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Evolution of transfusion practices

10 30 rule
AIDS
A patient specific approach to the decision to transfuse
blood components

RBC transfusion threshold


The rationale
???

What Hgb / Hct level poses greater risk to the patient than
the threat of contracting a transfusion-transmitted disease
greater degrees of anemia could be well tolerated
chronically anemic renal failure
Jehovahs witness
morbidity and mortality rates did not increase
until Hgb level fell below 7 g/dl

RBC transfusion threshold


The rationale
Adverse physiologic effects of anemia
No evidence that mild to moderate anemia impairs
wound healing
Hct < 15
increases bleeding
increases the length of hospital stay
increases the frequency or severity of postoperative infection

RBC transfusion threshold


The rationale

The cause of anemia is thought to be more important in influencing


the perioperative course than the severity of anemia
Maintaining of blood volume was more critical than correcting
anemia

RBC transfusion threshold


The rationale
The goal:
to anticipate, on a patient-by-patient basis, the minimum
Hgb level that will avoid organ damage due to O2 deprivation
Do2
Vo2
physiologic capacity for compensatory mechanism
The decision
should be based upon the clinical judgment that
oxygen-carrying capacity of the blood must be increased

Calculation of oxygen delivery (Do 2)

Do2 = Cao2 x CO x 10
Cao2 = Sao2 x Hg x 1.34 + Pao2 x 0.0031

Calculation of oxygen consumption (Vo2)


Vo2 = CO x (Cao2 - Cvo2)
normal arteriovenous oxygen content difference is 5 vol%
Svo2 = 75%
Vo2 :
sepsis
hyperthermia
metabolic activity
hyperthyroidism

Oxygen extraction ratio


Fraction of total oxygen delivered is consumed or extracted
by the tissues
ER = Vo2 / Do2
= [ CO x (Cao2 - Cvo2)] / Cao2 x CO
= (Cao2 - Cvo2) / Cao2

Oxygen extraction ratio


Global Regional
normal global oxygen delivery may occur in spite of critical
levels of regional ischemia
Svo2:
vo2 of many vascular beds (global)
heart, under basal condition : 55 70%
kidney and skin
: 7 10%
organ with the greatest ER will have the least O2 reserve

Compensatory mechanisms during anemia


1. Increased cardiac output
2. Redistribution of cardiac output
3. Increased oxygen extraction
4. Changes in Oxygen-Hemoglobin affinity

Compensatory mechanisms during anemia


Increased cardiac output
With isovolemic hemodilution
SV
SVR
vascular tone
viscocity
age
acute or develops slowly
self correcting
oxygen carrying capacity
oxygen transport

Compensatory mechanisms during anemia


Redistribution of cardiac output
to organ with greater O2 requirement (brain and heart)

The heart
has a high extraction ratio
must rely upon redistribution blood flow to O2 supply
greatest risk !!!

Compensatory mechanisms during anemia


Increased oxygen extraction
Play an important adaptive role
when the normovolemic Hct drops below 25%
mixed venous oxygen saturation
Organs with high ER under basal condition
limited capacity to increase Do2 by this mechanism

Compensatory mechanisms during anemia


Changes in Oxygen-Hemoglobin affinity
The sigmoid-shaped oxygen-Hemoglobin dissociation curve
P50 for normal adult Hgb at 370C and a pH of 7.4 : 27 mmHg
Left-shifting
hypothermia, alkalosis
Hgb molecule is more stingy and requires lower Po2
to release O2 to tissues
Hgb molecules does not release 50% of its O2

Compensatory mechanisms during anemia


Changes in Oxygen-Hemoglobin affinity
When anemia develops slowly
the affinity of Hgb for O2 may be decreased (right-shifted)
accumulation of 2,3 - DPG

Isovolemic anemia vs Acute blood loss


Acute blood loss
stimulation of adrenergic nervous system
vasoconstriction and tachycardia
! Increased CO does not contribute

Chronic anemia
CO may not change until Hgb decreases to 7 8 g/dl
synthesis of supranormal level of 2,3 DPG begin at Hgb 9 g/dl
right shifted

Establishing the RBC transfusion threshold


Transfusion trigger
the Hgb or Hct threshold that justifies RBC transfusion
for individual patient
it is presumed that the benefits of RBC transfusion
outweigh the risks

No single criterion could replace clinical judgment as the basis of


decision-making
No evidence that mild-moderate anemia contribute to
perioperative morbidity
NIH Consensus conference on Perioperative Red Cell Transfusion 1988

Establishing the RBC transfusion threshold


Guide therapy
clinical assessment
Hgb value
laboratory data (when indicated)
arterial oxygenation
mixed venous oxygen tension
cardiac output
oxygen extraction ratio
blood volume
estimation of the patients myocardial/coronary reserve !!!

Condition that may decrease tolerance for anemia


and influence the RBC transfusion threshold
Increased oxygen demand
Hyperthermia
Hyperthyroidism
Pregnancy

Limited ability to increase CO

Coronary artery disease


Myocardial dysfunction (infarction, cardiomyopathy)
-adrenergic blockade

Inability to redistribute CO

Low SVR state (sepeis, post-CPB)


Occlusive vascular disease (cerebral, coronary)

Left shift of O2-Hgb curve


Alkalosis
Hypothermia

Abnormal Hemoglobins

Presence of stored Hgb (decreased 2,3-DPG)


Hgb S

Acute anemia (limited 2,3-DPG compensation)


Impaired oxygenation
Pulmonary disease

Patient
consent

Low risk
younger patient

High risk
Atherosclerotic

slower blood loss


chronic anemia
temporary intra-op
hypothermia or
hemodilution

vasc. Dse
Perioperative
ischemia
pulmonary dse
rapid blood loss
Anticipated post-op
blood loss

Acute blood loss


and hypovolemia

10

Target hemoglobin concentration ( g/dl )

12

Compatibility testing
1. ABO Rhesus blood type identification
2. Antibody screening of donor plasma
3. Donor-Recipient cross-match

Compatibility testing
ABO Rhesus blood type identification
According to the antigens present on the surface of the RBC
Which antibodies are present in the serum
serum constitutively contains antibodies to the antigens
that are lacking on the RBC

Compatibility testing
ABO Rhesus blood type identification

Rh (D) antigen
when D antigen is not present on the surface of RBC,
anti-D antibodies are not constitutively present in the serum
Rh-negative exposes to donor RBCs with D antigen (Rh-pos)
will usually produce anti-D antibody (60-70%)
latent period
the reaction evolve slowly and may not be clinicall
apparent on first exposure
subsequent exposure of Rh-neg to Rh(D)-pos
acute hemolytic reaction

What donor blood group type may be compatible


For transfusion to a particular recipient ?
Focus on which antibodies will be present in the recipient serum !!!
reaction of these antibodies with donor RBC antigens
can activate complement
hemolysis of RBC
Type O-negative blood universal donors
Type AB-positive blood universal recipients

Compatibility testing
Antibody screening
Seek the presence of recipient antibodies against RBC antigens
commercially supplied RBCs

+ recipient serum
+ donor serum

The antibody screening should be repeated if patient has been


transfused since the last antibody screening test
may produce newly detectable antibodies

Compatibility testing
The cross-match
Donor RBCs mixed with recipient serum
simulating the actual anticipated transfusion
3 phases
1. Immediate phase
2. Incubation phase
3. Antiglobulin phase

Compatibility testing
The cross-match
The immediate phase

To ensure that there have been no errors in ABO-Rh typing


Donor RBCs + Patient serum macroscopic agglutination
(at room temperature)
Requires only 1-5 minutes
Detects incompatibilities
ABO system
MN, P, Lewis system
usually present in low titers
not reactive at physiologic temperature

Compatibility testing
The cross-match
The incubation phase
Requires 30-45 minutes
incubated in albumin or low-ionic strength salt solution
Detects
antibodies primarily in Rh system
incomplete antibodies
antibodies that attach to a specific antigen but do not
cause agglutination in a saline suspension of RBCs

Compatibility testing
The cross-match
The antiglobulin phase ( indirect antiglobulin test )

Addition of antiglobulin sera at the end of the incubation phase


contain antibodies that will bind to antiglobulin attached to
antigens on the surface of the donor RBCs
to identify the most incomplete antibodies from all blood
group system

Is cross-match necessary ?
ABO-Rh status alone

99.8 % compatible

With antibody screen

99.94% compatible

With complete cross-match

99.95% compatible

Those who have not previously exposed or pregnant


incompatibility : 1 in 1000
Those who have previously exposed or pregnant
incompatibility : 1 in 100

The administration, in emergency situation of uncross-matched


blood to patient with no history of pregnancy or transfusion
entails relatively low risk

Type and Screen orders


When blood is ordered preoperatively for surgical cases in which
transfusion is unlikely
If the need arises the blood can be cross-matched prior to transfusion
Advantages
if the blood is not needed
the additional expenses for cross-match is eliminated
if cross-match is performed and compatible unit identified
those unit are held in reserve
temporarily out of blood supply
if the blood is not used
wastage by outdating

Emergency transfusion
Choices
Type-specific partially cross-matched blood
Type-specific uncross-matched blood
O-negative (universal donor) PRBCs

O-negative (universal donor) whole blood


contains high titers of antibodies

Emergency transfusion
Even if the patients blood type become known and available
after 2 units of universal donor has been transfused

subsequent transfusion should continue with universal donor


even PRBC, contains some antibodies

reaction between antibodies in the plasma from the firs


donor and antigens on RBCs of the new donor unit
should not receive the type specific blood

until the transfused antibodies titers have fallen to the safe


level

Risk of blood product administration


1. Problems related to blood storage
2. Problems related to immune-mediated transfusion reaction
3. Infectious risks

Risk of blood product administration


Problems related to blood storage
Citrate intoxication
Citrate prevent coagulation of stored blood
by chelating ionized Calcium
large volume (> 1 blood volume)
administered rapidly (> 1 ml/kg/minor 1 unit/5 mins)
impaired liver function
temporary reduction of ionized Ca levels

Citrate intoxication
Signs
hypotension
narrow pulse pressure
VEDP
CVP
ECG
prolonged QT interval
widened QRS complexes
flattened T waves

Risk of blood product administration


Problems related to blood storage
Acid-base Changes
CPD pH to 7.0 7.1
during storage
ongoing metabolism of glucose to lactate
production of CO2
Citrate metabolized to bicarbonate

Risk of blood product administration


Problems related to blood storage
Decreases in 2,3-DPG
left shift of O2-Hgb dissociation curve
less efficient O2

Risk of blood product administration


Problems related to blood storage
Hyperkalemia
to maintain electrochemical neutrality
H+ generated during storage
RBCs lysis
with normal infusion rate K+ is distributed
rates > 90 120 ml/min hyperkalemia
aggravated by
hypovolemia
hypothermia
acidosis

Risk of blood product administration


Problems related to blood storage
Volume overload
occurs when blood or fluid transfused too rapidly for
compensatory fluid redistribution take place

Risk of blood product administration


Problems related to blood storage
Hypothermia
from rapid transfusion of large volumes of cold blood
stored at temp 1 60C
CO
tissue perfusion impaired
vasoconstriction
left-shifting of O2-Hgb dissociation curve
metabolic acidosis
shivering
O2 consumption by 300 - 400%
hemostatic dysfunction
ventricular irritability

Risk of blood product administration


Problems related to blood storage

Microaggregate delivery
2nd 5th day platelet aggregation
after 10th day larger aggregates, fibrin, degenerated white cells
pulmonary insufficiency
ARDS

Risk of blood product administration


Problems related to blood storage
Dilutional coagulopathy
platelets
clotting factors
V and VIII

Risk of blood product administration


Problems related to immune-mediated transfusion reaction
Reaction to RBC antigen
Immediate hemolytic transfusion reactions
anti-A
anti-B
anti-Kell
anti-Kidd
anti-Lewis
anti-Duffy
Incidence : 1 per 6000 7000 units transfused
Physician errors 20%
Mortality : 20 60 %

Immediate hemolytic transfusion reactions


Antibodies in the recipient plasma attack the corresponding antigen
on donor RBCs
activate Hageman factor (factor XII)
acts on kinin system bradykinin
capillary permeability
dilates the arterioles
hypotension
activate the complement system
release of histamine, serotonin from mast cell
bronchospasm

Immediate hemolytic transfusion reactions


hemolysis
release hemoglobin to the blood
bound to haptoglobin, albumin
circulate freely
renal damage
renal blood flow
mechanical obstruction in the renal tubule
free Hgb, RBC stroma
deposition of antigen-antibody complexes (G)
deposition of fibrin (DIC)

Immediate hemolytic transfusion reactions


Signs and symptoms
fever, chill, nausea and vomiting
hypotension and tachycardia
flushed and dyspneic
chest and back pain
restless
hemoglobinuria
diffuse bleeding
renal failure

Immediate hemolytic transfusion reactions


If transfusion reaction is suspected
transfusion should be stopped
recheck
repeat cross-match
direct anti-globulin test (Coombs test)
haptoglobin
only
for
hemolysis,
plasma & urine Hgb
not specifically of an immune reaction
bilirubin assays
examination of recipient plasma after brief centrifugation
pinkish discolorization
baseline coagulation status

Immediate hemolytic transfusion reactions


Management
maintenance of systemic blood pressure
volume
pressors
inotropes
preservation of renal function
promote urine output
volume
diuretic (mannitol/furosemide)
Sodium Bicarbonate
prevention of DIC

Risk of blood product administration


Problems related to immune-mediated transfusion reaction
Reaction to RBC antigen
Delayed hemolytic transfusion reactions

When the donor RBCs bear an antigen to which the recipient


has previously been exposed (transfusion/pregnancy)
over time, the recipient antibodies fall to levels too low
to be detected by compatibility testing
when transfused again with RBC containing
the original immunizing antigen
anamnestic response
produce more antibody
sequestered extrsvascularly (spleen, RES
symptoms are less severe

Delayed hemolytic transfusion reactions


Usually involves
Rh system
Kidd system
1 per 800 2500 transfusions
May be detected by the first or second week following transfusion
low-grade fever
bilirubin, with or without jaundice
unexplained reduction in Hgb concentration
Confirmed by + direct antiglobulin test (Coombs test)
Self-limiting, as transfused cells are removed

Risk of blood product administration


Problems related to immune-mediated transfusion reaction
Transfusion reaction to donor proteins
Urticarial reactions
0.2 2% of all transfusion
Due to the release of histamine
urticaria
itching
swelling
rash
Treatment
anti-histamine
Prevention
Saline-washed cell

Transfusion reaction to donor proteins


Anaphylaxis
when patients with hereditary Ig-A deficiency who have been
sensitized by previous transfusion or pregnancy are exposed
to blood with foreign Ig-A protein
symptoms
dyspnea
hypotension
bronchospasm
chest pain
laryngeal edema
shock
treatment
discontinuation of transfusion
epinephrine and steroids
prevention
washed RBCs, frozen deglycerolized RBCs,
RBCs from Ig-A deficient donor

Risk of blood product administration


Problems related to immune-mediated transfusion reaction
White cell-related transfusion reactions
Febrile reaction
Patient who receive multiple transfusions of PRBCs or platelets
may develop antibodies to HLA
during future transfusion : febrile reactions
antibody attack on donor leukocytes
lysis of donor granulocytes
release of chemical mediators
phagocytosis of donor leukocyte fragments
stimulate host macrophages to produce pyrogens

Febrile reaction
1% of all RBCs transfusions
Symptoms
temperature > 1o within 4 hours of transfusion
defervesces within 48 hours
Treatment
Acetaminophen

Risk of blood product administration


Problems related to immune-mediated transfusion reaction
White cell-related transfusion reactions
Graft-versus-Host Disease (GVHD)

When transfused (transplanted) into immunocompromised patients


the donor lymphocytes may become engrafted, proliferate and
established an immune response against the recipient
engrafted lymphocytes reject the host
progress rapidly to pancytopenia
high fatality rate

Graft-versus-Host Disease (GVHD)


Patient at risk
organ transplant patients
neonates undergone blood exchange transfusion
immunocompromised patients by other diseases
when a genetic relationship exists between donor and recipient
shares HLA haplotypes
although immunologically competent
fail to reject the transfused cell
do not recognize them as foreign body
however, the transfused donor lymphocyte
recognize the host as foreign body

Graft-versus-Host Disease (GVHD)


Whole blood
PRBC
Granulocytes
Platelets
Fresh plasma
But not
FFP
cryoprecipitate
frozen RBC
Donations from first-degree relatives
Transfusion in immunocompromised patients
irradiation to inactivate donor lymphocytes