Professional Documents
Culture Documents
Must Know Bloodbanking
Must Know Bloodbanking
Must Know Bloodbanking
Page | 237
Chromosome 7 Cartwright
Colton
Kell
Chromosome 9 ABO
Chromosome 11 Indian
Chromosome 17 Diego
Chromosome 18 Kidd
Chromosome 19 H
Lewis
Landsteiner-Weiner
Lutheran
Chromosome 22 P
Chromosome X Xg
Kx
Chromosome: Not known Dombrock
Von Descatello (Decastello) AB
Sturle (Sturli)
Blood groups (Most common) O > A > B > AB (Least common)
Page | 239
A2B A2B
B BB
BO
O OO
Gene Glycosyltransferase Immunodominant Sugar Ag Acceptor molecule
H L-fucosyltransferase L-fucose H Precursor subs.
A N-acetylgalactosaminyltransferase N-acetyl-D-galactosamine A H
B D-galactosyltransferase D-galactose B H
AB N-acetylgalactosaminyltransferase N-acetyl-D-galactosamine A H
D-galactosyltransferase D-galactose B
O -- -- -- Unchanged H
Amount of H Ag (Greatest) O > A2 > B > A2B > A1 > A1B (Least)
Bombay individual Bhende
(-) H gene
hh or Hnull
Lack H, A and B Ag’s
Designated as Oh
w/ anti-H, anti-A and anti-B Ab’s
Mistyped as group O
Parabombay Inherit weak H gene
w/ detectable A and B Ag’s but no detectable H Ag
Ah, Bh, ABh
Anti-H Differentiates Group O from Oh individuals
Ulex europaeus Lectin source of anti-H
ABO Histoblood group = present on all tissues and organs of the body
May be expressed in secretions depending on the secretor status (SeSe or
Sese)
Determination of Secretor Specimen: Saliva
Status Principle: Hemagglutination-inhibition
ABO antibodies Mixture of IgM, IgG and IgA (Henry)
Anti-A Predominantly IgM
Anti-B React at room temp
Naturally occurring
Anti-A,B (Group O) Predominantly IgG
React at 37’C
Immune Ab
Immune Ab’s Production is stimulated by:
1. Pregnancy
2. Incompatible transfusion and transplant
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ABO HDN Mother: Group O
Child: Group A or B
Group I discrepancies Weak reacting/missing Ab’s
Newborns
Elderly patients
Hypogammaglobulinemia/agammaglobulinemia
Group II discrepancies Weak reacting/missing Ag’s (Less frequent)
Leukemia
Acquired B phenomenon
Subgroups of A
Hodgkin’s disease
BGSS (Remedy: Wash RBCs)
Group III discrepancies Plasma abnormalities resulting to Rouleaux formation (Plasma factor)
! globulins: MM, WM, HL
! ^ibrinogen
Dextran and PVP
Wharton’s jelly (Remedy: Wash cord cells 6-8x (7x)
Group IV Miscellaneous:
Polyagglutination
Anti-I (cold agglutinin)
Cis “AB phenotype”
Unexpected ABO isoagglutinins:
= Anti-H: produced by A1 and A1B ("H Ag)
= Anti-A1: produced by A2 and A2B (No A1 Ag)
A Subgroups
A3 MF agglutination w/ anti-A & anti-A,B
Ax Weak MF agglutination w/ anti-A& anti-A,B
Aend MF agglutination w/ anti-A,B
Am (-) Agglutination, (+) AH substance in secretions
Ay (-) Agglutination, " AH substance in secretions
Ael (-) Agglutination, (+) H substance in secretions
B Subgroups
B3 MF agglutination w/ anti-B & anti-A,B
Bx MF agglutination w/ anti-A,B
Bm (-) Agglutination, (+) BH substance in secretions
Bel (-) Agglutination, (+) H substance in secretions
Rh Nomenclatures 1. Rosen^ield = no genetic basis, indicates the presence or absence of Rh Ag’s
2. Fisher-Race (DCE) = inheritance of 3 genes (d= amorph/silent)
3. Wiener (Rh-hr) = inheritance of 1 gene (Ex. R0), w/c codes for an
agglutinogen (Ex. Rh0), w/c contains 3 blood factors (Ex. Rh0hr’hr’’)
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Immunogenicity of Rh Ag’s (Most immunogenic) D > c > E > C > e (Least immunogenic)
R or r D or d
1 or ‘ Ce
2 or ‘’ cE
Z or y CE
G D+C+ red cell
Rh: 13, 14, 15, 16 4 different parts of the D mosaic
Genetic weak D D Ag’s expressed appear to be complete, but few in number
D Mosaic (Partial D) If one or more parts of D Ag is missing # weakened expression of D Ag
May produce anti-D (Ab against missing fragment)
4 fragments
C Trans D ---(trans)---> C (Ex. Dce/dCe)
f (ce) c ---(cis)---> e [Ex. Dce/DCE]
rhi (Ce) C ---(cis)---> e [Ex. DCe/DcE]
Hr0 “Common” Rh phenotypes (R1R1, R2R2, rr)
Rh Ab’s IgG1 and IgG3
React at 37’C
Immune Ab’s
(-) C’ binding = extravascular hemolysis (delayed HTR)
Rh HDN Mother: Rh (-)
Child: Rh (+), 2nd pregnancy
RhoGam or RhIg Puri^ied anti-D
Administer w/in 72 hrs after 1st delivery
Full dose RhoGam 300 μg anti-D
(>12 weeks gestation) Protect up to 30mL D+ WB or 15mL D+ RBCs
Minidose/Microdose 50 μg anti-D
RhoGam Protect up to 5mL of D+ WB or 2.5mL D+ RBCs
(<12 weeks gestation) Ex. Abortion
# RhIg vials Volume of FMH (mL) ÷ 30
Vol. FMH = % fetal cells x 50
---------------------------------------------
x = (% Fetal cells x 50) ÷ 30
x ≈ __ + 1 = # RhIg vials
As little as 1mL Rh(+) RBC Produces anti-D
Rh+ RBCs + anti-D = (+) agglutination
Perform test for Du (IAT) If RBCs + anti-D = (-) agglutination
= IAT is (+) agglutination = +Du (weak D)
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Rh- RBCs + anti-D + AHG reagent = (-) agglutination
2 conditions wherein an 1. No prior exposure to D Ag (males) or past childbearing age (females)
Rh- pt. can be transfused 2. Administer RhoGam
w/ Rh+ blood
Anti-LW Originally identi^ied as anti-Rh in early experiments involving rabbits
(Landsteiner-Weiner) immunized w/ Rhesus monkey blood
Anti-LW agglutinates Rh+ and Rh- cells except Rhnull cells
Rhnull No Rh Ag
Designated as ---/---
Stomatocytes
Rhdeleted No C/c and E/e Ag
Designated as D--/D--
Lewis system Le gene codes for the production of fucosyltransferase enzyme that catalyzes
addition of fucose to the 4th C of N-acetylglucosamine of type 1 precursor
Lewis Ag’s Lea ---(Se)---> Leb
Produced by tissue cells
Not well developed at birth = NB/cord cells = Le(a-b-)
Decreased expression during pregnancy
Genotype Substances Phenotype Le Ab’s
(Secretion)
ABH, lele, sese None ABH, Le(a-b-) Anti-Lea & Anti-Leb
ABH, lele, SeSe/Sese ABH ABH, Le(a-b-) Anti-Lea & Anti-Leb
ABH, LeLe/Lele, sese Lea ABH, Le(a+b-) Anti-Leb
ABH, LeLe/Lele, SeSe/Sese ABH, Lea, Leb ABH, Le(a-b+) none
Lewis Ab’s Anti-Lea & Anti-Leb
Naturally occurring
IgM
Activates the C’
MN Ag’s Glycophorin A (MN-SGP)
M = Ser-Ser-Threo-Threo-Gly
N = Leu-Ser-Threo-Threo-Glu
Well developed at birth
Important in paternity testing
Anti-M IgM, pH-dependent (6.5), glucose-dependent
Anti-N-like Ab IgM
Found in renal patients dialyzed w/ formaldehyde sterilized equipment
SS Ag’s Glycophorin B (Ss-SGP)
S = Methionine (29th)
s = Threonine (29th)
Page | 243
Ss Ab’s IgG
React at 37’C and AHG
Severe HTR w/ hemoglobinuria and HDN
Phenotype Detectable Ag’s Possible Ab’s
P1 P1 and P None
P2 P Anti-P1
p (p null) None Anti-P, P1, Pk (anti-Tja)
P1k Pk and P1 Anti-P
P2k Pk Anti-P, anti-P1
P1-like Plasma, pigeon and turtledove droppings, turtledove eggwhite
P1 substance Hydatid cyst ^luid, Lumbricoides terrestris, Ascaris suum
Anti-P1 IgM
Naturally occurring
Strong anti-P1 = Hydatid disease (E. granulosus)
Associated w/ fascioliasis, C. sinensis and O. viverrini infections
Anti-Tja Anti-P, P1, Pk
Spontaneous abortions in early pregnancy
Anti-P IgG
Naturally occurring
Biphasic hemolysin (PCH)
Test: Donath-Landsteiner
Ii Blood Group I: Individuality
Neonates = "I !I (Ag) = I-i+
Adults (18 mos.-adult) = !I "I = I+i-
HEMPAS !i Ag in adults
Anti-I Interfere w/ reverse typing (Group IV)
Benign anti-I = normal, IgM, naturally occurring, react at 4’C
Pathologic anti-I = IgM, react at 30/32’C (CAS = PAP)
Autoanti-I = M. pneumoniae, L. monocytogenes
Anti-i IgM
React at 4’C
EBV caused
Diseases of RES:
- Alcoholic cirrhosis
- Myeloid leukemia
- Reticuloses
Anti-IT Transition: from i # I
Yanomama Indians
Hodgkin’s lymphoma
K Kell
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k Cellano
Kpa Penney
Kpb Rautenberg
Jsa Sutter
Jsb Matthews
Kell Ag’s Immunogenicity: 2nd to D (D>K>c>E>C>e)
Synthesized on precursor Kx
= On WBCs: remain unconverted. If (-) # CGD
= On RBCs: converted to Kell Ag’s. If (-) # MacLeod phenotype
MacLeod phenotype Acanthocytosis
Muscular dystrophy
Anti-K IgG
React at 37’C and AHG
Fy(a+b-) Chinese (90.8%)
Fy(a-b-) American blacks
Resistant to P. vivax/P. knowlesi (malaria)
Fya and Fyb Receptors for malaria
Duffy gene 1st human gene to be assigned to speci^ic chromosome (1)
Anti-Fya IgG
Anti-Fyb React at AHG
Jka and Jkb Enhanced by enzymes
Anti-Jka Notorious antibody = not easily detected
Anti-Jkb Immune Ab’s (IgG)
Common cause of delayed HTR
Autoanti-Jk = Methyldopa (Aldomet)
Lua and Lub Development at age of 15
Anti-Lua IgG, IgM, IgA
Naturally occurring
React at room temp
Anti-Lub IgG4, IgM, IgA
Immune Ab
React at 37’C
Diego (Di) Mongolian ancestry
AE-1 = HCO3- <--> Cl-
Defect in AE molecule “ASO”
Acanthocytosis
Hereditary Spherocytosis
SEA Ovalocytosis
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Cartwright (Yt) Erythrocyte acetylcholinesterase = neurotransmission
Xg Sex-linked
!! Females
Short arm of X chromosome
Scianna Sc1, Sc2, Sc3
Dombrock Gregory (Gya)
Holley (Hy)
Joseph (Joa)
Colton (Co) CHIP, Aquaporin = water permeability
Chido/Rodgers (Ch/Rg) HLA system (Bg)
C4A (Rg) and C4B (Ch) = C’ component
HTLA = exhibit reaction only at high dilution
DAF (Cr)
Gerbich (Ge) GPC and GPD
Leach phenotype (GE: -2, -3, -4) = Elliptocytosis
Cromer (Cr) DAF
CROM Ab’s = black individuals
Knops (Kn) CR1 (C’ receptor 1)
Indian (In) CD44 (immune adhesion)
Benneth-Goodspeed (Bg) HLA Ag’s on RBCs (Class I MHC)
Bga = HLA-A7
Bgb = HLA-A17
Bgc = HLA-B28
Public Ag High-incidence Ag’s
Ena (99.9%)
Private Ag Low-incidence Ag’s (<1%)
HTLA Ab’s Anti-Ch
Anti-Rg
Anti-Kn
Anti-Yka
Anti-Csa
Anti-McC
Anti-JMH
Sources of Substances for Neutralization for Certain Antibodies
Anti-P1 Hydatid cyst ^luid, pigeon droppings, turtledoves’ egg whites
Anti-Le Plasma/serum, secretor saliva
Anti-Ch, Anti-Rg Plasma/serum
Anti-Sda Urine, guinea pig urine
Anti-I Mother’s milk
Page | 246
Anti-H Saliva
Effect of Proteolytic Enzymes on Select Antigen-Antibody Reactions
Enhanced P1
Rh
I
Kidd
Lewis
Destroyed MNS
Duffy
Chido
Rodgers
Cartwright
Xg
Donation Process
At least 2 persons Bleeder
Head (BB)
Donor registration 1st step
Interview & physical exam 2nd step
Actual donor selection and 3rd step
blood collection
Collection <15 mins (7-10mins)
>15 mins = (-) cryoprecipitate
Donor bleeding 450 angle # 10-200 angle
(Venipuncture: 150 angle)
Basic QualiOications of the Potential Blood Donor
Good health Purplish blue lesions # Kaposi’s sarcoma (HIV, HHV-8)
Age 18-65 yrs old
<18 yrs old = w/ parent’s consent
>65 yrs old = w/ physician’s consent
Body weight Max: 10.5mL/kg
Ideal: 110 lbs (50kg)
450mL blood + 30mL blood (serologic tests)
63mL anticoagulant
Page | 247
Vol. of anticoag. to be C = 63 – B
removed from blood bag
1:7 Anticoagulant: Blood ratio (Blood bag)
63mL AC = 450mL blood
31.5mL AC = 200mL blood
Temperature 37.5’C (99.5’F)
Pulse 50-100 beats/min (" athletes = acceptable)
BP cuff 40-60 mmHg (if used as tourniquet)
BP (DOH) 90-160 mmHg
60-100 mmHg
Min. H & H Allogeneic donation:
Hgb: ≥12.5 g/dL
Hct: ≥38%
Autologous donation:
Hgb: ≥11 g/dL
Hct: ≥33%
CuSO4 method Hgb determination
30mL container = 25 tests, solution changed daily
SG: CuSO4 = 1.053
1 cm = distance between blood and solution
Acceptable drop of blood # sink w/in 15 secs (Hgb: ≥12.5 g/dL)
Donor Deferral
Permanent Chagas’ disease
Babesiosis
Tegison (Tx: Psoriasis) = teratogenic
Recipient of human (pituitary)-derived GH = risk of transmitting CJD
[Recombinant GH = no deferral]
Recipient of cornea/dura mater = risk of transmitting CJD
3 years Malaria refugee/immigrant
1 year (12 months) Recipients of blood known to be possible sources of hepatitis
Tattoo
Rape
Incarceration in jail (3 days/72 hrs)
Blood transfusion
Major operation including dental surgery
Syphilis
Gonorrhea
Traveler # malaria-endemic places
Rabies vaccine
9 months (DOH) Childbirth (AABB: 6 weeks)
Page | 248
3 months (12 weeks) Recent blood donation (AABB: 8 weeks)
[DOH] = 450mL blood: 12 weeks
= 200mL blood: 6-8 weeks
1 month (4 weeks) Rubella vaccine
Isotretinoin/Accutane (Tx: Acne) = teratogenic
Proscar (Tx: Benign prostatic hyperplasia) = teratogenic
2-3 weeks After febrile episodes
2 weeks Rubeola vaccine
Polio vaccine
Mumps vaccine
2 days (48 hrs) After hemapheresis
12 hrs After alcohol intake
Cause: Arterial puncture Jet-like pulsating bleeding w/ bright red blood
Citrate Binds Ca2+
Massive transfusion (8-10 units) # Citrate toxicity # Hypocalcemia
Milk = !Ca2+
Dextrose/Glucose Provides energy for red cells
Citric acid Prevents caramelization ("pH)
Adenine For improved survival of red cells
Phosphate buffer ! ATP
Shelf-life: 21 days ACD (Apheresis)
CPD
CP2D
Shelf-life: 35 days CPDA-1
Shelf-life: 42 days CPDA-2 (DOH)
Additive solutions:
-Adsol (AS-1)
-Nutricel (AS-3)
-Optisol (AS-5)
Additive solutions SAGM:
-Saline
-Adenine
-Glucose
-Mannitol = RBC membrane stabilizing agent
Rejuvenation solutions ! ATP & 2,3-DPG (Rejuvesol)
PIGPA = Phosphate, Inosine, Glucose, Pyruvate, Adenine
PIPA = Phosphate, Inosine, Pyruvate, Adenine
Heavy spin 5000g for 5mins = pRBC, platelet concentrate
5000g for 7mins = cryo, cell-free plasma
Page | 249
Light spin 2000g for 3mins = platelet-rich plasma
6-8 hours processing To maximize the number of components derived from 1 unit of blood
Platelet concentrate Light spin # Heavy spin
Centrifuge at 20-24’C
[Other blood components: Ref. centrifuge (1-6’C)]
!Bacterial contamination
Separate from WB w/in 6-8 hrs
Blood Indication Storage Transport Shelf-life Other Info
Component
Whole blood 1. Blood vol. expansion & ! 1-6’C 1-10’C 21d (ACD, CPD) 1 unit:
RBC mass 35d (CPDA-1) !Hgb by 1 to 1.5g/
2. Massive transfusion & 42d (CPDA-2) dL
acute blood loss 2d (Heparin !Hct by 3-5%
Packed RBCs 1. ! RBC mass 1-6’C 1-10’C Open system: 24h ‡80% plasma
plasma (liver disease) -65’C 7 years (-65’C) all coag. factors and
2. Replace isolated factor complement
def. when speci^ic ‡FFP: Thaw at 37’C
Page | 250
Cryoprecipitate 1. Fibrinogen def. -18’C or 1 year ‡Contains:
37’C
‡Thawed cryoppt
hrs
Granulocyte 1. Granulocyte dysfunction 20-24’C 24h Contains 1 x 1010
concentrate (CGD) w/o granulocytes
2. Myeloid hypoplasia agitation
Platelet 1. Thrombocytopenia 20-24’C 5d (20-24’C w/ 1 unit will !
concentrate w/ agitation) platelet count by
agitation 2d (1-6’C) 5,000- 10,000/μL
1-6’C
Irradiated blood 1. Prevent GVHD 28 days from Usually RBCs and
component irradiation or orig. platelets are
exp. date irradiated
whichever comes
^irst
Factor VIII 1. For hemophilia A 1-6’C Varies Stored in
concentrate lyophilized form
Factor IX 1. For hemophilia B 1-6’C Varies ‡A.k.a. prothrombin
concentrate complex
‡Contains factors II,
VII, IX and X
NSA 1. Hypovolemic shock 2-10’C 5 years 96% Albumin
4% Globulin
Blood Indication Storage Transport Shelf-life Other Info
Component
PPF 1. Hypovolemic shock 2-10’C 5 years 80-85% Albumin
10-15% Globulin
SDP 5 years SDP: Single donor
plasma
Page | 251
Agglomeration Glycerol -80’C -65’C Mechanical
Glucose freezer
Fructose
EDTA
Cryoprotective agent Prevents rupture of RBCs during freezing
Ex. Glycerol
Deglycerolization Removal of glycerol
Hypertonic solution followed by an isotonic solution
High glycerol (DG) 12% NaCl -----> 1.6% NaCl -----> 0.9% NaCl
Low glycerol (DG) 45% NaCl in 15% mannitol
Agglomeration (DG) 50% Glucose + 5% Fructose -----> 0.9% NaCl
Cryoprecipitate After thawing = administer w/in 6 hours
After pooling = administer w/in 4 hours
Leukapheresis HES (Hydroxyethylstarch) = !Separation bet. WBCs and RBCs
Donor: administered w/ corticosteroids 12-24 hrs before donation
= !# of circulating granulocytes
Page | 252
Infusion IV ^luids:
a. NSS = the only ^luid allowed to start an IV line prior to transfusion
b. D5W (5% dextrose in H2O) = Not allowed to start (hypotonic # hemolysis)
c. Ringer’s lactate =not allowed to start (contains Ca2+ # promote coagulation)
Blood warmers 37’C
!Temp. >42’C = hemolyzed
Page | 253
Acquired Non-Microbially Associated Polyagglutination
Tn (-) β-3-D-galactosyltransferase enzyme needed for the normal structure of T
receptor (Tetrasaccharide of Thomas and Winzler)
Inherited Polyagglutination
Cad !Sda
Page | 254
Tn Cad T Tk
Arachis hypogaea - - + +
Salvia sclarea + - - -
Salvia horminum + + - -
Glycine soja + + + -
Autologous Donation
Predeposit AD Before anticipated transfusion
Requirements:
*No age limit
*No strict weight requirement ("vol. by 4mL/1 pound below 110)
*Hgb ≥ 11g/dL
*Hct ≥ 33%
*Frequency: every ≥ 3days
Intraoperative AD Collect blood during surgical procedure # reinfused immediately
Immediate preoperative Collect blood # replace patient volume w/ colloid/crystalloid # reinfuse
hemodilution during surgical procedure
Postoperative salvage Drainage tube
Postoperative bleeding # salvaged (saved) # clean and reinfused
Immediate Immune Transfusion Reactions
FNHTR !1’C in temperature
Cause: anti-leukocyte Ab’s (leukoagglutinins)
Prevention: Leukopoor RBCs
Allergic Cause: Donor plasma w/ foreign proteins
Prevention: Washed RBCs
Anaphylactic Afebrile (no fever)
Signs and symptoms occur only after the infusion of only few mL of blood
IgA de^iciency w/ anti-IgA antibody
Prevention: Washed RBCs | IgA-de^icient donor (rare)
Anaphylactoid Afebrile
Normal IgA w/ anti-IgA to donor IgA
Prevention: Washed RBCs | IgA-de^icient donor (rare)
TRALI (NCPE) Cause: Anti-leukocyte Ab’s (leukoagglutinins)
Signs and symptoms resemble respiratory distress
Prevention: Leukopoor RBCs
Hemolytic Bleeding, hypotension, hemoglobinuria, anuria
Delayed Immune Transfusion Reactions
Page | 255
TA-GVHD Cause: T lymphocyte proliferation
Prevention: Irradiated RBCs
PTP Onset of thrombocytopenia
Cause: anti-platelet Ab’s (HPA-1a negative platelets)
Prevention: Therapy
a. Administration of corticosteroid
b. Exchange transfusion
c. IV immunoglobulins
DHTR 7 days
Immediate Nonimmune Transfusion Reactions
TACO Administration of blood w/o equivalent blood loss
Iatrogenic: physician-caused
At risk:
a. Young children
b. Elderly patients
c. Patients w/ cardiac disease
Prevention: Therapy
a. Therapeutic phlebotomy
b. IV diuretics
c. O2 therapy
Bacterial contamination Cause: Endotoxin production by psychrophilic/cryophilic bacteria
Y. enterocolitica (most common)
E. coli
P. aeruginosa
Factors:
a. During phlebotomy
b. During preparation/processing
c. During thawing
Prevention:
a. Sterile technique
b. Visual inspection of unit
→ Blood unit = Brown, purple, hemolysis, clot
→ Plasma = Murky (dark brown) purple, red
PCITR Causes:
- Small bore needle
- Warming blood above 50’C
- Freezing blood w/o cryoprotective agent
- Citrate toxicity
Delayed Nonimmune Transfusion Reactions
Page | 256
Iron Overload Patients w/ normovolemic anemia
(Hemosiderosis) Transfusion-dependend patients:
- Aplastic anemia
- Congenital hemolytic anemia
Prevention:
a. Iron-chelating agent = Deferroxamine
b. Neocytes = young RBCs, has longer lifespan
Disease transmission HBV, HCV, HDV, CMV, EBV, HTLV-I and II, HIV, T. pallidum, Plasmodium spp., B.
microti, T. cruzi, T. gondii
Hemolytic Disease of the Newborn
In utero Anemia (! immature RBCs, enlarged spleen & liver = extramedullary
hematopoiesis)
Hydrops fetalis = cardiac insuf^iciency, edema
Neonatal period ! Unconjugated bilirubin # Brain # Kernicterus
Treatment 1. Intrauterine transfusion
- In utero
- Corrects anemia
- X-match: Mother’s serum
2. Exchange transfusion
- Neonatal period
- Removes bilirubin & Ab-coated RBCs
- X-match: Mother’s serum (preferred) or infant’s serum
Cross-Matching
Full X-match 2 hours
Can be shortened to 30 mins
Abbreviated X-match Type/screen + immediate spin
DC/PS = no agglutination/hemolysis
Electronic X-match Patient blood type is determined on 2 occasions
Emergency situation Patient blood type is unknown
Group O (Rh-) pRBCs
(+) Major X-match (-) Alloantibody control
(+) Autoantibody, autocontrol
Ratio of serum to cells Routine = 40:1
Det. weak Ab’s = 133:1
Saline for washing pH 7.2-7.4
Incubation period 30-120 mins (majority: 30 mins)
Enhancement media 1. Albumin
2. PEG
3. LISS (Incubation pd: 5-15 mins)
Lectin Sources
Page | 257
Anti-A1 Dolichos bi*lorus
Anti-H Ulex europaeus
Anti-M Iberis amara
Iberis umbellate
Iberis semperivens
Maclura aurantiaca
Anti-N Bauhinia variegate
Bauhinia purpura
Bauhinia bonatiana
Bauhinia candicans
Vicia graminea
Anti-B Bandeirae simplicifolia
Quality Control
Annually Mercury thermometers
Quarterly (Every 3 months) Speed timer (centrifuge)
Cell washers (speed, timer)
Blood warmers
Monthly Alarm Activation (refrigeration and freezers)
Temperature (refrigerated centrifuge)
Daily Refrigerators and freezers (continuous monitors)
Platelet incubators (enclosed, monitored chambers)
Daily when in use Transfusion service:
- Heating blocks
- Water baths
Donor facility:
- Donor unit agitators
- Scales
- Balances
- Hemoglobinometer
- Microhematocrit centrifuges
Every 4 hours Platelet incubators (ambient temperature storage)
Other Topics
Apheresis/Hemapheresis Whole blood is withdrawn, a desired component separated, and the remainder
of the tube returned to the donor
Intermittent-^low 1 venipuncture
centrifugation (IFC) Blood is withdrawn and reinfused through the same needle
Once the desired component is separated, the remaining components are
reinfused to the donor
Continuous-^low 2 venipunctures
centrifugation (CFC) Withdraw, process and return the blood to the individual simultaneously
Antibody screen Collect new specimen every 3 days in a series of transfusion
Page | 258
Donor & recipient samples Keep for 7 days after transfusion (at 1-6’C)
Compatibility testing Series of tests that ensure safety of transfusion to recipient and donor
1. Review of BB records
2. ABO and Rh
3. Ab screen
4. Cross matching
a. Major X-match = DC/PS
b. Minor X-match = PC/DS
DHTRs Occur 3 to 7 days after transfusion
Virus inactivation in plasma Heating in a liquid state w/ LMW stabilizers
products Heating in lyophilized state
UV irradiation
Y. enterocolitica !!! Bacterial contamination of blood
Density Separates neocytes from mature RBCs
Requirements for blood 1. (-) HbS
products to be transfused 2. <7 days
to infants 3. γ-irradiated
4. (-) CMV
Allogeneic donor blood Repeat ABO and Rh typing
from outside sources
w/in 30 mins Time limit when a unit of blood is removed from 2-8’C and returned back to
the refrigerator
Procedure when HTR 1. Stop transfusion
occurs 2. Keep IV line open
3. Notify the physician and BB
Specimens for investigation 1. Patient pre-transfusion blood sample
of HTR 2. Patient post-transfusion blood sample
= PT/PTT/DAT
= Pink: Hgb 0.2 g/L or 20 mg/dL
= Red: Hgb >1 g/L or 100 mg/dL
3. Patient post-transfusion urine
= Bilirubin/Urobilinogen
4. Blood bag
= GS/CS
LISS Glycine/glucose + saline
5-15 mins incubation
ZZAP Cysteine-activated papain
Mixture of DTT and papain
True chimerism Presence of 2 cell population
Ex. Twins
Mixed-^ield agglutination
Page | 259
Arti^icial chimerism After:
-BM transplantation
-Blood transfusion
-Exchange transfusion
-Fetomaternal hemorrhage
AB cis genotype Group IV discrepancy
Inheritance of 3 ABO genes (AB/O)
Acquired A antigen 1. Tn activation
2. P. mirabilis
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Elution Breaking of bonds between Ag and Ab by:
a. Physical: heating, shaking
b. Chemical: ether, acid
Adsorption Removal of Ab in serum using appropriate RBC
Biphasic hemolysin Cold = attaches to RBCs
Warm = RBC lysis
Per^luorocarbons O2 carrying capacity
RBC substitute
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