WEEK 7 is derived from the use of the blood of rhesus
monkeys in the basic test for determining the
Rh Blood Group System
RH BLOOD GROUP SYSTEM
 Second most important blood group system.
Most important is the ABO system
 Discovered in 1939
 Five principle antigens: D, C, E, c, and e
 The corresponding antibodies account for
most clinical transfusion issues
Importance of the Rh system
1. After the A and B antigens, the D antigen is the
most important red cell antigen in blood banking
2. The D antibody can cause transfusion reactions
and hemolytic disease of the newborn
(HDN)/Erythroblastosis fetalis
D Antigen
 The terms Rh-positive and Rh-negative refer
to the presence or absence of the D red blood
cell antigen
 Unlike the ABO system, the absence of the D
antigen does not have a corresponding
antibody
 The production of antibody requires red cell
stimulation from Rh-positive cells
Rh Blood Group
 Named Rh because of its similarity to the
antibody reacted to rhesus monkey cells
 85% of the population are Rh positive
 15% of the population are Rh negative
 Rh antigens have only been detected on red
cell membranes
 Consists of 45 different antigens
Rh Null Syndrome
 The lack of Rh system antigens - referred to
Rh null
 Causes an RBC membrane abnormality
 Shortened RBC life span
 patients with Rh null syndrome
 Osmotically fragile red cells called
stomatocytes
 Chronic haemolytic anaemia
History
 1939 Levine and Stetson defined D antigen (Rh
factor)
 1940 Landsteiner and Weiner discovered anti-Rh
(named after Rhesus monkey)
 Agglutinated 85% human RBCs
 15% RBCs did not agglutinate
 the presence or absence of the Rh antigen, often
called the Rh factor, on the cell membranes of the
red blood cells (erythrocytes). The designation Rh
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
that time a number of distinct Rh antigens have
been identified, but the first and most common
one, called RhD, causes the most severe immune
reaction and is the primary determinant of the Rh
trait.
Discovery of the Rh system:
 Levine and Stetson linked the Rh factor to HDN
 Weiner linked Rh factor to transfusion reactions
Rh Antigen Frequency
 D antigen – 85%
 d (absence o D)– 15%
 C antigen – 70%
 E antigen – 30%
 c antigen – 80%
 e antigen – 98%
Rh Genetics
 2 closely linked genes control the expression of
ALL Rh antigens (codominant alleles)
 RH - D gene - determines the expression of the D
antigen
 RH – C- E gene - determines the expression of the
C, c, E, and e antigens
Rh Nomenclature
 There are several different systems of
nomenclature that theorize the inheritance of the
Rh system
A. Fisher-Race – DCE Termiology
B. Wiener – Rh –Hr Terminology
C. Rosenfield – Alpha/Numeric Terminology
D. ISBT – International Society of Blood Transfusion
– Numeric terminology
FISHER-RACE TERMINOLOGY
 Fisher-Race postulated that the Rh system
antigens are inherited as a gene complex
(haplotype) that codes for three closely linked
sets of alleles
 D is inherited on one locus, no d
antigen; d is used to denote absence of
D
 C and c
 E and e
 Most commonly used (i.e. WHO)
  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
2. DCe/dcE individual is heterozygous for D, C, e, d, c,
and E genes
WEINER RH-HR TERMINOLOGY
 One gene is responsible for expression of all Rh
antigen on the red blood cells
Eight alleles:
 R0 - r
 R1 - r'
 R2 - r"
 Rz – ry
 Rarely used, but good for describing phenotype
 A single gene at the Rh locus leads to the expression of
the Rh antigens (next slide)
 Each parent contributes 1 Rh gene
 8 alleles exist at each gene locus
 Each gene controls production of an agglutinogen
composed of three factors (antigens)
 Wiener further theorized that 8 major genes led to
different combinations of antigens (D, C, E, c, e):
Blood Transfusion (ISBT)
 Attempts to standardize nomenclature
 Six digit numbers are assigned to each blood group
specificity
 1st three – blood group; last 3 antigenic specificity
 004 refers to the Rh system
 The remainder is the specific number
• Example: ISBT for the C antigen is 004002
Genotype vs. Phenotype
 The phenotype is the result of the reaction between the
red cells and antisera
 The genotype is the genetic makeup and can be
predicted using the phenotype and by considering the
race of an individual
 Only family studies can determine the true genotype
 Anti-D, anti-C, anti-E, anti-c, and anti-e is tested with
patient RBCs
 If a specimen gives the following reaction: 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
corresponding genes are present in the
heterozygous state
 If they express only C or c, or only E or e, the
person is assumed to be homozygous for that gene
Determining the Most Probably Genotype from the
Phenotype
Five antisera are used
 Anti-D
 Anti-C
 Anti-E
 Anti-c
 Anti-e
- Once the phenotype is known, the most probable
genotype can be determined from knowing the most
common genotypes
RH PHENOTYPES AND GENOTYPES
D Antigen
 D antigen is the most immunogenic antigen in
the Rh system
 85% of D-negative people receiving D-
positive blood transfusion produce the anti-D
antibody
 D-negative patients should receive only D-
negative blood
Weak D
 Anti-D is IgG
 Manufacturers have developed anti-D reagents
that react at room temperature and immediate
spin, like anti-A and anti-B tests
 When the D antigen is weakly expressed, its
detection requires indirect antiglobulin testing
(IAT)
 Older terminology refers to weak D or Du
WEAK D EXPRESSION
DUE TO:
 Weak D: Genetic. Quantitative variation of D
gene
 Weak D: Position effect. C is inherited in the
trans (opposite) chromosome
 Weak D: Partial D. Tests as positive, but after
transfusion with D-positive cells, develops
anti-D
 Partial D due to missing parts of the D
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
Rh Antibodies General Characteristics
 Usually made by exposure to Rh antigens
through transfusion or pregnancy
o Most are IgG and bind at 37°C
o Agglutination is observed by the IAT
o Enhancement with high protein, low
ionic strength solution (LISS),
enzymes, or polyethylene glycol are
useful
o May show dosage
Clinical Considerations in Transfusion Reactions
 Antibodies to the Rh system can cause
hemolytic transfusion reactions
o Antibody levels can fall below
detectable levels
o Upon re-exposure to the antigen, the
antibody produces a rapid secondary
response
o It is important to check patient history
HEMOLYTIC DISEASE OF THE FETUS AND
NEWBORN
 First observed in infants from D-negative
mothers and D-positive fathers
o Initial pregnancy, mom is usually not
affected; infants from subsequent
pregnancies are often stillborn or
jaundiced and anemic
o The initial pregnancy exposed the
mother to D-positive cells and to
produce anti-D
Rh Immune Globulin
 Anti-D can cross the placenta
o Rh immune globulin (RhIG) protects
D-negative mothers against production
of anti-D
o Antibody screen and D status of
mothers in early pregnancy are needed
to determine whether a mother is a
candidate for RhIG
LW Blood Group System
 Similar in serology properties to the Rh system but
not genetically related
o Alleles are Lwa, LWb, and LW
o LW gene uis an amorph
o Antibodies to the LW system are clinically
significant and rare
 
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
 The ONLY BLOOD GROUP SYSTEM not
manufactured by the red cells
 Chromosomal location – 19p
 ANTIGENS – Lea and Leb
 NOT INTRINSIC to RED BLOOD CELLS
 REVERSIBLY ADSORBED ONTO RED
CELLS FROM PLASMA
 Lea and Leb are NOT ANTITHETICAL
 Poorly developed at birth so neonates will type Le
(a− b−) regardless of the Lewis genes they
inherited
 Not found on cord blood or newborn red cells
 Lewis glycolipid detectable in plasma after ~10
days of life
 Transformation of Lewis phenotype after birth
seen in individuals who inherit Le and Se genes:
 Le(a−b−) to Le(a+ b−) to Le(a+ b+) to
Le(a−b+) [the true phenotype]

ANTIGENS MOST COMMON PHENOTYPES:

 Expression is affected by the genes – Le, Se and H
 Lewis gene – either Le or le (amorph)
 codes for L-fucosyltransferase,
which adds L fucose to type 1
chains
 If you inherit Le, you will have Lea
 If you inherit le, you will NOT
have Lea
 Le = Lea+
 le = Lea–
 Secretor gene – either Se or se (amorph)
 If you inherit Se, and you have Lea, it
will be converted to Leb
 Se, Le = Lea converted to Leb so you
will be Le (a–b+)
 If you inherit Se, and you don’t have
Lea, nothing will be converted to Leb
 Se, le = No Lea to be converted to Leb
so you will be Le (a–b–)
 If you inherit se, and you have Lea,
nothing will convert it to Leb
Le (a+b−), Le (a−b+), Le (a+b+) and Le (a−b−)
 lele genotype is more common among blacks
than among whites and results in the Le(a–b–)
phenotype
 Decrease in expression demonstrated in red
cells from many pregnant women, resulting in
Le(a−b−) phenotype during gestation
 Do not show dosage in serologic reactions
ANTIBODIES: Anti-Lea and Anti-Leb
Antibody type: IgM
 NATURALLY OCCURRING, SALINE-
REACTIVE
 Does not cross the placenta
 Source: Le (a–b–) people, without known red cell
stimulus
 Neutralized by: Lewis blood group substances in
plasma or saliva
 Characteristics:
 Enhanced by enzymes
 Sometimes reacts at 37°C and Coombs phase
 more weakly than at room temperature
 Rarely causes in vitro hemolysis; however, in vivo
posttransfusion hemolysis reported in cases which
Lewis Ab strongly reacts in Coombs phase
 May cause in vivo hemolysis of red cells
 Hemolysis/Disease Association
 NOT involved in HDN because Lewis antibodies
cannot cross the placenta and antigens are poorly
developed in newborns
Transfusion
 Donor cells assume Lewis phenotype of recipient
(Le antigens absorbed from plasma)
 Lewis antibodies in recipient’s plasma neutralized
by Lewis blood group substances
 in donor plasma
P (003) SYSTEM
 P ANTIGENS: P1, P2, Pk1, Pk2, p
 ▪ Structurally related to ABO antigens and exist as
glycoproteins and glycolipids
 ▪ MOST COMMON PHENOTYPES: P1 and
P2
 ▪ P1 individuals have both P and P1 antigens
 ▪ P2 individuals have only P antigens
 ▪ Rare phenotypes
 ▪ Pk1: have both P1 and Pk antigens
 ▪ Pk2: have both the P2 and Pk antigens
 ▪ p: negative for P, P1, and Pk antigens
 MOST COMMON ANTIGEN IN THE SYSTEM
 poorly expressed at birth and may take up to 7
years to be fully expressed
 varies in strength in adults
 deteriorates rapidly on storage – use fresh red cells
when typing donor units for patients with anti-
P1
 UNIVERSAL ANTIGEN on red cells, white cells,
tissue cells and in plasma
 Undetectable on red cells due to conversion to P
antigen
 Found on white cells, some tissue cells and in
plasma
 ▪ P ANTIBODIES: Anti-P1, Anti-P, Anti-PP,
Pk and anti-p
 ▪ Anti-P1 antibodies are naturally occurring, cold-
reacting, IgM anti-bodies often seen in
individuals with the P2 phenotype. They rarely
react at higher than room temperature, but they do
bind complement. Anti-P1 antibodies do not
cause HDN and are rarely associated with HTR
 ▪ Anti-P antibodies are produced by individuals
with Pk1 or Pk2 phenotypes and can trigger
severe HTR.
 ▪ Autoanti-P (the Donath-Landsteiner
antibody) is a cold-reacting antibody associated
with paroxysmal cold hemoglobinuria (PCH).
 ▪ Anti-PP, Pk, and anti-p antibodies occur only
rarely.
 p – absence of substance that codes for P1 and Pk
PHENOTYPES
 COMMON – P1 and P2
 RARE – p, P1k and P2k
P
 Platelets, epithelial cells, fibroblasts
P and Pk
 Plasma as glycosphingolipids
 Hydatid cyst fluid: glycoprotein
P1 Antigen
 Poorly expressed at birth
 May take up 7 years to be fully expressed
 Strength may vary w/ race
 Blacks stronger expression than white
 Deteriorates rapidly on storage
Anti-P1
 Naturally occurring IgM Ab
 Found in P1- individuals
 Weak, cold reactive saline agglutinins
 React at 4C, bind w/ complement
Anti-PP1PK
 IgM but sometimes Ig
 Originally called Anti-Tja
 First described in the serum of Mrs. Jay
 Produced early in life w/o sensitization
and reacts w/ all RBC’s except for a
person w/ p Phenotype
 Potential cause of severe HTR’s and
HDFN
Autoanti-P
 Associated with paroxysmal cold
hemoglobinuria
 An IgG autoantibody described as a
biphasic hemolysin
 Demonstrated by Donath-Landsteiner
Test
ANTIBODIES: Anti-P1, anti-P and anti-Tja (Anti-
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
OTHER BLOOD GROUP SYSTEM
(PART II)
The MNS (002) System
 MNS ANTIGENS: M, N, S, s, U
 determined by the MN and Ss loci
 MN is associated with glycophorin A while Ss
is associated with glycophorin B
 Important markers in paternity studies
MNS ANTIBODIES: Anti-M, Anti-N, Anti-S, Anti-s,
Anti-U
 Anti-M – relatively common usually naturally
occurring and may be both IgM and IgG
 do not bind complement and react optimally at
room temperature or below only rarely
associated with HDN or HTR
Anti-N – rare
 weak, naturally occurring IgM antibodies that
react best at room temperature or below
 not usually associated with HDN or HTR
 Anti-S, anti-s, and anti-U – rare
 IgG antibodies which usually develop
following RBC stimulation
 all have been associated with severe HDN and
HTR
LECTINS
o Anti-M lectin – Iberis amara
o Anti-N lectin – Vicia graminea, Bauhinia
variegata, Bauhinia purpura
I Blood Group System
I antigens: I and i
 At birth, infant red cells are rich in i antigen
 During first 18 months of life, i slowly
decreases, I increases
 Adult red cells, rich in I and only trace amount
of i
I antibodies: Anti-I and anti-i
 Benign anti-I – weak, naturally occurring
antibody, saline reactive IgM autoagglutinin
detectable only at 4C
 Pathologic anti-I – cold agglutinin that
demonstrates high titer reactivity and reacts
over a wide thermal range (0 to 30C)
 MYCOPLASMA PNEUMONIAE – may develop
strong cold agglutinins with auto-anti I specificity
 Anti-i – an IgM agglutinin reactive at 4°C
associated with IM infections
Lutheran Blood Group System (LU)
Antigens – Lua and Lub
 Poorly developed at birth
 Adult levels reached at 15 y/o
Antibodies – anti-Lua and anti-Lub
Anti-Lua
 Most are naturally occurring saline agglutinins
that react better at room temperatures than 37°C
Anti-Lub
 Most are IgG (often IgG4) reactive at 37°C and
the antiglobulin phase
 Made in response to pregnancy or transfusion
 Implicated with shortened survival of
transfused cells and posttransfusion jaundice
Other Blood Group System
XG Blood Group System (XG)
 SHORT ARM OF CHROMOSOME X
 Antigens – Xga – no known antithetical partner
Antibodies – anti-Xga
 IgG antibodies, red cell stimulated, but does
not cause transfusion reactions or HDN
 Reactive in IAT
 Sensitive to enzymes but not to dithiothreitol
Diego Blood Group System (DI)
 Chromosome 17, codominant alleles
Antigens – Dia/Dib
 Located on the anion-exchange molecule (AE-
1)
 MUTATION IN AE-1 can result in
HEREDITARY SPHEROCYTOSIS,
CONGENITAL ACANTHOCYTOSIS AND
SOUTHEAST ASIAN OVALOCYTOSIS
 Dia – USED IN MONGOLIAN ANCESTRY
ANTHROPOLOGICAL STUDIES
Antibodies – anti-Dia and anti-Dib
 Red-cell stimulated IgG antibodies that do not
bind complement
 Reactive in IAT
Cartwright Blood Group System (YT)
 Chromosome 7, codominant alleles
Antigens – Yta and Ytb
 Present in erythrocyte acetylcholinesterase
(AchE)
Yta
▪ High-incidence antigen
Ytb
▪ Low-incidence antigen
Antibodies – anti-Yta and anti-Ytb
 IgG antibodies, predominantly red cell
stimulated
 Reactive in IAT
Scianna Blood Group System (SC)
 Chromosome 1, codominant alleles
 Antigens – Sc1, Sc2, Sc3 and RADIN (Rg)
 Antibodies – anti-Sc1, anti-Sc2, anti-Sc3, anti-
Rg
Dombrock Blood Group System (DO)
 Chromosome 12, codominant alleles
 Resides in
GLYCOSYLPHOSPHATIDYLINOSITOL
(GPI) glycoprotein
Antigens – Doa and Dob, Gregory (Gya), Holley (Hy)
and Joseph (Joa)
 Total absence of DO expression is seen in
PNH III RBCs which are deficient in all GPI-
anchored glycoproteins
Colton Blood Group System (CO)
 Chromosome 7, codominant alleles
Antigens – Coa, Cob and Co3
 Present in aquaporin-1 (AQP1)
 Disease association: MONOSOMY-7 of the
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
Gerbich Blood Group System (GE)
 Chromosome 2
 Expressed on glycophorins C and D
 Antigens – 3 high incidence antigens (Ge2,
Ge3, and Ge4) and 4 low incidence antigens
(Wb, Lsa, Ana and Dha)
 Leach phenotype (GE: -2, -3, -4) –
ELLIPTOCYTOSIS
Cromer Blood Group System (CROM)
 Chromosome 1
 Antigens are carried by DECAY
ACCELERATING FACTOR (DAF)
Knops Blood Group System (KN)
 Chromosome 1
 Expressed on complement receptor one (CR1)
Indian Blood Group System (IN)
 Chromosome 11
 Antigens are carried by CD44 marker
Bg Blood Group System
 Bga antigen corresponds with HLA-B7
 Bgb with HLA-B17
 Bgc with HLA-A28
 Bg antibodies - NUISANCE ANTIBODIES
 Reactivity may be removed by
CHLOROQUINE or EDTA-GLYCINE HCl
HIGH TITER, LOW AVIDITY ANTIBODIES
Antibodies that exhibit reactivity at high dilutions of
serum, but the strength of agglutination is weak
at any dilution
 Anti-Ch (Chido)
 Anti-Rg (Rogers)
 Anti-Kn (Knops)
 Anti-JMH (John Milton Hagen)
 Anti-Yka (York)
 Anti-Csa (Cost)
 Anti-McC (McCoy)
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
patient
o Paid Donors- unsafest
DONOR SCREENING
 Process of ensuring the safety of both the
patient and donor
1. Donor Registration
 Must confirm donor’s identity and must link
the donor existing record.
 Need for Identification card (ID)
 List of information used in the registration
process:
 ◦Name (First, Last, MI)
 ◦Date and time of donation
 ◦Address
 ◦Telephone
 ◦Gender
 ◦Age or Date of Birth
 17 years old and above, (17y/o
Must have parent’s consent
Donor’s consent
 Additional information:
◦Name of patient for whom the blood is
intended
◦Race
◦Cytomegalovirus status
Medical History Questions
 Have you donated blood in the past 8 weeks or
plasma in the past 48 hours?
 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
taking antibiotics for an infection?
 Have you ever had heart problems, lung
problems (other than asthma) or a bleeding
problem?
 Have you ever had hepatitis? If yes, when?
 Have you ever had a positive test for HIV?
 In the past 48 hours, have you taken aspirin or
anything with aspirin in it?
 In the past 6 weeks, have you been pregnant or
are you pregnant now?
 In the past 8 weeks have you had any
vaccinations or other shots? Have you had
contact with someone who had a small pox
vaccination?
Physical Examination
 General appearance
 Weight: mandates a maximum of 10.5ml of
blood/kg
◦110Ibs (50kg)
◦If donor is less than 110Ibs:
 Temperature: Orally should not exceed 99.5’F
or 37.5’C
 Pulse: 50 to 100beats per minutes
 Blood Pressure: No greater than 180mmHg
Systolic
◦Diastolic: no greater than 100mmHg
 Hematocritand Hemoglobin:
◦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
DIAGNOSIS DEFERRAL
 3 years
DRUGS WITH 1 MONTH DEFERRAL
 -Proscar (prostate)
 -Propecia (baldness)
 -Accutane (acne)
 -Amnesteem (acne)
 -Claravis (acne)
 -Sotret (acne)
DRUGS WITH 6 MONTH DEFERRAL
 Avodart (prostate)
DRUGS WITH 3 YEAR DEFERRAL
 Soriatane (psoriasis)
DRUGS WITH PERMANENT DEFERRAL
 Tegison (psoriasis)
9 reasons for permanent deferral
 history of viral hepatitis after 11th
birthday
 confirmed + for HBsAg
 repeatedly reactive tests for anti-HBc
 past or present clinical evidence of
infection with HIV, HTLV, HCV
 history of babesiosis or Chagas
 risk of Creutzfeldt-Jacob disease
 family history of Creutzfeldt-Jacob
disease
 needle use to administer
nonprescription drugs
 recipient of dura mater or human
pituitary growth hormone
WEIGHT REQUIREMENT TO DONATE BLOOD
 110 lbs
PULSE REQUIREMENT TO DONATE BLOOD
 50-100 bpm
BLOOD PRESSURE REQUIREMENT TO
DONATE BLOOD
 <180 / <100
TEMPERATURE REQUIREMENT TO DONATE
BLOOD
 </= 99.5F (37.5C)
H&H REQUIREMENT TO DONATE WHOLE
BLOOD
 -Hbg >/= 12.5
 -Hct >/= 38%
PHLEBOTOMY VEIN LOCATION
 AC (antecubital or cephalic) vein
PHLEBOTOMY NEEDLE SIZE
 16-gauge
PHLEBOTOMY PREP COMPOUNDS
 -0.7% iodophor compound
 -10% povidone iodine
3 REASONS TO PERFORM AUTOLOGOUS
DONATION
 -rare blood type or antibodies
 -preventionof alloimmunization
 -prevention of transfusion-related diseases
MINIMUM TIME BLOOD CAN BE DRAWN
BEFORE PROCEDURE IN AUTOLOGOUS
DONATION
 no less than 72 hours beforehand difference in
criteria for autologous donations >
 no questions about high-risk behavior
 Hgb >/= 11
 Hct >/= 33%
 no infectious disease testing unless transfused
facility other than donation facility
 biohazardous units transfused with physician's
permission
 not restricted by age or weight

INTRAOPERATIVE COLLECTION
 -medical device collects blood lost during
surgery and reinfused
 -machine collects, washes, filters, and
concentrates
 -does not remove bacteria
 -blood washed with saline stored at RT for 4
hours or 1-6C for 24 hours
POSTOPERATIVE COLLECTION
 -collected in sterile canisters from surgical
drains and reinfused with or without
processing
 -transfusion must begin within 6 hours
DIFFERENCE BETWEEN ALLOGENIC AND
DIRECTED DONATIONS
 everything applies to both except 56 day
interval between donations may be waived for
directed
INTERMITTENT FLOW
 one venipuncture for apheresis
CONTINUOUS FLOW
 venipuncture in both arms for apheresis
FEMALE HEIGHT AND WEIGHT
REQUIREMENTS FOR DOUBLE RED CELL
DONATION
 5'1" and 130 lbs
MALE HEIGHT AND WEIGHT REQUIREMENTS
FOR DOUBLE RED CELL DONATION
 5'5" and 150 lbs
HCT REQUIREMENT FOR DOUBLE RED CELL
DONATION
 >/= 40%
DEFERRAL TIME AFTER DOUBLE RED CELL
DONATION
 16 weeks (double)
DONOR SCREENING & COMPONENT
PREPARATION
American Association of Blood Banks (AABB) –
established in 1947
 International association of blood banks that
includes hospital and community blood
centers, transfusion & transplantation centers,
and individuals involved in transfusion
medicine
 Mission is to establish and provide the highest
standard of care for patients and donors in all
aspects of transfusion medicine
 AABB Standards & AABB Technical Manual
– books published by AABB
DONOR SCREENING
 Encompasses the medical history requirements
for the donor, the (mini) physical
examination, and serologic testing of the
donor blood
AUTOLOGOUS DONORS
 Donations for self; NO AGE LIMIT
 Hematocrit: 33%
 Hemoglobin: 11 g/dL
 No have signs or symptoms of active
infection
 NO BACTEREMIA
 Preoperative collection must be labeled
“for autologous use only” and used only
for this patient
 Blood should not be donated within 72
hours of scheduled surgery or
transfusion
Blood Collection
WHOLE BLOOD COLLECTION
 For blood collection, most blood centers use an
iodine compound such as PVP-iodine or
polymeriodine complex.
 Using a tourniquet or bloodpressure cuff, the
venipuncture site is identified, and the
 area is scrubbed at least 4 cm in all directions
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)

Donor Unit Processing
ABO & Rh Typing
 Forward & reverse typing for ABO
 Testing Rh with anti-D reagent at immediate
spin phase
 Weak D testing performed if initial testing is
NEGATIVE
Antibody screen
 donors with a history of pregnancy or
transfusion – tested for presence of
UNEXPECTED antibodies to RBC antigens
 Pooled screening cell is tested against donor
serum or plasma
 Pooled screening cell contains antigens agains
significant ALLOANTIBODIES
HBsAg
 Methods currently approved are RIA, EIA,
ELISA & RPHA
 ELISA is the MOST COMMON procedure
used
 Serum or plasma is incubated with antigen to
HBsAg
 An enzyme-conjugate mixture is added
 If antibody is specific to the antigen, a
COLOR CHANGE develops & measured
spectrophotometrically
Anti-Hbc
 for prevention of post-transfusion
hepatitis B
 Has been implicated in Hepatitis C
disease
 Was once part of the surrogate testing
along with its counterpart ALT (alanine
aminotransferase)
 ALT was discontinued because of
increased sophistication & sensitivity of
anti- HCV testing
Anti-HCV & NAT
 SCREENING TEST – EIA which detects
antibodies to c200, c22-3 and NS-5 proteins
of HCV genome
 NAT – able to detect small amounts of viral
nucleic acid in blood before antibodies or
viral proteins such as HCV core antigen are
detectable by current methods
 Window period for detection of HCV is
reduced ~70% from a mean of 82 days to 25
days
 CONFIRMATORY TEST – include RIBA
(recombinant immunoblot assay)
▪ Fusion of HCV antigens to human superoxide
dismutase and a recombinant superoxide dismutase is
incorporated to detect nonspecific reactions
▪ Reported as positive, negative or indeterminate
▪ Positive = presence of HCV antibody
Anti-HIV-1/2 and NAT
 Screened by FDA-approved EIA method
 If negative, unit is suitable for transfusion
 If positive, test must be repeated in duplicate.
If any one of the duplicate tests is reactive,
UNIT MUST BE DISCARDED
 Confirmation tests for HIV include Western
Blot and immunofluorescence assay
WESTERN BLOT
o Performed using donor serum
o HIV material is separated into bands according
to their molecular weight
o Material is transferred to a
NITROCELLULOSE membrane and donor
serum is added
o If anti-HIV-1/2 antibodies are present, they
will bind to specific bands
o Results are expressed as positive, negative or
indeterminate
Anti-HTLV-I/II
 HTLV-I – causative agent of adult T-cell
leukemia & associated with neurologic
disorder called HTLV-associated myelopathy
 HTLV-II – 60% homologous to type I and is
prevalent among INTRAVENOUS drug users
in the US
 Persons can contract both viruses from
transfusion via infected lymphocytes
 Tested by EIA screening test that utilized viral
lysates from both viruses
 Confirmatory tests include Western Blot,
RIPA, & NAT testing
 A donation that is repeatedly reactive with
EIA – NOT USED FOR TRANSFUSION
 If tested with another EIA kit from a different
manufacturer, and the test is still reactive,
DONOR SHOULD BE INDEFINITELY
DEFERRED
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
are based on reagin, or antibody against
CARDIOLIPIN
 Cardiolipin-like antibodies have been
documented in persons with UNTREATED
syphilis infections
 Antibody will agglutinate cardiolipin carbon
particles in the form of VISIBLE
FLOCCULATION
 Confirmatory test is FTA-ABS or fluorescent
treponemal antibody absorption test
 INDIRECT IMMUNOFLUORESCENCE is
used to detect antibodies to spirochete T.
pallidum- agent of syphilis
 No documented cases of transfusion-
transmitted syphilis
 T. pallidum cannot survive more than 72 hours
in citrated blood stored at 1°C to 6°C
which would make PLATELETS the only
component capable of transmitting infection
AUTOLOGOUS DONOR UNIT PROCESSING
 Testing. In addition to ABO and Rh typing,
testing for HBsAg, syphilis, and HIV-1 are
required for processing autologous donor units.
Most donor facilities perform all tests normally
required for homologous units to allow unused
autologous units to be used for other transfusion
purposes.
 Labeling. Donor units dedicated for autologous
use must be clearly labeled “for autologous use
only,” and a biohazard label must be attached to
any unit repeatedly reactive for any of the
previously mentioned tests for infectious
diseases.
 Storage. In addition to being stored between 1◦C
and 6◦C, autologous units must be stored
separately from homologous units.

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
and platelets
Heavy- platelets in platelet rich plasma (PRP) will
be forced to the bottom of a satellite bag
 40-60 mL of plasma is expelled into another
satellite bag, while the remaining bag contains
platelet concentrate
 Storage Temperature
 20-24°C for 5 days (constant agitation)
 Each unit should contain at least 5.5 x 1010
platelets (platelet concentrate)
 Each unit should elevate the platelet count by
5-10,000 µL in a 165 lb person
Pooled platelets
 Used to reach therapeutic dose
 An “open system” occurs when pooling
platelets, resulting in an expiration of 4 hours
 Platelet, pheresis – therapeutic dose (from one
donor) without having to pool platelets
 3x1011 minumum
 HLA matched – for those with HLA
antibodies
 Leukocyte reduced - used to prevent febrile
non-hemolytic reactions and HLA
alloimmunization
Fresh Frozen Plasma (FFP)
 Plasma that is frozen within 8 hours of
donation
 -18°C or colder for 1 year
 Provides coagulation factors for
 Bleeding
 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
 Same storage as FFP (cannot be re-frozen as
FFP once it is separated); -18 for 1 year
 If thawed, store at room temp 4 hrs
 The leftover plasma is called cryoprecipitate
reduced or plasma cryo
 Good for thrombocytopenic purpura (TTP)
 CRYO is used for
 2° treatment for Factor VIII deficiency
(Hemophilia A)
 2 ° treatment for von Willebrand’s Disease
 Congenital or acquired fibrinogen
deficiency
 FXIII deficiency
“Fibrin Glue” applied to surgical sites
Granulocytes
 Neutrophils are the most numerous, involved
in phagocytosis of bacteria/fungi
 Although rare, it is useful for infants with
bacteremia
 Prepared by hemapheresis
 ≥ 1.0 x 1010
 Maintained at room temp for 24 hours
Rejuvenation Solution
 Restore 2,3 DPG and ATP
- During storage or up to 3 days after
expiration- pyruvate, inosine,
phosphate, adenine
- Extends expiration date for
freezing rare or autologous units
- Must be washed to remove inosine-
toxic

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