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Blood Products & Transfusion
Hani Sammour, MD, PB
Anesthesia and IC, Shifa hospital
Critical Care
Objectives
• Definition and preparation of blood components.
• Indications for blood components transfusion.
• Doses of blood components.
• Complications of blood transfusion.
Use of a transfusion algorithm guided by
appropriate laboratory testing, will reduce
unnecessary transfusion of precious (and
dangerous) blood components.
• There is a trend in major trauma care towards
transfusing blood products in equal ratios early
in resuscitation in order to prevent or correct
trauma-induced coagulopathy.
• This balanced approach to transfusion of blood
products, 1:1:1 (one unit of FFP and one unit of
platelets with each unit of PRBCs) is termed
damage control resuscitation.
BLOOD GROUPS
• Among at least 20 blood group antigen
systems in human red cell membranes, only
the ABO and the Rh systems are important in
the majority of blood transfusions.
• Individuals often produce antibodies
(alloantibodies) to the alleles they lack within
each system. Such antibodies are responsible
for the most serious reactions to transfusions.
The ABO System
• ABO blood group typing is determined by the
presence or absence of A or B red blood cell
(RBC) surface antigens:
– Type A blood has A RBC antigen.
– Type B blood has B RBC antigen.
– Type AB blood has both A and B RBC antigens.
– Type O blood has neither A nor B RBC antigen
present.
The Rh System
• Patients with the D Rhesus antigen are considered Rh-positive
and individuals lacking this antigen are called Rh-negative.
Approximately 85% of the white population and 92% of the
black population has the D antigen.
• Rh-negative patients usually develop antibodies against the D
antigen only after an Rh-positive transfusion or with pregnancy,
in the situation of an Rh-negative mother delivering an Rh-
positive baby.
Other Red Blood Cell Antigen Systems
• Other red cell antigen systems include Lewis, P, Ii, MNS,
Kidd, Kell, Duffy, Lutheran, Xg, Sid, Car-tright, YK, and
Chido Rodgers. Fortunately, with some exceptions (Kell,
Kidd, Duffy, and Ss), alloantibodies against these antigens
rarely cause serious hemolytic reactions.
COMPATIBILITY TESTING
• The purpose of compatibility testing is to
predict and to prevent antigen–antibody
reactions as a result of red cell transfusions.
ABO–Rh Testing
• The most severe transfusion reactions are due to
ABO incompatibility; naturally acquired antibodies
can react against the transfused (foreign) antigens,
activate complement, and result in intra-vascular
hemolysis.
• The patient’s red cells are tested with serum known
to have antibodies against A and against B to
determine blood type.
Cont.
• The patient’s red cells are also tested with anti-D
antibodies to determine Rh status. If the subject is
Rh-negative, the presence of anti-D antibody is
checked by mixing the patient’s serum against Rh-
positive red cells.
Antibody Screen
The purpose of this test is to detect in the serum the presence of the
antibodies that are most commonly associated with non-ABO hemolytic
reactions .
The test also known as the indirect Coombs test, requires 45 min and
involves mixing the patient’s serum with red cells of known antigenic
composition; if specific antibodies are present, they will coat the red cell
membrane, and subsequent addition of an antiglobulin antibody results in
red cell agglutination. Antibody screens are routinely done on all donor
blood and are frequently done for a potential recipient instead of a
crossmatch.
Crossmatch
• A crossmatch mimics the transfusion: donor
red cells are mixed with recipient serum.
• Crossmatching serves three functions:
(1) It confirms ABO and Rh typing.
(2) It detects antibodies to the other blood group
systems.
(3) It detects antibodies in low titers or those that
do not agglutinate easily.
Type & Crossmatch versus
Type & Screen
• In the situation of negative antibody screen without crossmatch, the
incidence of serious hemolytic reaction with ABO- and Rh-compatible
transfusion is less than 1:10.000.
• Crossmatching however, assures optimal safety and detects the
presence of less common antibodies not usually tested for in a screen .
• Because of the expense and time involved (45 min) crossmatches are
often now performed before the need to transfuse only when the
patient’s antibody screen is positive, when the probability of transfusion
is high, or when the patient is considered at risk for alloimmunization.
EMERGENCY TRANSFUSIONS
• When a patient is exsanguinating, the urgent need to
transfuse may arise prior to completion of a crossmatch,
screen, or even blood typing. If the patient’s blood type is
known, an abbreviated cross-match, requiring less than 5
min, will confirm ABO compatibility.
• If the recipient’s blood type and Rh status is not known
with certainty and transfusion must be started before
determination, type O Rh-negative (universal donor) red
cells may be used.
Definitions
• Blood product: any therapeutic substance prepared
from human blood.
• Whole blood: Unseparated blood collected into an
approved container containing an anticoagulant-
preservative solution.
Blood component
– A constituent of blood, separated from whole blood,
such as:
• Red cell concentrate
• Plasma
• Platelet concentrates
– Cryoprecipitate, prepared from fresh frozen plasma.
Plasma derivative
Human plasma proteins prepared under
pharmaceutical manufacturing conditions, such as:
– Albumin.
– Coagulation factor concentrates.
– Immunoglobulins.
1) Whole Blood
• There have been few widely accepted indications for whole blood
in modern transfusion practice.
• Whole blood is not available from most blood banks in the United
States.
• Dose: 6 ml/kg of WB raise Hemoglobin level 1 g/dl.
• One unit of WB will raise the hemoglobin of
an average-size adult by ~ 1g/dl
Whole Blood
• During donation, blood is collected into a sterile,
disposable, plastic pack which contains an anticoagulant-
preservative solution. This solution usually contains
citrate, phosphate, dextrose and often adenine (CPDA).
• There are variations in the volume of blood collected and
in the type of anticoagulant-preservative solution used in
different regions of the world.
• During storage, metabolism continues in the red cells and
platelets, while some plasma proteins lose their
biological activity.
Functions of anticoagulant-preservative solution in
blood collection pack
Functions
Solutions
Binds with calcium ions in blood in
exchange for the sodium salt so the
blood does not clot
C Sodium citrate
Supports metabolism of the red cells
during storage to ensure they release
oxygen readily at tissue level
P Phosphate
Maintains the red cell membrane to
increase storage life
D Dextrose
Provides energy source
A Adenine
Effects of storage on whole blood
• Reduction in the pH (blood becomes more acidic).
• Rise in plasma potassium concentration (extracellular K+).
• Progressive reduction in the red cell content of 2,3
diphosphoglycerate (2,3 DPG).
• Loss of all platelet function in whole blood within 48 hours of
donation.
• Reduction in Factor VIII to 10–20% of normal within 48 hours
of donation.
2) Red Blood Cells
Packed RBCs are the commonly utilized blood
product, providing oxygen-carrying capacity in
cases most of acute or chronic blood loss.
Preparation of red cell concentrate
Cont.
Advantages
• Simple and inexpensive to prepare.
Disadvantages
• It has a high ratio of red cells to plasma (high viscosity)
thereby increasing the time required for transfusion
through a small gauge needle or cannula.
• The white cells are a cause of febrile non-haemolytic
transfusion reactions in some patients.
Leukocyte-depleted red cells
• Special leukocyte filters can be used to remove
virtually all the white cells.
• The majority of red cells and platelet transfusions in
the United States & UK are currently leukocyte
reduced.
Cont.
Advantages
• Reduces acute transfusion reactions.
• Reduces cytomegalovirus infection (CMV).
Disadvantages
• Cost: special blood packs and equipment are required
• More skill and operator training is needed.
PRBCs transfusion guidelines
• Hemodynamic instability: Ongoing bleeding with unresponsive
(or incompletely responsive) to infusion of 2- 3 Liters crystalloid
• Hemodynamically Stable:
• ICU Patients: Hemoglobin <7 g/dL
• Post-Operative: Hgb ≤8 g/dL
• Cardiovascular Disease: Hgb ≤8 g/dL
AABB transfusion guideline
• A restrictive RBC transfusion threshold in which the transfusion
is not indicated until the hemoglobin level is 7 g/dL is
recommended for hospitalized adult patients who are
hemodynamically stable, including critically ill patients, rather
than when the hemoglobin level is 10 g/dL (strong
recommendation, moderate quality evidence).
• A restrictive RBC transfusion threshold of 8 g/dL is
recommended for patients undergoing orthopedic surgery,
cardiac surgery, and those with preexisting cardiovascular
disease (strong recommendation, moderate quality evidence).
Cont.
• The restrictive transfusion threshold of 7 g/dL is likely
comparable with 8 g/dL, but RCT evidence is not
available for all patient categories. These
recommendations do not apply to patients with acute
coronary syndrome, severe thrombocytopenia (patients
treated for hematological or oncological reasons who are
at risk of bleeding), and chronic transfusion-dependent
anemia (not recommended due to insufficient evidence).
AABB transfusion guideline
• For RBC transfusion thresholds, 31 RCTs included 12,587
participants and compared restrictive thresholds (transfusion
not indicated until the hemoglobin level is 7-8 g/dL) with
liberal thresholds (transfusion not indicated until the
hemoglobin level is 9-10 g/dL). The summary estimates across
trials demonstrated that restrictive RBC transfusion
thresholds were not associated with higher rates of adverse
clinical outcomes, including 30-day mortality, myocardial
infarction, cerebrovascular accident, rebleeding, pneumonia,
or thromboembolism.
Cont.
• For RBC storage duration, 13 RCTs included
5515 participants randomly allocated to
receive fresher blood or standard-issue blood.
These RCTs demonstrated that fresher blood
did not improve clinical outcomes.
Cont.
• Dose: 4 ml/kg of RBC increase Hemoglobin level 1 g/dl.
• One unit of RBC will raise the hemoglobin
of an average-size adult by ~ 1g/dl
• Transfuse slowly for first 15 minutes.
• Complete transfusion within 4 hours.
3) White cells (leukocytes)
• White cell transfusions have no proven clinical
uses.
• May be indicated in neutropenic patients with
bacterial infections not responding to antibiotics.
• Transfused granulocytes have a very short circulatory
life span, so that daily transfusions of 10 10
granulocytes are usually required.
4) Plasma
• This is separated from whole blood and frozen at –25°C or
colder within 6–8 hours of donation in order to preserve its
labile coagulation factors (Factors V and VIII).
• Fresh frozen plasma can be stored for at least one year or
longer if low temperatures can be maintained.
• When plasma is stored at a temperature of 2–6°C, the
labile clotting activity of Factors V and VIII will decline to
10–20% within 48 hours.
• Dosage: Initial dose of 15 ml/kg
Indications for transfusion of plasma
• International normalized ratio (INR) >1.5 with:
– Anticipated invasive procedure or surgery.
– Massive hemorrhage (over one blood volume)
• Emergent reversal of anticoagulant (warfarin)
therapy.
• Treatment of isolated factor deficiencies.
• The correction of coagulopathy associated with liver
disease.
Indications for transfusion of plasma
Coagulopathy (INR) >1.5 with:
1. Active bleeding.
2. Bleeding tendency:
• Anticipated invasive procedure or surgery.
• The correction of coagulopathy associated with liver disease.
• Emergent reversal of anticoagulant (warfarin) therapy.
• Treatment of isolated factor deficiencies.
5) Platelet
• The platelet count at 1 hour post transfusion of a unit of
platelets should increase by 5,000 to 10,000 platelets/µL.
• Platelets separated from plasma obtained from 4–6
donations of whole blood are often pooled to produce a
therapeutic dose of platelets for an adult platelet
apheresis unit, by 30,000–60,000 × 10 9/L.
• Dosage: 1 unit of platelet concentrate/10 kg body weight
Indications for transfusion of platelets
Thrombocytopenia or Dysfunctional platelets with:
1. Active bleeding
2. Bleeding tendency
• Neurosurgical procedures: 100,000 platelets/µL
• Vaginal delivery and minor surgical procedures: <50,000/µL
• Massive transfusion: < 50,000 platelets/µL
• Disseminated intravascular coagulation: 20,000–50,000 /µL
6. Cryoprecipitate
• Cryoprecipitate is obtained from a single donation of FFP
at about 4°C and is rich in factor VIII, von Willebrand factor
(VWF), factor XIII, and fibrinogen.
• Cryoprecipitate is usually administered as a transfusion of
10 single units.
• Each 5- to 15-mL unit contains over 80 units of factor VIII
and about 200 mg of fibrinogen.
Indications for transfusion of cryoprecipitate
• Hemophilia A
• von Willebrand disease
• Hypofibrinogemia
• Uremic bleeding
Component separation by apheresis
• Apheresis is an alternative method of producing blood
components. It is a sterile process in which a donor is
connected to a specialized device by which blood is
withdrawn, mixed with anticoagulant and centrifuged
and a specific component, usually plasma or platelets,
is mechanically separated and collected.
• The red cells and other components of the blood that
are not required are then reinfused back into the
donor.
Cont.
• The advantage of apheresis is that relatively large
amounts of plasma or platelets can be collected from
a donor.
• Since the red cells are returned to the donor’s
circulation, this avoids making the donor anemic and
the process can be repeated at frequent intervals.
Blood Component Characteristic
Red Cells Platelet Concentrate Fresh Frozen
Plasma
Cryoprecipita
te
Storage
Temperature
2-6°C 20-24°C -30°C -30°C
Shelf Life
Volume
35 day
200-350
5 day
30-50 ml/unit
1 yr (frozen)
150-200ml/unit
1 yr (frozen)
10-15 ml/unit
Transfusion
Interval
Transfuse within 30
min of removal
from blood
refrigerator.
Transfuse unit over
maximum of 4 hr
Start transfusion as soon as
received from blood bank.
Transfuse unit within 30
min
Once thawed,
should be
transfused
within 4 hr
884 hr
Compatibility
Testing
Requirement
Must be compatible
with recipient ABO
and Rh D type
Preferably ABO identical
with patient.
Rh negative females under
the age of 45 yr should be
given Rh negative platelets
FFP and cryoprecipitate
should be ABO compatible
to avoid risk of hemolysis
caused by donor anti-A or
anti-B
Administration Infuse through a blood administration set—platelet concentrates should not
be infused through blood sets that have been used for blood.
Complications of Blood Transfusion
1) IMMUNE Complications.
2) INFECTIOUS Complications.
3) MASSIVE BLOOD TRANSFUSION Complications.
Complications of Blood Transfusion
1) IMMUNE Complications
– Hemolytic reactions
• Acute hemolytic reaction.
• Delayed hemolytic reaction.
– Nonhemolytic reactions
• Febrile reactions • Urticarial reactions
• Anaphylactic reactions • Post-transfusion purpura
• Transfusion-Related Acute Lung Injury
• Graft-versus-host disease
Complications of Blood Transfusion
2) Infectious (all products)
Complications of Blood Transfusion
3) Complications of massive blood transfusion
– Coagulopathy
– Hypothermia
– Citrate Toxicity
– Acid–Base Balance
– Serum Potassium Concentration
IMMUNE COMPLICATIONS
Immune complications following blood transfusions are
primarily due to sensitization of the recipient to donor
red cells, white cells, platelets, or plasma proteins.
Less commonly, the transfused cells or serum may
mount an immune response against the recipient.
Immune complications
• Acute hemolytic transfusion reaction: ABO incompatibility.
• Delayed HTR: incompatible red cell antigen.
• Febrile non-HTR: anti-WBC antibodies in recipient.
• Urticarial reactions: antibody to donor plasma proteins.
• Anaphylactic: antibody to donor plasma proteins (IgA).
• Transfusion-related acute lung injury (TRALI): neutrophil
antibodies in donor product.
Hemolytic Reactions
• Hemolytic reactions usually involve specific
destruction of the transfused red cells by the
recipient’s antibodies. Less commonly,
hemolysis of a recipient’s red cells occurs as a
result of transfusion of red cell antibodies.
• Hemolytic reactions are commonly classified
as either acute (intravascular) or delayed
(extravascular).
Acute Hemolytic Reactions
• Acute intravascular hemolysis is usually due to ABO
blood incompatibility, and the reported frequency is
approximately 1:38,000 transfusions.
• The most common cause is misidentification of a patient,
blood specimen, or transfusion unit.
• These reactions are often severe, and may occur after
infusion of as little as 10–15 mL of ABO-incompatible
blood.
• The risk of a fatal hemolytic reaction is about 1 in
100,000 transfusions.
• In awake patients, symptoms include chills, fever, nausea,
and chest and flank pain.
Cont.
• In anesthetized patients, an acute hemolytic
reaction may be manifested by a rise in temperature,
unexplained tachycardia, hypotension, hemoglobinuria,
and diffuse oozing in the surgical field. Disseminated
intravascular coagulation, shock, and kidney failure can
develop rapidly.
• The severity of a reaction often depends upon the volume
of incompatible blood that has been administered.
Management of hemolytic reactions
1. If a hemolytic reaction is suspected, the transfusion should
be stopped immediately and the blood bank should be
notified.
2. The unit should be rechecked against the blood slip and the
patient’s identity bracelet.
3. Blood should be drawn to identify hemoglobin in plasma,
to repeat compatibility testing, and to obtain coagulation
studies and a platelet count.
4. A urinary catheter should be inserted, and the urine
should be checked for hemoglobin.
5. Osmotic diuresis should be initiated with mannitol and
intravenous fluids.
Delayed Hemolytic Reactions
Also called extravascular hemolysis, is generally mild and is
caused by antibodies to non-D antigens of the Rh system or to
foreign alleles in other systems such as the Kell, Duffy, or Kidd
antigens.
Following an ABO and Rh D-compatible transfusion, patients
have a 1–1.6% chance of forming antibodies directed against
foreign antigens in these other systems.
Cont.
• The hemolytic reaction is therefore typically delayed 2–21 days
after transfusion, and symptoms are generally mild, consisting
of malaise, jaundice, and fever.
• The patient’s hematocrit typically fails to rise, or rises only
transiently, in spite of the transfusion and the absence of
bleeding.
• The serum unconjugated bilirubin increases as a result of
hemoglobin breakdown.
Cont.
• Diagnosis of delayed antibody-mediated hemolytic reactions
may be facilitated by the antiglobulin (Coombs) test. The direct
Coombs test detects the presence of antibodies on the
membrane of red cells.
• Pregnancy (exposure to fetal red cells) can also be responsible
for the formation of alloantibodies to red cells.
• The frequency of delayed hemolytic transfusion reactions is
estimated to be approximately 1:12,000 transfusions.
• The treatment of delayed hemolytic reactions is primarily
supportive.
Nonhemolytic Immune Reactions
• Nonhemolytic immune reactions are due to
sensitization of the recipient to the donor’s white
cells, platelets, or plasma proteins.
• The risk of these reactions may be minimized by the
use of leukoreduced blood products.
Nonhemolytic Immune Reactions
A- Febrile Reactions:
• White cell or platelet sensitization is typically
manifested as a febrile reaction.
• Such reactions are relatively common (1–3% of transfusion
episodes) and are characterized by an increase in temperature
without evidence of hemolysis.
• Patients with a history of repeated febrile reactions should
receive leukoreduced transfusions only.
Cont.
B- Urticarial Reactions:
• Urticarial reactions are usually characterized by erythema,
hives, and itching without fever.
• They are relatively common (1% of transfusions) and are
thought to be due to sensitization of the patient to
transfused plasma proteins.
• Urticarial reactions can be treated with antihistaminic
drugs (H1 and perhaps H2- blockers) and steroids.
Cont.
C- Anaphylactic Reactions:
• Anaphylactic reactions are rare (approximately 1:150,000
transfusions).
• These severe reactions may occur after only a few milliliters of
blood has been given, typically in IgA-deficient patients with
anti-IgA antibodies who receive IgA-containing blood
transfusions.
• The prevalence of IgA deficiency is
estimated to be 1:600-800 in the general population.
• Such reactions require treatment with epinephrine, fluids,
corticosteroids, and H1 and H2 blockers.
Cont.
D- Transfusion-Related Acute Lung Injury (TRALI) :
• (TRALI) presents as acute hypoxia and noncardiac pulmonary
edema occurring within 6 h of blood product transfusion.
• It may occur as frequently as 1:5000 transfused units, and
with transfusion of any blood component, but especially
platelets and FFP.
• It is thought that transfusion of antileukocytic or anti-HLA
antibodies results in damage to the alveolar–capillary
membrane.
• Treatment is similar to that for acute respiratory distress
syndrome with the important difference that TRALI may
resolve within a few days with supportive therapy.
Cont.
E- Graft-Versus-Host Disease:
• This type of reaction may be seen in immunocompromised
patients. Cellular blood products contain lymphocytes capable
of mounting an immune response against the compromised
(recipient) host.
• Use of special leukocyte filters alone does not reliably
prevent graft -versus-host disease; irradiation(1500–3000
cGy) of red cell, granulocyte, and platelet transfusions
effectively eliminates lymphocytes without altering the
efficacy of such transfusions.
Cont.
F- Post-Transfusion Purpura:
• Rarely, profound thrombocytopenia may occur following
blood transfusions.
• This post-transfusion purpura results from the development
of platelet alloantibodies.
• For unknown reasons, these antibodies also destroy the
patient’s own platelets.
• The platelet count typically drops precipitously 5–10 days
following transfusion.
• Treatment includes intravenous IgG and plasmapheresis.
Cont.
G- Transfusion-Related Immunomodulation:
• Allogeneic transfusion of blood products may diminish
immunoresponsiveness and promote inflammation.
• Post-transfusion immunosuppression is clearly evident in
renal transplant recipients, in whom preoperative blood
transfusion improves graft survival.
INFECTIOUS COMPLICATIONS
A- Viral Infections:
Hepatitis:
• The incidence of post-transfusion viral hepatitis varies greatly,
from approximately 1:200,000 transfusions (for hepatitis B) to
approximately 1:1,900,000 (for hepatitis C).
• Most acute cases are anicteric.
Hepatitis C is the more serious infection; most cases progress
to chronic hepatitis, with cirrhosis developing in 20% of
chronic carriers and hepatocellular carcinoma developing in
up to 5% of chronic carriers.
Cont.
Acquired Immunodeficiency Syndrome (AIDS):
• The virus responsible AIDS, HIV-1, is transmissible by blood
transfusion. HIV-2 is a similar, but less virulent virus.
• All blood is tested for the presence of anti-HIV-1 and anti-HIV-
2 antibodies. The requirement for nucleic acid testing by the
Food and Drug Administration (FDA) has decreased the risk of
transfusion-transmitted HIV to approximately 1:1,900,000
transfusions.
Cont.
Other Viral Infections:
• Cytomegalovirus (CMV) and Epstein–Barr virus usually cause
asymptomatic or mild systemic illness.
• Some individuals infected with these viruses become
asymptomatic infectious carriers; the white cells in blood
units from such donors are capable of transmitting either
virus.
• Immunocompromised and immunosuppressed patients (eg,
premature infants, organ transplant recipients, and cancer
patients) are particularly susceptible to severe transfusion-
related CMV infections.
Cont.
B- Parasitic Infections:
• Parasitic diseases that can be transmitted by
transfusion include malaria, toxoplasmosis, and
Chagas’ disease. Such cases are very rare.
Cont.
C- Bacterial Infections:
• Bacterial contamination of blood products is the second leading
cause of transfusion-associated mortality.
• The prevalence of positive bacterial cultures in blood products
ranges from 1:2000 for platelets to 1:7000 for PRBCs and may be
due to transient donor bacteremia or inadequate antisepsis during
phlebotomy.
• The prevalence of sepsis due to blood transfusion ranges from
1:25,000 for platelets to 1:250,000 for PRBCs. Both gram-positive
(Staphylococcus) and gram-negative (Yersinia and Citrobacter)
bacteria can contaminate blood transfusions and transmit disease.
To avoid the possibility of significant bacterial contamination, blood
products should be administered over a period shorter than 4 h.
MASSIVE BLOOD TRANSFUSION
• Massive transfusion, historically defined as the
replacement by transfusion of 10 units of red cells in 24
hours, is a response to massive and uncontrolled
hemorrhage (Uptodate).
• Massive blood transfusion may be defined either as the
acute administration of more than 1.5 times the patient's
estimated blood volume, or as the replacement of the
patient's total blood volume by stored homologous bank
blood in less than 24 h (British Journal of Anaesthesia).
Cont.
Various definitions of massive blood transfusion (MBT)
have been published in the medical literature such as:
• Replacement of one entire blood volume within 24 h
• Transfusion of >10 units of packed red blood cells
(PRBCs) in 24 h
• Transfusion of >20 units of PRBCs in 24 h
• Transfusion of >4 units of PRBCs in 1 h when on-going
need is probable
• Replacement of 50% of total blood volume (TBV)
within 3 h.
Complications of massive blood transfusion
• Coagulopathy
• Hypothermia
• Citrate Toxicity
• Acid–Base Balance:
• Serum Potassium Concentration
Complications of massive blood transfusion
• Coagulopathy
The most common cause of nonsurgical bleeding
following massive blood transfusion is dilutional
thrombocytopenia, although clinically significant dilution
of coagulation factors may also occur.
Coagulation studies and platelet counts, if readily
available, should guide platelet and FFP transfusion.
BJA: British Journal of Anaesthesia, Volume 111, Issue suppl_1, December 2013, Pages i71–i82, https://doi.org/10.1093/bja/aet376
The content of this slide may be subject to copyright: please see the slide notes for details.
Pathogenesis of haemostasis abnormality in MT.
Dilutional coagulopathy, activation of inflammatory mediators.
Cont.
Hypothermia
• Massive blood transfusion is an absolute indication for
warming all blood products and intravenous fluids to
normal body temperature.
• Ventricular arrhythmias progressing to fibrillation often
occur at temperatures close to 30°C, and hypothermia can
hamper cardiac resuscitation.
• The use of rapid infusion devices with efficient heat
transfer capability has decreased the incidence of
transfusion-related hypothermia.
Cont.
Citrate Toxicity
• Because citrate metabolism is primarily hepatic, patients with
hepatic disease or dysfunction (and possibly hypothermic
patients) may demonstrate hypocalcemia and require calcium
infusion during massive transfusion, as may small children and
others with relatively impaired parathyroid–vitamin D
function.
• Clinically important hypocalcemia, causing cardiac depression,
will not occur in most normal patients unless the transfusion
rate exceeds 1 unit every 5 min, and intravenous calcium salts
should rarely be required in the absence of measured
hypocalcemia.
Cont.
Acid–Base Balance:
• Although stored blood is acidic due to the citric acid
anticoagulant and accumulation of red cell metabolites (carbon
dioxide and lactic acid), metabolic acidosis due to transfusion is
uncommon because citric acid and lactic acid are rapidly
metabolized to bicarbonate by the normal liver.
• In the situation of massive blood transfusion, acid-base status is
largely dependent upon tissue perfusion, rate of blood
transfusion, and citrate metabolism.
• Once normal tissue perfusion is restored, any metabolic acidosis
typically resolves, and metabolic alkalosis commonly occurs as
citrate and lactate contained in transfusions and resuscitation
fluids are converted to bicarbonate by the liver.
Cont.
Serum Potassium Concentration:
• The extracellular concentration of potassium in stored blood
steadily increases with time. The amount of extracellular
potassium transfused with each unit is typically less than 4
mEq per unit.
• Hyperkalemia can develop regardless of the age of the
blood when transfusion rates exceed 100 mL/min.
• Hypokalemia is commonly encountered
postoperatively, particularly in association with metabolic
alkalosis.
Cost of blood components
Netherland
2011
USA
2008
UK
2001
Product
€
210
300 $
82.5 £
Red cells
(leucocyte depleted)
€
102
233 $
£
156
Platelets
(leucocyte depleted)
€
181
160 $
£
19
Fresh frozen plasma
(leucocyte depleted)
117 $
£
23
Cryoprecipitate
(leucocyte depleted)
Compatible fluids and medications
• No medications or solutions should be added to or
infused through the same tubing as blood products
except for 0.9% Sodium Chloride, ABO compatible
plasma or 4% Albumin.
• It has been shown to be safe to co-administer
morphine (1mg/mL), pethidine (10mg/mL) and
ketamine (1mg/mL) if diluted in 0.9% Sodium Chloride
with red cells. In these situations, the blood product
should be administered via the closest to the patient
(distal lumen).
Cont.
• If other medications are required during a blood
transfusion, the transfusion must be stopped and the line
flushed with 0.9% Sodium Chloride before and after
administration of the medication. The blood transfusion
can then recommence.
• Fluids containing glucose are not compatible with red
blood cells, they cause clumping of the red blood
cells.
• Crystalloid or colloid solutions that contain calcium
should never be administered concurrently with any
blood product. Calcium reverses the anticoagulant citrate
causing red blood cells to clot.
References
• Morgan and Mikhail's Clinical Anesthesiology, 6th
edition
• The Clinical Use of Blood - World Health Organization
• Uptodate.com 2019

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blood_trans.pptx

  • 1. Blood Products & Transfusion Hani Sammour, MD, PB Anesthesia and IC, Shifa hospital Critical Care
  • 2. Objectives • Definition and preparation of blood components. • Indications for blood components transfusion. • Doses of blood components. • Complications of blood transfusion.
  • 3.
  • 4. Use of a transfusion algorithm guided by appropriate laboratory testing, will reduce unnecessary transfusion of precious (and dangerous) blood components.
  • 5. • There is a trend in major trauma care towards transfusing blood products in equal ratios early in resuscitation in order to prevent or correct trauma-induced coagulopathy. • This balanced approach to transfusion of blood products, 1:1:1 (one unit of FFP and one unit of platelets with each unit of PRBCs) is termed damage control resuscitation.
  • 6. BLOOD GROUPS • Among at least 20 blood group antigen systems in human red cell membranes, only the ABO and the Rh systems are important in the majority of blood transfusions. • Individuals often produce antibodies (alloantibodies) to the alleles they lack within each system. Such antibodies are responsible for the most serious reactions to transfusions.
  • 7. The ABO System • ABO blood group typing is determined by the presence or absence of A or B red blood cell (RBC) surface antigens: – Type A blood has A RBC antigen. – Type B blood has B RBC antigen. – Type AB blood has both A and B RBC antigens. – Type O blood has neither A nor B RBC antigen present.
  • 8. The Rh System • Patients with the D Rhesus antigen are considered Rh-positive and individuals lacking this antigen are called Rh-negative. Approximately 85% of the white population and 92% of the black population has the D antigen. • Rh-negative patients usually develop antibodies against the D antigen only after an Rh-positive transfusion or with pregnancy, in the situation of an Rh-negative mother delivering an Rh- positive baby.
  • 9. Other Red Blood Cell Antigen Systems • Other red cell antigen systems include Lewis, P, Ii, MNS, Kidd, Kell, Duffy, Lutheran, Xg, Sid, Car-tright, YK, and Chido Rodgers. Fortunately, with some exceptions (Kell, Kidd, Duffy, and Ss), alloantibodies against these antigens rarely cause serious hemolytic reactions.
  • 10. COMPATIBILITY TESTING • The purpose of compatibility testing is to predict and to prevent antigen–antibody reactions as a result of red cell transfusions.
  • 11. ABO–Rh Testing • The most severe transfusion reactions are due to ABO incompatibility; naturally acquired antibodies can react against the transfused (foreign) antigens, activate complement, and result in intra-vascular hemolysis. • The patient’s red cells are tested with serum known to have antibodies against A and against B to determine blood type.
  • 12. Cont. • The patient’s red cells are also tested with anti-D antibodies to determine Rh status. If the subject is Rh-negative, the presence of anti-D antibody is checked by mixing the patient’s serum against Rh- positive red cells.
  • 13. Antibody Screen The purpose of this test is to detect in the serum the presence of the antibodies that are most commonly associated with non-ABO hemolytic reactions . The test also known as the indirect Coombs test, requires 45 min and involves mixing the patient’s serum with red cells of known antigenic composition; if specific antibodies are present, they will coat the red cell membrane, and subsequent addition of an antiglobulin antibody results in red cell agglutination. Antibody screens are routinely done on all donor blood and are frequently done for a potential recipient instead of a crossmatch.
  • 14. Crossmatch • A crossmatch mimics the transfusion: donor red cells are mixed with recipient serum. • Crossmatching serves three functions: (1) It confirms ABO and Rh typing. (2) It detects antibodies to the other blood group systems. (3) It detects antibodies in low titers or those that do not agglutinate easily.
  • 15. Type & Crossmatch versus Type & Screen • In the situation of negative antibody screen without crossmatch, the incidence of serious hemolytic reaction with ABO- and Rh-compatible transfusion is less than 1:10.000. • Crossmatching however, assures optimal safety and detects the presence of less common antibodies not usually tested for in a screen . • Because of the expense and time involved (45 min) crossmatches are often now performed before the need to transfuse only when the patient’s antibody screen is positive, when the probability of transfusion is high, or when the patient is considered at risk for alloimmunization.
  • 16. EMERGENCY TRANSFUSIONS • When a patient is exsanguinating, the urgent need to transfuse may arise prior to completion of a crossmatch, screen, or even blood typing. If the patient’s blood type is known, an abbreviated cross-match, requiring less than 5 min, will confirm ABO compatibility. • If the recipient’s blood type and Rh status is not known with certainty and transfusion must be started before determination, type O Rh-negative (universal donor) red cells may be used.
  • 17. Definitions • Blood product: any therapeutic substance prepared from human blood. • Whole blood: Unseparated blood collected into an approved container containing an anticoagulant- preservative solution.
  • 18. Blood component – A constituent of blood, separated from whole blood, such as: • Red cell concentrate • Plasma • Platelet concentrates – Cryoprecipitate, prepared from fresh frozen plasma.
  • 19. Plasma derivative Human plasma proteins prepared under pharmaceutical manufacturing conditions, such as: – Albumin. – Coagulation factor concentrates. – Immunoglobulins.
  • 20. 1) Whole Blood • There have been few widely accepted indications for whole blood in modern transfusion practice. • Whole blood is not available from most blood banks in the United States. • Dose: 6 ml/kg of WB raise Hemoglobin level 1 g/dl. • One unit of WB will raise the hemoglobin of an average-size adult by ~ 1g/dl
  • 21. Whole Blood • During donation, blood is collected into a sterile, disposable, plastic pack which contains an anticoagulant- preservative solution. This solution usually contains citrate, phosphate, dextrose and often adenine (CPDA). • There are variations in the volume of blood collected and in the type of anticoagulant-preservative solution used in different regions of the world. • During storage, metabolism continues in the red cells and platelets, while some plasma proteins lose their biological activity.
  • 22. Functions of anticoagulant-preservative solution in blood collection pack Functions Solutions Binds with calcium ions in blood in exchange for the sodium salt so the blood does not clot C Sodium citrate Supports metabolism of the red cells during storage to ensure they release oxygen readily at tissue level P Phosphate Maintains the red cell membrane to increase storage life D Dextrose Provides energy source A Adenine
  • 23. Effects of storage on whole blood • Reduction in the pH (blood becomes more acidic). • Rise in plasma potassium concentration (extracellular K+). • Progressive reduction in the red cell content of 2,3 diphosphoglycerate (2,3 DPG). • Loss of all platelet function in whole blood within 48 hours of donation. • Reduction in Factor VIII to 10–20% of normal within 48 hours of donation.
  • 24. 2) Red Blood Cells Packed RBCs are the commonly utilized blood product, providing oxygen-carrying capacity in cases most of acute or chronic blood loss.
  • 25. Preparation of red cell concentrate
  • 26. Cont. Advantages • Simple and inexpensive to prepare. Disadvantages • It has a high ratio of red cells to plasma (high viscosity) thereby increasing the time required for transfusion through a small gauge needle or cannula. • The white cells are a cause of febrile non-haemolytic transfusion reactions in some patients.
  • 27. Leukocyte-depleted red cells • Special leukocyte filters can be used to remove virtually all the white cells. • The majority of red cells and platelet transfusions in the United States & UK are currently leukocyte reduced.
  • 28. Cont. Advantages • Reduces acute transfusion reactions. • Reduces cytomegalovirus infection (CMV). Disadvantages • Cost: special blood packs and equipment are required • More skill and operator training is needed.
  • 29. PRBCs transfusion guidelines • Hemodynamic instability: Ongoing bleeding with unresponsive (or incompletely responsive) to infusion of 2- 3 Liters crystalloid • Hemodynamically Stable: • ICU Patients: Hemoglobin <7 g/dL • Post-Operative: Hgb ≤8 g/dL • Cardiovascular Disease: Hgb ≤8 g/dL
  • 30. AABB transfusion guideline • A restrictive RBC transfusion threshold in which the transfusion is not indicated until the hemoglobin level is 7 g/dL is recommended for hospitalized adult patients who are hemodynamically stable, including critically ill patients, rather than when the hemoglobin level is 10 g/dL (strong recommendation, moderate quality evidence). • A restrictive RBC transfusion threshold of 8 g/dL is recommended for patients undergoing orthopedic surgery, cardiac surgery, and those with preexisting cardiovascular disease (strong recommendation, moderate quality evidence).
  • 31. Cont. • The restrictive transfusion threshold of 7 g/dL is likely comparable with 8 g/dL, but RCT evidence is not available for all patient categories. These recommendations do not apply to patients with acute coronary syndrome, severe thrombocytopenia (patients treated for hematological or oncological reasons who are at risk of bleeding), and chronic transfusion-dependent anemia (not recommended due to insufficient evidence).
  • 32. AABB transfusion guideline • For RBC transfusion thresholds, 31 RCTs included 12,587 participants and compared restrictive thresholds (transfusion not indicated until the hemoglobin level is 7-8 g/dL) with liberal thresholds (transfusion not indicated until the hemoglobin level is 9-10 g/dL). The summary estimates across trials demonstrated that restrictive RBC transfusion thresholds were not associated with higher rates of adverse clinical outcomes, including 30-day mortality, myocardial infarction, cerebrovascular accident, rebleeding, pneumonia, or thromboembolism.
  • 33. Cont. • For RBC storage duration, 13 RCTs included 5515 participants randomly allocated to receive fresher blood or standard-issue blood. These RCTs demonstrated that fresher blood did not improve clinical outcomes.
  • 34. Cont. • Dose: 4 ml/kg of RBC increase Hemoglobin level 1 g/dl. • One unit of RBC will raise the hemoglobin of an average-size adult by ~ 1g/dl • Transfuse slowly for first 15 minutes. • Complete transfusion within 4 hours.
  • 35. 3) White cells (leukocytes) • White cell transfusions have no proven clinical uses. • May be indicated in neutropenic patients with bacterial infections not responding to antibiotics. • Transfused granulocytes have a very short circulatory life span, so that daily transfusions of 10 10 granulocytes are usually required.
  • 36. 4) Plasma • This is separated from whole blood and frozen at –25°C or colder within 6–8 hours of donation in order to preserve its labile coagulation factors (Factors V and VIII). • Fresh frozen plasma can be stored for at least one year or longer if low temperatures can be maintained. • When plasma is stored at a temperature of 2–6°C, the labile clotting activity of Factors V and VIII will decline to 10–20% within 48 hours. • Dosage: Initial dose of 15 ml/kg
  • 37. Indications for transfusion of plasma • International normalized ratio (INR) >1.5 with: – Anticipated invasive procedure or surgery. – Massive hemorrhage (over one blood volume) • Emergent reversal of anticoagulant (warfarin) therapy. • Treatment of isolated factor deficiencies. • The correction of coagulopathy associated with liver disease.
  • 38. Indications for transfusion of plasma Coagulopathy (INR) >1.5 with: 1. Active bleeding. 2. Bleeding tendency: • Anticipated invasive procedure or surgery. • The correction of coagulopathy associated with liver disease. • Emergent reversal of anticoagulant (warfarin) therapy. • Treatment of isolated factor deficiencies.
  • 39. 5) Platelet • The platelet count at 1 hour post transfusion of a unit of platelets should increase by 5,000 to 10,000 platelets/µL. • Platelets separated from plasma obtained from 4–6 donations of whole blood are often pooled to produce a therapeutic dose of platelets for an adult platelet apheresis unit, by 30,000–60,000 × 10 9/L. • Dosage: 1 unit of platelet concentrate/10 kg body weight
  • 40. Indications for transfusion of platelets Thrombocytopenia or Dysfunctional platelets with: 1. Active bleeding 2. Bleeding tendency • Neurosurgical procedures: 100,000 platelets/µL • Vaginal delivery and minor surgical procedures: <50,000/µL • Massive transfusion: < 50,000 platelets/µL • Disseminated intravascular coagulation: 20,000–50,000 /µL
  • 41. 6. Cryoprecipitate • Cryoprecipitate is obtained from a single donation of FFP at about 4°C and is rich in factor VIII, von Willebrand factor (VWF), factor XIII, and fibrinogen. • Cryoprecipitate is usually administered as a transfusion of 10 single units. • Each 5- to 15-mL unit contains over 80 units of factor VIII and about 200 mg of fibrinogen.
  • 42. Indications for transfusion of cryoprecipitate • Hemophilia A • von Willebrand disease • Hypofibrinogemia • Uremic bleeding
  • 43. Component separation by apheresis • Apheresis is an alternative method of producing blood components. It is a sterile process in which a donor is connected to a specialized device by which blood is withdrawn, mixed with anticoagulant and centrifuged and a specific component, usually plasma or platelets, is mechanically separated and collected. • The red cells and other components of the blood that are not required are then reinfused back into the donor.
  • 44. Cont. • The advantage of apheresis is that relatively large amounts of plasma or platelets can be collected from a donor. • Since the red cells are returned to the donor’s circulation, this avoids making the donor anemic and the process can be repeated at frequent intervals.
  • 45. Blood Component Characteristic Red Cells Platelet Concentrate Fresh Frozen Plasma Cryoprecipita te Storage Temperature 2-6°C 20-24°C -30°C -30°C Shelf Life Volume 35 day 200-350 5 day 30-50 ml/unit 1 yr (frozen) 150-200ml/unit 1 yr (frozen) 10-15 ml/unit Transfusion Interval Transfuse within 30 min of removal from blood refrigerator. Transfuse unit over maximum of 4 hr Start transfusion as soon as received from blood bank. Transfuse unit within 30 min Once thawed, should be transfused within 4 hr 884 hr Compatibility Testing Requirement Must be compatible with recipient ABO and Rh D type Preferably ABO identical with patient. Rh negative females under the age of 45 yr should be given Rh negative platelets FFP and cryoprecipitate should be ABO compatible to avoid risk of hemolysis caused by donor anti-A or anti-B Administration Infuse through a blood administration set—platelet concentrates should not be infused through blood sets that have been used for blood.
  • 46. Complications of Blood Transfusion 1) IMMUNE Complications. 2) INFECTIOUS Complications. 3) MASSIVE BLOOD TRANSFUSION Complications.
  • 47. Complications of Blood Transfusion 1) IMMUNE Complications – Hemolytic reactions • Acute hemolytic reaction. • Delayed hemolytic reaction. – Nonhemolytic reactions • Febrile reactions • Urticarial reactions • Anaphylactic reactions • Post-transfusion purpura • Transfusion-Related Acute Lung Injury • Graft-versus-host disease
  • 48. Complications of Blood Transfusion 2) Infectious (all products)
  • 49. Complications of Blood Transfusion 3) Complications of massive blood transfusion – Coagulopathy – Hypothermia – Citrate Toxicity – Acid–Base Balance – Serum Potassium Concentration
  • 50. IMMUNE COMPLICATIONS Immune complications following blood transfusions are primarily due to sensitization of the recipient to donor red cells, white cells, platelets, or plasma proteins. Less commonly, the transfused cells or serum may mount an immune response against the recipient.
  • 51. Immune complications • Acute hemolytic transfusion reaction: ABO incompatibility. • Delayed HTR: incompatible red cell antigen. • Febrile non-HTR: anti-WBC antibodies in recipient. • Urticarial reactions: antibody to donor plasma proteins. • Anaphylactic: antibody to donor plasma proteins (IgA). • Transfusion-related acute lung injury (TRALI): neutrophil antibodies in donor product.
  • 52. Hemolytic Reactions • Hemolytic reactions usually involve specific destruction of the transfused red cells by the recipient’s antibodies. Less commonly, hemolysis of a recipient’s red cells occurs as a result of transfusion of red cell antibodies. • Hemolytic reactions are commonly classified as either acute (intravascular) or delayed (extravascular).
  • 53. Acute Hemolytic Reactions • Acute intravascular hemolysis is usually due to ABO blood incompatibility, and the reported frequency is approximately 1:38,000 transfusions. • The most common cause is misidentification of a patient, blood specimen, or transfusion unit. • These reactions are often severe, and may occur after infusion of as little as 10–15 mL of ABO-incompatible blood. • The risk of a fatal hemolytic reaction is about 1 in 100,000 transfusions. • In awake patients, symptoms include chills, fever, nausea, and chest and flank pain.
  • 54. Cont. • In anesthetized patients, an acute hemolytic reaction may be manifested by a rise in temperature, unexplained tachycardia, hypotension, hemoglobinuria, and diffuse oozing in the surgical field. Disseminated intravascular coagulation, shock, and kidney failure can develop rapidly. • The severity of a reaction often depends upon the volume of incompatible blood that has been administered.
  • 55. Management of hemolytic reactions 1. If a hemolytic reaction is suspected, the transfusion should be stopped immediately and the blood bank should be notified. 2. The unit should be rechecked against the blood slip and the patient’s identity bracelet. 3. Blood should be drawn to identify hemoglobin in plasma, to repeat compatibility testing, and to obtain coagulation studies and a platelet count. 4. A urinary catheter should be inserted, and the urine should be checked for hemoglobin. 5. Osmotic diuresis should be initiated with mannitol and intravenous fluids.
  • 56. Delayed Hemolytic Reactions Also called extravascular hemolysis, is generally mild and is caused by antibodies to non-D antigens of the Rh system or to foreign alleles in other systems such as the Kell, Duffy, or Kidd antigens. Following an ABO and Rh D-compatible transfusion, patients have a 1–1.6% chance of forming antibodies directed against foreign antigens in these other systems.
  • 57. Cont. • The hemolytic reaction is therefore typically delayed 2–21 days after transfusion, and symptoms are generally mild, consisting of malaise, jaundice, and fever. • The patient’s hematocrit typically fails to rise, or rises only transiently, in spite of the transfusion and the absence of bleeding. • The serum unconjugated bilirubin increases as a result of hemoglobin breakdown.
  • 58. Cont. • Diagnosis of delayed antibody-mediated hemolytic reactions may be facilitated by the antiglobulin (Coombs) test. The direct Coombs test detects the presence of antibodies on the membrane of red cells. • Pregnancy (exposure to fetal red cells) can also be responsible for the formation of alloantibodies to red cells. • The frequency of delayed hemolytic transfusion reactions is estimated to be approximately 1:12,000 transfusions. • The treatment of delayed hemolytic reactions is primarily supportive.
  • 59. Nonhemolytic Immune Reactions • Nonhemolytic immune reactions are due to sensitization of the recipient to the donor’s white cells, platelets, or plasma proteins. • The risk of these reactions may be minimized by the use of leukoreduced blood products.
  • 60. Nonhemolytic Immune Reactions A- Febrile Reactions: • White cell or platelet sensitization is typically manifested as a febrile reaction. • Such reactions are relatively common (1–3% of transfusion episodes) and are characterized by an increase in temperature without evidence of hemolysis. • Patients with a history of repeated febrile reactions should receive leukoreduced transfusions only.
  • 61. Cont. B- Urticarial Reactions: • Urticarial reactions are usually characterized by erythema, hives, and itching without fever. • They are relatively common (1% of transfusions) and are thought to be due to sensitization of the patient to transfused plasma proteins. • Urticarial reactions can be treated with antihistaminic drugs (H1 and perhaps H2- blockers) and steroids.
  • 62. Cont. C- Anaphylactic Reactions: • Anaphylactic reactions are rare (approximately 1:150,000 transfusions). • These severe reactions may occur after only a few milliliters of blood has been given, typically in IgA-deficient patients with anti-IgA antibodies who receive IgA-containing blood transfusions. • The prevalence of IgA deficiency is estimated to be 1:600-800 in the general population. • Such reactions require treatment with epinephrine, fluids, corticosteroids, and H1 and H2 blockers.
  • 63. Cont. D- Transfusion-Related Acute Lung Injury (TRALI) : • (TRALI) presents as acute hypoxia and noncardiac pulmonary edema occurring within 6 h of blood product transfusion. • It may occur as frequently as 1:5000 transfused units, and with transfusion of any blood component, but especially platelets and FFP. • It is thought that transfusion of antileukocytic or anti-HLA antibodies results in damage to the alveolar–capillary membrane. • Treatment is similar to that for acute respiratory distress syndrome with the important difference that TRALI may resolve within a few days with supportive therapy.
  • 64. Cont. E- Graft-Versus-Host Disease: • This type of reaction may be seen in immunocompromised patients. Cellular blood products contain lymphocytes capable of mounting an immune response against the compromised (recipient) host. • Use of special leukocyte filters alone does not reliably prevent graft -versus-host disease; irradiation(1500–3000 cGy) of red cell, granulocyte, and platelet transfusions effectively eliminates lymphocytes without altering the efficacy of such transfusions.
  • 65. Cont. F- Post-Transfusion Purpura: • Rarely, profound thrombocytopenia may occur following blood transfusions. • This post-transfusion purpura results from the development of platelet alloantibodies. • For unknown reasons, these antibodies also destroy the patient’s own platelets. • The platelet count typically drops precipitously 5–10 days following transfusion. • Treatment includes intravenous IgG and plasmapheresis.
  • 66. Cont. G- Transfusion-Related Immunomodulation: • Allogeneic transfusion of blood products may diminish immunoresponsiveness and promote inflammation. • Post-transfusion immunosuppression is clearly evident in renal transplant recipients, in whom preoperative blood transfusion improves graft survival.
  • 67. INFECTIOUS COMPLICATIONS A- Viral Infections: Hepatitis: • The incidence of post-transfusion viral hepatitis varies greatly, from approximately 1:200,000 transfusions (for hepatitis B) to approximately 1:1,900,000 (for hepatitis C). • Most acute cases are anicteric. Hepatitis C is the more serious infection; most cases progress to chronic hepatitis, with cirrhosis developing in 20% of chronic carriers and hepatocellular carcinoma developing in up to 5% of chronic carriers.
  • 68. Cont. Acquired Immunodeficiency Syndrome (AIDS): • The virus responsible AIDS, HIV-1, is transmissible by blood transfusion. HIV-2 is a similar, but less virulent virus. • All blood is tested for the presence of anti-HIV-1 and anti-HIV- 2 antibodies. The requirement for nucleic acid testing by the Food and Drug Administration (FDA) has decreased the risk of transfusion-transmitted HIV to approximately 1:1,900,000 transfusions.
  • 69. Cont. Other Viral Infections: • Cytomegalovirus (CMV) and Epstein–Barr virus usually cause asymptomatic or mild systemic illness. • Some individuals infected with these viruses become asymptomatic infectious carriers; the white cells in blood units from such donors are capable of transmitting either virus. • Immunocompromised and immunosuppressed patients (eg, premature infants, organ transplant recipients, and cancer patients) are particularly susceptible to severe transfusion- related CMV infections.
  • 70. Cont. B- Parasitic Infections: • Parasitic diseases that can be transmitted by transfusion include malaria, toxoplasmosis, and Chagas’ disease. Such cases are very rare.
  • 71. Cont. C- Bacterial Infections: • Bacterial contamination of blood products is the second leading cause of transfusion-associated mortality. • The prevalence of positive bacterial cultures in blood products ranges from 1:2000 for platelets to 1:7000 for PRBCs and may be due to transient donor bacteremia or inadequate antisepsis during phlebotomy. • The prevalence of sepsis due to blood transfusion ranges from 1:25,000 for platelets to 1:250,000 for PRBCs. Both gram-positive (Staphylococcus) and gram-negative (Yersinia and Citrobacter) bacteria can contaminate blood transfusions and transmit disease. To avoid the possibility of significant bacterial contamination, blood products should be administered over a period shorter than 4 h.
  • 72.
  • 73. MASSIVE BLOOD TRANSFUSION • Massive transfusion, historically defined as the replacement by transfusion of 10 units of red cells in 24 hours, is a response to massive and uncontrolled hemorrhage (Uptodate). • Massive blood transfusion may be defined either as the acute administration of more than 1.5 times the patient's estimated blood volume, or as the replacement of the patient's total blood volume by stored homologous bank blood in less than 24 h (British Journal of Anaesthesia).
  • 74. Cont. Various definitions of massive blood transfusion (MBT) have been published in the medical literature such as: • Replacement of one entire blood volume within 24 h • Transfusion of >10 units of packed red blood cells (PRBCs) in 24 h • Transfusion of >20 units of PRBCs in 24 h • Transfusion of >4 units of PRBCs in 1 h when on-going need is probable • Replacement of 50% of total blood volume (TBV) within 3 h.
  • 75. Complications of massive blood transfusion • Coagulopathy • Hypothermia • Citrate Toxicity • Acid–Base Balance: • Serum Potassium Concentration
  • 76. Complications of massive blood transfusion • Coagulopathy The most common cause of nonsurgical bleeding following massive blood transfusion is dilutional thrombocytopenia, although clinically significant dilution of coagulation factors may also occur. Coagulation studies and platelet counts, if readily available, should guide platelet and FFP transfusion.
  • 77. BJA: British Journal of Anaesthesia, Volume 111, Issue suppl_1, December 2013, Pages i71–i82, https://doi.org/10.1093/bja/aet376 The content of this slide may be subject to copyright: please see the slide notes for details. Pathogenesis of haemostasis abnormality in MT. Dilutional coagulopathy, activation of inflammatory mediators.
  • 78. Cont. Hypothermia • Massive blood transfusion is an absolute indication for warming all blood products and intravenous fluids to normal body temperature. • Ventricular arrhythmias progressing to fibrillation often occur at temperatures close to 30°C, and hypothermia can hamper cardiac resuscitation. • The use of rapid infusion devices with efficient heat transfer capability has decreased the incidence of transfusion-related hypothermia.
  • 79. Cont. Citrate Toxicity • Because citrate metabolism is primarily hepatic, patients with hepatic disease or dysfunction (and possibly hypothermic patients) may demonstrate hypocalcemia and require calcium infusion during massive transfusion, as may small children and others with relatively impaired parathyroid–vitamin D function. • Clinically important hypocalcemia, causing cardiac depression, will not occur in most normal patients unless the transfusion rate exceeds 1 unit every 5 min, and intravenous calcium salts should rarely be required in the absence of measured hypocalcemia.
  • 80. Cont. Acid–Base Balance: • Although stored blood is acidic due to the citric acid anticoagulant and accumulation of red cell metabolites (carbon dioxide and lactic acid), metabolic acidosis due to transfusion is uncommon because citric acid and lactic acid are rapidly metabolized to bicarbonate by the normal liver. • In the situation of massive blood transfusion, acid-base status is largely dependent upon tissue perfusion, rate of blood transfusion, and citrate metabolism. • Once normal tissue perfusion is restored, any metabolic acidosis typically resolves, and metabolic alkalosis commonly occurs as citrate and lactate contained in transfusions and resuscitation fluids are converted to bicarbonate by the liver.
  • 81. Cont. Serum Potassium Concentration: • The extracellular concentration of potassium in stored blood steadily increases with time. The amount of extracellular potassium transfused with each unit is typically less than 4 mEq per unit. • Hyperkalemia can develop regardless of the age of the blood when transfusion rates exceed 100 mL/min. • Hypokalemia is commonly encountered postoperatively, particularly in association with metabolic alkalosis.
  • 82. Cost of blood components Netherland 2011 USA 2008 UK 2001 Product € 210 300 $ 82.5 £ Red cells (leucocyte depleted) € 102 233 $ £ 156 Platelets (leucocyte depleted) € 181 160 $ £ 19 Fresh frozen plasma (leucocyte depleted) 117 $ £ 23 Cryoprecipitate (leucocyte depleted)
  • 83.
  • 84. Compatible fluids and medications • No medications or solutions should be added to or infused through the same tubing as blood products except for 0.9% Sodium Chloride, ABO compatible plasma or 4% Albumin. • It has been shown to be safe to co-administer morphine (1mg/mL), pethidine (10mg/mL) and ketamine (1mg/mL) if diluted in 0.9% Sodium Chloride with red cells. In these situations, the blood product should be administered via the closest to the patient (distal lumen).
  • 85. Cont. • If other medications are required during a blood transfusion, the transfusion must be stopped and the line flushed with 0.9% Sodium Chloride before and after administration of the medication. The blood transfusion can then recommence. • Fluids containing glucose are not compatible with red blood cells, they cause clumping of the red blood cells. • Crystalloid or colloid solutions that contain calcium should never be administered concurrently with any blood product. Calcium reverses the anticoagulant citrate causing red blood cells to clot.
  • 86. References • Morgan and Mikhail's Clinical Anesthesiology, 6th edition • The Clinical Use of Blood - World Health Organization • Uptodate.com 2019

Editor's Notes

  1. In theory, the goals of oxygen delivery and volume expansion can be achieved with packed RBCs and crystalloid solutions
  2. Transfused granulocytes have a very short circulatory life span, so that daily transfusions of 10 10 granulocytes are usually required.
  3. Plasma is separated from whole blood by centrifugation or by allowing the red cells to settle under gravity in a blood bank refrigerator.
  4. Incompatible units of platelet concentrates, FFP, clotting factor concentrates, or cryoprecipitate may contain small amounts of plasma with anti-A or anti-B (or both) alloantibodies. Transfusions of large volumes of such units can lead to intravascular hemolysis.
  5. By the time significant amounts of these antibodies have formed (weeks to months), the transfused red cells have been cleared from the circulation. Moreover, the titer of these antibodies subsequently decreases and may become undetectable.
  6. Reexposure to the same foreign antigen during a subsequent red cell transfusion, however, triggers an anamnestic antibody response against the foreign antigen.
  7. In this setting, however, this test cannot distinguish between recipient antibodies coated on donor red cells and donor antibodies coated on recipient red cells. The latter requires a more detailed reexamination of pretransfusion specimens from both the patient and the donor.
  8. Specific bacterial diseases rarely transmitted by blood transfusions from donors include syphilis, brucellosis, salmonellosis, yersiniosis, and various rickettsioses.
  9. Although most clinicians will be familiar with “routine” coagulation tests (eg, prothrombin time [PT], activated partial thromboplastin time [aPTT], international normalized ratio [INR], platelet count, fibrinogen), multiple studies show that viscoelastic analysis of whole blood clotting (thromboelastography, rotation thromboelastometry, and Sonoclot analysis) may be more useful in resuscitation, liver transplantation, and cardiac surgical settings.
  10. Fig 1 Pathogenesis of haemostasis abnormality in MT. Dilutional coagulopathy, activation of inflammatory mediators, hyperfibrinolysis, thrombocytopathy, and metabolic abnormalities (hypothermia, hypocalcaemia, and acidosis) all contribute to the pathogenesis of the haemostasis abnormality in massive haemorrhage. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author [2013]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oup.com