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Blood Banking & Immunohematology

Master blood group systems, compatibility testing, and transfusion medicine for the MedTech board exam.

1. ABO Blood Group System

Discovery and Genetics

  • Karl Landsteiner (1901): Discovered ABO system, Nobel Prize 1930
  • Chromosome location: 9q34
  • Inheritance: Codominant (A and B), O is recessive
  • H gene: Located on chromosome 19, produces H antigen (precursor)
  • Secretor gene (FUT2): Determines ABH antigens in body fluids

ABO Antigens and Antibodies

Blood TypeAntigens on RBCsAntibodies in PlasmaGenotypesFrequency (Filipino)
AA, HAnti-BAA, AO~27%
BB, HAnti-ABB, BO~25%
ABA, B, HNoneAB~7%
OH onlyAnti-A, Anti-BOO~41%

ABO Subgroups

A Subgroups

  • A1: 80% of type A, strong reactions
  • A2: 20% of type A, weaker reactions
  • • A2 cells may have anti-A1 in serum
  • • A1 lectin (Dolichos biflorus) differentiates
  • • Other weak A: A3, Ax, Aend, Am, Ael

B Subgroups

  • • Less common than A subgroups
  • • B3, Bx, Bm, Bel variants exist
  • • Weak B may be missed in routine testing
  • • Need extended incubation for detection

Bombay Phenotype (Oh)

Definition: Individuals lack H antigen due to homozygous hh genotype

  • • Cannot produce A, B, or H antigens
  • • Have anti-A, anti-B, and anti-H antibodies
  • • Can only receive blood from other Bombay individuals
  • • Forward typing: Appears as O
  • • Reverse typing: Reacts with all cells including O cells
  • • Discovered in Bombay (Mumbai), India

ABO Typing Methods

Forward (Cell) Typing

  • • Patient RBCs + known antisera
  • • Tests for antigens on RBCs
  • • Use anti-A and anti-B reagents

Reverse (Serum) Typing

  • • Patient serum + known cells
  • • Tests for antibodies in serum
  • • Use A1 cells, B cells, (O cells optional)

2. Rh Blood Group System

Discovery and Genetics

  • Landsteiner & Wiener (1940): Discovered using Rhesus monkey RBCs
  • Chromosome location: 1p36 (RHD and RHCE genes)
  • Most immunogenic antigen: D antigen (after ABO)
  • D-positive: ~85% Caucasians, ~95% Filipinos
  • D-negative: Lack D antigen, can develop anti-D

Rh Antigens (Fisher-Race Nomenclature)

Fisher-RaceWienerImmunogenicity RankNotes
DRho1stMost clinically significant
chr'2ndCommon cause of HDFN
Erh"3rdOften develops with anti-c
ehr"4thLess common antibody
Crh'5thLeast immunogenic of five

Weak D and Partial D

Weak D (Du)

  • • Reduced expression of complete D antigen
  • • Negative with direct typing, positive with IAT
  • • Usually cannot make anti-D
  • • Can donate as D-positive
  • • Can receive D-positive blood

Partial D

  • • Missing some D epitopes
  • • CAN make anti-D (against missing epitopes)
  • • Should receive D-negative blood
  • • Categories: DII, DIII, DIV, DV, DVI, DVII
  • • DVI most clinically significant

Rh Typing Methods

  • Slide/Tube method: Direct agglutination with anti-D
  • Weak D testing: Indirect antiglobulin test (IAT) required
  • Gel technology: Sensitive, standardized method
  • Monoclonal anti-D: IgM (immediate spin), IgG (IAT phase)

3. Other Blood Group Systems

Kell Blood Group System

  • K antigen: Third most immunogenic (after D and c)
  • Antibodies: IgG, clinically significant, cause HDFN
  • K-positive: ~9% Caucasians, rare in Asians
  • Kell null (Ko): McLeod syndrome association
  • Important antigens: K, k (cellano), Kpa, Kpb, Jsa, Jsb

Duffy Blood Group System

  • Antigens: Fya and Fyb
  • Fy(a-b-) phenotype: Common in African populations
  • Malaria resistance: Duffy antigens are receptors for Plasmodium vivax
  • Antibodies: IgG, can cause HDFN and HTR
  • Dosage effect: Stronger reactions with homozygous cells

Kidd Blood Group System

  • Antigens: Jka and Jkb
  • Antibodies: IgG, notorious for causing delayed HTR
  • Characteristics: "Disappearing antibody" - drops below detectable levels
  • Show dosage: Stronger with homozygous cells
  • Enhance detection: Use enzyme-treated cells, PEG

MNS Blood Group System

  • Antigens: M, N, S, s, U
  • Anti-M: Usually IgM, cold-reacting, clinically insignificant
  • Anti-N: Rare, usually from dialysis patients
  • Anti-S and anti-s: IgG, clinically significant
  • Anti-U: Can cause severe HDFN, found in S-s- individuals

Lewis Blood Group System

  • Antigens: Lea and Leb (adsorbed from plasma)
  • Not truly RBC antigens: Produced in plasma, adsorbed onto RBCs
  • Antibodies: IgM, NOT clinically significant
  • Do not cause HDFN: Antigens not developed on fetal cells
  • May change during pregnancy: Le(a-b-) phenotype common

P1PK and I Blood Group Systems

P1PK System

  • • Anti-P1: IgM, cold-reacting
  • • Usually clinically insignificant
  • • p phenotype: Very rare, anti-PP1Pk

I System

  • • I antigen: Adults; i antigen: Newborns
  • • Anti-I: Cold autoantibody (Mycoplasma)
  • • Anti-i: Associated with EBV infection

4. Antibody Screening & Identification

Antibody Screening Purpose

  • • Detect unexpected antibodies in patient serum/plasma
  • • Use 2-3 reagent red cell panel (screening cells)
  • • Screen cells must express common clinically significant antigens
  • • Perform at 37°C and AHG phase for IgG antibodies
  • • Required before transfusion and during pregnancy

Antibody Identification

Panel Cell Method

  • • Use 10-16 cell panel with known antigen profiles
  • • Test patient serum against each cell
  • • Match reaction pattern with antigram
  • • Rule out antigens: Cells negative for antigen, reaction negative
  • • Confirm antibody: At least 3 positive and 3 negative reactions

Enhancement Techniques

LISS (Low Ionic Strength Saline)

  • • Reduces zeta potential
  • • Speeds up antibody uptake
  • • Shorter incubation time
  • • May enhance non-specific reactions

PEG (Polyethylene Glycol)

  • • Removes water, concentrates antibodies
  • • Very sensitive method
  • • Cannot read immediate spin phase
  • • Must wash cells well before AHG

Enzyme Treatment

  • • Ficin, papain, bromelin
  • • Enhances: Rh, Kidd, Lewis, P, I
  • • Destroys: Fya, Fyb, M, N, S, s
  • • Useful for antibody identification

Gel Technology

  • • Standardized, stable endpoint
  • • Requires specialized cards/equipment
  • • No washing required
  • • Can store results for review

Antibody Characteristics

CharacteristicIgMIgG
Optimal temperature4°C - Room temp37°C
Detection phaseImmediate spinAHG phase
Complement activationStrongVariable
Crosses placentaNoYes
Causes HDFNNoYes

5. Compatibility Testing & Crossmatching

Pre-Transfusion Testing Steps

  1. Verify patient identity and sample labeling
  2. ABO and Rh typing (forward and reverse)
  3. Antibody screening
  4. Antibody identification (if screen positive)
  5. Crossmatch (major crossmatch)
  6. Selection of compatible units
  7. Issue and transfuse

Types of Crossmatches

Immediate Spin (IS)

  • • Patient serum + donor cells
  • • Centrifuge immediately
  • • Detects ABO incompatibility
  • • Used when antibody screen negative
  • • Fastest method

Full Crossmatch (AHG)

  • • Incubate at 37°C
  • • Add AHG reagent
  • • Detects IgG antibodies
  • • Required if antibody screen positive
  • • Most sensitive method

Electronic/Computer

  • • No serologic testing
  • • Computer verifies ABO compatibility
  • • Requires validated computer system
  • • Two ABO typings on record
  • • Negative antibody screen required

Major vs Minor Crossmatch

Major Crossmatch

  • • Patient SERUM + Donor CELLS
  • • Detects patient antibodies vs donor cells
  • • REQUIRED before transfusion
  • • Most important test

Minor Crossmatch

  • • Donor SERUM + Patient CELLS
  • • Detects donor antibodies vs patient cells
  • • NOT routinely performed
  • • Donor screening replaces this

Blood Selection Rules

Patient TypeCompatible RBC UnitsCompatible Plasma
OO onlyO, A, B, AB
AA, OA, AB
BB, OB, AB
ABAB, A, B, OAB only

* Universal donor (RBC): O negative | Universal recipient (RBC): AB positive

6. Blood Component Therapy

Blood Component Preparation

From 1 unit whole blood (450 mL ± 45 mL):

  • Packed RBCs: Centrifuge, remove plasma (Hct 65-80%)
  • Fresh Frozen Plasma: Freeze within 8 hours of collection
  • Platelets: From platelet-rich plasma or buffy coat
  • Cryoprecipitate: Thaw FFP at 4°C, collect precipitate

Blood Components Summary

ComponentStorageShelf LifeIndications
Packed RBCs1-6°C35-42 days (additive)Anemia, blood loss
Whole Blood1-6°C21-35 daysMassive transfusion
FFP≤-18°C1 yearClotting factor deficiency
Platelets20-24°C, agitation5 daysThrombocytopenia, bleeding
Cryoprecipitate≤-18°C1 yearFibrinogen deficiency, vWD
Granulocytes20-24°C24 hoursSevere neutropenia with sepsis

Special Products

Leukocyte-Reduced

  • • Filter removes WBCs (<5 × 10⁶)
  • • Prevents febrile reactions
  • • Reduces CMV transmission
  • • Prevents HLA alloimmunization

Irradiated Products

  • • 25 Gy gamma irradiation
  • • Prevents TA-GVHD
  • • For immunocompromised patients
  • • Directed donations from relatives

Washed RBCs

  • • Removes plasma proteins
  • • For IgA-deficient patients
  • • Severe allergic reactions
  • • Short shelf life (24 hours)

CMV-Negative

  • • Donor tests negative for CMV
  • • For CMV-negative transplant patients
  • • Leukoreduction is alternative
  • • Neonates, pregnant women

Cryoprecipitate Contents

  • Fibrinogen: 150-250 mg per unit
  • Factor VIII: 80-120 IU per unit
  • von Willebrand Factor (vWF)
  • Factor XIII
  • Fibronectin

7. Transfusion Reactions

Acute Hemolytic Transfusion Reaction (AHTR)

Most Serious Reaction!

  • Cause: ABO incompatibility (usually clerical error)
  • Mechanism: Intravascular hemolysis, complement activation
  • Symptoms: Fever, chills, flank pain, hypotension, hemoglobinuria, DIC
  • Lab findings: Positive DAT, hemoglobinemia, elevated bilirubin
  • Treatment: STOP transfusion immediately, maintain renal perfusion, supportive care

Delayed Hemolytic Transfusion Reaction (DHTR)

  • Onset: 3-14 days post-transfusion
  • Cause: Anamnestic response to foreign RBC antigens (Kidd, Rh, Kell)
  • Mechanism: Extravascular hemolysis
  • Symptoms: Mild fever, unexplained drop in hemoglobin, jaundice
  • Lab findings: Positive DAT, new antibody detected, elevated bilirubin
  • Treatment: Usually mild, supportive care

Non-Hemolytic Transfusion Reactions

Febrile Non-Hemolytic (FNHTR)

  • • Most common reaction
  • • Cytokines from stored WBCs
  • • Temperature rise ≥1°C
  • • Prevention: Leukoreduction
  • • Treatment: Antipyretics

Allergic Reaction

  • • Antibodies to plasma proteins
  • • Urticaria, hives, itching
  • • Usually mild
  • • Treatment: Antihistamines
  • • May resume transfusion if mild

Anaphylaxis

  • • IgA deficiency with anti-IgA
  • • Hypotension, bronchospasm
  • • Occurs within minutes
  • • Treatment: Epinephrine
  • • Future: Washed products or IgA-deficient donors

TRALI

  • • Transfusion-Related Acute Lung Injury
  • • Donor anti-HLA antibodies
  • • Within 6 hours of transfusion
  • • Non-cardiogenic pulmonary edema
  • • Treatment: Supportive, oxygen

Other Transfusion Complications

  • TACO: Transfusion-Associated Circulatory Overload - volume overload, CHF
  • TA-GVHD: Donor T-cells attack recipient tissues - prevented by irradiation
  • Bacterial contamination: Most common in platelets (room temp storage)
  • Iron overload: Chronic transfusion therapy, >20 units
  • Post-transfusion purpura: Severe thrombocytopenia 5-10 days post-transfusion

Transfusion Reaction Workup

  1. Stop transfusion, keep IV line open
  2. Clerical check - verify patient and unit identification
  3. Visual inspection of plasma (hemolysis?)
  4. Direct Antiglobulin Test (DAT)
  5. Repeat ABO/Rh on pre and post samples
  6. Antibody screen
  7. Urinalysis (hemoglobinuria)
  8. Bilirubin, LDH, haptoglobin
  9. Blood culture (if bacterial contamination suspected)

8. Special Topics in Blood Banking

Hemolytic Disease of the Fetus and Newborn (HDFN)

Pathophysiology

  • • Maternal IgG antibodies cross placenta
  • • Attack fetal RBCs if antigen positive
  • ABO HDFN: Most common, usually mild (Group O mother, A or B baby)
  • Rh HDFN: D-negative mother, D-positive fetus - more severe
  • • Other antibodies: c, K, Fy, Jk can cause HDFN

Rh Immune Globulin (RhIg)

  • Purpose: Prevent sensitization of D-negative mothers
  • Dosing: 300 mcg covers 30 mL whole blood (15 mL RBCs)
  • Antepartum: At 28 weeks gestation
  • Postpartum: Within 72 hours if baby is D-positive
  • Other indications: Abortion, amniocentesis, ectopic pregnancy, trauma
  • Rosette test: Screens for large fetomaternal hemorrhage
  • Kleihauer-Betke: Quantifies fetal cells in maternal blood

Direct and Indirect Antiglobulin Test

DAT (Direct Coombs)

  • • Tests for in-vivo sensitization
  • • Patient RBCs + AHG reagent
  • • Detects antibody/complement on RBCs
  • • Uses: AIHA, HDFN, HTR, drug-induced

IAT (Indirect Coombs)

  • • Tests for in-vitro sensitization
  • • Patient serum + reagent RBCs, incubate, add AHG
  • • Detects antibody in serum
  • • Uses: Antibody screen, crossmatch, weak D

Autoimmune Hemolytic Anemia (AIHA)

TypeWarm AIHACold Agglutinin DiseasePCH
AntibodyIgG (37°C)IgM (4°C)IgG (biphasic)
DATIgG positiveC3d positiveC3d positive
SpecificityRh-likeAnti-IAnti-P
HemolysisExtravascularIntravascularIntravascular

Donor Screening and Testing

Required Testing (Philippines - NVBSP)

  • ABO and Rh typing
  • Antibody screening
  • Hepatitis B surface antigen (HBsAg)
  • Hepatitis C antibody (anti-HCV)
  • HIV-1/2 antibody
  • Syphilis (VDRL/RPR or TPHA)
  • Malaria (in endemic areas)
  • NAT testing (where available)

Quality Control in Blood Banking

  • Reagent antisera: Test with known positive and negative cells daily
  • AHG reagent: Add IgG-coated check cells if negative test
  • Temperature monitoring: Refrigerators, freezers, platelet incubators
  • Centrifuge calibration: Timer, speed verification
  • Component QC: Hematocrit, platelet count, factor assays
  • Sterility testing: Culture of components
  • Proficiency testing: External quality assessment

Key Takeaways

  • ABO: Most important blood group system for transfusion safety
  • D antigen: Most immunogenic Rh antigen after ABO
  • Kidd antibodies notorious for delayed HTR (disappearing antibody)
  • Major crossmatch: Patient serum + donor cells (most important)
  • AHTR: Usually due to ABO incompatibility (clerical error)
  • RhIg prevents D sensitization in D-negative mothers
  • Platelets stored at room temp - highest bacterial contamination risk
  • DAT detects in-vivo sensitization; IAT detects serum antibodies