDURES
Major : one year after the recovery
Minor : 6 months
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

CROSS MATCHING
 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
 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
•Anticoagulants such as citrate and heparin
is used

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

PACKED REDCELLS
 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

INDICATIONS FOR PACKED RED CELLS
 In the field of orofacial surgery, a red blood cell
transfusion (RBCT) is occasionally required during double
jaw surgery, pan facial surgery and oncosurgery
 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
 The indications and triggers for RBCT are on-going issues.
There have been many studies and there are still on-going
research of an answer. Based on studies to date, there are
two strategies :
a) 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

PLATELET CONCENTRATES
 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 :
a) Platelet disorders
b) When massive blood loss has occurred
 One unit will usually raise the count to 5-10k / micro liter

FRESH FROZEN PLASMA
 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 clotting factors

CRYOPRECIPITATED ANTIHAEMOPHYLIC FACTOR
 Its an antihaemophyllic concentrate, Cryoprecipitate which is
produced by allowing FFP to thaw slowly at 1– 6°C
 It is prepared from plasma and is rich in clotting factors
 It is used in people with haemophillia and Von willebrand
disease to control bleeding
 Its contents are major portion of factor 8 which is present in
freshly drawn and separated plasma
 Indications for transfusion of cryoprecipitate include repletion
of fibrinogen levels activation of platelets; replacement of
factor VIII, vWF, or factor XIII when recombinant factors are
unavailable; and as part of a massive transfusion protocol

PROTHROMBIN COMPLEX CONCENTRATES
o PCCs are intermediate-purity pooled plasma products containing a
mixture of vitamin K–dependent proteins that are used for the
treatment of hemophilia A and B
o PCCs are produced by ionexchange chromatography
o Depending on the processing technique, either a 3-factor (eg,
factors II, IX, and X) or 4-factor (eg, factors II, VII, IX, and X)
concentrate contains a final overall clotting-factor concentration
that is approximately 25 times higher than in normal plasma
o PCCs were originally indicated for the treatment of patients with
hemophilia B. More recently, their indication has expanded as a
replacement therapy for congenital or acquired deficiency of
vitamin K–dependent clotting factors

FACTOR VIIA
oFactor VIIa is a recombinant agent that is used in the
treatment of patients with factor VII deficiency and in
patients with hemophilia A or B who have inhibitors.
oAt present, the accepted indications for the use of rFactor
VIIa are limited to hemophilia A and B with inhibitors,
acquired hemophilia, and factor VII deficiency

FACTOR VIII
o Hemophilia A is an X-linked disorder.
o The major clinical manifestations in this disease are arthropathy
secondary to spontaneous bleeding into joints with a risk of
mortality from hemorrhagic bleeds ranging from 20% to 50% of
patients
o The currently available plasma-derived concentrates are
classified as high purity (containing only the desired factor) or
intermediate purity (containing the desired factor as well as
other factors)

• Factor VIII replacement therapy in hemophilia A depends
on the type of surgery or bleeding event.
• For minor surgery, a desired level of factor VIII replacement
(20 U/kg) is greater than 30%, whereas replacement in the
trauma or major surgical setting requires levels of 100%.
• In general, the administration of 1 U of factor VIII
concentrate increases the level by 2%.
• Factor VIII therapy is continued for 1 to 3 days
postoperatively for minor procedures; however, 50%
replacement for 10 to 14 days is usually required for major
bleeds.

FACTOR IX
oHemophilia B or Christmas disease is an X-linked disorder that
affects 1 in 30,000 people.
oThree replacement therapies are presently available for the
treatment of factor IX deficiency
o1.Factor IX complex
o2. Coagulation factor IX concentrate, a high-purity plasma-
derived product
o3. Recombinant factor IX concentrate , a nanofiltered product
that is produced without animal or human proteins

oIn patients with hemophilia B undergoing minor surgical
procedures, the recommended replacement of factor IX is
greater than 30% (40 U/kg).
oPatients with major bleeds, trauma, or requiring major
surgical procedures should be replaced to 100% (125 U/kg)
and maintained throughout the postoperative period at a
level of 50% or greater

FACTOR XIII
o Once a fibrin clot is formed via the coagulation cascade it must
be stabilized in order to prevent premature fibrinolysis.
o The crosslinking of the alpha and beta chain fibrin monomers is
catalyzed by factor XIII.
o Inherited factor
o XIII deficiency is an autosomal recessive condition that manifests
with soft tissue bleeds, hemarthrosis, intracranial bleeding,
bleeding during surgery, and poor wound healing.
o Factor XIII concentrate is administered intravenously to a level of
5% to 20%.
o Dosing is recommended at 10 to 75 IU every 4 to 6 weeks

PRINCIPLES OF BLOOD TRANSFUSION
 1. Transfusion is only one part of the patient’s
management.
 2. Blood loss should be minimized to reduce
the patient’s need for transfusion.
 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 SterileApparatus.
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 following transfusion

Bill No:
Sticker No:
Pre Transfusion Vitals
BP
PR
Temp
SPO2
Post Transfusion Vitals
BP
PR
Temp
SPO2
Time Started : Time Ended:
Blood Transfusion Notes
Bld Grp Hb

• Transfuse blood at the rate of 2 drops/min for the first 5 mins.
In case of no reaction to 4 drops/min.
• Transfuse blood at the rate of maximum 16 drops/min till
transfusion is complete.
• Watch for any signs of anaphylaxis, hypotension,
breathlessness etc.
• In case of any reaction stop blood transfusion immediately.
• Administer : Inj Pheniramine Maleate 45.5gm IV stat
Inj hydrocortisone 100mg IV stat
• Inform blood bank

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.

 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 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.
PREVENTION IS BETTER THAN CURE

• Also known as Auto transfusion
• Defined as the collection and reinfusion of patients
own blood / blood components
• Safest form of blood transfusion
• More cost effective than allogenic transfusion

HISTORY
• First Autologous transfusion was done by James
Blundell in 1818 before the discovery of blood
groups.
• Anglo-saxon was the first to publish an article
reporting Autotransfusion in 1874.
• Blood salvage was first reported in American
literature in 1917.

3 Types of Autotransfusion
• Pre operative blood donation
• Intra operative and post operative blood recover
• Acute normovolemic Hemodilution

Predeposit autologous donation
(PAD)
• With a red cell storage-life of 35 days at 4°C, most
healthy adult patients can donate up to three red cell
units before elective surgery.
• Patients may be given iron supplements,
sometimes with erythropoietin.
• Given the current remote risk of viral transfusion-
transmitted infection by donor blood in developed
countries, the rationale, safety and cost-effectiveness of
routine PAD has been questioned.

Indications for Predeposit autologous donation PAD-
• Rare blood groups/ multiple blood group antibodies
where compatible allogenic (donor) blood is difficult
to obtain.
• Psychiatric risk because of anxiety about exposure to
donor blood.
• Patient refusal to donor blood transfusion but will
accept PAD.
• Children undergoing scoliosis surgery (other
options available).
• PAD should only be considered in surgery with a
significant likelihood of requiring transfusion,
• The patient’s ability to donate safely assessed.

68
Intraoperative cell salvage (ICS)
• For elective and emergency surgery with
significant blood loss and management of
major traumatic or obstetric haemorrhage.
• A 2010 Cochrane Collaboration review of
randomised trials of ICS, mainly in cardiac and
orthopaedic surgery, showed a 20% reduction in
donor blood exposure (an average saving of
0.7 units per patient).

Indications for ICS in adults and children (for whom low-volume
processing bowls are available)-
• Surgery where anticipated blood loss is >20% of the patient’s
estimated blood volume.
• Elective or emergency surgery in patients with risk factors for
bleeding or low preoperative Hb concentration.
• Major haemorrhage.
• Patients with rare blood groups or multiple blood group
antibodies for whom it may be difficult to provide donor blood.
• Patients who do not accept donor blood transfusions but
are prepared to accept, and consent to, ICS (this includes
most Jehovah’s Witnesses).

Postoperative cell salvage (PCS)
• Mainly used in orthopaedic procedures,
especially after knee or hip replacement and in
correction of scoliosis.
• Blood is collected from wound drains and then
either filtered or washed in an automated system
before reinfusion to the patient.
• The simple filtration systems for reinfusion of
unwashed red cells are mainly used when
expected blood losses are between 500 and
1000 mL.

• Collection of salvaged blood must be
completed within the specified time
(usually 6 hours) and the reinfusion
must be monitored and documented
in the same way as donor transfusions.
• PCS is relatively cheap, has the potential to
reduce exposure to donor blood and is
acceptable to most Jehovah’s Witnesses.

Acute normovolaemic haemodilution
(ANH)
• Several units of blood are collected into standard blood
donation packs immediately before surgery (usually in
the operating room) and the patient’s blood volume is
maintained by the simultaneous infusion of crystalloid
or colloid fluids.
• The blood is stored in the operating theatre at room
temperature and reinfused at the end of surgery or if
significant bleeding occurs.
• Often used in cardiac bypass surgery where the
immediate postoperative transfusion of ‘fresh whole
blood’ containing platelets and clotting factors is seen
as an advantage.

76
• Reported hazards of ANH include fluid
overload, cardiac ischemia and wrong blood
into patient errors.
• Mathematical modelling suggests ANH is most
effective as a blood conservation measure in
surgery with major blood loss.

COMPLICATIONS OF BLOOD TRANSFUSION
 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 classifiedinto:
a. Immunological complications
b. Non immunological complications
 Based on duration taken for the symptoms to occur they can be
classified as:
1. Acute
2. Delayed
 They can also be classified as
a. Non infectious complications
b. 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); 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,
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

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

DIFFERENCE BETWEEN TRALI AND TACO

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
 Pathophysiology : In contrast to intravascular hemolysis,
which is typically acute in 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 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 post- transfusion
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
 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 GRAFT-VERSUS- HOST DISEASE
 It is a rare disease 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.
 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
 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.

2. Febrile non-hemolytic transfusion reactions
 common transfusion reaction
 Etiology is not known
 Diagnostic criteria : to qualify as an FNHTR the fever
or chills/rigors must occur within 4 hours of
completion of the transfusion
 Treatment : transfusion should be stopped as soon
as reaction is suspected
 Supportive care
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 useof
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

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

Blood transfusion in OMFS

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