Tranfusion - RACHMAN

7/28/2019 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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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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Documents

Tranfusion - RACHMAN