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Blood Component Therapy

Speaker : Dr. Saikat Prasad Datta

Chairperson : Dr. Avas Chandra Roy
The Beginning of Component
In 1940 Edwin Cohn, a professor of biological chemistry at
Harvard Medical School, develops cold ethanol fractionation,
the process of breaking down plasma into components and
products. Albumin, a protein with powerful osmotic properties,
plus gamma globulin and fibrinogen are isolated and become
available for clinical use.
Blood Components

Other Components :-
1. Granulocytes
2. Coagulation Factor Concentrates
3. Immunoglobulins
Whole Blood
Whole blood collected from blood donor in CPDA-
1 Solution
399 ml ( 350 blood + 49 ml CPDA-1) and 513 ml
( 450 blood + 63 ml CPDA-1)
Indications :
Red cell replacement in acute blood loss with
Exchange transfusion
Patients needing red cell transfusions where red cell
concentrates or suspensions are not available
Hematocrit of 65% to 80% and a usual volume
between 225 mL and 350 mL.
Each unit of RBCs or Whole Blood contains enough
hemoglobin to increase the hemoglobin
concentration in an average-sized adult by
approximately 1 g/dL (increase hematocrit by
Iron overload is a complication of chronic RBC
transfusion therapy. Each transfusion contributes
approximately 250 mg of iron
Ref : Circular of Information for the Use of Human Blood and Blood - AABB
Physiology of PRBC Transfusion
DO=cardiac output CaO

Physiological Adaptation in Progressive (isovolumic) anaemia

-reduction of blood viscosity, which favours venous return to the heart and
facilitates ejection of stroke volume
-increases sympathetic stimulation of the heart
which contributes to the increase of cardiac output
-oxygen extraction also increases

VO2 remains constant

The limits of compensation

At a critical haemoglobin concentrationthe point at which compensatory
mechanisms for anaemia have been maximised and further reduction in haemoglobin
would result in compromised cellular metabolism.
In healthy humans, the critical haemoglobin is unknown but certainly below 5g/dL
Question 1

In hospitalized, hemodynamically stable patients, at what hemoglobin concentration

should a decision to transfuse RBCs be considered?


The AABB recommends adhering to a restrictive transfusion strategy. In adult and

pediatric intensive care unit patients, transfusion should be considered at hemoglobin
concentrations of 7 g/dL or less. In postoperative surgical patients, transfusion should be
considered at a hemoglobin concentration of 8 g/dL or less or for symptoms (chest pain,
orthostatic hypotension or tachycardia unresponsive to fluid resuscitation, or congestive
heart failure).

Quality of evidence: high; strength of recommendation: strong.

Question 2

In hospitalized, hemodynamically stable patients with preexisting cardiovascular

disease, at what hemoglobin concentration should a decision to transfuse RBCs be


The AABB suggests adhering to a restrictive transfusion strategy. Transfusion should be

considered at a hemoglobin concentration of 8 g/dL or less or for symptoms (chest pain,
orthostatic hypotension or tachycardia unresponsive to fluid resuscitation, or congestive
heart failure).

However, there was some uncertainty about the risk for perioperative myocardial infarction associated with a restrictive transfusion
strategy. There was moderate heterogeneity between the results of the 2 major trials, and they were not large enough to precisely define
the risks and benefits of transfusion in this setting.
Question 3

In hospitalized, hemodynamically stable patients with the acute coronary syndrome, at

what hemoglobin concentration should an RBC transfusion be considered?


The AABB cannot recommend for or against a liberal or restrictive RBC transfusion
threshold. Further research is needed to determine the optimal threshold.

Quality of evidence: very low; strength of recommendation: uncertain.

Question 4

Question 4 In hospitalized, hemodynamically stable patients, should transfusion be

guided by symptoms rather than hemoglobin concentration?


The AABB suggests that transfusion decisions be influenced by symptoms as well as

hemoglobin concentration.

Quality of evidence: low; strength of recommendation: weak.

Indication for PRBC Transfusion
The Transfusion Trigger : The threshold for transfusion of red
blood cells should be a hemoglobin level of 7 g per dL (70
g per L) in adults and most children.

Major exceptions to the use of a threshold of 7 to 8 g/dL

(where evidence is insufficient to guide therapy)
Symptomatic patients may be transfused at higher hemoglobin
levels to treat symptoms.
Patients with acute coronary syndrome
Threshold-based transfusion is not appropriate for patients
requiring massive transfusion, such as in the setting of trauma,
because it requires waiting for hemoglobin levels to be reported
Chronic transfusion-dependent anemia.

Ref : Carless PA, Henry DA, Carson JL, Hebert PP, McClelland B, Ker K. Transfusion thresholds and other strategies for guiding allogeneic red blood cell
transfusion. Cochrane Database Syst Rev. 2010;(10):CD002042
Transfusion in Thalassemia
Thalassemia major hypertransfusion strategy is suggested
Hypertransfusion regimen is designed to
maintain a relatively stable hemoglobin level
partially suppress ineffective erythropoiesis.

Pretransfusion hemoglobin level in the range of 9.5 to 10.5 g/dL

Generally avoid giving more than 10 mL per kg of packed RBCs in a single
day; this is a dose that should yield a post-transfusion hemoglobin increase
of about 3 to 3.5 g/dL
The post-transfusion hemoglobin should be approximately 12 to 13 and no
higher than 15 g/dL

Thalassemia intermedia Transfusions are given as needed; often, this

is during periods of erythropoietic stress such as acute infectious illnesses,
periods of rapid growth, surgery, or pregnancy.
FRESH FROZEN PLASMA is prepared from a whole blood
(within 6 hours after collection)or apheresis collection and
frozen at 18 C or colder.
On average, units contain 200 to 250 mL, but apheresis-
derived units may contain as much as 400 to 600 mL.
Fresh frozen plasma (FFP) contains plasma proteins including
all coagulation factors(AT LEAST 70% of the labile
coagulation Factors V and VIII)
Storage And shelf life : At 30C or colder for up to 1 year
FFP should be infused immediately after thawing or stored
at 1 to 6C. Labile coagulation factors rapidly degrade; use
within 6 hours of thawing .
Indications FFP is indicated in the following conditions:
Management of preoperative or bleeding patients who require
replacement of multiple plasma coagulation factors (eg, liver disease,
Patients undergoing massive transfusion who have clinically significant
coagulation deficiencies.
Patients taking warfarin who are bleeding or need to undergo an
invasive procedure before vitamin K could reverse the warfarin effect or
who need only transient reversal of warfarin effect.
Transfusion or plasma exchange in patients with thrombotic
thrombocytopenic purpura (TTP).
Management of patients with selected coagulation factor deficiencies,
congenital or acquired, for which no specific coagulation concentrates
are available.
Management of patients with rare specific plasma protein deficiencies,
such as C1 inhibitor, when recombinant products are unavailable.
One unit of Platelets derived from a whole blood collection
usually contains >5.5 1010 platelets suspended in 40 to
70 mL of plasma. Platelets may be provided either singly or
as a pool.
Platelet concentrate derived from blood donor using an
apheresis machine and disposable kit is called single donor
apheresis platelets (SDAP). Its volume is 200-300ml as
opposed to 50 to 90 ml, and platelet content is 6 to 8 times
the content in RDP.
Storage : 3 to 5 days at 20C to 24C (with agitation).

Do not store at 2C to 6C in Refrigerators as it makes them non-functional

Platelet (Contd.)
Thrombocytopenia is unlikely to be the cause of bleeding in
patients with platelet counts of at least 50,000/L. Higher
transfusion thresholds may be appropriate for patients with
platelet dysfunction.
For the clinically stable patient with an intact vascular system
and normal platelet function, prophylactic platelet
transfusions may be appropriate at <5000 to 10,000/L.
Prophylactic platelet transfusion may not be of therapeutic
benefit when thrombocytopenia is related to destruction of
circulating platelets secondary to autoimmune disorders [eg,
immune thrombocytopenic purpura (ITP)]; however,
transfusion may be indicated for active bleeding in these
Platelet : Dose
The number of platelet units to be administered
depends on the clinical situation of each patient. One
unit of Platelets would be expected to increase the
platelet count of a 70-kg adult by 5000 to 10,000/L
and increase the count of an 18-kg child by 20,000/L.
The therapeutic adult dose is 1 unit of Apheresis
Platelets or 4 to 6 units of whole blood-derived
platelets, either of which usually contain 3.0 1011
This dose may need to be repeated in 1 to 3 days
because of the short lifespan of transfused platelets (3
to 4 days)
Platelet transfusion refractoriness

Platelet Alloimmunization
Nonimmune events may also contribute to reduced platelet survival.
intravascular devices

In immune refractory states secondary to serologic incompatibility,

there is poor recovery in the early postinfusion interval. In nonimmune
mechanisms) platelet recovery within 1 hour of infusion may be
adequate while longer-term survival (ie, 24-hour survival) is reduced.
Serologic tests may confirm the presence of alloimmunization.
Corrected Count Increment (CCI)
CCI = (postcount precount) BSA / platelets transfused

eg. A patient with acute myelogenous leukemia with a nomogram-

derived BSA of 1.40 meter2 is transfused with a unit of Apheresis
Platelets (a platelet dose of 4.5 1011). The pretransfusion platelet
count is 2000/L. The patients platelet count from a sample of
blood collected 15 minutes after platelet transfusion is 29,000/L.
The CCI is calculated as (29,000 2000) 1.4 / 4.5 = 8,400/L
per 1011 per m2 .
In the clinically stable patient, the CCI is typically greater than 7500
at 10 minutes to 1 hour after transfusion and remains above 4500 at
24 hours. Both immune and nonimmune mechanisms may contribute to
reduced platelet recovery and survival.
RBC Alloimmunization in Platelet
Immunization to red cell antigens may occur because of
the presence of residual red cells in Platelets.
Red cell compatibility testing is necessary only if the
platelet component is prepared by a method that results in
the component containing 2 mL or more of red cells,
making the unit appear pink to salmon in color. This occurs
more frequently with whole blood-derived platelets than
apheresis platelets.
When platelet components from Rh-positive donors
must be given to Rh-negative females , prevention of
Rh (D) immunization by use of Rh Immune Globulin
should be considered.
Cryoprecipitated Antihemophilic Factor (AHF) is prepared by
thawing whole blood-derived FFP between 1 and 6 C and
recovering the precipitate. The cold-insoluble precipitate is placed in
the freezer within 1 hour after removal from the refrigerated
centrifuge. Cryoprecipitated AHF contains fibrinogen, Factor VIII,
Factor XIII, vWF, and fibronectin
This component is used in the control of bleeding associated with
fibrinogen deficiency and to treat Factor XIII deficiency when volume
considerations preclude the use of frozen plasma and recombinant
proteins are not available. It is also indicated as second-line therapy
for von Willebrand disease and hemophilia A (Factor VIII
deficiency). Also as a source of fibrinogen in acquired
coagulopathies: e.g.disseminated intravascular coagulation (DIC)
Can be transfused across ABO barrier.
The First Blood Bank
Lewisohn's contribution, in 1915, was to determine the optimal concentration of sodium
citrate for preserving blood products without inducing toxicity.

His research was put into use during the First World War
Preservative solutions
The first anticoagulant preservative was citrate-glucose solution
The next important development occurred during the Second World
War when acidifieditrate dextrose (ACD) solution was introduced
1957 : Citrate-phosphate-dextrose (CPD), which was less acidic than
ACD and maintained 2,3-diphosphoglycerate (2,3-DPG) level better
than in ACD solution. Shelf-life of blood stored in CPD at 2-4 C was
21 day.
In 1978 : CPDA-1. The addition of adenine improved the synthesis of
adenosine triphosphate (ATP) in the stored blood,which prolonged
the storage of blood/red cells at 2-4 C to 35 days.
Additive Solutions : Traditional preservatives were put into use when
whole blood was the major product. With the advent of component
therapy use of red cells increased. Additive solutions provide
nutirents to the RBC for better viability. Addition of such solutions
increases the storage time to 42 days.
Bottle to Bag
In one of the single most influential technical
developments in blood banking, Carl Walter and
W.P. Murphy, Jr., introduce the plastic bag for
blood collection in 1950.
Replacing breakable glass bottles with durable
plastic bags allows for the evolution of a collection
system capable of safe and easy preparation of
multiple blood components from a single unit of
whole blood.
Today blood bags are made of high tensile
strength PVC.
In vitro RBC changes during storage
2,3 BPG concentration After five to six weeks of storage, levels in the RBC
progressively fall toward 10 percent of normal. As a result, the oxyhemoglobin
dissociation curve progressively shifts to the left, resulting in reduced oxygen release
by hemoglobin at any given tissue pO2.
Potassium leakage Potassium is not actively transported back into the RBC
because membrane ATPase is inhibited at 1 to 6C, the temperature range
employed for storage of red cells. The potassium concentration peaks at
approximately 30 to 50 mEq/L in whole blood (90 mEq/L in packed RBC
products), and as high as 70 mEq/L in 28-day-old irradiated blood

Hyperkalemia Risk factors for transfusion-related hyperkalemia include the rate

and volume of the transfusion, the use of a central venous
infusion and/or pressure pumping, the use of irradiated blood, and the age of
the blood infused.
Transfusion-related Hyperkalemia
There are three clinical settings in which there is an increased risk
of transfusion-related hyperkalemia:
Severe trauma Hyperkalemia is a common occurrence in patients with severe
trauma. Although blood product transfusion plays an important role, other risk
factors include tissue breakdown with the release of cellular potassium into the
extracellular fluid, a low cardiac output which impairs renal function, and
hypocalcemia which can increase the severity of the manifestations of
hyperkalemia [43,44
Impaired renal function Renal excretion of the potassium load provided in
blood transfusions limits the elevation in serum potassium. This protective effect is
diminished in patients with moderate to severely impaired renal function. Such
patients may require modifications in transfusion practices, such as the use of
fresher or washed red cells.
Infants and newborns Infants and newborns are another group at increased
risk for transfusion-related hyperkalemia due to the low rate of urinary
excretion of a potassium load.
Q. What is Leucoreduction?
A unit of whole blood generally contains 1 to 10
109 white cells.
Leukocyte reduction filters variably remove other
cellular elements in addition to white cells.
Leukoreduction has the inadvertent effect of removing
approximately 10% of red blood cells from a
processed unit of Red Blood Cells.
Leukocyte-reduced components are indicated to
decrease the frequency of recurrent febrile nonhemolytic
transfusion reaction.
Reduce the risk of transfusion-transmitted CMV
Reduce the incidence of HLA alloimmunization
Q. What is Washing
Washed components are typically prepared using 0.9% Sodium Chloride,
Injection (USP) with or without small amounts of dextrose. Washing removes
unwanted plasma proteins, including antibodies and glycerol from previously
frozen units. Washed red blood cells are red blood cells which have had
most of the plasma, platelets and white blood cells removed and replaced
with an electrolyte solution
It is indicated to reduce exposure to constituents that predispose patients to
significant or repeated transfusion reactions (eg, the removal of IgA-
containing plasma in providing transfusion support for an IgA-deficient
recipient or in rare recipients experiencing anaphylactoid/ anaphylactic
reactions to other plasma components).
Q. What is Irradiation
Blood components that contain viable lymphocytes may be
irradiated to prevent proliferation of T lymphocytes, which is
the immediate cause of TA-GVHD
The standard dose of gamma irradiation is 2500 cGy
targeted to the central portion of the container with a
minimum dose of 1500 cGy delivered to any part of the
Irradiation induces erythrocyte membrane damage.
Irradiated red cells have been shown to have higher
supernatant potassium levels than nonirradiated red cells.
The expiration date of irradiated red cells is changed to 28
days after irradiation if remaining shelf life exceeds 28
days. There are no known adverse effects following
irradiation of platelets; the expiration date is unchanged.
Need for warming of blood before
Need for warming of blood before transfusion There is
no need of warming of blood in elective transfusion
where a unit of blood is transfused over 2 to 4 hours.
However, warming of blood can be useful when rapid
transfusion of components is required
Warmed blood is most commonly required in:
Large volume rapid transfusions: Adults: greater than 50
ml/kg/hour Children: greater than 15 ml/kg/hour
Transfusions to neonates
Exchange transfusion in infants
Patients with clinically significant cold agglutinins.
Blood Warmer
Blood should not be warmed by placing it in a
microwave, on a heat source, or in hot water or by
using other devices not specifically approved for
blood warming. Blood should only be warmed in a
blood warmer. Blood warmers should have a
visible thermometer and an audible warning alarm
and should be properly maintained. Blood should
never be warmed in a bowl of hot water as this
could lead to haemolysis of the red cells which
could be life-threatening.
The Blood Transfusion Set
170 micron filter to capture any fibrin debris
BT Set must be changed after every 2-4 units and
at least 12-hourly during blood component
Platelets are best transfused through blood tubing
not previously used for red cells. Platelets will
adhere to fibrin captured in the filter.
Used blood tubing can be a breeding ground for
bacteria. Do not leave it attached to the patient.
Compatible fluids No other intravenous solutions or medications except
0.9 percent sodium chloride for injection, ABO compatible plasma, or
albumin should be administered through the same tubing concurrently with
the RBCs.
Infusion rate Suggested rates for adults are 1 to 2 mL per minute (60 to
120 mL per hour) for the first 15 minutes and then as rapidly as tolerated;
the complete infusion should not exceed four hours. However, slower
rates of infusion (possibly combined with administration of a smaller unit to
comply with the four-hour infusion requirement) and/or the administration of
diuretics may be indicated for patients who are predisposed to circulatory
Post-transfusion hemoglobin level The post-transfusion hemoglobin level
may be accurately measured as early as 15 minutes following transfusion,
as long as the patient is not actively bleeding. This practice is based on
studies showing a high degree of concordance between values measured 15
minutes after the transfusion versus longer intervals
Complications of Blood Transfusion
Transfusion reaction
Circulatory overload
Metabolic toxicity
Graft-versus-host disease
Iron overload
Transfusion-transmitted bacterial infection (TTBI) is an
important complication of blood product administration. The
incidence of TTBI is higher than the incidence of transfusion-
transmitted viral infection. A wide spectrum of organisms has
been associated with TTBI
skin and enteric and environmental organisms. Reports in the
older literature emphasized the importance of cryophilic
organisms, especially Yersinia enterocolitica and Pseudomonas
Tickborne infections (eg, Babesia, Anaplasma
phagocytophilum, Rickettsia rickettsii, Colorado tick fever virus,
and tickborne encephalitis virus)
Parasitic infection in endemic countries (eg, malaria,
trypanosomiasis, and leishmaniasis).
HIV-1 antibody testing was first implemented in 1985
Data obtained in 1985 prior to the availability of HIV
testing showed that approximately 90 percent of
transfused recipients acquired HIV infection when given an
HIV seropositive blood component.
Despite these procedures, HIV transmission may still occur
for three theoretical reasons:
Donations may be collected during the window period of
infection, defined as the interval of time shortly after HIV
infection, when the donor is infectious but has not yet developed
positive HIV laboratory tests.
Infection with variant strains of HIV that may escape detection by
current screening assays.
Testing or clerical errors.
Group O
In mid-1994, French investigators reported that some persons
infected with HIV-1 group O, a variant endemic in some central
African countries, tested negative on a number of HIV-1 antibody
and HIV-1/HIV-2 antibody combination assays [1].
In July 1996, the first case of group O infection in North America
was reported. Due to the rarity of group O infection and the ability
of current HIV antibody assays to crossreact with most group O
infected donors, the contribution of such genetically divergent
infections to transfusion transmitted HIV risk will be negligible.
Nevertheless, the FDA in December 1996 implemented policies to
exclude from donation persons from countries in Africa in which
group O variants are endemic.

Lancet. 1994 . HIV-1/HIV-2 seronegativity in HIV-1 subtype O infected patients. Loussert-Ajaka Iet al.
HIV (Contd.)
Although HIV-1 has had an extremely prominent
role in blood safety, this is not the case for HIV-2.
While there have been thousands of cases of
transfusion transmitted HIV-1 infection, there have
been fewer than 50 such cases attributed to HIV-
HIV is inactivated by the purification process used
to produce plasma derivatives such as albumin
and IVIg. There has never been a documented
case of HIV transmission from albumin or immune
globulin preparations.
Blood transfusion was a major risk factor for acute post
transfusion infectious hepatitis in the past.
The screening of blood donors for historical risk factors,
serologic evidence of hepatitis B infection, and elevated
serum ALT caused a striking reduction in the rates of
non-A, non-B post-transfusion hepatitis, even before
HCV was identified.
The subsequent initiation of donor screening for anti-
HCV antibodies in 1990 has nearly eliminated the risk
of post-transfusion acute HCV infection. The estimated
risk is now less than one in a million per unit transfused
Febrile nonhemolytic transfusion reactions (FNHTRs) are the most
common of all transfusion reactions. They occur in approximately 0.1
to 1 percent of transfusions.
FNHTRs are commonly caused by cytokines that are generated and
accumulate during the storage of blood components
Clinical manifestations of FNHTR occur within one to six hours after
initiation of a transfusion
These include fever, often a chill, occasionally severe rigors, and
sometimes mild dyspnea. The temperature increase is typically in the
range of 1 to 2C.
The major means of preventing FNHTRs is pre-storage leukoreduction
of the product.
Usage of premedications is not recommended.
Transfusion Associated ALI is defined as new
acute respiratory distress syndrome (ARDS)
occurring during or within six hours after blood
product administration
TRALI has been associated with virtually all blood
products, high-plasma-volume components such as
plasma, apheresis platelet concentrates, and whole
blood have been consistently shown to carry the
greatest risk
female sex and increased parity of the donor
1. Neutrophil sequestration
and priming

2. Neutrophil Activation
Diagnostic Criteria : TRALI
The possibility of Transfusion-associated
circulatory overload
(TACO) should be considered in any patient who
has respiratory distress or hypertension within six
hours of completing a transfusion.
Patient risk factors include pre-existing cardiac
and possibly renal dysfunction, small stature, low
body weight, extremes of age (eg, <3 years,
>60 years), and hypoalbuminemia, number of
units transfused
Unlike TACO, the risk of TRALI is not related to the
volume of the transfusion.
TRALI may occur closer in time to the initiation of the
transfusion (before significant volume is infused)
TRALI is often associated with hypotension, fever, and
transient leukopenia. TRALI is not associated with an
elevated N terminal Pro-BNP (NT Pro-BNP), central
venous pressure, or pulmonary artery wedge pressure.
In TRALI, the ratio of protein in the edema fluid to
plasma is high, reflecting an exudate rather than a
Hemolytic Transfusion Reactions
Acute HTRs (AHTRs) are usually due to ABO incompatibility, most often the result of clerical or
procedural error
Patterns of hemolysis :
hemolysis of the transfused cells by a host immune response against a foreign (to the recipient) antigen on the
these RBCs.
In some cases, transfusion of plasma-containing antibodies directed against a recipient's RBC antigen leads to
hemolysis of the recipient's RBCs. This is less common primarily because the incompatible donor plasma is
instantly diluted upon transfusion, reducing the strength of the transfused antibodies.
Rarely, both donor and recipient RBCs can be destroyed : hyperhemolytic crisis. The mechanism by which
hemolysis of RBCs lacking the implicated antigen (bystander hemolysis) occurs is not well understood.
Only a small amount of exposure (<1 mL of blood) is required to elicit an antibody response
The abundance of the antigen on the RBC surface also influences the severity of the reaction. Antigen
density varies significantly for different RBC antigens. As an example, ABO antigens are present at
approximately 200,000 to 800,000 per cell, while Kell antigens are present at approximately 3000
to 6000 per cell, a 100-fold difference
Site of RBC destruction (intravascular or extravascular) is determined chiefly by nature of antibody
response. This has clinical implications
Non-immune hemolysis from RBC injury :
Acute HTR (AHTR) refers to transfusion-associated hemolysis that
occurs during the transfusion or within the first 24 hours after
AHTR is a medical emergency that requires immediate cessation of
the transfusion
An ABO-associated AHTR may be suspected when a patient
develops chills, fever, hypotension, hemoglobinuria, renal failure,
back pain, or signs of disseminated intravascular coagulation (DIC).
The serum or urine may be pink due to the presence of free hemoglobin.
In a patient under anesthesia or in a coma, oozing from venipuncture
sites due to DIC or change in the urine color to red or brown due to
Stop transfusion, Normal saline (avoid RL/ DNS) should be infused
immediately to reduce the risks of hypotension and renal injury.
Delayed HTRs (DHTRs) are defined as HTRs that
occur more than 24 hours following transfusion
DHTRs most commonly present one to two weeks
after transfusion of RBCs, although the interval can
range from 3 to 30 days. These reactions are most
commonly due to an amnestic response to a
foreign RBC antigen to which the recipient was
previously exposed. Common routes of previous
exposure include prior transfusions and pregnancy
RBC antigens most commonly responsible for
DHTRs include those of the Kidd or Rh system.
Transfusion-associated graft versus host disease (ta-GVHD) does not occur
after most transfusions because the donor lymphocytes are destroyed by the
recipient's immune system before they can mount a response against the
host. However, this protective response does not occur in two settings:
when the recipient is immunodeficient
when there is a specific type of partial HLA matching between the donor and
Ta-GVHD develops 4 to 30 days after blood transfusion.
Patients typically present with fever and rash. Other symptoms include
anorexia, vomiting, abdominal pain, profuse diarrhea, and cough.
Distinguishing transfusion-associated GVHD (ta-GVHD) from transplantation-
associated disease. Ta-GVHD is poorly responsive to any available form of
therapy and is almost always a fatal complication.
Prevention : Irradiation, (?) 4th Generation Leucodepleton
1. Blood Substitutes
For more than 100 years researchers have
pursued the Holy Grail of trauma medicine: a
blood substitute. The ideal blood substitute
would retain all the functions of blood and
none of the transfusion problems associated
with blood.
Blood Substitutes (Contd.)
Research exploring alternatives to blood began
approximately 150 years ago.
Searching for a blood substitute, T. Gaillard Thomas posited
that intravenous infusion of cows milk, a process he
termed lacteal injections, might have the potential to save
Thomas presented three case studies of moribund patients
into whom he injected about 8 ounces of fresh cows milk. In
these case studies, one patient survived and two died. He
attributed their deaths to other complications unrelated to
the lacteal injections and claimed the injections were safe
provided that fresh milk was used.
1. Blood Substitutes
Native tetrameric hemoglobin, when removed from the red cell, breaks down into dimers, which are rapidly
cleared by glomerular filtration, resulting in a short vascular half-life.
Furthermore, free hemoglobin has reduced contact with phosphates, causing the P50 curve to shift to the left,
resulting in hemoglobin with a high oxygen affinity and limited oxygen unloading.
Significant renal damage
Three HBOCs that have progressed to Phase II or III clinical trials: HemAssist, PolyHeme, and
Cross linking and Polymerization

The fundamental difference in O2 transfer by Hb and PFC is that the former binds O2, while the latter
dissolves it.
Oxygen is dissolved in PFCs at a concentration of about 40%50%, which is 20 times higher than the
capacity of water and 2 times higher than plasma.
Their small sizes enable them to easily pass through the vessels occluded in some diseases, where
RBCs cannot pass; hence, their application helps improving the oxygenation rate. An in vitro study
showed that use of PFCs as artificial blood is considerably advantageous in occluded coronary artery
to maintain myocardial function.
Other Experimental approaches
Elimination of blood group antigens Enzymatic conversion of A,
B, and AB red cells to group O has been achieved in vitro via the use
of exoglycosidases derived from bacterial sources. This enzymatic
conversion (ECO) technique, if proven to be safe and effective, has
the potential to simplify blood transfusion by eliminating the risk for
ABO-incompatible transfusion errors and creating a more universal
blood inventory.
Ex vivo generation of red cells Limited numbers of viable red
cells can be generated ex vivo in culture systems from CD34+
hematopoietic stem cells.

Although this is an exciting first step, there are formidable barriers to

the large-scale production of such red cells for therapeutic
transfusion purposes.
The First Transfusion

Sanguis ovis symbolicam quandam facultatem habet cum sanguine Christi, quia
Christus est agnus Dei

Sheeps blood has some symbolic power, like the blood of Christ, for Christ is the Lamb of God.
2. Xenotransfusion
From 2000, because of progress in
xenotransplantation and the need of blood supply,
xenotransfusion is again in th limelight.
Pigs are the best potential donors.
RBC diameters (pig 6 m: human 7.2 m)
The pig blood group AO system is related to the human
ABO system
uniform pig herds in which all animals are of blood
type O already exist
Genetic Modification to further the phenotype and
immunotype can be undertaken
3. Blood Doping
"Blood doping" was banned by the IOC in 1985.
On August 23, 2012 Lance Armstrong was
stripped of his seven Tour de France titles and
banned for life.
More potent for use in blood doping is
Co2+ (administered as Cobalt chloride).
Cobalt chloride has been known to be useful in
treating anemic patients.
Studies have shown that Co2+ induces hypoxia like
responses, the most relevant response being
Cobalt Chloride in Refractory Anemia
The 5 Rights of Transfusion Ensure that the
Right Patient is getting the
Right Product
in the Right Amount
at the Right Rate
at the Right Time
Why you wont find a tattoo on
Christiano Ronaldo
Ronaldo, skips the ink so that he can continue to
donate blood. In many countries, a new tattoo
can affect how often a person donates blood,
with a waiting period between six months and
a year employed as a precaution against
cross-contamination and diseases like hepatitis.

I dont have tattoos because I donate blood

very often. He reportedly gives twice a year.