These slides were presented at Department of Surgery, Kathmandu Model Hospital

1. Blood products and BLOOD TRANSFUSION
Dr Kiran Pandey
MS GS Resident (NAMS)
Kathmandu Model Hospital

3. 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

4. INTRODUCTION
 Blood is a connective tissue in liquid form .
 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

5. FUNCTIONS OF BLOOD

6. 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

7. HISTORY OF BLOOD TRANSFUSION
As early as the 17th century
 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.

8.  1907
Blood typing and cross matching between donors and patients.
 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.

9. 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

10. LANDSTEINER'S LAW
Based on his observations Karl Landsteiner in 1900 framed a
law called Landsteiner's Law
It has 2 major components ,
 If an agglutinogen is present in the RBCs of an individual , the
correspondingagglutinin 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

12. RHESUS BLOOD GROUP
 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.
 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
 In Rh negative individuals , anti – D antibodies are not
naturally present in the plasma

13. OTHER BLOOD GROUPS
 There are 34 other known blood groups systems
with more than 300 known variants .
 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.

14. 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

15. Plasma compatibility
RBC compatibility

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

17. 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

18. 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

19. 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.

20.  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%

21. 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

23. 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

24. 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

25. 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

26. APHERESIS
Apheresis refers to the process of separating the cellular and soluble
components of blood using a machine.
Donor 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 and
Selective collection of plasma is called plasmapheresis
oHere the anticoagulants such as citrate and heparin is used

27. BLOOD PRODUCTS

28. 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

29. 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

30. 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

31. 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

32. 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

33. 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

34. 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
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

36. 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

37. 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
for 10 mins

38. 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.

39.  Perioperative blood loss and anaemia is best dealt
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

40. BLOOD SALVAGE

42. COMPLICATIONS OF BLOOD TRANSFUSION
 A carefully prepared and supervised blood transfusionis
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 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

44. 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

45. 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
 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

46. 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

47. 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

48. DIFFERENCE BETWEEN TRALI AND TACO

49. 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 treatmeAnt 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

50. HEMOLYTIC REACTIONS
 Transfusions leading to RBC hemolysis can be among
the most devastating and feared complications of blood
product administration
 With 1 hour
 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

51. INTRAVASCULAR HEMOLYSIS
 Pathophysiology :
 complement cascade are fixed and activated
 The 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)

53.  Complement generation and RBC release of
hemoglobin can induce acute kidney injury and renal
failure
 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

54. EXTRAVASCULAR HAEMOLYSIS
 Pathophysiology :
In contrast to intravascular hemolysis, is generally associated with
a more subdued, slower RBC clearance
 RBC clearance occurs as incompatible cells are coated by IgG
class antibodies, which are 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

55. TREATMENT OF HEMOLYTIC DISEASES
 Approaches
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) of fully compatible blood 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

56. ANAPHYLAXIS
 Within minutes to 2-3 hours.
 severe and extreme reactions in the spectrum of allergic
reactions
 Pathophysiology :
 Mostly 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

57. Anaphylactic reactions
characterized by rapid onset of
 respiratory distress,
 laryngeal edema,
 hypotension
 gastrointestinal symptoms
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

58. 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.

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

61. 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

62. 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

63. 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

64. 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

65. 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

66. 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

67. Complication of massive blood
Transfusion
• Coagulopathy
• Hypocalcema
• Hyperkalemia and Hypokalemia
• Hypothermia

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

71. 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

72. DEVELOPMENT OF IN VITRO BLOOD CELLS

73. LABORATORY DERIVED PLATELETS

74. REFERENCES
Baily and Love
 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