5/13/2015

Immunohematology
A Student Review

Scott C. Wise, MS, MT(ASCP)SBB
Associate Professor, Georgia Regents University
American Society for Clinical Laboratory Science – Georgia
2015 Annual Meeting 
May 16, 2015

Part I
Blood Group Systems

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Genetics

Inheritance Patterns:

Autosomal Codominant: (most)
Autosomal Dominant:  A/O, B/O
Recessive (silent/amorphic):  O/O, dd, 
Fy, Jk)
Suppressor:  In(Jk), In(Lu)

Zygosity:  homozygous or 
heterozygous? (e.g., Fy(a‐b+) or 
Fy(a+b+)

QC ‐ ?
Antibody Rule Outs ‐ ? Fig. 3‐2 Difference between phenotype and genotype. The 
difference between the genotype and phenotype is illustrated 
in this diagram of ABO system inheritance patterns.

Chemistry/Antigens (general structures)

Fig. 4‐1  Model of red cell membrane that carries blood group antigens from blood 
group systems and collections. The red cell antigens are molecules that form part 
of the red cell membrane's lipid bilayer or extend from the surface of the red cell.

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Chemistry/Antigens (precursor substances)

Fig. 4‐4: Type 1 and type 2 oligosaccharide chain structures. Gal, Galactose; GlcNAc, 
N‐acetylglucosamine; *, most type 2 chains are located on the red cells.

Chemistry/Antigens (Secretor Status)

Secretor Status:  SeSe, Sese, sese

• Depends upon inheritance of the Se gene  
• Influences presence of ABO/Lewis antigens in body secretions (e.g., saliva, 
mucus in digestive tract and respiratory cavities, tears, sweat); does not 
influence expression of antigens on red cell membrane
• 80% of population are secretors
• The determination of secretor status is important because secretor status 
is associated with a wide variety of diseases (like urinary tract infections, 
diabetes, digestive disorders) and in organ transplantation (renal 
vasculature antigen expression – graft rejection)

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Chemistry/Antigens (ABO)
Fig. 4‐5 Biochemical 
structures of the H, A, 
and B antigens. Gal, D‐
Galactose; GlcNAc, N‐
acetylglucosamine; Fuc, 
L‐fucose; GalNAc, N‐
acetylgalactosamine.

Genetics:  Expression of 
A and/or B on RBCs 
requires the presence 
of H; no H = ? 
phenotype

Chemistry/Antigens (H)

Fig. 4‐6 Variation of H‐antigen concentrations in ABO phenotypes. 
Group O red cells possess the most H antigens; group A1B red cells 
possess the fewest H antigens.

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Chemistry/Antigens (ABO Phenotyping)

TABLE 4‐6 ABO Phenotype Reactions

Chemistry/Antigens (ABO 
Discrepancies)

TABLE 4-9 Overviews of ABO Discrepancies

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Grouping

Forward Reverse

Chemistry/Antigens
(ABO Discrepancy 
Flowchart)
Missing/Weak Extra Mixed Field Missing/Weak Extra

Young
Cold
A/B Subgroup Acquired A/B O Transfusion Elderly
Autoantibody
Immunocompromised

Disease Bone Marrow Cold

B(A) Phenotype
(cancer) Transplant Alloantibody

Rouleaux Rouleaux

Anti-A1

Chemistry/Antigens (ABO Discrepancies – see attachment for 
possible causes/resolutions)
Discrepancy Anti‐A Anti‐B A1 cells B cells O Cells Autocontrol
1 0 0 0 0 0 0
2* 4+ 0 1+ 4+ 0 0
3 4+ 4+ 2+ 2+ 2+ 2+
4 4+ 4+ 1+ 0 0 0
5* 4+ 0 0 4+ 3+ 0
6 0 0 4+ 4+ 4+ 0
7 0 0 2+ 4+ 0 0
8 4+ 2+ 0 4+ 0 0
9 4+ 4+ 2+ 0 2+ 0
10 0 4+ 4+ 1+ 1+ 1+

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Chemistry/Antigens (Methodologies – Traditional Tube/Microwell 
Testing)
Fig. 2-5 Summary of ABO reagents. Fig. 9-4 Results and interpretation of an ABO/Rh
Blood banks are using monoclonal phenotype. In the hemagglutination test,
antibodies for ABO reagents in routine agglutination is a positive result, and no
testing. agglutination is a negative result.

Chemistry/Antigens (Methodologies – Solid Phase Red Cell 
Adherence Assay ‐ SPRCA)
Fig. 9-6 Reactions and interpretation of SPRCA.

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Chemistry/Antigens (Methodologies – Gel Test)
Fig. 9-14 ID-MTS Gel Test procedure for the detection of A, B, and D antigens.

A Subgroup Resolution

TABLE 4-3 Serologic Characteristics

of A3, Ax, and Ael Subgroups

Anti‐A1 Lectin (Dolichos biflorus)

Anti‐ H Lectin (Ulex Europeus)

Fig. 4‐8 Comparison of A1 and A2 red cells.

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Chemistry/Antigens(Lewis)

Fig. 6‐2  Formation of the Lewis antigens

Chemistry/Antigens (Rh Inheritance)

Fig. 5-1 Comparison of Rh genetic theories. Comparison of three Rh genetic theories that have influenced the
nomenclature of the Rh blood group system. Modern molecular techniques have established that the Rh blood
group system antigens are determined by two genetic loci.

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Chemistry/Antigens (RhoD inheritance)

Rh Inheritance:

Fig. 5‐4 Inheritance of the D antigen. Predicting the probability of 
D‐positive offspring from a D‐negative mother and a heterozygous 
(Dd) father. The d gene does not exist and is being used only for 
illustrative purposes. From this mating, it is shown that 50% of the 
children could be D‐positive.

Fig. 5‐5 D antigen concentration. The D antigen concentration 
varies with the antigens inherited at the RHCE gene. The D‐
deletion phenotype has the most D antigen sites. The C gene 
weakens the D antigen expression if inherited on the opposite 
chromosome. R2R2 cells show a higher D expression than R1R1 
cells. If anti‐D was reacted with R2R2 cells, they would typically 
demonstrate a stronger pattern of agglutination.

Chemistry/Antigens (Rh Phenotype & Conversions)

TABLE 5-2 Wiener Theory: Genes and Antigens TABLE 5-3 Converting Fisher-Race Terminology to
Wiener Terminology

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Chemistry/Antigens (Weak D)

TABLE 5-7 Weak D Summary Fig. 5-7 Weak D caused by Ce inherited in trans. D-
antigen expression is weaker when the D and Ce
genes are inherited on the opposite chromosome.

Chemistry/Antigens (Weak D Testing)

TABLE 5-6 Weak D Test: Interpretation with Control Results

Fig. 5‐6 Weak D test procedure

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Chemistry/Antigens (HLA – Antigens and Significance)
Fig. 1-16 Major histocompatibility complex (MHC). Transfusion:

Platelet refractoriness – ↓post 1 hour count;   
HLA matched or crossmatched platelets (50/50)

Transplantation:

Graft survival – depends on number of Class I     
& Class II mismatches; HPC ‐ GVHD

Diagnosis:

Disease markers – B27 (Ankylosing Spondylitis), 

Location: most nucleated cells (leukocytes), tissues, platelets, weak  DQ2 (Celiac disease) 
expression on red cells (Bga, Bgb, Bgc)

Sensitizing Events ‐ Pregnancy, Blood Transfusion, Prior Transplant

Chemistry/Antigens (HLA ‐ Testing)
Fig. 1-18 Lymphocytotoxicity test for
identification of HLA antigens. Complement
and a dye are used to determine whether
there is antigen-antibody recognition.
Complement-mediated cell membrane
damage occurs if the antigen and antibody
form a complex. The damaged membrane
becomes permeable to the dye, which enters
the cell, allowing a positive reaction to be
observed. Dye exclusion is a negative reaction.

Other:  Flow Cytometry, Luminex, DNA testing (SSO, SSP)

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Chemistry/Antigens (Platelets)
Testing:

Requires specialized testing (solid phase 
immunoassay) usually only available through 
reference laboratories

Condition Associations:

Platelet Refractoriness
Neonatal Alloimmune Thrombocytopenia (NAIT)
Posttransfusion Purpura (PTP)

Chemistry/Antigens (Other Blood Group Systems – see 
attachment)
• System
• Antigen frequency (high or low)
• Phase most likely to be detected at (class)
• Reactivity with enzyme treated cells
• Clinically significant – capable of causing hemolytic transfusion reactions and/or HDFN
• Disease associations (phenotypic):
Hemolytic anemias (Rhnull, McLeod phenotype)
McLeod Syndrome (Chronic Granulatomous Disease)
Malaria (Duffy)
Cold Hemagglutinin Disease (I, IH)
Paroxysmal Cold Hemoglobinuria (P – IgG biphasic hemolysin; Donath Landsteiner 
antibody test)

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Part II
Antibody Screening and Identification

Immunogenecity & Antigen Frequency

• Immunogenicity:
Definition? 
Factors?
What is the most immunogenic blood group antigen? 2nd?

• Antigen Frequency (%):
ABO (O = ? A = ? B = ? AB = ?)
Other (low?  high?)

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Immune System (B & T Cell Interactions)

Immune Response (Macrophages)

Fig. 1‐4  Antibody attaches to the Fc receptor on a macrophage to 
signal clearance. The variable portion of the immunoglobulin 
attaches to the antigen on the red cell, while the macrophage 
attaches to the Fc portion. The red cell is transported to the spleen 
and liver for clearance.

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Immune Response 
(Primary vs Secondary)

Fig. 1‐6 Primary and secondary 
immune responses. The initial 
exposure to an antigen elicits 
the formation of IgM, followed 
by IgG antibodies and memory 
B cells. The second response to 
the same antigen causes much 
greater production of IgG 
antibodies and less IgM 
antibody secretion.

Immunoglobulin Structure

TABLE 1-2 Comparison of IgM and IgG

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Immunoglobulin Structure

Complement
Serum proteins that assist with 
the clearance of antibody‐coated 
red cells.  Biologic functions 
include:

Opsonization – enhancing 
phagocytosis of antigens
Chemotaxis – attracting 
macrophages and neutrophils
Cell Lysis – rupturing membranes 
of foreign cells
Agglutination – clustering and 
binding of pathogens together 
(sticking)

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Agglutination Reactions ‐ Stages

TABLE 1-5 Factors Affecting Agglutination

Agglutination Reactions ‐ Potentiators

TABLE 2-14 Summary of Antibody Potentiators

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Direct and Indirect Antiglobulin Tests

TABLE 2‐10 Comparison of Direct Antiglobulin Test and Indirect 
Antiglobulin Test

Sources of Error in Antiglobulin Testing

TABLE 2-11 Common Sources of False-Positive

Error in Antiglobulin Testing

TABLE 2-12 Common Sources of False-Negative Error in

Antiglobulin Testing

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Applications of DAT and IAT

TABLE 2-8 Clinical Examples Causing a Positive

TABLE 2-9 Applications of Indirect
Direct Antiglobulin Test
Antiglobulin Test in the
Immunohematology Laboratory

Antibody Screening

• Methodology (Tube, Gel, Solid Phase)

Fig. 7-1 Screening cell antigram.

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Antibody Screening

Fig. 7-2 Screen interpretations. Tentative

interpretations that can be made after
testing of the antibody screen and direct
antiglobulin test. IS, Immediate-spin; 37° C,
37° C incubation; AHG, antihuman globulin;
CC, check cells; ✓, check cells agglutinate;
NT, not tested; Poly, polyspecific antiglobulin
reagent; C3, anticomplement reagent.

Antibody Identification

TABLE 7‐3 Guidelines for Interpretation of a Panel

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Antibody Identification

Antibody Identification

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Antibody Identification

Antibody identification

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Antibody Identification

Antibody Identification

Fig. 7-4 Mini-cold panel.

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Antibody Identification

Antibody Identification

Fig. 7-6 Principle of the elution technique.

*Never assume that the antibody in the serum is the same as the antibody coating the red cells.  

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Antibody Identification – Special Procedures/Reagents

Neutralization – good for Lewis (Lewis Substance); P1 antibodies (hydatid cyst fluid), anti‐

Sda (fresh urine) Ch and Rg (plasma).

Adsorptions:
Autologous – can only be performed if patient has not been recently transfused or 
unless cell separation procedure is performed.  If DAT is positive, antibody must be 
removed before procedure can be performed.  
Allogeneic – use R1R1, R2R2 and rr cells.  Must be careful during interpretation as 
clinically significant antibodies can be excluded.

Commercially available W.A.R.M and RESt kits are available.    

RBC Phenotyping – DAT must be negative.  If DAT is positive and patient has not been 
recently transfused, Chlorquin Diphosphate can be used to remove IgG from patient’s red 
cells.  Recent transfusion requires cell separation procedure to be performed prior to 
phenotyping.  

Antibody Identification – Special Procedures/Reagents

• 2‐ME (2‐Mercaptoethanol) and DTT (Dithiothreitol) – cleaves disulfide 

bonds of IgM antibody molecules.  Helps distinguish between IgM 
and IgG.
• AET (2‐aminoethylisothiouronium bromide) – creates red cells that 
lack Kell antigens
• ZZAP (DTT + papain) –used to remove immunoglobulins and 
complement from the surface of red blood cells, commonly when 
evaluating a potential autoantibody. ZZAP also deactivates a 
multitude of red cell antigens on the red cell surface. 

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Antibody Identification

Fig. 7-5 Prewarm technique.

Antibody Identification

Fig. 7‐3 Strategies for the weak antibody or one that does not fit a pattern. 

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Antibody Identification

Fig. 4-10 Saline replacement technique. Rouleaux

causing false-positive reactions can be
distinguished from agglutination through the use
of this simple technique.

Part III

Crossmatch and Special Tests

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Compatibility Testing

Fig. 8-1 Process of compatibility testing. The process begins at the Fig. 8-5 Recipient sample labeling.
recipient and ends with a safe transfusion into the recipient.

Compatibility Testing

Fig. 8-4 Comparison of immediate-spin, computer, and antiglobulin crossmatch

requirements. XM, Crossmatch.

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Compatibility Testing

TABLE 8-3 Unexpected Incompatibilities in Immediate-Spin Crossmatch

Compatibility Testing

Antibodies can be missed in compatibility testing if:

• The corresponding antigen is absent from screening cells
• The antibody is so weak that it detects only homozygous expressions 
of the antigen (dosage effect)
• The antibody is detectable only by a method not routinely employed 
(e.g., in the presence of a particular enhancement medium)
• Antibody history is unknown

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Compatibility Testing

TABLE 8-5 ABO Compatibility for Whole Blood, Red Blood Cells,
and Plasma Transfusions

Compatibility Testing - Incorrect ABO Grouping

Crossmatch:
Resolution:
IS 37oC AHG CC
• Check all tube labeling
against positive ID of donor Patient
and patient serum 4+
• Repeat ABO/Rh of patient +
and donor Donor
• Request new sample if cells
necessary

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Compatibility Testing - Rh Incompatibility

Crossmatch:
• will not be detected unless
IS 37oC AHG CC
prior sensitization has
occurred Patient
serum
+ 0 0 0 2+
Donor
cells

Compatibility Testing - Alloantibodies in patient

serum reacting with Donor RBC
IS 37oC AHG CC
• Check reaction(s) of screening cells
• Perform antibody panel I 0 0 2+ NT
• Phenotype patient* and donor units II 0 0 0 2+
III 0 0 0 2+
*if not transfused within last 3 months
AC 0 0 0 2+

Dr1 0 0 0 2+
Dr2 0 0 2+ NT

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Compatibility Testing - Autoantibodies in patient

serum reacting with Donor RBC
IS 37oC AHG CC
• Check reaction(s) of screening cells
• Check autocontrol I 0 0 2+ NT
• Perform antibody panel
II 0 0 2+ NT
• Adsorb out autoantibody
• Run same panel on adsorbed serum III 0 0 2+ NT
• If underlying alloantibodies, AC 0 0 2+ NT
phenotype donor units
• Remove IgG from patient cells
before phenotyping (if not recently Dr1 0 0 2+ NT
transfused) Dr2 0 0 2+ NT

Compatibility Testing – Antibodies to low incidence antigens

• Panel studies usually not helpful IS 37oC AHG CC

• Specific antiserum sometimes not I 0 0 0 2+

available
II 0 0 0 2+
• Easy to find compatible blood
III 0 0 0 2+
• May have to rely on reference lab
for ID AC 0 0 0 2+
Dr1 0 0 0 2+
Dr2 0 0 0 2+
Dr3 0 0 0 2+
Dr4 0 0 1+ 2+

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Compatibility Testing – Antibodies to high-incidence antigens

• Panel studies usually not able IS 37oC AHG CC

to resolve
I 0 0 2+
• Specific antiserum sometimes
not available II 0 0 2+
• Hard to find compatible blood III 0 0 2+
• May have to rely on reference AC 0 0 0 2+
lab for ID and to find
compatible blood Dr1 0 0 2+
Dr2 0 0 2+
Dr3 0 0 2+
Dr4 0 0 2+

Serological Steps to Resolution of Incompatibility

• Verify integrity of specimen (patient identification, labeling)

• Check patient history (diagnosis, medications)
• Perform antibody ID
• If panel results are inconclusive (or cannot rule out all
possibilities) must run selected cells, special techniques
(neutralizations, absorption, elution, enzymes, etc.)
• Type antibody-producer for corresponding antigen (if not
transfused within last 3 months)
• Screen for antigen negative (ABO/Rh) compatible units

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Part IV
Blood Donation, Transfusion Therapy
Transfusion Reactions, and Hemolytic 
Disease of Fetus and Newborn

Donor Selection

• Registration (positive identification)
• Educational Materials
• Screening (Health History Interview – see attachment)
• Physical Examination
• Informed consent 
• Self‐exclusion

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Donor Collection

• 0.7% aqueous scrub solution of iodophor compound to remove surface dirt and bacteria 
and begin germicidal action
• 10% povidone‐iodine is applied beginning at the intended venipuncture site and 
continuing outward in a concentric spiral. 
• The area is allowed to air dry for 30 seconds before being covered with sterile gauze
• For donors sensitive to these solutions, another method should be designated by the 
blood bank physician, such as chlorhexidine (ChloraPrep 2%) and 70% isopropyl alcohol
• ABBB standards require the use of collection containers that divert the first 10 to 20 mL 
of blood into a “diversion pouch” when platelet products are to be prepared from whole 
blood donation
• Primary bag used for blood collection, all attached satellite bags, sample tubes, and the 
donor registration form must be labeled with a unique identification number. 

Physical Examination

TABLE 12-6 Physical Examination Requirements

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Donor Deferrals (see attachments)

• Temporary
• Permanent 
• Indefinite

Donor Adverse Reactions

TABLE 12-7 Adverse Donor Reactions and Appropriate Treatment

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Special Donations

Directed/Desginated:

• A patient must give consent and have his/her 
physician submit a written request for the Red Cross to 
collect blood from the selected donors.
• No evidence that patients can select safer donors than 
Autologous :
a volunteer blood system provides.
• Doctor’s prescription • All donated blood products are tested with the same 
• No age limit tests for HIV and other infectious diseases, which 
• Lower hemoglobin (11.0 g/dL) further enhances the safety of the blood supply.
• Cannot donate within 72 hours of 
• Social pressure associated with directed donations 
surgery may compromise the reliability of the donor’s answers 
• Abbreviated testing per AABB standards to health‐history questions.

Donor Processing
FDA Regulations:

• Blood is classified as a drug under the Federal Food, Drug and Cosmetic Act and is 
therefore subject to strict regulatory requirements during the manufacturing 
process as well as subsequent handling by transfusion facilities including labeling.  
It may only be dispensed with a prescription from a physician.  
• Any equipment used in the manufacturing of blood products is also regulated 
under Medical Devices by the FDA (e.g., blood collection scales, apheresis 
machines, computer hardware/software).
• Any adverse reactions during donation or during subsequent transfusion must be 
reported to FDA (Biological Product Deviation Reporting)
• Fatalities attributable to blood component transfusion must be reported verbally 
to FDA within 24 hours and a written report filed within 7 days.  

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Donor Processing

AABB Standards
Testing:
ABO/Rh
Antibody Screening
Infectious Disease Testing
Component preparation:
Storage
Quality control

Donor Testing

TABLE 13‐1 Required Donor Blood Tests

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Storage of Blood Components

Fig. 14‐3 Storage lesion

Donor Labeling

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Transfusion Therapy ‐
Summary

Transfusion Therapy – Expected Increments with Component 
Transfusions
In a 70‐kg adult (per unit):
• Whole Blood and RBCs:  Hgb 1 g/dL, Hematocrit 3% 
• Random Donor Platelets:  5‐10K per unit
• Apheresis Platelets:  30‐60K per unit
• Fresh Frozen Plasma (FFP)* – coagulation factors 20% (3‐6 units)
• Cryoprecipitate (CRYO)*:  fibrinogen 5‐10 mg/dL

*FFP and CRYO should only be given in the event that there are no 
suitable coagulation factor concentrates that are available.

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Transfusion Therapy ‐ Neonatal

<4 months of age do not have to repeat compatibility testing if initial 
screen and DAT are negative

Fresh blood < 7 days
CMV seronegative 
Leukoreduced
Irradiated
Hgb S negative

Transfusion Therapy ‐ Emergency

• RBCs ‐ Group O (Rh positive or Rh negative selection may be sex 
dependent in some facilities)  
• Plasma – Group AB
• Uncrossmatched – no sample or not enough time to complete 
testing; donor blood must be conspicuously labeled and segments 
pulled for later compatibility testing (when sample received and 
testing completed) 

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Transfusion Therapy – Massive Transfusion

• Massive transfusion defined as the replacement of one or more blood 
volumes within a 24 hour period.  
• Adult EBV 5000 mL (about 10 units whole blood)
• Will also develop deficiencies of clotting factors and platelets so these 
will need to be replaced as well
• Switching blood types may be necessary to avoid depleting blood 
supply of a particular type (e.g. A+ to O+).  Care must be taken when 
switching back to original type.  Why?

Transfusion Therapy – Sickle Cell Patients

• Sickle cell patients tend to make antibodies more readily than do 
other patients.  This is due to the fact that Sickle Cell disease is a 
disease that occurs in the black population who share antigenic 
similarities.  The majority of the donor population is white with 
antigenic dissimilarities. This fact alone contributes to the increased 
immunogenicity of donor blood antigens in Sickle Cell patients.
• Sickle cell patients should be given blood that is ABO/Rh compatible 
and negative for C, E, and K antigens.  Blood must also be Hgb S 
negative.  

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Transfusion Therapy ‐ Summary

Adverse Complications of Transfusion ‐ Instructions

Fig. 10‐5 Instructions to medical staff when a transfusion reaction is suspected.

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Adverse Complications of Transfusion ‐ Workup

Fig. 10-6 Postreaction work-up. Initial investigation to TABLE 10-9 Additional Testing in a Transfusion
determine if a hemolytic transfusion reaction is Reaction Investigation
occurring.

Adverse Complications of 
Transfusion ‐ Summary

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Hemolytic Disease of Fetus and Newborn (HDFN)

Fig. 11-1 Metabolism of

bilirubin. A, Before delivery,
fetal bilirubin produced by the
breakdown of sensitized red
cells in the fetal spleen is safely
metabolized by the maternal
liver. B, After delivery, the
newborn's liver does not
produce glucuronyl transferase
and cannot convert bilirubin to
an excretable form. As a result,
it collects in tissues and causes
brain damage.

Fig. 11-2 Twofold serial dilutions of the serum

HDFN containing the antibody are prepared with saline as the
diluent. Saline is first added to tubes 1:2→1:256. Serum is
then added to tube 1 and 1:2. The serum is transferred
TABLE 11-2 Prenatal Testing: Tests to Identify from 1 to 1:2 and then to 1:4 continuing to the last
Women at Risk of Hemolytic Disease of the Fetus tube, changing pipette tips to prevent carryover. The red
and Newborn cell selected for testing is usually homozygous and
tested by the antiglobulin technique using anti-IgG. The
titer is reported as the reciprocal of the highest dilution
that gives a 1+ reaction.

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TABLE 11-3 Testing at Delivery (Postpartum Testing)

HDFN

HDFN

Fig. 11-5 Liley graph and Queenan

et al modification. A, Liley graph
for evaluating data from
spectrophotometric analysis of
amniotic fluid. The change in
optical density at 450 (∆OD 450)
and weeks of gestation are plotted
to estimate the severity of HDFN. A
reading of 0.206 at 35 weeks
correlates with severe HDFN, which
may necessitate immediate
delivery. B, Modification by
Queenan et al. of the Liley graph to
include four zones beginning at 14
weeks of gestation.

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TABLE 11-4 Decisions for Rh Immune Globulin Administration

HDFN ‐ RhIG

HDFN
Fig. 11-6 Rosette test for detection of fetomaternal Fig. 11-7 Acid elution test for determination of hemoglobin F.
hemorrhage. RhIG, Rh immune globulin; lpf, low power field. After staining, fetal red cells appear dark pink, and adult cells
appear as pale ghost cells. Fetal hemoglobin resists acid elution
and remains intact, whereas the adult cells lose the hemoglobin
and do not take up the stain.

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Fig. 11-8 Calculating the dosage of RhIG

HDFN

The End.

REVIEW BOC STUDY GUIDE QUESTIONS

Good Luck on the Certification Exam!
References (tables and figures):
Blaney, Kathy, Paula Howard. Basic & Applied Concepts of Blood Banking and Transfusion Practices, 3rd 
Edition. Mosby, 2013. 

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