This document discusses blood coagulation and blood transfusions. It covers several key points: 1) Only 30% of countries have nationwide transfusion services, and 80% of the world's population only has access to 20% of safely collected and tested blood. 2) The main indications for blood transfusions are to increase oxygen-carrying capacity and intravascular volume when a patient is hemorrhaging. 3) There are several potential complications from blood transfusions like changes in oxygen transport, coagulopathy, allergic reactions, and hemolytic transfusion reactions. Proper testing and protocols are important to minimize risks.

1. Blood coagulation &
its component
therapy
Dr. Anup kumar Harichandan
PG, 2nd yr

2. • Eighty percent of the world's population has access
to only 20% of the world's “safe” blood, that is blood
that is properly collected and tested.
• Only 30% of the world's countries have a
nationwide transfusion service.
• The anesthesiologist should be an expert on the
implications and the complications associated with
blood transfusions and should be a leader of acute
transfusion medicine in the hospital setting as
approx. 70% of blood transfusions carried by them.

3. Indications for Transfusion
Allogeneic (Homologous) Blood
• Blood transfusions are given to increase oxygen-
carrying capacity and intravascular volume.
• Theoretically, increasing vascular volume is not an
indication for blood transfusions because volume
can be augmented with administration of fluids that
do not transmit infections (e.g., crystalloids or
some colloids).
• On the practical side, when a patient is
hemorrhaging, blood is given to increase oxygen-
carrying capacity and intravascular volume.

4. • The goals should be to restore intravascular
volume, cardiac output, and organ perfusion to
normal levels.
• But by using crystalloids and/or colloids to treat
hypovolemia, normovolemic dilutional anemia
will be created.
• Thus,Increasing oxygen-carrying capacity is the
only real indication for blood transfusions.

5. American College of Surgeons' Classes
of Acute Hemorrhage
Factors Class I Class II Class III Class IV
Blood loss (mL) 750 750-1500 1500-2000 2000 or more
Blood loss (%
blood volume)
15 15-30 30-40 40 or more
Pulse
(beats/min)
100 100 120 140 or higher
Blood pressure Normal Normal Decreased Decreased
Pulse pressure
(mm Hg)
Normal or
increased
Decreased Decreased Decreased
Capillary refill
test
Normal Positive Positive Positive
Respirations per
minute
14-20 20-30 30-40 35
Urine output
(mL/hr)
30 20-30 5-10 Negligible
Central nervous
system: mental
status
Slightly anxious Mildly anxious
Anxious,
confused
Confused,
lethargic
Fluid
replacement
Crystalloid Crystalloid
Crystalloid +
blood
Crystalloid +
blood

6. • The following indications were recommended in the 6th
edition of Anesthesia with the rule of thumb that
administration of 1 unit of packed RBCs will increase
hematocrit value by 3% to 5%:
1. Blood loss greater than 20% of blood volume when
more than 1000 mL
2. Hemoglobin level less than 8 g/dL
3. Hemoglobin level less than 10 g/dL with major disease
(e.g., emphysema, ischemic heart disease)
4. Hemoglobin level of less than 10 g/dL with autologous
blood
5. Hemoglobin level less than 12 g/dL and ventilator
dependent

7. Autologous Blood :
• Autologous blood is assumed to be much safer
than allogeneic blood, mainly because of the
decreased risk of infection.
• Because of a marked decrease in infectivity from
allogeneic blood the difference in safety
compared with autologous blood is much less.
• Not surprisingly, the proportion of autologous
blood collected has significantly decreased since
the peak in 1992.

8.  Complications associated with autologous blood
transfusions include the following:
• Anemia
• Preoperative myocardial ischemia from anemia
induced by preoperative donation
• Autologous units given to wrong patient (1 per 13,000
to 62,000)
• Need for more frequent blood transfusions
In fact, transfusion-related bacterial sepsis may be more frequent with
use of autologous blood because of the underlying medical
condition of the donor and less stringent donor selection. Also,
autologous blood must be tested the same as allogeneic blood.

9. Compatibility Testing
• The ABO-Rh type, crossmatch, and antibody screen
are frequently referred to as compatibility tests .
• These tests were designed to demonstrate harmful
antigen-antibody interactions in vitro so that harmful in-
vivo antigen-antibody interactions could be prevented.
• All donor &recipient blood must be tested for the correct
ABO and Rh type and screened for unexpected
antibodies.
• Proper selection of donor blood requires a test for
compatibility between recipient blood and donor blood;
this test is known as a crossmatch

10. ABO-Rh Typing
• Determination of the patient's correct blood type
is exceedingly important because the most
serious and tragic reactions are usually caused
by accidental transfusion of ABO-incompatible
blood.
• These reactions result from naturally occurring
antibodies (i.e., anti-A and anti-B), which
activate complement and lead to rapid
intravenous hemolysis.

11. • Anti-A or anti-B antibodies, or both, are formed
whenever the individual lacks either or both of
the A and B antigens.
• Antibodies are directed against those antigens
that are lacking in the individual's own cells.
ABO typing is performed by testing RBCs for the
A and B antigens and the serum for the A and B
antibodies before transfusion

12. Blood Group
Red Cells Tested With Serum Tested With
Anti-A Anti-B A Cells B Cells
A + - - +
B - + + -
AB + + - -
O - - + +
ABO Compatibility Testing

13. • Crossmatching:
• A crossmatch is essentially a trial transfusion
within a test tube in which donor RBCs are
mixed with recipient serum to detect a potential
for serious transfusion reaction.
• The crossmatch can be completed in 45 to 60
minutes and is carried out in three phrases:
I. immediate phase,
II. incubation phase,
III. antiglobulin phase.

14. • The immediate phase is conducted at
room temperature and is a check against
errors in ABO typing.
• It detects ABO incompatibilities and those
caused by naturally occurring antibodies in
the MN, P, and Lewis systems.
• This takes 1 to 5 minutes to complete.

15. • The incubation phase involves incubation at 37°C
in albumin or low-ionic strength salt solution.
• The addition of albumin and low-ionic-strength salt
solution aids in the detection of incomplete
antibodies or those antibodies that are able to attach
to a specific antigen (i.e., sensitization) but are
unable to cause agglutination in a saline suspension
of RBCs.
• This phase primarily detects antibodies in the Rh
system.
• The incubation period is 30 to 45 minutes in albumin
and of 10 to 20 minutes in low-ionic-strength salt

16. • The antiglobulin phase of the crossmatch, the
indirect antiglobulin test, involves the addition of
antiglobulin sera to the incubated test tubes.
• With this addition, antihuman antibodies present
in the sera become attached to the antibody
globulin on the RBCs, causing agglutination.
• This antiglobulin phase detects most incomplete
antibodies in the blood group systems, including
the Rh, Kell, Kidd, and Duffy blood group
systems.

17. Donor Recipient
O O, A, B, AB
A A, AB
B B, AB
AB AB
Donor Blood Groups that Patients Can Receive
Although all three phases of the crossmatch are important,
the first two stages are of prime importance in preventing
serious hemolytic transfusion reactions

18. • Antibody Screening :
• The antibody screen is also carried out in three
phases and is similar in length to the
crossmatch.
• The screen, however, is a trial transfusion
between the recipient's serum and commercially
supplied RBCs that are specifically selected to
contain optimal numbers of RBC antigens or
those antigens that will react with antibodies that
are commonly implicated in hemolytic

19. • Emergency Transfusion:
• Specific Recommended Protocol
The following steps are recommended for patients who are
hypovolemic and require blood transfusion:
1. Infuse crystalloids or colloids.
2. Draw a blood sample for typing and crossmatching.
3. If crossmatched blood is not ready to give, use type-
specific or type O Rh-negative cells or type O Rh-
positive cells for males or postmenopausal females
without a history of transfusions; type-specific, partially
crossmatched blood; or type-specific, crossmatched
blood.

20. Storage of Blood
• Citrate phosphate dextrose adenine (CPDA)
is an anticoagulant preservative in which blood
is stored at 1°C to 6°C.
• Citrate is an anticoagulant, phosphate serves as
a buffer, and dextrose is a red cell energy
source, adenine allows RBCs to resynthesize
adenosine triphosphate (ATP), which extends
the storage time from 21 to 35 days.
• The shelf life can be extended to 42 days when
AS-1 (Adsol), AS-3 (Nutricel), or AS-5 (Optisol)
is used

21. Complications
Changes in oxygen transport
• RBCs are transfused primarily to increase
transport of oxygen to tissues.
• The respiratory function of red cells may be
impaired during preservation, making it difficult for
them to release oxygen to the tissues immediately
after transfusion due to increase in 2,3 DPG in
RBC.

23. Parameter
Days of Storage
0 35 (Whole Blood) 35 (Packed Cells)
pH 7.55 6.73 6.71
Plasma hemoglobin
(mg/dL)
0.50 46.00 246.00
Plasma potassium
(mEq/L)
4.20 17.20 76.00
Plasma sodium
(mEq/L)
169.0 153.00 122.00
Blood dextrose
(mg/dL)
440.0 282.00 84.00
2,3-
Diphosphoglycerate
(µM/mL)
13.20 1.00 1.00
Percent survival * — 79.00 71.00
Properties of Whole Blood and Packed Red Cell Concentrates Stored in CPDA-1

24. Complications
i. Coagulopathy & Dilutional thrombocytopenia
ii. Low level of factor V & factor VIII
iii. DIC like syndrome
iv. Citrate intoxication
v. Acid base abnormality
vi. Electrolyte imbalance(hyperkalemia,hypocalcemia)
vii. Hypothermia
viii. Transfusion associated Graft Vs Host disease
ix. Transfusion related Acute lung injury(TRALI)
x. Adverse ocular reaction
xi. Transfusion related Immunomodulation

25. • Massive Transfusion :
• Massive transfusion is defined, in adults, as
replacement of >1 blood volume in 24 hours or
>50% of blood volume in 4 hours (adult blood
volume is approximately 70 mL/kg).
• In children, it is defined as transfusion of >40
mL/kg (blood volume in children over 1 month
old is approximately 80 mL/kg).
• Massive transfusion occurs in settings such as
severe trauma, ruptured aortic aneurysm,
surgery and obstetrics complications etc.

26. Parameters Values to aim for
Temperature >35 °C
Acid-base status ph >7.2, base excess <–6, lactate <4 mmol/L
Ionised calcium
(Ca)
>1.1 mmol/L
Haemoglobin (Hb)
This should not be used alone as transfusion trigger;
and, should be interpreted in context with
haemodynamic status, organ & tissue perfusion.
Platelet (Plt) ≥ 50,000 /cc
PT/APTT ≤ 1.5x of normal
Fibrinogen ≥ 1.0 g/L
Parameters in Massive Transfusion Investigation & Monitoring

27. Transfusion Reactions
• Hemolytic Transfusion Reaction :
Sign & Symptoms :
• The classic signs and symptoms of a hemolytic
transfusion reaction—chills, fever, chest and flank
pain, and nausea—are masked by anesthesia.
• Under general anesthesia, the only signs may be
hemoglobinuria, bleeding diathesis, or hypotension.
The presenting sign is usually hemoglobinuria.
• Consequeces : ARF,DIC,Hypovolemic shock

28. Factors that affect degree of reaction
•volume of transfused blood
•number of antigenic sites on the red cell
membrane
•activity of the reticuloendothelial system.
•The properties of the antibody, including
concentration and ability to activate complement

29. • Treatment :
1. STOP THE TRANSFUSION.
2. Maintain the urine output at a minimum of 75 to 100 mL/hr by
the following methods:
a. Generously administer fluids intravenously and possibly
mannitol (12.5 to 50 g, given over 5 to 15 minutes).
b. If intravenously administered fluids and mannitol are
ineffective, administer furosemide (20 to 40 mg) intravenously.
3. Alkalinize the urine; because bicarbonate is preferentially
excreted in the urine, only 40 to 70 mEq of sodium bicarbonate per
70 kg of body weight is usually required to raise the urine pH to 8,
whereupon repeat urine pH determinations indicate the need for
additional bicarbonate.

30. 4. Assay urine and plasma hemoglobin
concentrations.
5. Determine platelet count, partial
thromboplastin time, and serum fibrinogen
level.
6. Return unused blood to blood bank for
repeat crossmatch.
7. Send patient's blood and urine sample to
blood bank for examination.
8. Prevent hypotension to ensure adequate
renal blood flow.

31. • Delayed Hemolytic Transfusion
Reaction(Immune Extravascular Reaction)
• In many cases of hemolytic transfusion reaction, the
transfused donor cells may survive well initially, but
after a variable delay (2 to 21 days) they are
hemolyzed.
• This type of reaction occurs mainly in recipients
sensitized to RBC antigens by previous blood
transfusions or pregnancy. As a result, this type of
delayed reaction is more common in females who have
a known disposition of alloimmunization.

32. • These reactions are those in which the level of antibody at
the time of transfusion is too low to be detected or too low
to cause RBC destruction. RBC destruction occurs only
when the level of antibody is increased after a secondary
stimulus (i.e., anamnestic response).
• These delayed reactions are often manifested only by a
decrease in the post-transfusion hematocrit value.
• Jaundice and hemoglobinuria can occur in these patients
and can cause some impairment in renal function but only
rarely do they lead to death. Unlike immediate reactions,
antibodies most commonly involved in delayed hemolytic
reactions are those in the Rh and Kidd systems rather
than the ABO system

33. • Nonhemolytic Transfusion Reactions :
• The most common adverse reactions to blood
transfusions are the less serious febrile reactions.
• The symptoms consist of chills, fever, headache,
myalgia, nausea, and nonproductive cough occurring
shortly after blood transfusion caused by pyrogenic
cytokines and intracellular contents released by donor
leukocytes.
• Use of leukoreduced blood will reduce the incidence of
febrile reactions

34. • Because febrile reactions obviously involve fever,
they can be easily confused with a hemolytic
transfusion reaction.
• A direct antiglobulin test readily differentiates a
hemolytic reaction from a febrile reaction because
this test rules out the attachment of an RBC
antibody to transfused donor RBCs.

35. • Allergic reactions can be minor, anaphylactoid,
or anaphylactic.
• Most allergic transfusion reactions are minor and
are thought to be caused by the presence of
foreign protein in the transfused blood.
• The most common symptom is urticaria
associated with itching.
• When these reactions are not a serious hemolytic
reaction,transfusion not need to be discontinued.
Antihistamines are used to relieve symptoms.

36. • Anaphylactoid reactions (Pseudoanaphylaxis) is
similar to anaphylaxis clinically but are not mediated
by IgE,rather caused by direct mast cell degranulation.
• Anaphylaxis occurs in which the patient has
dyspnea,hypotension, laryngeal edema, chest pain,
and shock.
• These are anaphylactic reactions caused by the
transfusion of IgA to patients who are IgA deficient
and have formed anti-IgA.

37. • This type of reaction does not involve red cell
destruction and it occurs very rapidly, usually
after the transfusion of only a few milliliters of
blood or plasma.
• The patients who experience these anaphylactic
reactions can be given transfusions with washed
RBCs from which all traces of donor IgA have
been removed or with blood lacking the IgA
protein.
• Treatment : im epinephrine (1:1000),steroids

38. Infectivity Of Blood
Risk of transfusion transmitted Infection
•Human immunodeficiency virus-1
•Human T-lymphotropic virus
•Cytomegalovirus (CMV)
•Hepatitis C virus (HCV)
•Hepatitis B virus (HBV)
•West Nile virus (WNV)
•Others: Y. enterocolitica,malaria,syphilis,chaga’s
disease,Parvovirus B19,SARS
•Rare :Cruetzfeldt Jakob’s disease,Herpes,Infectious
mononucleosis,toxoplasmosis,trypanosomiasis,leismaniasis,brucellosis
,typhus,filaria,measles,salmonellosis,Colorado tick fever.

39. Infectious disease testing for blood
transfusion in India
•HIV
•HBV
•HCV
•Malaria
•Syphilis

40. Blood Coagulation
• Hemostasis comprises cellular and biochemical
processes that limit blood loss resulting from injury,
maintain intravascular blood fluidity, and promote
revascularization of thrombosed vessels after injury.
• Normal physiologic hemostasis necessitates a delicate
balance between procoagulant pathways and
anticoagulnt mechanisms inhibiting thrombus formation
beyond the injury site.
• Vascular endothelium,platelets,& plasma
coagulation proteins play important roles in
hemostasis.
• Failure to maintain balance commonly leads to
excessive bleeding or pathologic thrombus formation.

41. • Primary Hemostasis :In this Vascular
endothelial injury, mechanical or biochemical
alteration, leads to platelet deposition at the
injury site,which adequate in minor injury.
• Secondary Hemostasis : mediated by
activation of plasma clotting factors for the
control of more significant bleeding which
necessitates stable clot formation incorporating
cross-linked fibrin.

42. Role Of Endothelium :
•Under normal conditions, vascular endothelium provides a
nonthrombogenic surface to promote blood fluidity. Healthy
endothelial cells possess antiplatelet, anticoagulant, and
profibrinolytic effects to inhibit clot formation.
• Negatively charged vascular endothelium repels platelets
and produces prostacyclin (PGI2) and nitric oxide (NO),
which are potent platelet inhibitors.
•Adenosine diphosphatase (ADPase) synthesized by
vascular endothelial cells degrades adenosine diphosphate
(ADP), another potent platelet activator.

43. • Vascular endothelium further expresses several
inhibitors of plasma-mediated hemostasis,
including thrombomodulin (an indirect thrombin
inhibitor), heparin-like glycosaminoglycans,
and tissue factor pathway inhibitor
(TFPI),tissue plasminogen activator (t-PA),
which is responsible for activating fibrinolysis—a
primary counterregulatory mechanism limiting
clot propagation.

44. • Damage to vascular endothelial cells exposes the
underlying extracellular matrix (ECM) including collagen,
von Willebrand factor (vWF),& other platelet-adhesive
glycoproteins.
• Platelets bind to and are activated by exposure to ECM
components which activates plasma-mediated
coagulation pathways to generate thrombin and,
ultimately, fibrin clot.
• Certain cytokines (i.e., interleukin-1, tumor necrosis
factor, and γ-interferon) and hormones (i.e.,
desmopressin acetate or endotoxin) induce
prothrombotic changes in vascular endothelial cells.

45. Role of Platelets :
•Under normal circumstances, platelets do not bind
vascular endothelium; however, when injury exposes ECM,
platelets undergo a series of biochemical and physical
alterations characterized by three major phases
Adhesion :
vWF proves particularly important as a bridging molecule
between ECM and platelet glycoprotein Ib receptor
complexes. Absence of either vWF (von Willebrand
disease) or glycoprotein Ib receptors (Bernard-Soulier
syndrome) results in a clinically significant bleeding
disorder.

46.  Activation :
• During the activation phase, platelets release granular
contents, resulting in recruitment and activation of
additional platelets as well as propagation of plasma-
mediated coagulation.
• Platelets contain two specific types of storage granules:
alpha granules and dense bodies.
• Alpha granules contain numerous proteins essential to
hemostasis like fibrinogen, coagulation factors V and
VIII, vWF, platelet-derived growth factor, and others.
• Dense bodies contain ADP and ATP as well as calcium,
serotonin, histamine, and epinephrine.

47.  Aggregation :
• During the final phase of platelet aggregation,
activators released during the activation phase
serve to recruit additional platelets to the site of
injury.
• Newly active glycoprotein IIb/IIIa receptors on the
platelet surface bind fibrinogen to provide for cross-
linking with adjacent platelets.
• The importance of these receptors is reflected by
the bleeding disorder associated with their
hereditary deficiency: Glanzmann thrombasthenia.

49. Role Of Plasma :
Plasma-mediated hemostasis might best be
summarized as an amplification system to
accelerate thrombin generation from an inactive
precursor (i.e., prothrombin).
Extrinsic Pathway of Coagulation
Intrinsic Pathway of Coagulation
Common Pathway of Coagulation

53. • Intrinsic Anticoagulant Mechanisms:
• Once activated, regulation of hemostasis proves
essential to limit clot propagation beyond the
injury site.
• Four major counterregulatory pathways that
appear particularly crucial for downregulating
hemostasis: fibrinolysis, TFPI, the protein C
system, and serine protease inhibitors.

54. Fibrinolysis system

55. Tissue Factor Plasminogen Inhibtor system
inhibits the tissue factor/factor VIIa complex and
thereby the extrinsic coagulation pathway.
•TFPI and factor Xa form phospholipid membrane-
bound complexes that incorporate and inhibit tissue
factor/factor VIIa complexes.
•Most TFPI is bound to vascular endothelium but
released into circulation by heparin administration.

56. The protein C system
•It is important in downregulating hemostasis
because it inhibits thrombin as well as the essential
cofactors Va and VIIIa.
•Thrombin initiates this inhibitory pathway by binding
a membrane-associated protein, thrombomodulin,
to activate protein C.Protein C, complexed with the
cofactor protein S degrades both cofactors Va and
VIIIa.
• Thrombin, once bound to thrombomodulin, is
inactivated and removed from circulation.

57. Serine Protease inhibitors system:
It includes antithrombin (AT) and heparin
cofactor II.
• Antithrombin binds to and inhibits thrombin as
well as factors IXa, Xa, XIa, and XIIa.
•Heparin cofactor II inhibits thrombin alone.
•Heparin, a catalyst accelerator, binds
antithrombin to promote inhibition of targeted
enzymes.

58. Disorders of Hemostasis :
•Inherited- Hemophilia A,Hemophilia B,Von
willebrand’s disease,Bernand Soulier’s
disease,Glanzman’s thrombosthenia
•Acquired-Drugs like
warfarin,heparin,fibrinolytic agents &
coexisting medical illness like liver
disease,renal disease,DIC

59. • Hypercoagulable States and Risk for Perioperative Thrombosis
• High Risk
• Heparin-induced thrombocytopenia (HIT)
• Antithrombin deficiency
• Protein C deficiency
• Protein S deficiency
• Antiphospholipid antibody syndrome
• Moderate Risk
• Factor V Leiden genetic polymorphism
• Prothrombin G20210A genetic polymorphism
• Hyperhomocysteinemia
• Dysfibrinogenemia
• Postoperative prothrombotic state
• Malignancy
• Immobilization

60. • Monitoring Coagulation :
Activated partial Thromboplastin Time:
• The aPTT assesses integrity of the intrinsic and common
pathways of plasma-mediated hemostasis.
• It measures the time required in seconds for clot formation to
occur after mixing a sample of patient plasma with
phospholipid, calcium, and an activator of the intrinsic pathway
of coagulation (i.e., celite, kaolin, silica, or ellagic acid).
• Prolongation of the aPTT is evaluated further with mixing
studies to determine whether delayed clot formation is
attributable to a coagulation factor deficiency or an inhibitor
(i.e., heparin, antiphospholipid antibody, fibrin split products).

61. •The mixing study performed by mixing the patient's plasma
sample with “normal” donor plasma. In case of a coagulation
factor deficiency, time to clot formation will correct and
sequential assays for specific coagulation factor
concentrations allow for identification of the deficiency.
•A common means of confirming heparin prolongation of the
aPTT is to perform a thrombin clotting time (TCT). In this
test, the patient's citrate-containing plasma sample is mixed
with thrombin and time to clot formation is measured in sec.
•The most common mechanism underlying prolongation of the
TCT is presence of heparin or a direct thrombin inhibitor
anticoagulant.

62. • Prothrombin Time:
• The PT assesses integrity of the extrinsic and common
pathways of plasma-mediated hemostasis. It measures time
required in seconds for clot formation to occur after mixing a
sample of patient plasma with tissue factor (thromboplastin)
and calcium.
• Given the importance of monitoring PT results for patients on
long-term warfarin therapy, the INR was introduced as a means
of normalizing PT results among different laboratories.
• INR = (patient PT/standard PT) in which the “standard PT”
represents the geometric mean of multiple normal samples
from the testing laboratory.

63. • Platelet Count & Bleeding Time :
• The platelet count remains a standard
component in screening for coagulation
abnormalities.
• Normal value-1.5 lakh-3 lakh/cc
• Bleeding Time, as a test of platelet dysfunction
• Normal value-1-5 min
• Clotting Time :
• It is a indicator of coagulation cascade function
• Normal Value-3- 8 min

64. Blood Component Therapy
• A major advance in the field of blood
banking has been the development of
blood component therapy
• The basic philosophy is based on the
concept that patients are best treated by
administration of the specific fraction of
blood that they lack

65. Scheme for separation of whole blood for component therapy.

66. • Packed Red Blood Cells :
• Whole blood provides oxygen-carrying capacity
and intravascular blood volume expansion.
• PRBC increases oxygen carrying capacity
without increasing intravascular blood volume.
• Other than severe hemorrhage, most indications
for red blood cells can be effectively treated with
packed RBCs, retaining the plasma and the
components thereof for other patients .

67. Value Whole Blood Packed Red Blood Cells
Volume (mL) 517 300
Erythrocyte mass (mL) 200 200
Hematocrit (%) 40 70
Albumin (g) 12.5 4
Globulin (g) 6.25 2
Total protein (g) 48.8 36
Plasma sodium (mEq) 45 15
Plasma potassium (mEq) 15 4
Plasma acid (citric-lactic) 80 25 (mEq)
Donor-to-recipient ratio 1 unit per patient 1 unit per 4-6 patients
Comparison of Whole Blood and Packed Red Blood Cells

68. • The administration of packed RBCs is facilitated by
reconstituting them with a crystalloid or colloid;
• If the solution contains calcium, clotting occurs.
• Therefore Lactated Ringer's solution is not
recommended for use as a diluent for packed RBCs.
• If the diluent is hypotonic with respect to plasma the
RBCs will swell and eventually lyse.
• Solutions recommended for reconstituted packed
erythrocytes are 5% dextrose in 0.4% saline, 5%
dextrose in 0.9% saline, 0.9% saline, and Normosol-R
with a pH of 7.4.

69. • Platelet Concentrates :
• Platelet concentrates are prepared by differential
centrifugation from freshly drawn units of blood
or from donors who specifically donate large
amounts of platelets by plateletpheresis.
• If platelets are stored at room temperature, they
are satisfactory to use within 7 days of
collection.
• 1 Unit-60 ml random donor platelet inc
platelets by 5K to 10K/cc where as single donor
platelets inc by 30 K-60 K/cc.

70. • PC are primarily effective at room temperature (20°C to
24°C), which enhances bacterial growth.
• Bacterial contamination, mainly from platelet
concentrates, is the third leading cause of transfusion-
related deaths.
• For any patient who develops a fever within 6 hours after
receiving platelets, sepsis from platelets should be
considered.
• Hence,platelet concentrates are routinely tested for
bacteria and are the only blood product that is stored
at room temperature.

71. • Indications for the use of platelets are somewhat difficult to
define.
• In the July 1989 FDA Drug Bulletin it was stated that platelets
should not be given to patients with
1. Immune thrombocytopenic purpura (unless there is life-
threatening bleeding),
2. Prophylactically with massive blood transfusion.
3. Prophylactically after cardiopulmonary bypass.

72. • The American Society of Anesthesiologists (ASA)
Task Force provided the following recommendations:
1. Prophylactic platelet transfusion is ineffective and
rarely indicated when thrombocytopenia is due to
increased platelet destruction (e.g., idiopathic
thrombocytic purpura).
2. Prophylactic platelet transfusion is rarely indicated in
surgical patients with thrombocytopenia due to
decreased platelet production when the platelet count is
greater than 1 lakh/cc and is usually indicated when the
platelet count is less than 50,000/cc. The determination
of whether patients with intermediate platelet counts
(50,000 to 1 lakh/cc) require therapy should be based on
the patient's risk of bleeding.

73. 3. Surgical and obstetric patients with microvascular
bleeding usually require platelet transfusion if the
platelet count is less than 50,000/cc and rarely require
therapy if it is greater than 1lakh/cc. With intermediate
platelet counts (50,000 to 1 lakh/cc), the determination
should be based on the patient's risk for more
significant bleeding.
4. Vaginal deliveries or operative procedures ordinarily
associated with insignificant blood loss may be
undertaken in patients with platelet counts less than
50,000/cc.
5. Platelet transfusion may be indicated despite an
apparently adequate platelet count if there is known
platelet dysfunction and microvascular bleeding.

74. • Fresh Frozen Plasma :
• It contains all the plasma proteins, particularly
factors V and VIII, which gradually decline during
the storage of blood.
• The major risk is transmission of infectious
diseases, such as hepatitis B, hepatitis C, and
AIDS.
• Other risks include sensitization to foreign
proteins.
• Shelf life :1 yr

75. • The only indications for FFP administration the ASA
Task Force agreed on were the following:
1. Replacement of isolated factor deficiencies
2. Reversal of warfarin effect
3. In cases of antithrombin III deficiency
4. Treatment of immunodeficiencies
5. Treatment of thrombotic thrombocytopenia purpura
6. Massive blood transfusion (rarely and only when
factors V and VIII are less than 25% of normal)
7. Requirements for indications 1 and 6 are
prothrombin and partial thromboplastin times at least 1.5
times longer than normal.

76. • Cryoprecipitate :
Cryoprecipitate contains factor VIII:C (i.e.,
procoagulant activity), factor VIII:vWF (i.e.,
von Willebrand factor), fibrinogen, factor
XIII, and fibronectin, which is a
glycoprotein that may play a role in
reticuloendothelial clearance of foreign
particles and bacteria from the blood.

77. • Cryoprecipitate should be administered through
a filter and as rapidly as possible.
• The rate of administration should be at least
200 mL/hr, and infusion should be completed
within 6 hours of thawing.
• Indication : Haemophilia A ,Von Willbrand’s
disease,Fibrinogen deficiency,Factor XIII
deficiency.

78. • Prothrombin Complex :
Factor IX can be recovered from plasma or plasma
fractions by absorption with ion exchanges or
inorganic chemicals. These products are all
complexes of factors II, VII, IX, and X.
• The main indication for these products is treatment
of factor IX deficiency, or hemophilia B (i.e.,
Christmas disease).
• Factor IX or prothrombin complex has also been
used for the treatment of acquired
hypoprothrombinemic bleeding disorders, principally
sodium warfarin overdose

79. • Single donor plasma :
• Single-donor plasma is plasma that has been
removed from stored blood without any effort
being made to preserve coagulation factors.
• Single-donor plasma is very effective as a
volume expander.
• It obviously cannot be used to correct
deficiencies in coagulation factors.

80. Synthetic Oxygen-Carrying
Substances
• Other Than Human Red Blood Cells (Blood)
• Two concepts of synthetic blood have been attempted. The
first approach uses linear binding kinetics, unlike the nonlinear
binding of hemoglobin.
• The most notable is the perfluorochemical emulsion called
Fluosol-DA. However, it had little use because it carries
oxygen (i.e., a small amount) only when the PaO2 is more than
300 mm Hg.
• A newer perfluoro compound, perfluorooctyl bromide,
carries 3 to 4 times more oxygen and has a longer half-life and
presumably fewer problems than are associated with Fluosol-
DA. Other related products are Oxygent (Alliance), Oxycyte
(synthetic blood), several other perfluorocarbon emulsions.

81. • The remaining synthetic blood or oxygen therapeutics
are labeled as hemoglobin-based oxygen carriers
(HBOCs).
• These products modify the hemoglobin molecule from
humans, animals, or recombinant technology.
• The most serious are kidney toxicity due to stroma,
an increase in affinity for oxygen (i.e., left shift in the
oxygen dissociation curve), and arteriolar
vasoconstriction from nitric oxide scavenged by the
infused hemoglobin.

82. • Genetic engineering has provided hope for blood
products. Initially, recombinant erythropoietin was
developed for treatment of anemias and facilitation of
autologous blood donation.
• In 1992, a human recombinant hemoglobin (rHb 1.1)
was designed as a blood substitute,with the use of
genetic engineering techniques, it was made from
Escherichia coli. It functions as normal hemoglobin
in terms of oxygen-carrying capacity, but it does not
require crossmatching, nor does it transmit disease or
become rapidly outdated.

83. Parameter Synthetic Allogeneic
Oxygen delivery Rapid and consistent Dependent on 2,3-DPG
Risk of disease
transmission
None Very high
Storage
Room temperature
Stable efficacy
Refrigeration
Loss of efficacy
Shelf life 1-3 years 42 days
Preparation Ready to use Crossmatch
Compatibility Universal Type specific
Duration of action 1-3 days 60-90 days
Comparison of Synthetic Blood in General with Allogeneic Blood

84. • References:
• Miller’s textbook of anaesthesiology(7th
edn)
• Guyton’s text book of physiology

85. Thank you...