It consists of slides about blood, various blood groups , pre-transfusion testing , blood products , conditions where blood transfusion is indicated and the various complications of blood transfusion in the field of oral and maxillofacial surgery.

1. BLOOD TRANSFUSION
By Dr.Amith
1st yr PG
OMFS
RRDCH

2. 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

3. 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

4. FUNCTIONS OF BLOOD

5. COMPOSITION OF BLOOD
Blood
Cells (45%)
Erythrocytes
[5
million/cumm]
Leucocytes
[4000 – 11000/
cumm]
Agranulocytes Granulocytes
Thrombocytes
[1.5-4 lakhs]
Plasma(55%)
91% Water 9% solids
1% inorganic 8% organic

6. HISTORY OF BLOOD TRANSFUSION
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.

7.  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.

8. 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

9. 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

11. RHESUS BLOOD GROUP
 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

12.  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

13. 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

15. CLINICAL PICTURE OF ERYTHROBLASTOSIS FETALIS

16. 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

17. 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.

18.  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.

19.  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.

20. 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 phenotype.
It is observed to occur in 1 out
of every 250,000 people
It was discovered by Y.M
Bhende

21. Plasma compatibility
RBC compatibility

22. 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
 PURPOSE: a. To prevent coagulation.
b. To preserve the life and survival of RBCs so as to
have the maximum post transfusion survival.

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

24. 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

25. 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

26. 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.

27.  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 : 6months
LABORATORY EXAMINATION :
 Haemoglobin : not less than 12.0 gm/dl
 Hematocrit : not less than 36%

28. 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

30. 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

31. 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

32. 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

33. 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

34. BLOOD PRODUCTS

35. 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

36. 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

37. INDICATIONS FOR PACKED RED CELLS
 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

38. TRANSFUSION STRATEGY & TRIGGER
 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 :
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
b) 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

39. 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

40. 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

41. 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 CF

42. 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 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

44. 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

45. 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

46. 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.

47.  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
PREVENTION IS BETTER THAN CURE

48. BLOOD SALVAGE

49. 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 classified into
:
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

51. 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

52. 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

53. 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

54. 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

55. DIFFERENCE BETWEEN TRALI AND TACO

56. 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

57. 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

58. 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)

60.  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

61. EXTRAVASCULAR HAEMOLYSIS
 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

62. 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 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

63. 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

64. 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.

65. TRANSFUSION-ASSOCIATED GRAFT-VERSUS-
HOST DISEASE
 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

67. 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

68. 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

69. 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

70. 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

71. 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

72. 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

73. INFECTIOUS COMPLICATIONS
 Based on the etiology , the infectious complications
can be broadly classified into complications caused
by :
 Viruses
 Bacteria
 Parasites
 Prions

76. 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

77. DEVELOPMENT OF IN VITRO BLOOD CELLS

78. LABORATORY DERIVED PLATELETS

79. 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