WEEK 7 is derived from the use of the blood of rhesus

monkeys in the basic test for determining the

Rh Blood Group System presence of the Rh antigen in human blood.
 The Rh blood group system was discovered in
1940 by Karl Landsteiner and A.S. Weiner. Since
RH BLOOD GROUP SYSTEM that time a number of distinct Rh antigens have
 Second most important blood group system. been identified, but the first and most common
Most important is the ABO system one, called RhD, causes the most severe immune
 Discovered in 1939 reaction and is the primary determinant of the Rh
 Five principle antigens: D, C, E, c, and e
 The corresponding antibodies account for trait.
most clinical transfusion issues
Discovery of the Rh system:
Importance of the Rh system
 Levine and Stetson linked the Rh factor to HDN
1. After the A and B antigens, the D antigen is the  Weiner linked Rh factor to transfusion reactions
most important red cell antigen in blood banking Rh Antigen Frequency
2. The D antibody can cause transfusion reactions  D antigen – 85%
and hemolytic disease of the newborn  d (absence o D)– 15%
(HDN)/Erythroblastosis fetalis  C antigen – 70%
 E antigen – 30%
D Antigen  c antigen – 80%
 The terms Rh-positive and Rh-negative refer  e antigen – 98%
to the presence or absence of the D red blood
cell antigen
 Unlike the ABO system, the absence of the D Rh Genetics
antigen does not have a corresponding
antibody  2 closely linked genes control the expression of
 The production of antibody requires red cell ALL Rh antigens (codominant alleles)
stimulation from Rh-positive cells  RH - D gene - determines the expression of the D
antigen
Rh Blood Group
 Named Rh because of its similarity to the  RH – C- E gene - determines the expression of the
antibody reacted to rhesus monkey cells C, c, E, and e antigens
 85% of the population are Rh positive
 15% of the population are Rh negative Rh Nomenclature
 Rh antigens have only been detected on red
cell membranes  There are several different systems of
 Consists of 45 different antigens nomenclature that theorize the inheritance of the
Rh Null Syndrome Rh system
 The lack of Rh system antigens - referred to
Rh null A. Fisher-Race – DCE Termiology
 Causes an RBC membrane abnormality B. Wiener – Rh –Hr Terminology
 Shortened RBC life span C. Rosenfield – Alpha/Numeric Terminology
 patients with Rh null syndrome D. ISBT – International Society of Blood Transfusion
 Osmotically fragile red cells called
stomatocytes – Numeric terminology
 Chronic haemolytic anaemia

History FISHER-RACE TERMINOLOGY

 Fisher-Race postulated that the Rh system
 1939 Levine and Stetson defined D antigen (Rh antigens are inherited as a gene complex
(haplotype) that codes for three closely linked
factor) sets of alleles
 1940 Landsteiner and Weiner discovered anti-Rh  D is inherited on one locus, no d
(named after Rhesus monkey) antigen; d is used to denote absence of
 Agglutinated 85% human RBCs D
 15% RBCs did not agglutinate  C and c
 E and e
 the presence or absence of the Rh antigen, often
called the Rh factor, on the cell membranes of the  Most commonly used (i.e. WHO)
red blood cells (erythrocytes). The designation Rh
  Developed by Ronald Fisher and Robert Race of
Conversion to Fisher-Race
England  R presence of D, 1 or '
 They theorized that the Rh antigens are controlled  Signifies the presence of E
by a complex of 3 sets of genes with closely linked  Z or y signifies the presence of both C
loci (i.e. Dce gene complex codes for D, c, e and E on the gene
antigens)  Individual antigens are
 Rho corresponds to - D
 rh' corresponds to - C
 rh" corresponds to - E
5- Antigens of the system:  hr' corresponds to - c
o D  hr" corresponds to – e
o C
o c
o E NOTE!!!!!!!!!!!!!!!!!!!
o e
o d – silent allele - amorph

Rosenfield Nomenclature
 No genetic basis – but indicates the absence or
There are 8 gene complexes at the Rh locus presence
 Antigens are designated by number
Fisher-Race uses DCE as the order/ Others alphabetize the  Rh1:D
genes as CDE  Rh2:C
 Rh3:E
1. Rh deletion - - De or –DE, CD- or cD-
 Rh4:c
2. Rh null – -D-; the person expresses no Rh antigen.  Rh5:e
Phenotype is written as ---/---.
3. Rh mod – all Rh antigen is weak; no phenotype Example
expression
D+, C+, E-, c+, e+ is written as Rh:1,2,-3,4,5
Fisher-Race Example:

1. DCe/DCe individual is homozygous for D, C, and e International Society of

genes Blood Transfusion (ISBT)
2. DCe/dcE individual is heterozygous for D, C, e, d, c,
and E genes  Attempts to standardize nomenclature
 Six digit numbers are assigned to each blood group
specificity
WEINER RH-HR TERMINOLOGY  1st three – blood group; last 3 antigenic specificity
 One gene is responsible for expression of all Rh  004 refers to the Rh system
antigen on the red blood cells  The remainder is the specific number
Eight alleles:
 R0 - r • Example: ISBT for the C antigen is 004002
 R1 - r' Genotype vs. Phenotype
 R2 - r"
 Rz – ry  The phenotype is the result of the reaction between the
red cells and antisera
 Rarely used, but good for describing phenotype
 The genotype is the genetic makeup and can be
 A single gene at the Rh locus leads to the expression of
predicted using the phenotype and by considering the
the Rh antigens (next slide)
race of an individual
 Each parent contributes 1 Rh gene
 Only family studies can determine the true genotype
 8 alleles exist at each gene locus
 Anti-D, anti-C, anti-E, anti-c, and anti-e is tested with
 Each gene controls production of an agglutinogen
patient RBCs
composed of three factors (antigens)
 If a specimen gives the following reaction: D+, C+, E-,
 Wiener further theorized that 8 major genes led to
c+, e+
different combinations of antigens (D, C, E, c, e):
 The phenotype would be DCce
 the most probable genotype would be
 White population: DCe/dce
 Black population: DCe/Dce
Probable genotype

 If the RBCs express both C and c or E and e, the Rh Antibodies General Characteristics
corresponding genes are present in the  Usually made by exposure to Rh antigens
heterozygous state through transfusion or pregnancy
 If they express only C or c, or only E or e, the o Most are IgG and bind at 37°C
person is assumed to be homozygous for that gene o Agglutination is observed by the IAT
o Enhancement with high protein, low
ionic strength solution (LISS),
Determining the Most Probably Genotype from the enzymes, or polyethylene glycol are
Phenotype useful
Five antisera are used o May show dosage
 Anti-D
 Anti-C Clinical Considerations in Transfusion Reactions
 Anti-E  Antibodies to the Rh system can cause
 Anti-c hemolytic transfusion reactions
 Anti-e o Antibody levels can fall below
- Once the phenotype is known, the most probable detectable levels
genotype can be determined from knowing the most o Upon re-exposure to the antigen, the
common genotypes antibody produces a rapid secondary
response
RH PHENOTYPES AND GENOTYPES o It is important to check patient history
D Antigen HEMOLYTIC DISEASE OF THE FETUS AND
 D antigen is the most immunogenic antigen in NEWBORN
the Rh system  First observed in infants from D-negative
 85% of D-negative people receiving D- mothers and D-positive fathers
positive blood transfusion produce the anti-D o Initial pregnancy, mom is usually not
antibody affected; infants from subsequent
 D-negative patients should receive only D- pregnancies are often stillborn or
negative blood jaundiced and anemic
o The initial pregnancy exposed the
Weak D mother to D-positive cells and to
 Anti-D is IgG produce anti-D
 Manufacturers have developed anti-D reagents
that react at room temperature and immediate Rh Immune Globulin
spin, like anti-A and anti-B tests  Anti-D can cross the placenta
 When the D antigen is weakly expressed, its o Rh immune globulin (RhIG) protects
detection requires indirect antiglobulin testing D-negative mothers against production
(IAT) of anti-D
 Older terminology refers to weak D or Du o Antibody screen and D status of
mothers in early pregnancy are needed
WEAK D EXPRESSION to determine whether a mother is a
DUE TO: candidate for RhIG
 Weak D: Genetic. Quantitative variation of D
gene LW Blood Group System
 Weak D: Position effect. C is inherited in the  Similar in serology properties to the Rh system but
trans (opposite) chromosome not genetically related
 Weak D: Partial D. Tests as positive, but after o Alleles are Lwa, LWb, and LW
transfusion with D-positive cells, develops o LW gene uis an amorph
anti-D o Antibodies to the LW system are clinically
 Partial D due to missing parts of the D significant and rare
complex - rare
 Older terminology - D variant or D mosaic

SIGNIFICANCE OF TESTING FOR WEAK D

 AABB Standards
 All donors who do not directly test positive for
D must be tested for weak D
 Weak D positive units are labeled positive
o A "D control" must be run each time a
weak D testing is performed
o Patients are usually not tested for weak
D
 
WEEK 8 se, Le = Lea will not be converted to
Leb so you will be Le (a+b–)
OTHER BLOOD GROUP SYSTEM  If you inherit se, and you don’t have
Lea, nothing will happen
(PART I)  se, le = You will be Le (a–b–)
 H gene – either H or h (amorph)
 If you inherit H, you will have ABH
REMINDER!!!!!!!!!!!!!!!!!! antigens on RBCs and secretions (if you
001-ABO have Se gene, if not, you will not have
002-MNS any on secretions)
003-P  If you inherit h, you will have NO ABH
antigens on RBCs and secretions
004-Rh
005-Lutheran IN SHORT:
006- Kell  Le gene is required for the presence of Lea
antigen on RBCs and secretions
007- Lewis  Le and H genes are required for presence of
008- Duffy Leb antigen on RBCs and secretions
009- Kidd  Le and hh – only Lea antigen on RBCs or in
010- Diego secretions
 Se is not contributory in absence of H gene
 Se and H genes are required for presence of A,
MNEMONIC!! B and H antigens on RBCs and secretions
Ang Mens Po (ni) Rhea Lumabas Kaya  H gene WITHOUT Se gene – A, B and H
Lang Di Kita (ni) Diego antigens on RBCs but NOT on secretions
 In absence of H (hh), no ABH antigens on
RBCs or in secretions

Other characteristics of Lewis antigens

LEWIS (007) SYSTEM  Poorly developed at birth so neonates will type Le
(a− b−) regardless of the Lewis genes they
 The ONLY BLOOD GROUP SYSTEM not inherited
manufactured by the red cells  Not found on cord blood or newborn red cells
 Chromosomal location – 19p  Lewis glycolipid detectable in plasma after ~10
 ANTIGENS – Lea and Leb days of life
 NOT INTRINSIC to RED BLOOD CELLS  Transformation of Lewis phenotype after birth
 REVERSIBLY ADSORBED ONTO RED seen in individuals who inherit Le and Se genes:
CELLS FROM PLASMA  Le(a−b−) to Le(a+ b−) to Le(a+ b+) to
 Lea and Leb are NOT ANTITHETICAL Le(a−b+) [the true phenotype]

ANTIGENS MOST COMMON PHENOTYPES:

 Expression is affected by the genes – Le, Se and H Le (a+b−), Le (a−b+), Le (a+b+) and Le (a−b−)
 Lewis gene – either Le or le (amorph)  lele genotype is more common among blacks
 codes for L-fucosyltransferase, than among whites and results in the Le(a–b–)
which adds L fucose to type 1 phenotype
chains
 If you inherit Le, you will have Lea  Decrease in expression demonstrated in red
 If you inherit le, you will NOT cells from many pregnant women, resulting in
have Lea Le(a−b−) phenotype during gestation
 Le = Lea+  Do not show dosage in serologic reactions
 le = Lea–
ANTIBODIES: Anti-Lea and Anti-Leb
 Secretor gene – either Se or se (amorph) Antibody type: IgM
 If you inherit Se, and you have Lea, it  NATURALLY OCCURRING, SALINE-
will be converted to Leb REACTIVE
 Se, Le = Lea converted to Leb so you  Does not cross the placenta
will be Le (a–b+)  Source: Le (a–b–) people, without known red cell
 If you inherit Se, and you don’t have stimulus
Lea, nothing will be converted to Leb  Neutralized by: Lewis blood group substances in
 Se, le = No Lea to be converted to Leb plasma or saliva
so you will be Le (a–b–)  Characteristics:
 If you inherit se, and you have Lea,  Enhanced by enzymes
nothing will convert it to Leb  Sometimes reacts at 37°C and Coombs phase
 more weakly than at room temperature  ▪ Anti-PP, Pk, and anti-p antibodies occur only
 Rarely causes in vitro hemolysis; however, in vivo rarely.
posttransfusion hemolysis reported in cases which
Lewis Ab strongly reacts in Coombs phase
 May cause in vivo hemolysis of red cells  p – absence of substance that codes for P1 and Pk
 Hemolysis/Disease Association
 NOT involved in HDN because Lewis antibodies PHENOTYPES
cannot cross the placenta and antigens are poorly  COMMON – P1 and P2
developed in newborns  RARE – p, P1k and P2k
Transfusion
 Donor cells assume Lewis phenotype of recipient P
(Le antigens absorbed from plasma)
 Lewis antibodies in recipient’s plasma neutralized  Platelets, epithelial cells, fibroblasts
by Lewis blood group substances
 in donor plasma P and Pk

P (003) SYSTEM  Plasma as glycosphingolipids

 P ANTIGENS: P1, P2, Pk1, Pk2, p
 Hydatid cyst fluid: glycoprotein
 ▪ Structurally related to ABO antigens and exist as
glycoproteins and glycolipids
 ▪ MOST COMMON PHENOTYPES: P1 and
P1 Antigen
P2
 Poorly expressed at birth
 ▪ P1 individuals have both P and P1 antigens
 May take up 7 years to be fully expressed
 ▪ P2 individuals have only P antigens
 ▪ Rare phenotypes  Strength may vary w/ race
 ▪ Pk1: have both P1 and Pk antigens  Blacks stronger expression than white
 ▪ Pk2: have both the P2 and Pk antigens  Deteriorates rapidly on storage
 ▪ p: negative for P, P1, and Pk antigens
 MOST COMMON ANTIGEN IN THE SYSTEM Anti-P1
 poorly expressed at birth and may take up to 7  Naturally occurring IgM Ab
years to be fully expressed  Found in P1- individuals
 varies in strength in adults  Weak, cold reactive saline agglutinins
 deteriorates rapidly on storage – use fresh red cells  React at 4C, bind w/ complement
when typing donor units for patients with anti-
P1 Anti-PP1PK
 UNIVERSAL ANTIGEN on red cells, white cells,  IgM but sometimes Ig
tissue cells and in plasma  Originally called Anti-Tja
 Undetectable on red cells due to conversion to P  First described in the serum of Mrs. Jay
antigen  Produced early in life w/o sensitization
 Found on white cells, some tissue cells and in and reacts w/ all RBC’s except for a
plasma person w/ p Phenotype
 ▪ P ANTIBODIES: Anti-P1, Anti-P, Anti-PP,  Potential cause of severe HTR’s and
Pk and anti-p HDFN
 ▪ Anti-P1 antibodies are naturally occurring, cold-
reacting, IgM anti-bodies often seen in Autoanti-P
individuals with the P2 phenotype. They rarely  Associated with paroxysmal cold
react at higher than room temperature, but they do hemoglobinuria
bind complement. Anti-P1 antibodies do not  An IgG autoantibody described as a
cause HDN and are rarely associated with HTR biphasic hemolysin
 ▪ Anti-P antibodies are produced by individuals  Demonstrated by Donath-Landsteiner
with Pk1 or Pk2 phenotypes and can trigger Test
severe HTR.
 ▪ Autoanti-P (the Donath-Landsteiner
antibody) is a cold-reacting antibody associated ANTIBODIES: Anti-P1, anti-P and anti-Tja (Anti-
with paroxysmal cold hemoglobinuria (PCH). P1PPk)
Anti-P1 KELL BLOOD GROUP
 Cold-reacting (usually IgM) weak antibody  First blood group system discovered after the
 Present in 2/3 of P2 individuals introduction of antiglobulin testing
 Very rare cause of HTR  Identified in 1946 in serum of Mrs.Kelleher
 Hydatid cyst fluid (rich in P1) will neutralize  Chromosomal location – 7q
anti-P1 but not anti-P  Kell antigens: K, k, Kpa, Kpb, Jsa, Jsb
 Well-developed at birth
Anti-P  Not destroyed by common proteolytic
 Very rare antibody enzymes
 2 types
o One that is produced by Pk individuals (they Kell antigens: K, k, Kpa, Kpb, Jsa, Jsb
lack P antigen so they produce anti-P)  Well-developed at birth
o Potent IgM hemolysin  Not destroyed by common proteolytic
o May be IgG – involved in CHRONIC enzymes
ABORTION  Kell antigen is SECOND to D antigen in
o One that is from patients with immunogenicity
o Also known as AUTO-ANTI-P or Kell antibodies: Anti-K
o IgG BIPHASIC HEMOLYSIN  Most common antibody seen in blood bank
o Binds complement to red cells at COLDER after ABO and Rh
TEMPERATURE  IgG “immune” antibodies reactive in AHG
o Hemolyzes red cells at 37°C phase
o Weakly positive DAT – cells coated with  Can cause HTR and HDN
complement only Ko or K null phenotype
o Antibody does not interfere with routine serum-  Lacks Kell antigens, have no membrane
cell tests abnormality
o Paroxysmal Cold Hemoglobinuria (PCH)  Expresses no autosomal Kell antigens but
o Historically seen in patients with tertiary carries Kx in abundance
syphilis
o It now more commonly presents as a transient, MacLeod phenotype
acute condition secondary to viral infection,  Lacks Kx antigen, with abnormal red cell
especially in young children morphology
 Common among males with X-linked CGD
K null MacLeod
Anti-Tja (anti-PP1Pk) Kx antigens Present Lacking
o First described in the serum of Mrs. Jay (a p Autosomal Lacking Decreased expression
individual with adenocarcinoma of the Kell
stomach, T in Tja refers to tumor) antigens
o anti-P, anti-P1, and anti-Pk components of Red cell NO YES
anti-PP1Pk are separable through adsorption abnormality (ACANTHOCYTOSIS)
o Hemolytic IgM/IgG antibody
o Produced by individuals with p phenotype
o Associated with an increased
incidence of spontaneous abortions in early THE DUFFY (008) SYSTEM
pregnancy
o Hemolytic in vivo and in vitro  Named for Mr. Duffy – multiply transfused
o Has caused severe HTR hemophiliac
o Has been associated with CHRONIC  Chromosomal location – 1q
ABORTION and HDN  1950 was found to have the first described anti-
Disease Associations Fya
Antibodies  1955 – Sanger and colleagues
 Anti-P1 – parasitic infections
 Anti-PP1Pk or anti-P – early abortions
 Autoanti-P – PCH Duffy antigens: Fya and Fyb
Antigens  Well-developed at birth
 P – serve as receptors for P-fimbriated  Easily destroyed by common proteolytic
uropathogenic E. coli—a cause of urinary tract enzymes
infections
 Pk – receptor for shiga toxins, which cause  Null phenotype: Fy (a-b-) : important
shigella dysentery and E. coli–associated anthropological marker for AFRICAN
hemolytic uremic syndrome BLACKS
 P – receptor of human parvovirus B19  Resist infection by P. vivax (humans) and P.
 Pk provides some protection against HIV knowlesi (monkeys)
infection of peripheral blood mononuclear  Makes anti-Fy3 antibody
cells  Predominant in West Africa
Duffy antibodies: Anti-Fya and Anti-Fyb Chromosomal Assignment of Genes for
 Usually IgG and react best at AHG
 Both are implicated in DELAYED HTR and HDN Common Blood Group System

BLOOD GROUP SYSTEM

THE KIDD (009) SYSTEM
CHROMOSOME
 Chromosomal location – 18q Rh , 1
 Kidd antigens: Jka, Jkb Duffy
 Jk(a-b-) or Jk null phenotype RBCs resist lysis MNS 4
in 2M urea Chido/Rodgers 6
 Organisms with Jkb-like specificity include Kell 7
Enterococcus faecium, Micrococcus and ABO 9
Proteus mirabilis Kidd 18
Lewis, 19
Kidd antibodies: Anti-Jka and Anti-Jkb Landsteiner,
 NOTORIUS REPUTATION in blood bank due Wiener,
to its association to delayed hemolytic Lutheran,
transfusion reaction
 Demonstrate dosage effect Hh
 ENHANCED BY ENZYME TREATMENT P 22
 Usually IgG

Hemolytic Disease of the Fetal/Newborn

 HDFN occurs when:

 Fetal red cells, carrying antigens inherited from
the father, stimulate the mother to produce IgG
 antibodies.
 Maternal IgG antibodies destroy fetal red cells

Hemolytic processes can cause the following:

 In utero, this destruction can cause severe anemia,

which can result in heart failure and possibly
death.
 After delivery, red cell destruction continues with
the increase of bilirubin, causing jaundice and
possible damage to the CNS (kernicterus)
 WEEK 9  Anti-i – an IgM agglutinin reactive at 4°C
associated with IM infections
OTHER BLOOD GROUP SYSTEM
(PART II)
Lutheran Blood Group System (LU)
Antigens – Lua and Lub
The MNS (002) System  Poorly developed at birth
 MNS ANTIGENS: M, N, S, s, U  Adult levels reached at 15 y/o
 determined by the MN and Ss loci
 MN is associated with glycophorin A while Ss Antibodies – anti-Lua and anti-Lub
is associated with glycophorin B Anti-Lua
 Important markers in paternity studies  Most are naturally occurring saline agglutinins
that react better at room temperatures than 37°C
MNS ANTIBODIES: Anti-M, Anti-N, Anti-S, Anti-s, Anti-Lub
Anti-U  Most are IgG (often IgG4) reactive at 37°C and
 Anti-M – relatively common usually naturally the antiglobulin phase
occurring and may be both IgM and IgG  Made in response to pregnancy or transfusion
 do not bind complement and react optimally at  Implicated with shortened survival of
room temperature or below only rarely transfused cells and posttransfusion jaundice
associated with HDN or HTR

Anti-N – rare Other Blood Group System

 weak, naturally occurring IgM antibodies that
react best at room temperature or below XG Blood Group System (XG)
 not usually associated with HDN or HTR  SHORT ARM OF CHROMOSOME X
 Anti-S, anti-s, and anti-U – rare  Antigens – Xga – no known antithetical partner
 IgG antibodies which usually develop
following RBC stimulation Antibodies – anti-Xga
 all have been associated with severe HDN and  IgG antibodies, red cell stimulated, but does
HTR not cause transfusion reactions or HDN
 Reactive in IAT
LECTINS  Sensitive to enzymes but not to dithiothreitol
o Anti-M lectin – Iberis amara
o Anti-N lectin – Vicia graminea, Bauhinia Diego Blood Group System (DI)
variegata, Bauhinia purpura  Chromosome 17, codominant alleles

I Blood Group System Antigens – Dia/Dib

I antigens: I and i  Located on the anion-exchange molecule (AE-
 At birth, infant red cells are rich in i antigen 1)
 During first 18 months of life, i slowly  MUTATION IN AE-1 can result in
decreases, I increases HEREDITARY SPHEROCYTOSIS,
 Adult red cells, rich in I and only trace amount CONGENITAL ACANTHOCYTOSIS AND
of i SOUTHEAST ASIAN OVALOCYTOSIS
 Dia – USED IN MONGOLIAN ANCESTRY
I antibodies: Anti-I and anti-i ANTHROPOLOGICAL STUDIES
 Benign anti-I – weak, naturally occurring
antibody, saline reactive IgM autoagglutinin Antibodies – anti-Dia and anti-Dib
detectable only at 4C  Red-cell stimulated IgG antibodies that do not
 Pathologic anti-I – cold agglutinin that bind complement
demonstrates high titer reactivity and reacts  Reactive in IAT
over a wide thermal range (0 to 30C)

 MYCOPLASMA PNEUMONIAE – may develop

strong cold agglutinins with auto-anti I specificity
Cartwright Blood Group System (YT) Gerbich Blood Group System (GE)
 Chromosome 7, codominant alleles  Chromosome 2
 Expressed on glycophorins C and D
Antigens – Yta and Ytb  Antigens – 3 high incidence antigens (Ge2,
 Present in erythrocyte acetylcholinesterase Ge3, and Ge4) and 4 low incidence antigens
(AchE) (Wb, Lsa, Ana and Dha)
 Leach phenotype (GE: -2, -3, -4) –
Yta ELLIPTOCYTOSIS
▪ High-incidence antigen
Cromer Blood Group System (CROM)
Ytb  Chromosome 1
▪ Low-incidence antigen  Antigens are carried by DECAY
ACCELERATING FACTOR (DAF)
Antibodies – anti-Yta and anti-Ytb
 IgG antibodies, predominantly red cell Knops Blood Group System (KN)
stimulated  Chromosome 1
 Reactive in IAT  Expressed on complement receptor one (CR1)

Scianna Blood Group System (SC) Indian Blood Group System (IN)
 Chromosome 1, codominant alleles  Chromosome 11
 Antigens – Sc1, Sc2, Sc3 and RADIN (Rg)  Antigens are carried by CD44 marker
 Antibodies – anti-Sc1, anti-Sc2, anti-Sc3, anti-
Rg Bg Blood Group System
 Bga antigen corresponds with HLA-B7
Dombrock Blood Group System (DO)  Bgb with HLA-B17
 Chromosome 12, codominant alleles  Bgc with HLA-A28
 Resides in  Bg antibodies - NUISANCE ANTIBODIES
GLYCOSYLPHOSPHATIDYLINOSITOL  Reactivity may be removed by
(GPI) glycoprotein CHLOROQUINE or EDTA-GLYCINE HCl

Antigens – Doa and Dob, Gregory (Gya), Holley (Hy)

and Joseph (Joa) HIGH TITER, LOW AVIDITY ANTIBODIES
 Total absence of DO expression is seen in Antibodies that exhibit reactivity at high dilutions of
PNH III RBCs which are deficient in all GPI- serum, but the strength of agglutination is weak
anchored glycoproteins at any dilution
 Anti-Ch (Chido)
Colton Blood Group System (CO)  Anti-Rg (Rogers)
 Chromosome 7, codominant alleles  Anti-Kn (Knops)
 Anti-JMH (John Milton Hagen)
Antigens – Coa, Cob and Co3  Anti-Yka (York)
 Present in aquaporin-1 (AQP1)  Anti-Csa (Cost)
 Disease association: MONOSOMY-7 of the  Anti-McC (McCoy)
bone marrow

Chido/Rodgers Blood Group System (CH/RG)

 C4a and C4b of chromosome 6
 Antigens – 6 Ch antigens, 2 Rodgers antigens
and WH antigen
 Anti-Ch/Rg antibodies - collectively known as
HIGH-TITER, LOW-AVIDITY (HTLA)
 Presence confirmed by (1) Ab screening with
C4 coated cells and (2) plasma inhibition
CLINICALLY INSIGNIFICANT MINOR Some approximate Dates of
BLOOD GROUP Discovery of Blood
Ch/Rg, KN and Bg Groups (according to Turgeon)
 1900 – ABO
901 SERIES/HIGH INCIDENCE SERIES  1927 – MN
Anti-Sda– SHINY & REFRACTILE, mixed-  1927 – P
field agglutination reaction, under the  1939 – Rh
microscope, inhibited by Sd-positive urine  1945 – Lutheran
 1946 – Kell
Anti-Vel – associated with severe immediate  1946 – Lewis
HTR  1950 – Duffy
 1951 – Kidd
 WEEK 10
VOLUNTARY BLOOD DONATION Medical History
(Donor Screening & Component Preparation)  Essential to ensure protection of the donor and
benefit to the recipient
 The questionnaire was designed to be self-
TYPES OF DONORS administered by the donor but if preferred may
be administered by a trained medical
 Autologous
historian or physician
 The interviewer should be familiar with the
 Allogenic
question.
o Voluntary Non Remunerated Donors-safest  The interview should be conducted in a
type of blood secluded area.

o Directed Donors- have the same blood type of the Medical History Questions
patient  Have you donated blood in the past 8 weeks or
plasma in the past 48 hours?
o Paid Donors- unsafest  In the past 12 months have you been under a
doctors care, been pregnantsor had a major
illness or surgery? If yes, what and when?
 Do you currently have an infection or are you
DONOR SCREENING taking antibiotics for an infection?
 Have you ever had heart problems, lung
 Process of ensuring the safety of both the problems (other than asthma) or a bleeding
patient and donor problem?
 Have you ever had hepatitis? If yes, when?
1. Donor Registration  Have you ever had a positive test for HIV?
 In the past 48 hours, have you taken aspirin or
 Must confirm donor’s identity and must link
anything with aspirin in it?
the donor existing record.
 In the past 6 weeks, have you been pregnant or
 Need for Identification card (ID) are you pregnant now?
 In the past 8 weeks have you had any
 List of information used in the registration vaccinations or other shots? Have you had
process: contact with someone who had a small pox
vaccination?
 ◦Name (First, Last, MI)
 ◦Date and time of donation Physical Examination
 ◦Address  General appearance
 ◦Telephone  Weight: mandates a maximum of 10.5ml of
 ◦Gender blood/kg
 ◦Age or Date of Birth ◦110Ibs (50kg)
 17 years old and above, (17y/o ◦If donor is less than 110Ibs:
Must have parent’s consent  Temperature: Orally should not exceed 99.5’F
or 37.5’C
Donor’s consent  Pulse: 50 to 100beats per minutes
 Additional information:  Blood Pressure: No greater than 180mmHg
◦Name of patient for whom the blood is Systolic
intended ◦Diastolic: no greater than 100mmHg
◦Race  Hematocritand Hemoglobin:
◦Cytomegalovirus status ◦38% Hct(12.5g/dLHgb)
TYPES OF DEFERRAL DONOR REACTIONS
 Syncope (fainting)
TEMPORARY DEFERRALS  Remove needle immediately
 Certain immunizations  Hyperventilation
 2 weeks -MMR, yellow fever, oral polio, typhoid  Have donor rebreathe into paper bag.
 4 weeks -Rubella, Chicken Pox  Nausea/vomiting
 2 months – small pox  Twitching/muscle spasms
 Pregnancy – 6 weeks upon conclusion  Hematoma
 Certain medications  Convulsions – rare, get immediate assistance
 Proscar/Propecia, Accutain – 1 month  Cardiac difficulties
 Avodart – 6 months POST-PHLEBOTOMY CARE
 Soriatane – 3 years  Donor applies pressure for 5 minutes
 Tegison - permanent  Check and bandage site
 Have donor sit up for few minutes
 Have donor report to refreshment area for
additional 15 minutes of monitoring
PERMANENT DEFERRALS
 HIV, HBV, or HCV positive
POST-PHLEBOTOMY INSTRUCTIONS
 Protozoan diseases such as Chagas disease or
 Eat/drink before leaving
Babesiosis  Wait until staff releases you
 Received human pituitary growth hormone
 Drink more fluids next 4 hours
 Donated only unit of blood in which a
 No alcohol until after eating
recipient contracted HIV or HBV  Refrain from smoking for 1 hour
 Was the only common donor in 2 cases of
 If bleeding continues apply pressure and raise
post-transfusion HIV or HBV in recipient arm
 Lived in a country where Creutzfeld-Jacob
 Faint or dizzy sit with head between knees
disease is prevalent  Abnormal symptoms persist contact blood
 Most cancers except minor skin cancer and
center.
carcinoma in-situ of the cervix  Remove bandage
 Severe heart disease, liver disease
PROCRESSING OF DONOR’S BLOOD
 ABO/Rh
 Antibody Screen
WHOLE BLOOD COLLECTION
 HBsAg
 Donor Identification
 Anti-HBc
 Aseptic technique
 Anti-HCV and NAT
 Post-donation instructions
 Anti-HIV-1/2 and NAT
 Donor reactions
 Anti-HTLV-I/II
◦Mild reactions
 WNV RNA
◦Moderate reactions
 Syphilis
◦Severe reactions
 Malaria

RESULTS OF TESTING
 Tests for disease markers must be negative or
BLOOD COLLECTION UNIT
 Materials used are sterile and single use. within normal limits.
 Most important step is preparing the site to a  Donor blood which falls outside these
state of almost surgical cleanliness. parameters must be quarrantined.
 Bacteria on skin, if present, may grow well in
stored donor blood and cause a fatal sepsis in
6 pieces of info in donor registration
recipient
 donor ID
 Use 16-17 gauge needle to collect blood from
 -prescreening
a single venipuncture within 15 minutes
 -donor history
 Collect 450 +/- 45 mLs of blood
 -contact info
  -written consent
 -photo or other ID MUCUS MEMBRANE OR SKIN
PENETRATION BLOOD EXPOSURE
5 donor safety questions > DEFERRAL

 -general health  12 months

 -surgeries
 -heart/lung disease
 -bleeding problems
 -pregnancy SEXUAL CONTACT WITH PERSON
HIGH-RISK FOR HIV DEFERRAL

 12 months
required time between whole blood donations >

 56 days (8 weeks)

INCARCERATION FOR 72 HOURS

DEFERRAL
VACCINES REQUIRING 2 WEEKS
DEFERRAL  12 months

 -Measles
RETURN FROM MALARIAL EPIDEMIC
 -Mumps AREA DEFERRAL
 -Polio (oral)
 -Typhoid (oral)  12 months
 -Yellow fever

COMPLETION OF SYPHILIS THERAPY

DEFERRAL
VACCINES REQUIRING 4 WEEK
DEFERRAL  12 months
 -Rubella
 -Varicella-Zoster
TRANSFUSION DEFERRAL

 12 months
CONCLUSION OF PREGNANCY
DEFERRAL
TRAVEL TO IRAQ (LEISHMANIA)
 6 weeks DEFERRAL

 12 months
TATTOOS AND PERMANENT MAKEUP
(UNLICENSED) DEFERRAL
ANIMAL BITE TREATED WITH HUMAN
 12 months DIPLOID CELL-RABIES VACCINE
DEFERRAL

 12 months
ASYMPTOMATIC AFTER MALARIA WEIGHT REQUIREMENT TO DONATE BLOOD
DIAGNOSIS DEFERRAL  110 lbs

 3 years PULSE REQUIREMENT TO DONATE BLOOD

 50-100 bpm

DRUGS WITH 1 MONTH DEFERRAL BLOOD PRESSURE REQUIREMENT TO

DONATE BLOOD
 -Proscar (prostate)  <180 / <100
 -Propecia (baldness)
 -Accutane (acne) TEMPERATURE REQUIREMENT TO DONATE
 -Amnesteem (acne) BLOOD
 -Claravis (acne)  </= 99.5F (37.5C)
 -Sotret (acne)
H&H REQUIREMENT TO DONATE WHOLE
BLOOD
 -Hbg >/= 12.5
DRUGS WITH 6 MONTH DEFERRAL  -Hct >/= 38%

 Avodart (prostate) PHLEBOTOMY VEIN LOCATION

 AC (antecubital or cephalic) vein

PHLEBOTOMY NEEDLE SIZE

DRUGS WITH 3 YEAR DEFERRAL  16-gauge
 Soriatane (psoriasis) PHLEBOTOMY PREP COMPOUNDS
 -0.7% iodophor compound
 -10% povidone iodine
DRUGS WITH PERMANENT DEFERRAL
3 REASONS TO PERFORM AUTOLOGOUS
 Tegison (psoriasis) DONATION
 -rare blood type or antibodies
 -preventionof alloimmunization
 -prevention of transfusion-related diseases
9 reasons for permanent deferral
MINIMUM TIME BLOOD CAN BE DRAWN
 history of viral hepatitis after 11th BEFORE PROCEDURE IN AUTOLOGOUS
birthday DONATION
 confirmed + for HBsAg  no less than 72 hours beforehand difference in
 repeatedly reactive tests for anti-HBc criteria for autologous donations >
 past or present clinical evidence of  no questions about high-risk behavior
infection with HIV, HTLV, HCV  Hgb >/= 11
 history of babesiosis or Chagas  Hct >/= 33%
 risk of Creutzfeldt-Jacob disease  no infectious disease testing unless transfused
 family history of Creutzfeldt-Jacob facility other than donation facility
disease  biohazardous units transfused with physician's
 needle use to administer permission
nonprescription drugs  not restricted by age or weight
 recipient of dura mater or human
pituitary growth hormone
 DONOR SCREENING & COMPONENT
INTRAOPERATIVE COLLECTION PREPARATION
 -medical device collects blood lost during
surgery and reinfused American Association of Blood Banks (AABB) –
 -machine collects, washes, filters, and established in 1947
concentrates  International association of blood banks that
 -does not remove bacteria includes hospital and community blood
 -blood washed with saline stored at RT for 4 centers, transfusion & transplantation centers,
hours or 1-6C for 24 hours and individuals involved in transfusion
medicine
POSTOPERATIVE COLLECTION  Mission is to establish and provide the highest
 -collected in sterile canisters from surgical standard of care for patients and donors in all
drains and reinfused with or without aspects of transfusion medicine
processing  AABB Standards & AABB Technical Manual
 -transfusion must begin within 6 hours – books published by AABB

DIFFERENCE BETWEEN ALLOGENIC AND DONOR SCREENING

DIRECTED DONATIONS  Encompasses the medical history requirements
for the donor, the (mini) physical
 everything applies to both except 56 day
examination, and serologic testing of the
interval between donations may be waived for
donor blood
directed

INTERMITTENT FLOW AUTOLOGOUS DONORS

 Donations for self; NO AGE LIMIT
 one venipuncture for apheresis
 Hematocrit: 33%
 Hemoglobin: 11 g/dL
CONTINUOUS FLOW
 No have signs or symptoms of active
 venipuncture in both arms for apheresis
infection
 NO BACTEREMIA
FEMALE HEIGHT AND WEIGHT
 Preoperative collection must be labeled
REQUIREMENTS FOR DOUBLE RED CELL
“for autologous use only” and used only
DONATION
for this patient
 5'1" and 130 lbs  Blood should not be donated within 72
hours of scheduled surgery or
MALE HEIGHT AND WEIGHT REQUIREMENTS transfusion
FOR DOUBLE RED CELL DONATION
 5'5" and 150 lbs
Blood Collection
WHOLE BLOOD COLLECTION
HCT REQUIREMENT FOR DOUBLE RED CELL
 For blood collection, most blood centers use an
DONATION
iodine compound such as PVP-iodine or
 >/= 40% polymeriodine complex.
 Using a tourniquet or bloodpressure cuff, the
DEFERRAL TIME AFTER DOUBLE RED CELL venipuncture site is identified, and the
DONATION  area is scrubbed at least 4 cm in all directions
 16 weeks (double)
from the site for a minimum of 30 seconds.
 The area is then covered with a dry sterile gauze
pad until the venipuncture is performed.
 Donors who are allergic or sensitive to iodine
compounds may use chlorhexidrine gluconate
and isopropyl alcohol.
COMMON BLOOD ANTICOAGULANTS,
ADDITIVES & REJUVENATING SOLUTIONS –
prevent physical changes to maintain the viability &
function of the blood constituents, preventing
bacterial contamination and minimizing cell lysis

A. ACD/CPD/CPD2 – anticoagulant: 21 day

expiration when stored between 1 to 6°C
B. CPDA-1 – anticoagulant: 35 day expiration
C. Heparin – anticoagulant: 2 day expiration
D. Additive solutions: 42 day expiration
E. Rejuvenating solutions: restores 2,3-DPG and
ATP

DONOR RECORDS – minimum retention time for

donor records varies from 5 to 10 years to
indefinite retention
DEFERRALS (HENRY’S)
  CONFIRMATORY TEST – include RIBA
Donor Unit Processing (recombinant immunoblot assay)
ABO & Rh Typing
 Forward & reverse typing for ABO ▪ Fusion of HCV antigens to human superoxide
 Testing Rh with anti-D reagent at immediate dismutase and a recombinant superoxide dismutase is
spin phase incorporated to detect nonspecific reactions
 Weak D testing performed if initial testing is ▪ Reported as positive, negative or indeterminate
NEGATIVE ▪ Positive = presence of HCV antibody

Antibody screen Anti-HIV-1/2 and NAT

 donors with a history of pregnancy or  Screened by FDA-approved EIA method
transfusion – tested for presence of  If negative, unit is suitable for transfusion
UNEXPECTED antibodies to RBC antigens  If positive, test must be repeated in duplicate.
 Pooled screening cell is tested against donor If any one of the duplicate tests is reactive,
serum or plasma UNIT MUST BE DISCARDED
 Pooled screening cell contains antigens agains  Confirmation tests for HIV include Western
significant ALLOANTIBODIES Blot and immunofluorescence assay
HBsAg WESTERN BLOT
 Methods currently approved are RIA, EIA, o Performed using donor serum
ELISA & RPHA o HIV material is separated into bands according
 ELISA is the MOST COMMON procedure to their molecular weight
used o Material is transferred to a
 Serum or plasma is incubated with antigen to NITROCELLULOSE membrane and donor
HBsAg serum is added
 An enzyme-conjugate mixture is added o If anti-HIV-1/2 antibodies are present, they
 If antibody is specific to the antigen, a will bind to specific bands
COLOR CHANGE develops & measured o Results are expressed as positive, negative or
spectrophotometrically indeterminate

Anti-Hbc Anti-HTLV-I/II
 for prevention of post-transfusion  HTLV-I – causative agent of adult T-cell
hepatitis B leukemia & associated with neurologic
 Has been implicated in Hepatitis C disorder called HTLV-associated myelopathy
disease  HTLV-II – 60% homologous to type I and is
 Was once part of the surrogate testing prevalent among INTRAVENOUS drug users
along with its counterpart ALT (alanine in the US
aminotransferase)  Persons can contract both viruses from
 ALT was discontinued because of transfusion via infected lymphocytes
increased sophistication & sensitivity of  Tested by EIA screening test that utilized viral
anti- HCV testing lysates from both viruses
 Confirmatory tests include Western Blot,
Anti-HCV & NAT RIPA, & NAT testing
 SCREENING TEST – EIA which detects  A donation that is repeatedly reactive with
antibodies to c200, c22-3 and NS-5 proteins EIA – NOT USED FOR TRANSFUSION
of HCV genome  If tested with another EIA kit from a different
 NAT – able to detect small amounts of viral manufacturer, and the test is still reactive,
nucleic acid in blood before antibodies or DONOR SHOULD BE INDEFINITELY
viral proteins such as HCV core antigen are DEFERRED
detectable by current methods
 Window period for detection of HCV is
reduced ~70% from a mean of 82 days to 25
days
SYPHILIS
 done because it is a sexually-transmitted disease  ProVue – FIRST FULLY AUTOMATED
and places the donor at higher risk for possible BLOOD BANKING SYSTEM for use with
exposure to hepatitis & HIV the ID-Micro Typing System Gel Test

 Screening tests include RPR & VDRL – both AUTOLOGOUS DONOR UNIT PROCESSING
are based on reagin, or antibody against  Testing. In addition to ABO and Rh typing,
CARDIOLIPIN testing for HBsAg, syphilis, and HIV-1 are
 Cardiolipin-like antibodies have been required for processing autologous donor units.
documented in persons with UNTREATED Most donor facilities perform all tests normally
syphilis infections required for homologous units to allow unused
 Antibody will agglutinate cardiolipin carbon autologous units to be used for other transfusion
particles in the form of VISIBLE purposes.
FLOCCULATION
 Confirmatory test is FTA-ABS or fluorescent  Labeling. Donor units dedicated for autologous
treponemal antibody absorption test use must be clearly labeled “for autologous use
 INDIRECT IMMUNOFLUORESCENCE is only,” and a biohazard label must be attached to
used to detect antibodies to spirochete T. any unit repeatedly reactive for any of the
pallidum- agent of syphilis previously mentioned tests for infectious
 No documented cases of transfusion- diseases.
transmitted syphilis
 T. pallidum cannot survive more than 72 hours  Storage. In addition to being stored between 1◦C
in citrated blood stored at 1°C to 6°C and 6◦C, autologous units must be stored
which would make PLATELETS the only separately from homologous units.
component capable of transmitting infection

AUTOMATION – used to increased efficiency and

productivity of donor testing

 SOLID PHASE TECHNOLOGY

 ABS2000 – credited as being the FIRST
FULLY AUTOMATED walk-away system
designed to automate routine, labor-intensive
processing, thus allowing technologists to
complete other tasks Performs ABO/Rh using
hemagglutination & antibody
screens/crossmateches using solid phase
technology

 ROSYS Plato & ABSHV – can perform

medium-to-high-volume testing

 Dias Plus System – performs high-volume

testing (more than 300 tests per hour) designed
for 24- hour operation

 Galileo – fully automated, bidirectional

interface, capable of medium- to high volume
testing for ABO

 THE GEL SYSTEM – developed by Dr. Yves

Lapierre in 1985. Gel chambers have dextran
acrylamide gel particles that facilitate trapping
agglutinates if agglutination of antibody and
RBCs has occurred
 WEEK11 Dextrose
supports ATP generation by glycolytic pathway
COMPONENT PREPARATION &
THERAPY Adenine
BLOOD COMPONENT acts as a substrate for red cell ATP synthesis
PREPARATION
Citrate
prevents coagulation by chelating calcium, also
COMPONENT PREPARATION – manufacturing protects red cell membrane
process of all components used in
transfusion therapy Sodium biphosphate
prevents excessive decrease in pH
Why Do We Separate Blood into Components?
Helps to provide appropriate therapy for each patient Mannitol
• Allows for optimal storage of each component Osmotic diuretic acts as a membrane stabilizer
• Maximizes a limited resource
• Because we can (materials science) Red Blood Cells ‐ Apheresis
Allows for the collection of two units of red cells
Components of Whole Blood
from one donor every 16 weeks
When centrifuged, whole blood can be separated into
• Saline is used to replace the fluid lost
the following layers due to varying specific gravities:
• Double unit is placed in inventory as two separate
• Plasma: upper layer
units
• "Buffy coat" contains
• Can be leukoreduced by apheresis instrument or by a
• Platelets
leukoreduction filter
• White blood cells
• Red Blood Cells
Apheresis Platelets
Types of Anticoagulant‐Preservative Solutions
• Prepared from a single donor during a 90 minute
• CPD (Citrate‐phosphate‐dextrose)
procedure.
• CP2D (Citrate‐phosphate‐2x Dextrose)
• In a continuous process, blood is collected, spun
• CPDA‐1 (Citrate‐phosphate‐dextrose‐adenine)
down, platelets are harvested, red cells and most
Any one of these agents can be used as the
plasma are returned to the donor.
anticoagulant in the primary bag
• Procedure can be repeated in 7 days (a person can
donate 24 times/year)
Use of Additive Solutions
• After the plasma is expressed off the PRBCs, about
Blood Component Preparation
100 mLs of an additive solution is added
 Components of whole blood are centrifuged:
• Purpose: Extends the storage limit of RBCs
 “light spin” – short time, low RPM
• AS‐1 or AS‐5 (Dextrose, adenine, mannitol and
 “heavy spin” – longer spin, high RPM
saline)
 Procedures are in the AABB Technical
• Mannitol is a sugar that maintains osmotic pressure
Manual
during storage and decreases RBC lysis
Blood component preparation- Light Spin
• AS‐3 (Dextrose, adenine, saline, citrate)
- Platelet rich plasma (PRP)
• AS‐7 (Dextrose, adenine, mannitol, sodium
- Expressed into satellite bag
bicarbonate + phosphate)
- RBC (remain in original bag), sealed and split-
additives
preservative/anticoagulant storage limits
CPD- 21 days
Blood component preparation- Heavy spin of PRP
CP2D- 21 days
- PPP- platelet poor plasma
CPDA-1- 35 days
- Plasma (all removed but 50-70mLs are kept with
AS-1- 42 days
plts- to reconsitiute and to maintain pH of 6.2 or
AS-3- 42 days
higher)
AS-7- 42 days
- Platelets (sediment on bottom of bag, rest for 1 hr)
- 50-70mLs of plasma with platelets maintain pH of
6.2 or higher
- Stored at RT on rotator (only the platelets)  RBCs (deglycerolized or washed)
- 20-24C for up to 5 days (because of possibility of  Good at 1-6°C for 24 hours
contamination and overgrowth)  RBCs (irradiated)
 1-6°C for 28 days
Whole blood- closed system
 Sterile Leukocyte-Reduced RBCs are for:
- Allows for maximum expiration date  patients who receive a lot of transfusions to
- Anticoagulant- preservative mixture prevent antibody production toward WBC
- Integral satellite bags antigens
Whole blood- open system  Patients transfused outside of a hospital
 Break in the seal  Patients who have reacted to leukocytes in the
- Prone to contamination past
- Expiration date- 24 hrs
Frozen RBCs
Anticoagulant- Preservative- Citrate phosphate  Glycerol is added to cryoprotect the unit
dextrose (CPD)  Glycerol prevents cell lysis
21 days
1-6C Deglycerolized RBCs
 RBCs that have had the glycerin removed
Anticoagulant- Preservative- Citrate phosphate  Thawed at 37°C
2 dextrose (C2PD)  A blood cell processor washes the cells with
21 days varying concentrations of saline
1-6C  Considered “open”, expires in 24 hrs.

Anticoagulant- Preservative- Citrate phosphate Washed RBCs

dextrose adenine (CPDA-1)  Not effective in reducing WBCs
35 days  For patients (with anti-IgA) that may react
1-6C with plasma proteins containing IgA
Requires Hct of less than 80%  Reactions may be allergic, febrile, or
Whole Blood anaphylactic
 Component Requirements
 Stored: 1-6° C Irradiated RBCs
 Shipping: 1-10° C  Prevents T-cell proliferation that may cause
 21 or 35 days depending on preservative transfusion-associated graft versus host
(CPD, CP2D, or CPDA-1 disease (GVHD)
 Consists of RBCs, WBCs, platelets and  GVHD is fatal in 90% of those affected
plasma (with anticoagulant)  Used for:
 1 unit increases Hgb 1 g/dL and Hct 3%  Donor units from a blood relative
 When is it used?  HLA-matched donor unit
 Patients who are actively bleeding and lost  Intrauterine transfusion
>25% of blood volume  Immunodeficiency
 Exchange transfusion  Premature newborns
 Chemotherapy and irradiation
Red Blood Cells  Patients who received marrow or stem cells
RBCs
 1-6° C (stored); 1-10° C (shipped) Platelets
 21, 35, or 42 days depending on preservative  Important in maintaining hemostasis
or additive  Help stop bleeding and form a platelet plug
 Hematocrit should be ≤80% (primary hemostasis)
 One unit increases hematocrit 3%  People who need platelets:
 Once the unit is “opened” it has a 24 hour  Cancer patients
expiration date!  Bone marrow recipients
 Postoperative bleeding
RBCs (frozen)  Requires 2 spins:
 ≤ -65°C for 10 years
 Soft – separates RBCs and WBCs from plasma  Same storage as FFP (cannot be re-frozen as
and platelets FFP once it is separated); -18 for 1 year
Heavy- platelets in platelet rich plasma (PRP) will  If thawed, store at room temp 4 hrs
be forced to the bottom of a satellite bag  The leftover plasma is called cryoprecipitate
 40-60 mL of plasma is expelled into another reduced or plasma cryo
satellite bag, while the remaining bag contains  Good for thrombocytopenic purpura (TTP)
platelet concentrate  CRYO is used for
 Storage Temperature  2° treatment for Factor VIII deficiency
 20-24°C for 5 days (constant agitation) (Hemophilia A)
 Each unit should contain at least 5.5 x 1010  2 ° treatment for von Willebrand’s Disease
platelets (platelet concentrate)  Congenital or acquired fibrinogen
 Each unit should elevate the platelet count by deficiency
5-10,000 µL in a 165 lb person  FXIII deficiency
“Fibrin Glue” applied to surgical sites
Pooled platelets
 Used to reach therapeutic dose Granulocytes
 An “open system” occurs when pooling  Neutrophils are the most numerous, involved
platelets, resulting in an expiration of 4 hours in phagocytosis of bacteria/fungi
 Platelet, pheresis – therapeutic dose (from one  Although rare, it is useful for infants with
donor) without having to pool platelets bacteremia
 3x1011 minumum  Prepared by hemapheresis
 HLA matched – for those with HLA  ≥ 1.0 x 1010
antibodies  Maintained at room temp for 24 hours
 Leukocyte reduced - used to prevent febrile
non-hemolytic reactions and HLA Rejuvenation Solution
alloimmunization  Restore 2,3 DPG and ATP
- During storage or up to 3 days after
Fresh Frozen Plasma (FFP) expiration- pyruvate, inosine,
 Plasma that is frozen within 8 hours of phosphate, adenine
donation - Extends expiration date for
 -18°C or colder for 1 year freezing rare or autologous units
 Provides coagulation factors for - Must be washed to remove inosine-
 Bleeding toxic
 Abnormal clotting due to massive transfusion
 Patients on warfarin who are bleeding
 Treatment of TTP and HUS
 Factor deficiencies
 ATIII deficiency
 DIC when fibrinogen is <100 mg/dL
 FFP is thawed before transfusion
 30-37°C waterbath for 30-45 minutes
 Stored 1-6°C and transfused within 24 hours
 Needs to be ABO compatible

Cryoprecipitate
 Cryoprecipitated antihemophilic factor (AHF)
or “Cryo” is the precipitated protein portion
that results after thawing FFP
 Contains:
 von Willebrand’s factor (plt. adhesion)
 Fibrinogen
 150 mg in each unit
 Factor VIII
 About 80 IU in each unit
 Fibrinonectin
Transport- Whole blood or RBCs Granulocytes- Apheresis
o Kept at 1-10C o Storage temp= 20-24C
o On ice o Storage duration= 24 hrs
o Shipping temp= 20-24C with gel packs
Transport- FFP and Cryoprecipitate o Has to be irradiated
o Shipped on dry ice

Transport- Platelets
o 20-24C
o NO ice

Transport containers should be

o Validated periodically

RBC- Liquid
o Storage temp= 1-6C
o Storage duration:
o CPD, CP2D= 21 days
o CPDA-1= 35 days
o AS-1, 3, 5= 42 days
o Shipping temp= 1-10C on ice

RBC- Frozen
o Storage temp= -65- -80C
o Storage duration= 10 yrs
o Shipping temp= frozen, on dry ice

FFP- liquid (after thawing)

o Storage temp= 1-6C
o Storage duration= 24 hrs

FFP- Frozen
o Storage temp= -18- -20C
o Storage duration= 1 yr
o Shipping temp= frozen on dry ice

Cryoprecipitate- Liquid (after thawing, pooled)

o Storage temp= 20-24C
o Storage Duration= 4 hrs

Cryoprecipitate- Frozen
o Storage temp= -18- -20C
o Storage Duration= 1 yr
o Shipping temp- frozen on dry ice

Platelets from whole blood or Apheresis

o Storage temp= 20-24C
o Storage duration= 5 days
o Shipping temp= 20-24C with gel packs

Platelets- pooled
o Storage temp= 20-24C
o Storage duration= 4 hrs
o Shipping temp= 20-24C with gel packs