15 blood banking and transfusion disorders

8/11/2019 15 Blood Banking and Transfusion Disorders

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15 Blood Banking and Transfusion Disorders

ABO Blood Group Antigens

Definition of ABO blood group antigens

• They are glycoproteins attached to the RBC surface.

ABO Blood Group Antigens


• They are glycoproteins attached to the RBC surface.


•

They are glycoproteins attached to the RBC surface.

Blood group O characteristicsBlood group antibodies are natural antibodies that are synthesized in Peyer'spatches. A and B antigens that are normally present in food are trapped byspecialized epithelial cells called cells that o!erlie Peyer's patches. cells ha!eclose pro"imity to B lymphocytes lying #ithin the epithelium. cells transport the Aand B antigens to these lymphocytes$ resulting in the de!elopment of naturalantibodies against the antigens. %atural antibodies de!elop against antigens thatare not present on the RBC$ #hich e"plains #hy blood group O patients ha!eantibodies against both A and B antigens.

&. ost common blood groupo No blood group antigens are present on the RBC membrane.

. %atural antibodies (isohemagglutinins) in serum

a. Anti*A*+g$ anti*B*+g

b. ost people ha!e anti*AB*+g, antibodies.

. +ncreased incidence of duodenal ulcers

Blood group A characteristics

&. Anti*B*+g antibodies

. +ncreased incidence of gastric carcinoma

Blood group Bcharacteristics



• Anti*A*+g antibodies

Blood group ABcharacteristics

&. -east common blood group

2. No natural antibodies

%e#borns

&. Do not ha!e natural antibodies at birth. +g, antibodies are of maternal origin.

o +g, antibodies cross the placenta.

lderly peoplepage /0

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lderly patients may not ha!e a hemolytic transfusion reaction if they are transfused#ith the #rong blood group because they fre2uently lose their natural antibodies.

• 3re2uently lose their natural antibodies

Paternity issues in ne#borns

&. Blood group AB parents cannot ha!e an O child.. Blood group O parents cannot ha!e an AB$ A$ or B child.

4. Blood group A and B parents can ha!e O children if both ha!e AO and BO phenotypes.

Determining the ABO group&. 3or#ard type

a. +dentifies the blood group antigen Patient RBCs are added to test tubes that contain either anti*A or anti*B test

serum.b. "ample*blood group A RBCs

Agglutination reaction #ith anti*A test serum but not #ith anti*B test serum

. Bac5 typea. +dentifies the natural antibodies

Patient serum is added to test tubes containing either A or B test RBCs.

b. "ample*blood group A serum Patient anti*B*+g antibodies agglutinate B test RBCs but not A test RBCs.



Rh and Non-Rh Antigen Systems

Rh antigen systempage /1

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&. +t has three ad6oining gene loci.a. -ocus coding for D antigen (no d antigen)b. -ocus coding for C and c antigenc. -ocus coding for and e antigen

. Autosomal codominant inheritancea. One of the sets of three Rh antigens from each parent is transmitted to each child.

i. "ample*child #ith CDe from the father and cde from the mother %ote that the child lac5s antigen.

ii. Absence of D antigen on a chromosome is designated d e!en though the antigendoes not e"ist.

b. Possible Rh antigen profiles

i. DD$ Dd$ or ddii. CC$ Cc$ or cciii. $ e$ or ee

4. An indi!idual #ho is Rh positi!e is D antigen positi!e.a. Appro"imately 708 of the population has D antigen.b. +ndi!iduals lac5ing D antigen are considered Rh negati!e.

9. Rh phenotype of an indi!iduala. RBCs are reacted #ith test antisera against each of the Rh antigens.

b. "ample*Rh phenotype that is positi!e for C$ c$ D$ and antigens but negati!e for eantigen (phenotype is CcD)

Rh antigen systempage /1

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&. +t has three ad6oining gene loci.a. -ocus coding for D antigen (no d antigen)b. -ocus coding for C and c antigenc. -ocus coding for and e antigen

. Autosomal codominant inheritancea. One of the sets of three Rh antigens from each parent is transmitted to each child.

i. "ample*child #ith CDe from the father and cde from the mother %ote that the child lac5s antigen.

ii. Absence of D antigen on a chromosome is designated d e!en though the antigendoes not e"ist.

b. Possible Rh antigen profilesi. DD$ Dd$ or ddii. CC$ Cc$ or cciii. $ e$ or ee

4. An indi!idual #ho is Rh positi!e is D antigen positi!e.a. Appro"imately 708 of the population has D antigen.



b. +ndi!iduals lac5ing D antigen are considered Rh negati!e.9. Rh phenotype of an indi!idual

a. RBCs are reacted #ith test antisera against each of the Rh antigens.

b. "ample*Rh phenotype that is positi!e for C$ c$ D$ and antigens but negati!e for eantigen (phenotype is CcD)

Alloimmunization

&. Production of an antibody against a foreign antigen not present on an indi!idual's RBCsa. Patient e"posure to Rh antigen he is lac5ing (e.g.$ D antigen)b. Patient e"posure to non*Rh antigen she is lac5ing (e.g.$ :ell antigen)c. These antibodies are called atypical antibodies.

The indi!idual is considered sensitized if atypical antibodies are present.

. ;ignificance of atypical antibodiesa. ay produce a hemolytic transfusion reaction (<TR)

ii Occurs #hen blood containing the foreign antigen is infused into an indi!idualiii "ample*indi!idual #ith anti*:ell antibodies is e"posed to :ell antigen positi!e

RBCs.iiii +g, antibodies are more li5ely to produce an <TR than +g antibodies.

+g, antibodies react best in #arm temperatures$ but +g antibodies react

best in cold temperatures.b. Transfusion re2uirements in an indi!idual #ith atypical antibodies

ii +ndi!idual must recei!e blood that is negati!e for the foreign antigen.

iii "ample*indi!idual #ith anti*:ell antibodies must recei!e :ell antigen negati!e

blood.

Clinically important non*Rh antigenspage //

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&. Duffy (3y) antigensa. 3y antigens are the binding site for infestation of RBCs by Plasmodium vivax. b. a6ority of blac5 Americans lac5 the 3y antigen.

Offers protection against contracting P. vivax malaria

. + and i antigen systemsa. +g antibodies (cold agglutinins) may de!elop against + or i antigen.b. +ncreased ris5 for de!eloping a cold autoimmune hemolytic anemia

ii Anti*i hemolytic anemia may occur in infectious mononucleosis.

iii Anti*+ hemolytic anemia may occur in Mycoplasma pneumoniae infections.

Blood Transfusion Therapy



Blood donorsThere is a ris5 for transmitting infection #hen transfusing blood because there is anincubation period before specific antibodies are de!eloped against the pathogen.The ris5 for de!eloping an infection per unit of blood for different pathogens is asfollo#s= &=44>> for hepatitis C? &=>>$>>> for hepatitis B? and$ &=$>>>$>>> for <[email protected] most common infectious agent transmitted by blood transfusion is

cytomegalo!irus (C@)$ #hich is present in donor lymphocytes.

&. Autologous transfusiona. Process of collection$ storage$ and reinfusion of the indi!idual's o#n bloodb. ;afest form of transfusion

. Tests performed on donor blooda. ,roup (ABO) and type (Rh)b. Antibody screen (indirect Coombs' test)

Detects atypical antibodies (e.g.$ anti*D$ anti*:ell)

c. ;creening tests for infectious disease

"amples*syphilis$ hepatitis B and C$ <+@*& and $ <T-@*&

Blood donorsThere is a ris5 for transmitting infection #hen transfusing blood because there is anincubation period before specific antibodies are de!eloped against the pathogen.The ris5 for de!eloping an infection per unit of blood for different pathogens is asfollo#s= &=44>> for hepatitis C? &=>>$>>> for hepatitis B? and$ &=$>>>$>>> for <[email protected] most common infectious agent transmitted by blood transfusion iscytomegalo!irus (C@)$ #hich is present in donor lymphocytes.

&. Autologous transfusiona. Process of collection$ storage$ and reinfusion of the indi!idual's o#n bloodb. ;afest form of transfusion

. Tests performed on donor blooda. ,roup (ABO) and type (Rh)b. Antibody screen (indirect Coombs' test)

Detects atypical antibodies (e.g.$ anti*D$ anti*:ell)

c. ;creening tests for infectious disease

"amples*syphilis$ hepatitis B and C$ <+@*& and $ <T-@*&

Patient crossmatchPatients #ith a negati!e antibody screen should ha!e a compatible crossmatch.<o#e!er$ a compatible crossmatch does not guarantee that the recipient #ill notde!elop atypical antibodies$ a transfusion reaction$ or an infection.

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Before blood is transfused into ne#borns or patients #ith T*cell deficiencies$ it must



be irradiated to 5ill donor lymphocytes. This pre!ents the patient from de!eloping agraft*!ersus*host reaction or a C@ infection.

&. Components of a standard crossmatcha. ABO group and Rh typeb. Antibody screen for atypical antibodiesc. Direct Coombs' test to identify atypical +g, antibodies on patient RBCsd. a6or crossmatch

. a6or crossmatcha. Purpose of a ma6or crossmatch

Detect atypical antibodies that are directed against foreign antigens on donor

RBCsb. Patient serum is mi"ed #ith a sample of RBCs from a donor unit.

ii ach unit of donor blood must ha!e a separate crossmatch.

iii -ac5 of RBC agglutination or hemolysis indicates a compatible crossmatch.

. se of blood group O pac5ed RBCs for transfusiona. Can be transfused into any patient$ regardless of the blood group

ii

Blood group O RBCs lac5 A and B antigens.iii Blood group O indi!iduals are considered uni!ersal donors.

b. Blood group O indi!iduals can recei!e only O blood.

Anti*A*+g and anti*B*+g #ill hemolyze transfused A$ B$ or AB RBCs.

ii Blood group AB indi!iduals can be transfused #ith blood from any blood group.

a. They lac5 natural antibodies.

b. They are considered uni!ersal recipients.

Blood component therapy

Tale 15-1! Blood "omponents

"omponent Dis#ussion

Pac5ed RBCs Purpose= increase O transport to tissuesPac5ed RBCs ha!e less !olume and a higher <ct than #hole bloodach unit of pac5ed RBCs should raise the <b by & gd- and the <ct by 48? lac5 of an incrementimplies a hemolytic transfusion reaction or blood loss in the patientYersinia enterocolitica, a pathogen that thri!es on iron$ is the most common contaminant of storedblood

Platelets Purpose= stop medically significant bleeding related to thrombocytopenia or 2ualitati!e plateletdefects (e.g.$ aspirin)Platelets ha!e <-A antigens and ABO antigens on their surface? ho#e!er$ they lac5 Rh antigensach unit of platelets should raise the platelet count by 0>>>*&>$>>> cells-

3resh frozenplasma

Purpose= treatment of multiple coagulation deficiencies (e.g.$ D+C? cirrhosis) or treatment of #arfarino!er*anticoagulation if bleeding is life*threatening

Cryoprecipitate Purpose= treatment of coagulation factor deficiencies in!ol!ing fibrinogen and factor @+++ (e.g.$ D+C)Cryoprecipitate contains fibrinogen$ factor @+++$ and factor E+++Desmopressin acetate is used instead of cryoprecipitate in treating mild hemophilia A and !onFillebrand disease

D+C$ disseminated intra!ascular coagulation? <ct$ hematocrit? <b$ hemoglobin.



Transfusion reactions

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+ndi!iduals #ho are deficient in +gA and #ho ha!e antibodies directed against +gAfrom pre!ious e"posure to a blood product may de!elop a se!ere anaphylacticreaction. +gA deficient indi!iduals must recei!e blood or blood products that lac5 +gA.

Anti*<-A antibodies de!elop #hen indi!iduals are e"posed to foreign <-A antigens(e.g.$ pre!ious blood transfusion or organ transplant). Fomen commonly ha!e thesereactions o#ing to pregnancy$ #hen there is an increased ris5 for e"posure to fetalblood during deli!ery or after a spontaneous abortion.

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+ndi!iduals #ho ha!e been infused #ith blood in the past may ha!e been e"posed toa foreign blood group antigen and de!eloped atypical antibodies that are no longercirculating? therefore$ the pretransfusion antibody screen is negati!e. <o#e!er$memory B cells are present and ree"posure to the foreign antigen causes them toproduce antibodies$ resulting in an e"tra!ascular hemolytic anemia. This reactionmay occur #ithin hours to 4 to &> days after the transfusion.

&. Allergic reactionsa. ost common transfusion reactionb. Type + +g*mediated hypersensiti!ity reaction against proteins in the donor bloodc. Clinical findings

i. rticaria #ith pruritusii. 3e!er$ tachycardia$ #heezing

iii. Potential for anaphylactic shoc5i!. ild cases are treated #ith antihistamines.

. 3ebrile reactiona. Pathogenesis

i. Recipient has anti*human leu5ocyte antigen (<-A) antibodies directed againstforeign <-A antigens on donor leu5ocytes.

There are no <-A antigens on RBCs.

ii. Type ++ hypersensiti!ity reactionb. Clinical findings

i. 3e!er$ chills$ headache$ and flushingii. Treated #ith antipyretics

4. Acute hemolytic transfusion reaction (<TR)a. ay be intra!ascular or e"tra!ascular hemolytic reactions

b. +ntra!ascular hemolysisi. ABO blood group incompatibilityii. "ample*group B patient recei!es group A donor blood.

Anti A*+g attaches to A positi!e donor RBCs producing intra!ascular

hemolysis.iii. Type ++ hypersensiti!ity reaction

c. "tra!ascular hemolysisi. An atypical antibody reacts #ith a foreign antigen on donor RBCs.

acrophage phagocytosis and destruction of donor RBCs coated by the



atypical antibodyii. Gaundice commonly occurs.

ncon6ugated bilirubin is the end product of macrophage degradation of

<b.iii. Type ++ hypersensiti!ity reaction

d. Clinical findings

i. 3e!er$ bac5 pain$ hypotensionii. Disseminated intra!ascular coagulation$ oliguria (renal failure)

e. -aboratory findingsi. Positi!e direct Coombs' test

+g, antibody andor C4b is coating donor RBCs.

ii. Positi!e indirect Coombs' test Atypical antibody is present in serum.

iii. No significant increase in <b o!er pretransfusion le!els.i!. <emoglobinuria (sign of intra!ascular hemolysis)

!. Gaundice (sign of e"tra!ascular hemolysis)

$emolyti# disease of the ne%orn &$DN'

• <D% results from the transplacental passage of maternal +g, antibodies (e.g.$ anti*D antibodies$

anti*AB antibodies in O mothers) resulting in an e"tra!ascular hemolytic anemia in the fetus.

ABO <D%

&. pidemiologya. ost common <D%

Present in >8 to 08 of all pregnancies

b. others are blood group O and the fetus is either blood group A or B.. Pathogenesis

a. Blood group O indi!iduals ha!e anti*AB*+g, antibodies.

ii +g, antibodies cross the placenta and attach to fetal A or B RBCs.

iii 3etal splenic macrophages phagocytose RBCs$ causing anemia.

iiii ncon6ugated bilirubin from e"tra!ascular hemolysis is disposed of in the

mother's li!er.b. ay affect the firstborn or any future pregnancy if ABO incompatibility e"ists

. Clinical and laboratory findingsa. Gaundice de!elops #ithin the first 9 hours after birth.

ii ABO <D% is the most common cause of 6aundice in this period.

%e#born li!er cannot handle the e"cess bilirubin load.

iii Ris5 for 5ernicterus is !ery small (see belo#).

b. Anemiaii ild normocytic anemia or no anemia at all

iii "change transfusions are rarely indicated.

c. Positi!e direct Coombs' test on fetal cord blood RBCs

Due to anti*AB*+g, antibodies coating fetal A or B RBCs



b. ;pherocytes are present in the cord blood peripheral smear.

Due to macrophage remo!al of a portion of the RBC membrane

Rh <D%;pecial tests are performed on the mother's blood that detect fetal RBCs in herblood. The amount of fetal blood is 2uantified so that the appropriate amount of anti*D globulin is gi!en to the mother. Anti*D globulin mas5s the antigenic sites on thefetal RBCs or destroys the fetal RBCs so that the mother does not host an antibodyresponse against the D antigen. +f the patient de!elops anti*D antibodies$ there is noindication for gi!ing the globulin either during or after deli!ery$ because its mainpurpose is to pre!ent sensitization.

:ernicterus refers to deposition of free (not bound to albumin) lipid*solubleuncon6ugated bilirubin in the basal ganglia o#ing to an incompletely formed blood*brain barrier. Bilirubin damages neurons in the brain$ causing se!ere dysfunction.

ABO incompatibility protects the mother from de!eloping Rh sensitization. 3ore"ample$ in a mother #ho is O negati!e and carrying a fetus #ho is A positi!e$ any Apositi!e fetal RBCs entering her circulation #ill be destroyed by maternal anti*A*+gantibodies$ thereby pre!enting sensitization.

&. Pathogenesisa. other is Rh (D antigen) negati!e and the fetus is Rh positi!e.b. other is e"posed to fetal Rh positi!e blood (fetomaternal bleed).

Occurs during the last trimester or during childbirth itself

c. Cytotrophoblast is absent during the last trimester. +ncreases the ris5 for a fetomaternal bleed

d. other de!elops anti*D*+g, antibodies #hen e"posed to fetal Rh positi!e cells.

3irst Rh incompatible pregnancy does not affect the firstborn.e. ;ubse2uent Rh incompatible pregnancies result in e"tra!ascular hemolytic anemia in the

fetus.

ii Anti*D*+g, antibodies cross the placenta and attach to fetal Rh positi!e RBCs.

iii 3etal splenic macrophages phagocytose RBCs$ causing se!ere anemia.

3etus may de!elop high*output cardiac failure leading to hydrops fetalis

and death. <ydrops fetalis is a combined left* and right*sided heart failure #ith

ascites and edema. "tramedullary hematopoiesis is present in the li!er and spleen.

ncon6ugated bilirubin is con6ugated in the mother's li!er.

. Pre!ention of Rh <D% in Rh negati!e mothers #ithout anti*Da. Recei!e anti*D globulin (Rh immune globulin) during the 7th #ee5 of pregnancyb. Anti*D globulin does not cross the placenta.c. Anti*D globulin protects the mother from sensitization to fetal Rh positi!e cells that may

enter her circulation during the last trimester.d. Anti*D globulin lasts ∼4 months in the mother's blood.e. Additional anti*D globulin is gi!en to the mother after deli!ery if the baby is Rh positi!e.

4. Clinical and laboratory findingsa. Degree of anemia is more se!ere than #ith ABO <D%.



b. Gaundice de!elops shortly after birth.ii -e!el of uncon6ugated bilirubin is much higher than #ith ABO <D%.

ost of the uncon6ugated bilirubin is not bound by albumin and circulates

free in the blood.iii +ncreased ris5 for 5ernicterus

The free$ unbound lipid soluble uncon6ugated bilirubin poses the greatest

ris5 for bilirubin entry into the brain .c. Positi!e direct and indirect Coombs' tests on fetal cord bloodd. ;pherocytes are not present in cord blood.

acrophages phagocytose the entire RBC.

b. "change transfusions are re2uired.

ii %e#born's blood is remo!ed and replaced #ith fresh blood.

iii Transfusion corrects anemia and remo!es antibodies and uncon6ugated bilirubin.

se of blue fluorescent light

&. sed as a treatment of 6aundice in the ne#born. ncon6ugated bilirubin in the s5in absorbs light energy from blue fluorescent light.4. Photoisomerization con!erts uncon6ugated bilirubin to a nonto"ic #ater*soluble dipyrrole (called

lumirubin).

o -umirubin is e"creted in bile or urine.

15 blood banking and transfusion disorders

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