BLOOD BANKING NOTES – BY: GERARD ANDREW RAMOS, RMT

1492 Pope Innocent VIII – recipient of first blood transfusion in history, but he & the donors died.
1869 Braxton Hicks – recommended sodium phosphate as nontoxic anticoagulant
1901 Karl Landsteiner – discovered ABO blood groups and explained transfusion reaction.
1902 Von Decastello and Sturli – discovered the fourth ABO blood group, AB
1913 Edward E. Lindemann – used vein-to-vein transfusion of blood by using multiple syringes
1913 Lester Unger – designed syringe-valve apparatus; permitted unassisted physician
1914 Albert Hustin – reported the use of sodium citrate Anticoagulant
1915 Richard Lewisohn – determined the minimum amount of citrate anticoagulant to be used
1916 Rous and Turner – introduced citrate-dextrose solution for preservation of blood
1941 Charls Drew – his techniques has led to widespread system of blood banks in WWII
1943 Loutit and Mollison – introduced the formula for acid-citrate-dextrose (ACD)
1957 Gibson – introduced an improved preservative solution, citrate-phosphate-dextrose (CPD)

ANTICOAGULANT PRESERVATIVE SOLUTIONS

1 unit of whole blood = 450 mL of blood (one pint) and 63 mL of Ac-preservative solution

*As storage time increases = red cell viability decreases

“Lesion of Storage” – loss of red cell viability

Biochemical changes seen in stored whole blood:

↑ plasma potassium ↓ ATP levels
↑ plasma hemoglobin ↓ 2,3-DPG
↑ lactic acid ↓ pH

APPROVED PRESERVATIVE SOLUTIONS

Storage
Name Abbreviation Shelf-life temperature
Acid-citrate-dextrose ACD 21 1 – 6 °C
Citrate-phosphate-dextrose CPD 21 1 – 6 °C
Citrate-phosphate-adenine CPDA-1 35 1 – 6 °C
Citrate-phosphate-double dextrose CP2D 21 1 – 6 °C

*Plasticized Polyvinyl chloride (PVC) plastic bags – blood containers

Plasticizer: DEHP - di(ethylhexl)phthalate

Additive Solutions
 Prolongs red cell survival for up to 42 days
 Generally contains: SALINE, ADENINE, GLUCOSE, MANNITOL (AS-1, AS-5)
 100 mL additive solution is used for a 450 mL blood bag
 Solution must be added to RBCs within 72 hours of storage

Name Abbreviation Storage Time (Days) Primary Bag

Adsol (Fenwal Laboratories) AS-1 42 CPD
Nutricel (Medsep Corporation) AS-3 42 CP2D
Optisol (Terumo Corporation) AS-5 42 CPD

Rejuvenation Solutions
 used to restore levels of ATP and 2,3-DPG levels in red cells stored in CPD, CPDA-1, AS-1
 Generally contains: PHOSPHATE, INOSINE, PYRUVATE, ADENINE
 Solution can be used up to 3 days after expiration of red cells
 REJUVESOL : the FDA-approved rejuvenation solution in US
Red Cell Freezing
 primarily used for autologous units and storage of rare blood types
 involves addition of cryoprotective agent to red cells that are < 6 days old.
 Glycerol is most commonly used as cryoprotective agent
 Long term storage : 10 yrs. at -65 °C

Deglycerolization
 to be done prior transfusion to avoid infusing the hypertonic glycerol
 red cell washing with decreasing conc. of saline (12 % saline, 1.6 % saline, 0.2 % dextrose with
saline) or commercially available cell-washing system.

*24 hrs. = outdating period for thawed red cells stored at 1-6 °C

Positive sign of an Antigen-Antibody reaction in blood banking:

1. HEMAGGLUTINATION – most common
2. HEMOLYSIS

Grading of Agglutination Reactions:

Macroscopically observed findings Grade

One solid agglutinate, clear supernatant 4+

Several large agglutinates, clear supernatant 3+

Medium-sized agglutinates, clear background 2+

Small agglutinates, turbid background 1+

Barely visible agglutination, turbid background w+ or (-/+)

No agglutination 0

Factors that influence agglutination reactions

1. High Speed Centrifugation

 simplest and most common technique to enhance agglutination

2. Effect of Antigen-Antibody Ratio

 Zone of equivalence should be obtained
 Prozone (Ab excess) and Postzone (Ag excess) reactions will lead to FALSE NEGATIVE results
 Remedies:
o Prozone = serum dilution
o Postzone = increase serum to cell ratio in the test system

3. Effect of pH
 Ideal pH 6.5 to 7.5

4. Effect of temperature
 IgM react best at cold temperature (4-22°C)
 IgG react best at warm temperature (37°C)

5. Effect of Immunoglobulin type

 IgM = capable of agglutinating red cells in 0.85% saline medium
 IgG = cannot agglutinate red cells in saline; requires enhancement media or potentiators
6. Effect of Enhancement media and potentiators
 Primarily used to help detect IgG antibodies
 Aimed at REDUCING the Zeta Potential of the red cell membrane

Zeta potential
 expression of the difference in electrostatic potential at the surface of the red cells & the ionic
cloud of positive cations that are attracted to the negative charges on the surface

ID of IgM Antibody
1. Saline
 4-22°C immediate spin (IS) up to 60 mins.
 primarily identifies IgM

ENHANCEMENT MEDIA / POTENTIATORS

ID of IgG Antibody
1. Protein Media
 increases the dielectric constant, w/c reduces the zeta potential
 Examples of protein media:
o 22 % albumin
 causes agglutination by adjusting zeta potential between Red cells
 incubation at 37°C for 15 – 60 mins
o Polybrene
 can detect ABO incompatibility & clinically significant IgG alloAb
o Polyethylene glycol
 reduces false-positive reactions
 more effective than albumin, LISS, or manual polybrene
 incubation at 37°C for 10 – 30 mins; cell washing before IAT
 NOTE: Test mixture CANNOT be centrifuged & examined for aggl’n
o Polyvinylpyrrolidone (PVP)
o Protamine

2. LISS – Low ionic strength solution

 decrease the ionic strength of a reaction medium and so reduce the zeta potential
 increase the attraction bet. (+) charge Ab & (-) red cells
 contain 0.2 % NaCl and often used because of increase rate of Ab uptake during sensitization
 incubation at 37°C for 5 - 15 mins

3. Enzymes
 ENHANCES antibody reactivity to Rh, Kidd, P1, Lewis and I antigens
 DESTROYS reactivity to red cell antigens Fya, Fyb, M, N, & S.
 Examples:
o Ficin (plant)
o Papain (papaya)
o Trypsin (pig stomach)
o Bromelin (pineapple)

4. Anti-Human Globulin (AHG)

 designed to detect red cells coated w/ antibody or complement, or both.

DTT & 2 ME
 sulfhydryl compounds that break the disulfide the bonds of the J chain of IgM molecule,
but leave IgG molecule intact

ZZAP reagent
 thiol reagent + proteolytic enzyme
 causes dissociation of IgG molecules from the surface of sensitized red cells
SEROLOGIC SYSTEMS USED IN TRADITIONAL LAB. METHODS
FOR RED CELL ANTIBODY DETECTION

Reaction Phase Ig Class Mechanism of Action

Detcted
IMMEDIATE SPIN IgM IgM react best at cold temperature (4-22°C)
IgM is very efficient in agglutination reactions

37°C INCUBATION IgG IgG react best at warm temperature (37°C)

NO VISIBLE AGGLUTINATION commonly seen

ANTIGLOBULIN TEST IgG AHG has specificity for the Fc portion of heavy chain of IgG
It acts as a bridge cross-linking red cells.

ANTIGLOBULIN TEST
 “Coombs Test”, discovered by Robin Coombs in 1945
 based on the principle that anti-human globulins (AHG) obtained from immunized nonhuman
species bind to human globulins such as IgG or complement, either in free state or attached to
RBCs
 Primarily detect IgG and / or complement-sensitized RBCs.

Polyspecific AHG
 contains anti-IgG & anti-C3d component of complement system.

Monospecific AHG
 contain only one Ab specificity: anti-IgG or anti-C3d

Polyclonal AHG
 produced by immunizing a colony of rabbits (for large volume productions)
 there is heterogeneity of IgG molecules (use of serum from many donors)
 there is also pooling of anti-IgG from many immunized rabbits

Monoclonal AHG
 technique devised by Kohler & Milstein
 prepared by “Hybridoma Technology”; uses mice as lab animals
 has been used to produce AHG with high-titer antibodies and well-defined specificities
 Advantage: pure & uncontaminated reagent

Polyspecific Reagent Polyclonal-Monoclonal Blend

 AHG reagent of choice
 potent and give fewer false (+) results

Direct Antiglobulin Test

 detects in vivo sensitization of RBCs w/ IgG and/or complement components.
 Clinical conditions that can result in “in vivo” coating of red cells:
o Hemolytic Disease of the Newborn (HDN)
o Hemolytic Transfusion Reaction (HTR)
o Autoimmune Hemolytic Anemia (AIHA)
o Drug-induced Hemolytic Anemia (DIHA)

Indirect Antiglobulin Test

 determine in vitro sensitization of red cells
 Applications of IAT include:
o Antibody detection (Compatibility tests and Antibody screening tests)
o Antibody identification (Antibody Panel test)
o Antibody Titration
o Red Cell Phenotype
.FACTORS THAT AFFECT ANTIGLOBULIN TEST
1. Ratio of Serum to Cells
 ratio should be 40:1 or 2 drops of serum & 1 drop of 5 % RCS.
 when using saline, it is useful to increase the ratio to detect weak Ab
o 4 drops of serum & 1 drop of 3% RCS or 133:1
2. Reaction Medium
 Albumin
o allow Ab-coated cells to come into closer contact w/ each other
 LISS
o enhance Ab uptake and allow incubation time to be decreased.
 PEG
o action is to remove water thereby concentrating antibody
3. Temperature
 IgG activity and complement activation optimum at 37°C

4. Incubation Time
 for cells suspended in saline: 30 – 120 mins.
 for LISS: 10 – 15 mins. (extended incubation = decreased sensitivity)

5. Washing of Cell
 wash RBCs 3 times before immediate addition of AHG
 purpose is to REMOVE free unbound globulins
 inadequate washing will result to false (-) results, because of neutralization by free globulins
 washing should be performed in as short time as possible to minimize elution of low-affinity Abs

6. Saline for Washing

 should have a pH of 7.2 – 7.4
 saline stored for long periods in plastic containers = decrease in pH
 monoclonal Ab – sensitive in pH changes; bacterial contamination = false (+) results
7. Addition of AHG
 add AHG immediately after washing
 neutralization of AHG is only a problem w/ free IgG left in serum
8. Centrifugation for Reading
 Recommended for AHG = 1000 RCF for 20 sec.

SOURCES OF ERROR IN AHG TECHNIQUE

False – Positive Results
1. Improper specimen (refrigerated, clotted) may cause in vitro complement attachment
2. Autoagglutinable cells
3. Bacterial contamination of cells or saline used in washing
4. Cells w/ a positive DAT used for the IAT
5. Saline contaminated by heavy metals or colloidal silica
6. Dirty glassware
7. Overcentrifugation & Overreading
8. Polyagglutinable cells
9. Preservative-dependent Antibody in LISS reagents
10. Contaminating antibodies in the AHG

False – Negative Results

1. Inadequate or improper washing of cells
2. Nonreactive AHG
3. AHG not added
4. Serum not added in the indirect test
5. Serum nonreactive because of deterioration of complement
6. Inadequate incubation conditions in IAT
7. Cell suspension either too weak or too heavy
8. Undercentrifuged or overcentrifuged
9. Poor reading technique
ABO Blood Group System

Karl Landsteiner
 first described blood groups A, B, O (1901)
 first individual to perform forward & reverse grouping

Von Decastello & Sturli

 discovered the 4th ABO blood group = AB

Important facts for ABO:

 The ABO antigens and antibodies remain the most significant for transfusion practice
 ABO gene – located in chromosome 9
 ABH antigens develop as early as 37TH DAY OF FETAL LIFE
 ABO antibodies can be detected in serum after 3-6 months of life,reach adult levels at 5-10 yrs old
 Patients older than 65 yrs of age = Low titers of ABO antibodies
 ABO blood group is unique because individuals have antibodies in their serum to antigen they
lack on their red cells, thus, REVERSE TYPING is unique on ABO blood group system.
 ABO antibodies are generally IgM, with some mixture of IgG

A B O AB
Antigen present on A antigen B antigen No A or B antigen A and B antigens
red cells
Antibody present Anti-B Anti-A Anti-A, Anti-B, NO Anti-A and
on serum Anti-A,B NO Anti-B

Phenotype = outward expression of genes (A,B,O)

Genotype = actual genetic make-up (AA, BO, OO)

Type O
 both phenotype & genotype are the same
 individual would have to be HOMOZYGOUS for O gene.

ABO MATINGS
A A
Ex. Father = BO B AB AB Chances of Offspring:
Mother = AA AB = 50%
O AO AO AO = 50%

ABO GENETICS
 ABO genes code for the production of SPECIFIC GLYCOSYLTRANSFERASES (enzymes)
that add sugars to a basic precursor substance
 The ABH glycolipid antigens are built upon a common carbohydrate residue w/c represents a
PARAGLOBOSIDE (Precursor Substance)

Paragloboside or Precursor Substance:

RBC precursor structure: lacto-N-neotetraosylceramide (TYPE 2 CHAIN PARAGLOBOSIDE)

“Beta 1 → 4 linkage”
H gene
 now known as the “FUT-1 gene”
 present in greater than 99.99% of the random population
 H substance must be formed for the other sugars to be attached in response to an inherited A/B gene

Bombay Phenotype
 LACKS normal expression of ABH antigen because α-2-L-fucosyltransferase is NOT produced
 devoid of antigens of the ABO system
Immunodominant sugar
 sugar that occupy the terminal positions of the precursor chain & confer the blood group specificity

GalNAC D-galactose

D-galactose L-fucose D-galactose L-fucose D-galactose L-fucose

GlcNAC GlcNAC GlcNAC

D-galactose D-galactose D-galactose

Glucose Glucose Glucose

“H Ag” “A Ag” “B Ag”

Immunodominant
Gene Glycosyltransferase (enzyme) Sugar donor sugar Antigen

H α-2-L-fucosyltransferase GDP-Fuc L-fucose H

α-3-N-acetylgalactosaminyl
A transferase UDP-GalNAc N-acetyl-galactosamine A

B α-3-D-galactosyltransferase UDP-Gal D-galactose B

O allele
 AMORPH
 H substance remains unmodified
 Blood Group O has the HIGHEST CONCENTRATION OF H ANTIGEN

ABH antigens
 also referred to as “Histoblood Group Antigens”
 present in all organs if the human body
SeSe or Sese
 “Secretor” (ABH blood group-specific substances can be found in all body secretions)
 78% of random population

sese
 “Nonsecretor”
 22% of random population

Secretor Gene (Se gene)

 also called “FUT-2”
 codes for the production of α-2-L-fucosltransferase, w/c is expressed in tissues
related to exocrine secretions
 this transferase utilize Type-1 precursor to form Type-1 H determinants, w/c are the major
carriers of the ABH molecules in secretions
 The Se gene DOES NOT AFFECT the formation of A, B, or H antigens on the red cell and does
not control the presence of ABH transferases in hematopoietic tissue

Fluids in w/c ABH substances can be detected in secretions:

 Saliva, Tears, Milk
 Digestive juices, Bile, Urine
 Amniotic fluid, Pathologic fluids

A Subgroups

A1
 80% of all Group A individuals
 very potent gene (810,000 – 1,170,000 antigen sites)
 greater activity of GalNAC

A2
 20% of all Group A individuals
 produces only 240,000 – 290,000 antigen sites
 lesser activity of GalNAC

Anti-A1 and Anti-A from B

Blood Group Antigens present sera Anti-A1 Lectin

A1 A1, A Positive Positive

A2 A Positive Negative

Sources of Anti-A1
 Absorbed serum from Group B individuals
 DOLICHOS BIFLORUS (Anti-A1 Lectin)
o agglutinates A1 and A1B

Lectins
 seed extracts that agglutinate human cells w/ some degree of specificity
o DOLICHOS BIFLORUS (Anti-A1 Lectin)
o ULEX EUROPAEUS (anti-H Lectin)
Reactivity of Anti-H Antisera or Lectin w/ ABO Blood Groups:

O > A2 > B > A2B > A1 > A1B

* O = greatest amount of H Ag
* A1B = least amount of H Ag

H antigen is found in greatest conc. on Group O individuals

BOMBAY PHENOTYPE
 very rare, does NOT produce α-2-L-fucosyltransferase necessary for formation of H structure
 can be genetically expressed as hh or Hnull or Oh
 ABH antigens are absent, no agglutination w/ Anti-A, Anti-B or Anti-H
 They are A,B,H nonsecretor (No ABH substance in saliva)
 A Recessive mode of inheritance
 Red cells of Bombay will NOT REACT w/ anti-H Lectin
 Red cells of Bombay are compatible only w/ the serum from another Bombay individual

Anti-A Anti-B Anti-H Lectin

Type O Negative Negative POSITIVE

Bombay Negative Negative Negative

ABO TYPING DICREPANCIES

Group 1 Discrepancy
 WEAKLY REACTING OR MISSING ANTIBODIES
 Reason: Patient has depressed antibody production
 Examples:
o Newborns
o Elderly patients
o Patients demonstrating Hypogammaglobulinemia caused by:
 CLL
 Malignant lymphoma
 Immunosuppressive drugs
o Patients w/ Congenital Agammaglobulinemia
o Patients w/ Immunodeficiency states
o Patents w/ bone marrow transplantations
o CHIMERISM (presence of two cell populations in a single individual & occurs in twins)
 Resolutions:
o Incubate px serum w/ reagent A1 & B cells at room temp. for 15 – 30 mins

Group 2 Discrepancy
 WEAKLY REACTING OR MISSING ANTIGENS
 Examples:
o Subgroups of A or Subgroups of B
o Leukemia – may yield weakened A or B antigen
o Hodgkin’s disease – mimic the depression of Ag found in leukemia
o Acquired B phenomenon
o Excess amounts of BGSS (blood-group specific-soluble substances) present in plasma
 Resolution:
o Washing the patient’s cells free of the BGSS w/ saline should alleviate the problem
Group 3 Discrepancy
 PROTEIN OR PLASMA ABNORMALITIES
 Result in Rouleaux Formation
 Examples:
o Elevated levels of globulin:
 Multiple Myeloma
 Waldenstrom’s Macroglobulinemia
 Plasma cell dyscrasias
 Advanced cases of Hodgkin’s lymphomas
o Elevated levels of fibrinogen
o Plasma expanders such as Dextran and Polyvinyl-pyrrolidone
o WHARTON’S JELLY

 Resolution:
o Performing a saline dilution or saline replacement technique will free the cells in the
case of rouleaux formation in the reverse type
o In true agglutination, red cell clumping will still remain after addition of saline

Group 4 Discrepancy
 MISCELLANEOUS PROBLEMS
 Examples:
o Polyagglutination
o Cold Reactive antibodies (allo & auto)
o Warm autoantibodies
o Unexpected ABO isoagglutinins
o Ab other than Anti-A and Anti-B
o RBCs with cis-AB phenotype

Polyagglutination
 Red cells agglutinating w/ all human sera
 Genetic inheritance or bacterial infection
 Example:
o T polyagglutination
 exposure of a hidden RBC Ag (T Ag) occurs in patient w/ bacterial / viral infection

cis-AB phenotype
 refers to the inheritance of both AB genes from one parent carried on one chromosome, and an O
gene inherited from the other parent.
 Genotype: ABO
 Usually the B antigen yields a weaker reaction w/ the anti-B

Rh Blood Group System

Levine & Stetson

 described a hemolytic transfusion reaction in an obstetrical patient (Rh incompatibility)

Rh Genetics
 The genes that control the system are autosomal codominant located on the short arm of
chromosome 1.
 The Rh Ag are inherited as CODOMINANT ALLELES
o Offspring inherit one Rh haplotype from each parent

Rh Biochemical structure
 Nonglycosylated protein (no carbohydrate attached to the protein)
 Rh antigens are transmembrane polypeptides & are integral part of RBC membrane
Rh TERMINOLOGIES

I. Fisher-Race: “The DCE Terminology”

 Rh inheritance is controlled by 3 closely linked loci on each chromosome of a homologous pair
 Each locus has its own set of alleles which are: Dd , Cc , and Ee .

D Gene D

Production
Close Linkage C/c Gene C/c
Pathway

E/e Gene E/e

RBC surface

Gene Frequency of Rh Antigen

Gene Frequency (%)

D 85%
(d or absence of D) 15%
C 70%
c 80%
E 30%
e 98%

II. WIENER: “The Rh-Hr Terminology”

 There is one Rh locus at which occurs one Rh gene, but this gene has multiple alleles producing
one agglutinogen composed of three factors.

Agglutinogen

Factor Rh0 Rh0

Rh0 gene Factor hr’ hr’

Factor hr’’ hr’’

RBC surface

Gene Agglutinogen Blood Factors Short Desig. Fisher-Race Ag

Rh0 Rh0 Rh0 hr' hr'' R0 Dce

Rh1 Rh1 Rh0 rh' hr'' R1 DCe
Rh2 Rh2 Rh0 hr' rh'' R2 DcE
Rhz Rhz Rh0 rh' rh'' Rz DCE
rh rh hr' hr'' r dce
rh' rh' rh' hr'' r' dCe
rh'' rh'' hr' rh'' r'' dcE
rhy rhy rh' rh'' ry dCE
III. Rosenfield: “Alpha / Numeric Terminology”
 This system has NO genetic basis
 It simply demonstrates the presence or absence of the Ag on the red cell
 A minus sign preceding a number designates “Absence of an Ag”
 If the Ag has not been typed for, its number will NOT appear in the sequence
 Advantage: red cell phenotype is succinctly described

D = Rh1 Ex. Wiener Fisher-Race Rosenfield

C = Rh2 R1r DCe / dce Rh: 1, 2, -3, 4, 5
1 1
E = Rh3 RR DCe / DCe Rh: 1, 2, -3, -4, 5
c = Rh4 rr dce / dce Rh: -1, -2, -3, 4, 5
1 2
e = Rh5 RR DCe / DcE Rh: 1, 2, 3, 4, 5

IV. ISBT: Numeric Terminology

 Universal language (both eye and machine readable)
 Adopted a 6-digit number for each authenticated blood group specificity
o 1st three = represent “system”
o 2nd three = represent “antigen specificity”
 Rh blood group system: 004

Ex. Numeric Fisher-Race Wiener ISBT Number

Rh1 D Rh0 004001
Rh2 C rh’ 004002
Rh3 E rh’’ 004003
Rh4 c hr’ 004004
Rh5 e hr’’ 004005

WEAK D
 Red cells carrying Weak D Ag have historically been referred to as having the Du type

1. Genetic Weak D
 inheritance of D genes that code for a weakened expression of the D antigen
 appears to be COMPLETE, but few in number
 seen mostly frequently in Blacks

2. C Trans
 “Position Effect” or “Gene interaction effect”
 the allele carrying D is trans C or in the opposite haplotype to the allele carrying C
o e.g. Dce / dCe
 Interference does not occur when C gene is inherited in the cis position to D e.g. DCe / dce
 They can receive D-positive cells with no adverse effects

3. D Mosaic
 one or more parts of the D Ag is MISSING
 Anti-D made by D-mosaic individuals can cause HDN or transfusion reactions

Rh Antibodies
 IgG; react at 37ºC or in AHG
 exposure to less than 1 mL of Rh(+) red cells can stimulate Ab production in an Rh(-) person
 IgG1 and IgG3 are of the greatest clinical significance because RES rapidly clears red cells
coated with them in the circulation
 Rh antibodies DO NOT BIND COMPLEMENT
o Rh antigens are not situated on the red cell surface this closely. Red cell destruction resulting from
antibodies is primarily EXTRAVASCULAR

Immunogenicity of common Rh Antigens

D > c > E > C > e

Rhnull syndrome (---/---)
 LACKS all Rh antigens
 Characteristics:
o mild compensated hemolytic anemia
o Reticulocytosis
o decrease in Hb and Hct
o decrease in Haptoglobin
o increased bilirubin
o STOMATOCYTOSIS
o Increase in Hb F
o Rh null red cells are negative for Fy5

Rhmod
 exhibit features similar to those with Rhnull
 however, the clinical symptoms are usually less severe

Exalted D
 DO NOT demonstrate Cc and / or Ee reactivity
 unusually strong D expression
 represented as D-- / D--

IgM cold-reacting antibodies

 Anti-Lea
 Anti-Leb
 Anti-I
 Anti-P1
 Anti-M
 Anti-A, Anti-B
 Anti-N

IgG warm-reacting antibodies

 Anti-Rh
 Anti-K
 Anti-Fya, Anti-Fyb
 Anti- Jka, Anti-Jkb
 Anti-S, anti-s
 Anti-P

Enhanced by Enzymes:
 Kidd
 Rh
 Lewis
 I
 P1

Destroyed by Enzymes:
 Duffy
 M,N,S,s

Shows Dosage:
 Duffy
 M,N,S,s
 Kidd
 Rh
BLOOD DONOR DEFERRAL

PERMANENT
 HIV (+) / AIDS
 HBsAg (+) , anti-HBc (+)
 Hemophilia, von Willebrand’s disease, receiving clotting factors
 Sickle cell anemia, Thalassemia, Polycythemia
 Kaposi sarcoma
 Malignant Tumors (except for basal cell carcinoma of skin & carcinoma in situ of cervix)
 Chronic cardiopulmonary, liver or renal disease
 History of Babesiosis or Chaga’s disease
 Recipient of human dura mater grafts, pituitary-derived growth hormone
 Donors who injected bovine insulin manufactured since 1980 from cattle in the UK
 Have taken the drug TEGISON for treatment of Psoriasis

FOR 3 YEARS
 Immigrant or refugee coming from an area endemic for Malaria, 3 years after departure, or those
who have had a Diagnosis of Malaria, 3 years after becoming asymptomatic
 Have taken the drug SORIATANE for treatment of Psoriasis

FOR 1 YEAR
 Sexual contact w/ a prostitute or persons in a high-risk group for AIDS
o Sexual worker
o IV drug users
 Rape victims
 After Hepatitis B immune globulin administration
 Close contact with someone with symptomatic viral hepatitis
 Tatoo, skin piercing, accidental needle sticks
 Recipient of blood components thru transfusion
 Recipeint of organ transplants
 Treatment of syphilis/gonorrhea (deferral starts after completion of therapy)
 After therapeutic rabies vaccination
 After bite from an animal
 Health care workers w/ percutaneous exposure to blood / body fluids
 Incarceration in a jail for more than 72 consecutive hours

FOR 6 MONTHS (After cessation of the drug Avodart for prostate gland enlargement)

FOR 2 MONTHS (Recent blood donation)

FOR 1 MONTH –
 German measles (Rubella) vaccination
 After cessation of the drug Proscar for treatment of Benign Prostatic Hyperplasia
 After cessation of the drug Accutane for Acne treatment
 After cessation of the drug Propecia for baldness

FOR 2 WEEKS
 After vaccination with: Yellow fever, Oral polio, Measles (Rubeola), Mumps, Typhoid

FOR 48 HOURS (Whole blood donation deferred after Hemapheresis)

For 3 days (Recent Aspirin intake)
For 12 hours (After Alcohol intake)

TEMPORARY
 Active disease under treatment: Cold, Flu, TB, Syphilis, infections
 Curable disease of the heart, lung, kidney, liver, and GI tract
 Treatment w/ ANTIBIOTICS
QUALIFICATIONS OF A POTENTIAL BLOOD DONOR

1. Age = minimum is 17 yrs old

2. Body weight
 110 lbs or 50 kg
 Standards mandates a maximum of 10.5 mL/kg of donor weight for whole blood collection
inclusive of pilot tubes for testing

Calculations for Drawing Donors Weighing Less than 50 kg (110 lb)

A. Volume to draw = (Donor’s weight in kg/50) × 450 mL

B. Amount of anticoagulant needed = (A/100) × 14
C. Amount of anticoagulant to remove from collection bag = 63 mL – B

3. Temperature
 Oral temperature should not exceed 37.5ºC or 99.5ºF

4. Pulse
 50 – 100 beats / min
 Lower pulse rate is acceptable for athletes

5. Blood Pressure
 Systolic: < 180
 Diastolic: < 100

6. Minimum Hemoglobin
 Hct: > 38%
 Hb: > 12.5 g/dL

REQUIREMENT FOR PRE-DEPOSIT AUTOLOGOUS TRANSFUSION

 Hct = 33%
 Hb = 11 g/dL
 Last donation must be completed 3 days before the anticipated operation
 Tests to be done: ABO & Rh

Hemoglobin Determination (Manual method for Mass Blood Donation)

 Copper sulfate method:
 Solution of CuSO4 has a specific gravity of 1.054
 The SG of blood correlates with the hemoglobin
 A small blood sample is dropped in the solution to see if it floats or sinks