BLOOD GROUP

Dr.H.Abd Rachman Tanjung AIFM

BAGIAN FISIOLOGI FAKULTAS KEDOKTERAN UNIVERSITAS ISLAM SUMATERA UTARA

Blood groups
Antibodies in the plasma of one blood react

with 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.

Antigens of the ABO blood group Number of antigens Antigen specificity Antigen carrying Molecules 4: A, B, AB, and A1 Carbohydrate The sequence of oligosaccharides determines whether the antigen is A, B, or A1 Glycoproteins and glycolipids of unknown function The ABO blood group antigens are attached to oligosaccharide chains that project above the RBC surface. These chains are attached to proteins and lipids that lie in the RBC membrane The ABO gene indirectly encodes the ABO blood group antigens. The ABO locus has three main allelic forms: A, B, and O. The A and B alleles each encode a glycosyltransferase that catalyzes the final step in the synthesis of the A and B antigen, respectively. The A/B polymorphism arises from several SNPs in the ABO 4 gene, which result in A and B transferases that differ

Molecular basis

Antigens of the ABO blood group Frequency of ABO blood A: 43% Caucasians, 27% Blacks, 28% Asians B: 9% Caucasians, 20% Blacks, 27% Asians A1: 34% Caucasians, 19% Blacks, 27% Asians Note: Does not include AB blood groups (1) Blood group O is the most common phenotype in 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, rare Note: Blood group A is divided into two main phenotypes, A1 and A2

Frequency of ABO phenotypes

Antibodies produced against ABO blood group antigen Antibody type IgG and IgM Naturally occurring. Anti-A is found in the serum of people with blood groups O and B. Anti-B is found in the serum of people with blood groups O and A Capable of hemolysis Anti-A and anti-B bind to RBCs and activate the complement cascade, which lyses the RBCs while they are still in the circulation (intravascular hemolysis)

Antibody reactivity

Transfusion reaction Yes typically causes an acute hemolytic transfusion reaction Most deaths caused by blood transfusion are the result of transfusing ABOincompatible blood
Hemolytic disease of the newborn No or mild disease HDN may occur if a group O mother has more than one pregnancy with a child with blood group A, B, or AB. Most cases are mild and do not require treatment
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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
H fucosotransferasa

AGGLUTININS When type A agglutinogen is not present in a person's red blood cells, antibodies known as anti-A agglutinins develop in the plasma. Also, when type B agglutinogen is not present in the red blood cells, antibodies known as anti-B agglutinins develop in the plasma. Type O blood, although containing no agglutinogens, does contain both anti-A and anti-B agglutinins; type A blood contains type A agglutinogens and anti-B agglutinins; type B blood contains type B agglutinogens and anti-A agglutinins. Finally, type AB blood contains both A and B agglutinogens but no agglutinins.

Frequency of ABO Blood Groups. O 47% A 41% B 9% AB 3%

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 gene determines 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

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

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.

RBC ANTIGENS & BLOOD TYPING

Antigens present on RBC surface specify blood type Major antigen group is ABO system 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

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RH SYSTEM II
Landsteiner 1940 C, D, E antigens (D is most immunogenic) 85 % white people Rh+, 99 % Asians Rh+, African black 100 % Rh+ clinical importance: 1. blood transfusion 2. pregnancy: mother Rh negative and fetus Rh positive, 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-Rh antibodies are NOT normally produced Rh antigen is not often present in the nature

OTHER SYSTEMS
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

TRANSFUSION REACTIONS
People with Type A blood make antibodies to Type B RBCs, but not to Type A Type B blood has antibodies to Type A RBCs but not to Type B Type AB blood doesnt have antibodies to A or B Type O has antibodies to both Type A & B If different blood types are mixed, antibodies will cause mixture to agglutinate

Fig 13.5

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TRANSFUSION REACTIONS CONTINUED

If blood types don't match, recipients antibodies agglutinate donors RBCs Type O is universal donor because lacks A & B antigens

Insert

fig. 13.6

Recipients antibodies wont agglutinate donors Type O RBCs

Type AB is universal recipient because doesnt make anti-A or anti-B antibodies

Wont agglutinate donors RBCs

Fig 13.6

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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, bu the person missing the C antigen always has the c antigen. Th 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 to be Rh negative. About 85 per cent of all white people are Rh positive and 15 p cent, Rh negative..

Rh Immune Response
Formation of Anti-Rh Agglutinins. When red blood cells containing Rh factor are injected into a person whose blood does not contain the Rh factor-that is, into an Rh-negative person-anti-Rh agglutinins develop slowly, reaching maximum concentration of agglutinins about 2 to 4 months later. This immune response occurs to a much greater extent in some people 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 Rhnegative person has never before been exposed to Rh-positive blood, transfusion of Rh-positive blood into that person will likely cause no immediate reaction. However, anti-Rh antibodies can develop in sufficient quantities during the next 2 to 4 weeks to cause agglutination of those transfused cells that are still circulating in the blood.

These cells are then hemolyzed by the tissue macrophage system. Thus, a delayed transfusion reaction occurs, although it is usually mild. On subsequent transfusion of Rh-positive blood into the same person, who is now already immunized against the Rh factor, the transfusion reaction is greatly enhanced and can be immediate and as severe as a transfusion reaction caused by mismatched type A or B blood.

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 instances of 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 sufficient anti-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

2.Effect of the Mother's Antibodies on the Fetus. After anti-Rh antibodies have formed in the mother, they diffuse slowly through the placental membrane into the fetus's blood. There they cause agglutination of the fetus's blood. The agglutinated red blood cells subsequently hemolyze, releasing hemoglobin into the blood. The fetus's macrophages then convert the hemoglobin into bilirubin, which causes the baby's skin to become yellow (jaundiced). The antibodies 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 the anti-Rh agglutinins from the mother usually circulate in the infant's blood for another 1 to 2 months after birth, destroying more and
more red blood cells.

The hematopoietic tissues of the infant attempt to replace the hemolyzed red blood cells. The liver and spleen become greatly enlarged and produce red blood cells in the same manner that they normally do during the middle of gestation. Because of the rapid production of red cells, many early forms of red blood cells, including many nucleated blastic forms, are passed from the baby's bone marrow into the circulatory system, and it is because of the presence of these nucleated blastic red blood cells that the disease is called erythro-blastosis fetalis. Although the severe anemia of erythroblastosis fetalis is usually the cause of death, many children who barely survive the anemia exhibit permanent mental impairment or damage to motor areas of the brain because of precipitation of bilirubin in the neuronal cells, causing destruction of many, a condition called kernicterus.

The mechanism by which Rh immunoglobulin globin prevents sensitization of the D antigen is not completely understood, but one effect of the anti-D antibody is to inhibit antigen-induced B lymphocyte antibody production in the expectant mother. The administered anti-D antibody also attaches to D-antigen sites on Rh-positive fetal red blood cells that may cross the placenta and enter the circulation of the expectant mother, thereby interfering with the immune response to the D antigen.

BLOOD TRANSFUSION

BAGIAN FISIOLOGI FAKULTAS KEDOKTERAN UISU

Communication between clinicians and the Blood Bank is vital!

ROLE OF THE CLINICIAN

Ensure that the right blood gets to the right patient at the right time Follow the correct procedures for the ordering, collection and administration of blood/ blood products

Complete the blood request form Order blood in advance, if possible Provide clear information on blood products being requested, #units requested, reason for transfusion, urgency
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COMPTABILITY

The clinician should; 1. complete all required details on the blood request form 2. accurately label blood sample tubes 3. check the identity of the patient, the product and the documentation at the patients bedside before transfusion.

SAFE TRANSFUSIONS
Depends on avoiding incompatibility between the donors red cells and the antibodies in the patients plasma Severe acute hemolytic transfusion reactions are nearly always caused by transfusing red cells that are incompatible with the patients ABO type and can be fatal Most often result from errors made in identifying the patient

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2 MAIN REASONS FOR TRANSFUSING BLOOD

Restore or maintain bodys oxygen-carrying capacity Maintain the volume of blood circulating around the body
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STORING BLOOD

The storage temperature for blood is +2C and +8C Red cells or whole blood must never be allowed to freeze

PLASMA
Fresh frozen plasma (FFP) plasma that has been separated from a unit of whole blood within 6-8 hours of donation, maintained at a temperature 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 a life-saving procedure) Plasma contains water, electrolytes, clotting factors and proteins mostly albumin.
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Factors VIII and V deteriorate if plasma is not stored at -20C or less Other clotting factors stable at refrigerator 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
Before use, fresh frozen plasma must be 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
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 slow Cold blood can cause spasm in the vein used for infusion so apply warm towels locally

On average, it takes 30 minutes for a unit of blood to reach 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 of red cells and liberation of K+ which could be life-threatening
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WARMED BLOOD IS MOST COMMONLY REQUIRED IN

Large volume rapid transfusions Adults: infusion of greater than 50ml/kg/hour Children: greater than 15ml/kg/hour Exchange transfusion in infants Patients 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

Must be kept at a temperature of 20C to 24C 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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Time Limits for Infusion

Blood/ infusion blood product
Whole blood/ red cells

Start infusion

Complete

within 30 min. of removing pack from refrigerator immediately within 30 min

within 4 hour (less in high ambient temp) within 20 min within 20 min
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Platelet concentrates FFP

THERE IS A RISK OF BACTERIAL PROLIFERATION OR LOSS OF FUNCTION IN BLOOD PRODUCTS ONCE THEY HAVE BEEN REMOVED FROM THE CORRECT STORAGE CONDITIONS
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CHECK THE PATIENTS IDENTITY AND THE BLOOD PRODUCT BEFORE TRANSFUSION

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IDENTITY CHECKLIST
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 label medical 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 49 blood group

RECORDING OF TRANSFUSION
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, transfusion commenced,signature of person administering the transfusion 50 Any transfusion reaction

BLOOD CHECKLIST
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. leakage unusual color signs of hemolysis 51

MONITORING THE TRANSFUSED PATIENT

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MONITOR THE PATIENT AT THE FOLLOWING STAGES:

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
Monitor carefully ESPECIALLY during the first 15 minutes to detect early signs & symptoms of adverse effects

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CHART AT EACH STAGE, RECORD THE FOLLOWING INFO IN THE PATIENTS :

Patients general appearance Temperature Pulse rate Blood pressure Respiratory rate Fluid balance Oral and IV fluid intake Urinary output

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RECORD
Time transfusion is started Time 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

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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