Tranfusion - RACHMAN
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B L O O D G R O U P
Dr.H.Abd Rachman Tanjung AIFM
BAGIAN FISIOLOGI
FAKULTAS KEDOKTERAN
UNIVERSITAS ISLAM SUMATERA UTARA
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Blood groups
Antibodies in the plasma of one blood reactwith antigens on the surface of the red cells of
another blood
more than 30 commonly occurring antigens two particular groups of antigens:AB0 and Rh
systems are immunogenic enough to cause
hemagglutination
Blood transfusion often resulted in
agglutination and hemolysis, often led to
death.
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4
Antigens of the ABO blood group
Number ofantigens
4: A, B, AB, and A1
Antigenspecificity
CarbohydrateThe sequence of oligosaccharides determines whetherthe antigen is A, B, or A1
Antigen carryingMolecules
Glycoproteins and glycolipids of unknownfunctionThe ABO blood group antigens are attached tooligosaccharide chains that projectabove the RBC surface. These chains are attached toproteins and lipids that lie in theRBC membrane
Molecular basis
The ABO gene indirectly encodes the ABO
blood group antigens.The ABO locus has three main allelic forms: A, B, andO. The A and B alleles eachencode a glycosyltransferase that catalyzes the finalstep in the synthesis of the A andB antigen, respectively. The A/B polymorphism arises
from several SNPs in the ABOgene, which result in A and B transferases that differ
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Antigens of the ABO blood group
Frequency ofABO blood
A: 43% Caucasians, 27% Blacks, 28% AsiansB: 9% Caucasians, 20% Blacks, 27% Asians
A1: 34% Caucasians, 19% Blacks, 27% AsiansNote: Does not include AB blood groups (1)
Frequency ofABOphenotypes
Blood group O is the most common phenotypein most populations.Caucasians: group O, 44%; A1, 33%; A2, 10%; B, 9%;A1B, 3%; A2B, 1%
Blacks: group O, 49%; A1, 19%; A2, 8%; B, 20%; A1B,3%; A2B, 1%Asians: group O, 43%; A1, 27%; A2, rare; B, 25%;A1B, 5%; A2B, rareNote: Blood group A is divided into two mainphenotypes, A1 and A2
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Antibodies produced against ABO blood group antigen
Antibody type IgG and IgMNaturally occurring. Anti-A is found in the
serum of people with blood groupsO and B. Anti-B is found in the serum ofpeople with blood groups O and A
Antibody reactivity Capable of hemolysisAnti-A and anti-B bind to RBCs and activate thecomplement cascade, which lyses the RBCs while they
are still in the circulation (intravascular hemolysis)
Transfusion reaction Yes typically causes an acute hemolytictransfusion reactionMost deaths caused by blood transfusion are theresult of transfusing ABOincompatible blood
Hemolytic disease ofthe newborn
No or mild diseaseHDN may occur if a group O mother has more thanone pregnancy with a childwith blood group A, B, or AB. Most cases are mild anddo not requiretreatment
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ABO system
four groups: A, B, AB, O
two (3) agglutinogens = antigens on the surface of
RBC
two agglutinins = antibodies present in the plasma agglutinogens = glycoprotein, oligosaccharides
having different carbohydrate at their endings
A N-acetylgalactosamin
B galactose
Hfucosotransferasa
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Frequency of ABO Blood Groups.
O 47%
A 41%
B 9%
AB 3%
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AB0 agglutinogens determined by two genes, one on each of two
paired chromosomes 0 is functionless gene; O = ohne
A gene determines A group; B genedetermines B group
codominancy: blood type A: genotype AA, A0 blood type B: genotype BB, B0 blood type AB: genotype AB blood type 0: genotype 00
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AB0 AGGLUTININS
Antibodies present in the plasma
-globulins, IgM molecules
group A antibodies anti-B
group B antibodies anti-A
group AB no antibodies group 0 antibodies anti-A and anti-B
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O-A-B Blood Types
When neither A nor B agglutinogen is present, the
blood is type O. When only type A agglutinogen is
present, the blood is type A. When only type B
agglutinogen is present, the blood is type B. When
both A and B agglutinogens are present, the blood is
type AB.
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RBC ANTIGENS & BLOOD TYPING
Antigens present on RBC surface specify blood type
Major antigen group isABOsystem
Type A blood has only A antigens
Type B has only B antigens Type AB has both A & B antigens
Type O has neither A or B antigens
13-15
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RH SYSTEM II
Landsteiner 1940
C, D, E antigens (D is most immunogenic)
85 % white people Rh+, 99 % Asians Rh+, Africanblack 100 % Rh+
clinical importance:1.blood transfusion
2.pregnancy: mother Rh negative and fetus Rhpositive, antibodies diffuse trough the placenta(erythroblastosis fetalis, new-born hemolysis,
kernicterus, jaundice)in both cases the exposition to the antigen is
needed first (sensitization), because anti-Rhantibodies are NOT normally produced Rhantigen is not often present in the nature
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OTHERSYSTEMS
MNSs: very low immunogens, normally no natural
antibodies in blood occur, Landsteiner 1927
P system: Landsteiner, low immunogens ( 80%
people); subtypes
Kell, Duffy, Kidd, Lutheran, Diego
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TRANSFUSION REACTIONS
People with Type A bloodmake antibodies to Type BRBCs, but not to Type A
Type B blood has antibodies
to Type A RBCs but not toType B
Type AB blood doesnt haveantibodies to A or B
Type O has antibodies to
both Type A & B
If different blood types aremixed, antibodies will causemixture to agglutinate
Fig 13.513-16
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TRANSFUSION REACTIONSCONTINUED
If blood types don't match,
recipients antibodiesagglutinate donors RBCs
Type O is universal donorbecause lacks A & Bantigens Recipients antibodies wont
agglutinate donors Type ORBCs
Type AB is universalrecipient because doesnt
make anti-A or anti-Bantibodies Wont agglutinate donors
RBCs
Insert fig. 13.6
Fig 13.6 13-17
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RH BLOOD TYPES
Rh Antigens-"Rh-Positive" and "Rh-Negative" People.There are six common types of Rh antigens, each of which is
called an Rh factor. These types are designated C, D, E, c, d,
and e.
A person who has a C antigen does not have the c antigen, bthe person missing the C antigen always has the c antigen. T
same is true for the D-d and E-e antigens.
Anyone who has this type of antigen is said to be Rh positive,
whereas a person who does not have type D antigen is said tbe Rh negative.
About 85 per cent of all white people are Rh positive and 15 p
cent, Rh negative..
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Rh Immune Response
Formation of Anti-Rh Agglutinins. When red blood cells
containing Rh factor are injected into a person whose blooddoes not contain the Rh factor-that is, into an Rh-negativeperson-anti-Rh agglutinins develop slowly, reaching maximumconcentration of agglutinins about 2 to 4 months later. Thisimmune response occurs to a much greater extent in somepeople than in others. With multiple exposures to the Rh factor,an Rh-negative person eventually becomes strongly"sensitized" to Rh factor.
Characteristics of Rh Transfusion Reactions. If an Rh-negative person has never before been exposed to Rh-positiveblood, transfusion of Rh-positive blood into that person will
likely cause no immediate reaction. However, anti-Rhantibodies can develop in sufficient quantities during the next 2to 4 weeks to cause agglutination of those transfused cells thatare still circulating in the blood.
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These cells are then hemolyzed by the tissue
macrophage system. Thus, a delayedtransfusionreaction occurs, although it is usually mild. Onsubsequent transfusion of Rh-positive blood intothe same person, who is now already immunizedagainst the Rh factor, the transfusion reaction is
greatly enhanced and can be immediate and assevere as a transfusion reaction caused bymismatched type A or B blood.
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Erythroblastosis Fetalis ("Hemolytic Disease of the
Newborn") Erythroblastosis fetalis is a disease of the fetus
and newborn child characterized by agglutination and
phagocytosis of the fetus's red blood cells. In most instancesof erythroblastosis fetalis, the mother is Rh negative and the
father Rh positive. The baby has inherited the Rh-positive
antigen from the father, and the mother develops anti-Rh
agglutinins from exposure to the fetus's Rh antigen. In turn,the mother's agglutinins diffuse through the placenta into the
fetus and cause red blood cell agglutination.
1. Incidence of the Disease. An Rh-negative mother having
her first Rh-positive child usually does not develop sufficientanti-Rh agglutinins to cause any harm. However, about 3 per
cent of second Rh-positive babies exhibit some signs of
erythroblastosis fetalis; about 10 per cent of third babies
exhibit the disease; and the incidence rises progressively
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2.Effect of the Mother's Antibodies on the Fetus. After anti-Rhantibodies have formed in the mother, they diffuse slowly through
the placental membrane into the fetus's blood. There they causeagglutination of the fetus's blood. The agglutinated red blood cellssubsequently hemolyze, releasing hemoglobin into the blood. Thefetus's macrophages then convert the hemoglobin into bilirubin,which causes the baby's skin to become yellow (jaundiced). Theantibodies can also attack and damage other cells of the body.
3.Clinical Picture of Erythroblastosis. The jaundiced,erythroblastotic newborn baby is usually anemic at birth, and theanti-Rh agglutinins from the mother usually circulate in the infant'sblood for another 1 to 2 months afterbirth, destroying more andmore red blood cells.
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The hematopoietic tissues of the infant attempt to replacethe hemolyzed red blood cells. The liver and spleenbecome greatly enlarged and produce red blood cells in
the same manner that they normally do during the middleof gestation. Because of the rapid production of red cells,many early forms of red blood cells, including manynucleated blastic forms, are passed from the baby's bonemarrow into the circulatory system, and it is because ofthe presence of these nucleated blastic red blood cells
that the disease is called erythro-blastosis fetalis.Although the severe anemia of erythroblastosis fetalis isusually the cause of death, many children who barelysurvive the anemia exhibit permanent mental impairmentor damage to motor areas of the brain because of
precipitation of bilirubin in the neuronal cells, causingdestruction of many, a condition called kernicterus.
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The mechanism by which Rh immunoglobulinglobin prevents sensitization of the D antigen isnot completely understood, but one effect of theanti-D antibody is to inhibit antigen-induced Blymphocyte antibody production in the expectantmother. The administered anti-D antibody alsoattaches to D-antigen sites on Rh-positive fetalred blood cells that may cross the placenta andenter the circulation of the expectant mother,
thereby interfering with the immune response tothe D antigen.
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BLOOD
TRANSFUSION
BAGIAN FISIOLOGI
FAKULTAS KEDOKTERAN UISU
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Communication
between clinicians andthe Blood Bank is vital!
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ROLE OF THE CLINICIAN
Ensure that the right blood gets
to the right patient at the righttime
Follow the correct procedures for
the ordering, collection and
administration of blood/ blood
products C l h bl d
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Complete the blood requestform
Order blood in advance,
if possible
Provide clear information onblood products being requested,
#units requested, reason fortransfusion, urgency
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COMPTABILITY
The clinician should;1. complete all required details on
the blood request form
2. accurately label blood sampletubes
3. check the identity of the patient,
the product and the
documentation at the patients
bedside before transfusion.
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SAFE TRANSFUSIONS
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Depends on avoiding incompatibilitybetween the donors red cells and the
antibodies in the patients plasma
Severe acute hemolytic transfusionreactions are nearly always caused by
transfusing red cells that are incompatible
with the patients ABO type and can befatal
Most often result from errors made in
identifying the patient
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2 MAIN REASONS
FOR TRANSFUSING
BLOOD
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Restore or maintain bodysoxygen-carrying capacity
Maintain the volume of blood
circulating around the body
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STORING BLOOD
The storage temperature forblood is +2C and +8C
Red cells or whole blood mustnever be allowed
to freeze
PLASMA
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PLASMA
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Fresh frozen plasma (FFP) plasmathat has been separated from a
unit of whole blood within 6-8
hours of donation, maintained at atemperature of -20C or lower
(given to a patient to restore or to
help maintain clotting factors)
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For plasma volume replacement
crystalloids and colloids are
recommended.
(FFP should be given only when
these are unavailable, and as alife-saving procedure)
Plasma contains water,
electrolytes, clotting factors andproteins mostly albumin.
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Factors VIII and V deteriorate if plasma is
not stored at -20C or less
Other clotting factors stable atrefrigerator temperatures.
Plasma must be frozen solid at all times
There is no lower limit for storage of
frozen plasma.
It is not important how low the
temperature is as long as it is -20C or
lower.
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Temperature must be
maintained at negative 20
degrees Centigrade or lower
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THAWING
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Before use, fresh frozen plasma mustbe thawed in water which is between
30C and 37C (Use a thermometer)
Do not heat to more than 37C.(destroys clotting factors and proteins)
While thawing, put inside another
plastic bag and keep upright.
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AFTER THAWING
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Store in refrigerator at +2C and+8C.
Infuse within 30 minutes if not,
transfuse within 24 hours.
Unused thawed unit, should be
discarded, not refrozen.
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WARMING BLOOD
No evidence that warming blood is
beneficial to the patient when
infusion is slowCold blood can cause spasm in the
vein used for infusion so apply
warm towels locally
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On average, it takes 30
minutes for a unit of blood toreach 10 degrees Centigrade
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Blood should be warmed in a blood
warmer with visible thermometer and
audible warning alarm.
Should not be warmed in a bowl of hot
water as this could lead to hemolysis ofred cells and liberation of K+ which
could be life-threatening
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WARMED BLOOD IS MOST COMMONLY
REQUIRED IN
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Large volume rapid transfusions
Adults: infusion of greater than
50ml/kg/hourChildren: greater than
15ml/kg/hour
Exchange transfusion in infantsPatients with clinically significant
cold agglutinins
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If ambient temperature is greater than
+25C or if there is a chance that the
blood will not be transfused
immediately, blood should be placed in a
refrigerator or should be issued in a cold
box or insulated carrier that will keep
the temperature under +8C
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PLATELET CONCENTRATES
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Must be kept at a temperature of 20C to24C on a platelet agitator to maintain
platelet function
Storage life is restricted to 3 or 5 days(risk of bacterial proliferation)
Platelets held at lower temperature lose
blood clotting capability
Platelet concentrates should NEVER BE
PLACED IN A REFRIGERATOR!
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Blood/ Start infusion Completeinfusionblood product
Whole blood/ within 30 min. of within 4 hour
red cells removing pack (less in highfrom ambient temp)refrigerator
Platelet immediately within 20 minconcentrates
FFP within 30 min within 20 min
Time Limits for Infusion
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THERE IS A RISK OF BACTERIALPROLIFERATION OR LOSS OF
FUNCTION IN BLOOD
PRODUCTS ONCE THEY HAVE
BEEN REMOVED FROM THE
CORRECT STORAGECONDITIONS
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CHECK THE PATIENTS
IDENTITY AND THEBLOOD PRODUCT
BEFORE TRANSFUSION
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IDENTITY CHECKLIST
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IDENTITY CHECKLIST
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Ask patient to identify himself by family name, given
name, date of birth and other information
If unconscious, ask a relative or a second member of
staff to state patients identity
Check patients identity and gender against:
identity wristband or labelmedical notes
Check that details on compatibility label attached to
blood pack exactly match details on patients
documentation and identity wristband:Name, hospital reference number, ward, operating
room or clinic
blood group
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RECORDING OF TRANSFUSION
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Consent from patient and/or relatives
Reason for transfusion
Signature of the prescribing clinician
Pre-transfusion checks of :
patients identity, blood pack, compatibility label.signature of the person performing the check
Transfusion
type and volume of component, donation number,
blood group, time at which, transfusioncommenced,signature of person administering
the transfusion
Any transfusion reaction
BLOOD CHECKLIST
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BLOOD CHECKLIST
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1.No discrepancies between ABO and Rh group on:
blood pack, compatibility label
2. No discrepancies between unique donation number
on: blood pack, compatibility label
3. Check expiry date on blood pack.4. Examine pack before transfusion. Do not administer
if pack is damaged or there is any evidence of
deterioration.
leakageunusual color
signs of hemolysis
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MONITORING THE
TRANSFUSED PATIENT
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MONITOR THE PATIENT AT THE
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MONITOR THE PATIENT AT THE
FOLLOWING STAGES:
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Monitor carefully ESPECIALLY duringthe first 15 minutes to detect earlysigns & symptoms of adverse effects
Before starting the infusion
As soon as the infusion is started
15 min after starting the infusion
at least every hour during the infusion
on completion of the infusion
4 hrs after completing the transfusion
CHART AT EACH STAGE RECORD
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CHART AT EACH STAGE, RECORD
THE FOLLOWING INFO IN THE
PATIENTS :
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Patients general appearance
Temperature
Pulse rateBlood pressure
Respiratory rate
Fluid balanceOral and IV fluid intake
Urinary output
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RECORD
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Time transfusion is startedTime the transfusion is
completed
Volume & type of all products
transfused
Unique donation no of all
products transfused
Any adverse effects
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PHARMACEUTICALS &
BLOOD PRODUCTS
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No meds and infusion solutions
other than normal saline should be
added to any blood component .They may contain additives such as
calcium which can cause citrated
blood to clot.Dextrose solution (5%) can lyze red
cells.Last word of advice
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