Ebook Immunohematology and transfusion medicine - A case study approach: Part 1

(BQ) Part 1 book Immunohematology and transfusion medicine - A case study approach presents the following contents: Basic single antibody identification - how hard can it be, rhesus pieces, cold case, hide and seek, the transfusion reaction, what the kell,...

Immunohematology and Transfusion Medicine

Mark T Friedman • Kamille A West

Peyman Bizargity

Immunohematology and Transfusion Medicine

A Case Study Approach

The views expressed do not necessarily represent the views of the National Institutes of Health, the Department of Health and Human Services, or the U.S Federal Government.

ISBN 978-3-319-22341-4 ISBN 978-3-319-22342-1 (eBook)

DOI 10.1007/978-3-319-22342-1

Library of Congress Control Number: 2015945233

Springer Cham Heidelberg New York Dordrecht London

© Springer International Publishing Switzerland 2016

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Mark T Friedman

St Luke’s-Roosevelt Hospital and Beth

Israel Medical Centers

Department of Pathology, Blood Bank

and Transfusion Service

The Mount Sinai Health System

New York

New York

USA

Kamille A West

Department of Transfusion Medicine

National Institutes of Health Clinical Center

New York USA

Preface

Pre-transfusion testing, including ABO/Rh typing, identification of unexpected antibodies, and compatibility testing, is an important measure in the provision of blood that may be transfused to the patient in the safest possible manner This brief introduction is not intended to give the trainee a detailed instruction on solving immunohematology cases; rather, it is intended to give an overview on how to ap-proach the immunohematology problems (Chaps 1–28) of this workbook The au-thors of this workbook presume that the reader has had at least basic instruction in immunohematology before engaging in these cases

Although one may be tempted to jump right to the antibody panel after noting

a positive antibody screen in the presented cases, it is recommended to review the clinical history for important clues that may be helpful in solving the case For example, a history of prior transfusions suggests that the patient could have made clinically significant alloantibodies (i.e., warm-reactive IgG alloantibodies capable

of causing hemolytic transfusion reactions or hemolytic disease of the fetus or born) Alternatively, the use of phrases such as “routine clinic visit” may suggest that the patient is clinically stable despite significant anemia In these practice cases,

new-as in the real medical world, obtaining clinical history is an important step not to be overlooked, though in some of these cases (as sometimes occurring in actual prac-tice), scant history is provided

After reviewing the medical history, the next step is to interpret the ABO/Rh ing results In most cases, this will be straightforward, though one should be alert

typ-to any discrepancy in the forward and reverse typing results For example, noting a positive result with the A1 cell in the back type may be the result of anti-A1 antibody

in an individual of A2 blood type or the result of a cold allo- or autoantibody.Next, one should review the antibody screen It should be noted that in this work-book, we present a two-cell screen in either standard tube or gel (column aggluti-nation) methods Although typically, the antibody screen is interpreted simply as positive or negative, limited additional information can be gleaned by noting dif-ferences in reactions between the two cells (i.e., whether both cells or only one cell reacting) or differences in the testing phases (i.e., if tube method is used, differences

in reactions between 37 °C vs AHG phase) Additionally, the antigen profiles of

Preface vi

the antibody screen cells are listed in the beginning which may also provide useful information when ruling out antibodies

After review of the clinical history, ABO/Rh typing, and antibody screen, one is ready to move on to the antibody panels if performed in the case (see Fig 1) Al-though traditionally one is taught to interpret the antibody panels through a process

of crossing out antigens, it is prudent to first take a moment to get a “landscape” view of the panel reactions That is, one should look to see whether there are reac-tions at cold temperatures (i.e., 4 °C, RT, IS) or warm temperatures (37 °C, IgG), whether there are many cells that are positive (perhaps all cells are positive as in a panagglutinin reaction) or only few and whether the autocontrol is positive or nega-tive Such consideration may help to narrow the possible specificities of the present antibodies In that light, for example, if reactions are only evident at 4 °C in the panel, then warm-reactive antibodies (such as anti-D, -K, -Jka, etc.) can promptly

be excluded Finally, after this initial review, one should then move on to the thodical exclusion of antibody specificities This is traditionally taught as “crossing out” antigens in which the reactions are negative with attention toward dosage (i.e., homozygous vs heterozygous antigen expression) Figure 2 demonstrates crossing out with respect to negative reactions, dosage, and the patient’s RBC antigen phe-notype The effect of enzyme treatment (e.g., papain or ficin) may also be of value

me-as antibody reactivity to some antigens may be enhanced or destroyed Ultimately, after consideration of all of the clinical information and antibody identification test-ing, the identity of the antibody or antibodies may be determined so that the most compatible blood can be provided for the patient in case transfusion is necessary

In the end, these cases are not necessarily meant to be difficult (though they do become more challenging as one progresses through the workbook) but are selected based on principle to introduce the practical concepts of and methods used in im-munohematology antibody identification Once the learner has grasped these basic techniques, he/she can apply them to more interesting cases that may be presented

to them within the actual clinical practice of the transfusion service

Finally, Chaps 29–35 are designed to engage the learner in other aspects of transfusion medicine including use of massive transfusion, therapeutic apheresis, factor concentrates, and blood management

Preface viii

1 Basic Single Antibody Identification: How Hard Can It Be? 1

2 Rhesus Pieces 5

3 Cold Case 9

4 Child’s Play 13

5 I Can “See” Clearly Now 17

6 You Really “Oughta” Get This 21

7 What the Kell 27

8 EeeeeK!!! 33

9 Are You Kidding? 39

10 G-Force 45

11 Hide and Seek 51

12 The Transfusion Reaction 57

13 What’s This Junk? 63

14 Playing with Enzymes 67

15 The Platelet Transfusion 73

16 Differential Alloadsorption 79

ix

Contents x

17 Hey, How Did That Antibody Get There? 87

18 I Can’t Stop the Hemolysis! 91

19 Just Another Autoantibody 97

20 I Got You Baby 101

21 “You” Got that Right 105

22 The Case of Low Platelets 109

23 The Perils of Transfusing the Sickle Cell Patient 115

24 To KB or Not to KB, That is the Question 123

25 It May Do Harm 127

26 Fuggedaboutit 133

27 Bad Medicine 141

28 In the Clouds 147

29 Emergency! 153

30 Time to Change the Plasma 157

31 Do the Math! 161

32 Eight is Enough! 165

33 Cruising for a Bruising 167

34 Help, I Cannot Stop the Bleeding! 171

35 Saving Blood 175

Index 179

List of Abbreviations

ADAMTS13 A disintegrin and metalloproteinase with a thrombospondin type 1

motif, member 13

aHUS Atypical hemolytic uremic syndrome

CHF Congestive heart failure

CPDA Citrate–phosphate–dextrose–adenine

CPOE Computer physician order entry

C-section Cesarean section

DAT Direct antiglobulin test

DIC Disseminated intravascular coagulation

DTT Dithiothreitol

EDTA Ethylenediaminetetraacetic acid

ELISA Enzyme-linked immunosorbent assay

GERD Gastroesophageal reflux disease

GVHD Graft versus host disease

HDFN Hemolytic disease of the fetus/newborn

HTLA High titer/low avidity

IAT Indirect antiglobulin test

List of Abbreviations xii

MICU Medical intensive care unit

NHSN National Healthcare Safety Network

NOACS Novel anticoagulants

PBM Patient blood management

PCC Prothrombin complex concentrate

PEG Polyethylene glycol

PTP Posttransfusion purpura

RBC Red blood cell

RESt Rabbit erythrocyte stroma

RhIg Rh immune globulin

TTP Thrombotic thrombocytopenic purpura

vWF von Willebrand Factor

WAIHA Warm autoimmune hemolytic anemia

WBC White blood cell

List of Abbreviations xiii

Table of laboratory normal values

of red cell antibodies and in the clinical management of patient transfusions The questions accompanying each case are presented in an open-ended format rather than in the traditional single-best-answer multiple-choice format; though some may prefer the latter format for convenience, it is wise to remember that patients do not come with multiple choices Furthermore, the open-ended style should hopefully encourage learners to engage in further reading and discussion of the subject matter Over the years, many clinical pathology trainees have benefitted from the use of this type of workbook problem-solving learning, both in the preparation for their board certification exam as well as for their careers Finally, the authors are indebted to Oanh Nguyen and Olga Kruty for their technical review in the preparation of this workbook.

© Springer International Publishing Switzerland 2016

M T Friedman et al., Immunohematology and Transfusion Medicine,

DOI 10.1007/978-3-319-22342-1_1

Chapter 1

Basic Single Antibody Identification:

How Hard Can It Be?

Clinical History

A 52-year-old male with a history of hypertension, type 2 diabetes mellitus, and three-vessel coronary artery disease is admitted to the hospital for a coronary ar-tery bypass graft surgery An ethylenediaminetetraacetic acid (EDTA) anticoagulant sample is submitted to the blood bank for type and crossmatch of four red blood cell (RBC) units No transfusion history is given

ABO/Rh/Antibody Screen

ABO/Rh (tube method)

Reaction scale = 0 (no reaction) to 4+ (strong reaction)

RBC red blood cells, LISS low ionic strength solution, AHG antihuman globulin, CC check cells,

NT not tested, SC screen cell

1 Basic Single Antibody Identification: How Hard Can It Be? 2

Answers 3

Questions

1 What is the patient’s ABO/Rh blood type?

2 What antibodies did you identify?

3 Are the antibodies clinically significant? Why or why not?

4 How many RBC units would you need to screen in order to find four ible (i.e., negative for the corresponding antigen) units as requested? (Refer to the table of RBC antigen frequencies, using antigen frequencies listed under Caucasian population)

is group O since both anti-A and anti-B isoantibodies are detected in the plasma

of the patient Testing with reagent anti-D serum shows that the D antigen is present on the patient’s RBC; therefore, the patient is Rh D positive

2 What antibodies did you identify? Anti-E alloantibody is present; E antigen

(Rh3) is a part of the Rh blood group system Although the “rule of three” applies

in the identification of antibodies, for simplicity of working up the cases in this workbook, the learner will find that the rule cannot be consistently applied The “rule of three” states that at least three antigen-positive and three antigen-negative RBCs that react and do not react, respectively, are necessary to achieve

a statistically significant p value (or probability value) of 0.05 In this case,

however, only two of the panel cells are E antigen positive and so a third cell technically should be tested [1]

3 Are the antibodies clinically significant? Why or why not? Anti-E is a

clini-cally significant alloantibody since it is IgG, is warm temperature reactive (i.e.,

37 °C), and is capable of causing delayed hemolytic transfusion reactions as well

as hemolytic disease of the newborn In general, clinically significant antibodies are warm-reacting, immune IgG antibodies while cold-reacting IgM antibodies are not considered to be clinically significant Antibodies to the following blood group antigens are usually IgG: Duffy, Kell, Kidd, Rh, and Ss Antibodies to the following blood group antigens are usually IgM: Lewis, MN, and P1

4 How many RBC units would you need to screen in order to find four

com-patible (i.e., negative for the corresponding antigen) units as requested?

About 29 % of the Caucasian population carries E antigen (see table of RBC antigen frequencies) on their red cells; thus, 71 % are negative and the chances

of finding a compatible donor red cell unit for the patient with anti-E antibody are about seven out of ten units A total of 4 RBC units were requested for the

1 Basic Single Antibody Identification: How Hard Can It Be? 4

patient; thus, dividing 4 by 0.71 (i.e., 4/ 0.71), we find that 5.6 or, essentially, 6 RBC units need to be screened in order to find 4 E-antigen-negative, compatible RBC units for the patient

Reference

1 Blaney KD Antibody detection and identification In: Blaney KD, Howard PR, editors Basic and applied concepts of immunohematology 1st ed St Louis: Mosby, Inc; 2000 p 164.

Recommended Reading

1 Avent ND, Reid ME The Rh blood group system: a review Blood 2000;95:375–87.

2 Trudell KS Detection and identification of antibodies In: Harmening DM, editor Modern blood banking and transfusion practices 6th ed Philadelphia: F.A Davis; 2012 p 216–26.

3 Walker PS, Hamilton JR Identification of antibodies to red cell antigens In: Roback JD, Grossman BJ, Harris T, Hillyer CD, editors Technical manual 18th ed Bethesda: AABB;

© Springer International Publishing Switzerland 2016

M T Friedman et al., Immunohematology and Transfusion Medicine,

to the blood bank

ABO/Rh/Antibody Screen

ABO/Rh (tube method)

Reaction scale = 0 (no reaction) to 4+ (strong reaction)

RBC red blood cell, LISS low ionic strength solution, AHG antihuman globulin, CC check cell, NT

not tested, SC screen cell

2 Rhesus Pieces 6

Answers 7

Questions

1 What is the patient’s ABO/Rh blood type?

2 What antibodies did you identify?

3 Can the weaker reaction strength on cell #11 seen in the panel be explained?

4 What are the possible causes or sources of the antibodies in this patient?

5 What additional testing would you do in the blood bank to help you determine

the nature or source of the antibodies?

Answers

1 What is the patient’s ABO/Rh blood type? The patient is group A, Rh-negative

blood type Refer to Chap #1, question 1 answer for further information on ward and reverse ABO typing

for-2 What antibodies did you identify? Alloantibody against the D antigen (Rh1) is

present

3 Can the weaker reaction strength on cell #11 seen in the panel be explained?

Cell #11 is an R0r′ (Dce/Ce) red cell, meaning that the D antigen is in the trans

position (i.e., on the opposite allele) relative to the C antigen D antigen pression is weakened by the steric arrangement of the C antigen (known as the

ex-“Ceppellini” effect) [1] Thus, the panel shows weaker reactions with these cells from the anti-D antibody present in the patient’s serum It is best to use R2R2cells when testing for weak or low-titer anti-D antibodies In reality though, this effect is not commonly seen on panels but is illustrated here as a learning point See the table below for a review of the Rh haplotypes [2]

4 What are the possible causes or sources of the antibodies in this patient? We

are not given a transfusion history in this pregnant patient, but it is possible that she was transfused with D-positive blood products in the past, either mistakenly

or in the case of an emergency when sufficient Rh-negative blood was not able It is also possible that the patient developed anti-D antibodies as a result

avail-of fetal–maternal hemorrhage, either during current pregnancy or during prior pregnancies (including abortion or fetal loss) Given that the current pregnancy

is uncomplicated, the most likely explanation for the anti-D antibodies is passive administration of anti-D (i.e., Rh immune globulin, RhIg) RhIg (300 mcg dose)

is routinely given at 28 weeks of gestation to Rh-negative women who have not been previously sensitized [2]

2 Rhesus Pieces 8

5 What additional testing would you do in the blood bank to help you

deter-mine the nature or source of the antibodies? Besides careful history taking,

including all pregnancies, abortions, transfusions, and RhIg injections, the titer

of anti-D antibodies could be helpful in distinguishing anti-D from active munization (i.e., exposure to Rh-positive red blood cells, RBCs) versus passive immunization (i.e., Rh immune globulin) A low titer of anti-D (i.e., titer ≤ 4) would favor passively acquired anti-D versus higher titers of the antibody A room temperature indirect antiglobulin test (IAT) may also be of value since the presence of such reactions would indicate the presence of immunoglobulin M (IgM) anti-D (i.e., newly developing anti-D); IgM is not present in manufacturer RhIg preparations and thus would indicate active immunization In any case, a history of RhIg injection should always be elicited to confirm the suspicion of passively acquired anti-D [2]

im-References

1 Ceppellini R, Dunn LC, Turri M An interaction between alleles at the Rh locus in man which

2 Denomme GA, Westhoff CM The Rh system In: Roback JD, Grossman BJ, Harris T, Hillyer

CD, editors Technical manual 18th ed Bethesda: AABB; 2014 p 320.

© Springer International Publishing Switzerland 2016

M T Friedman et al., Immunohematology and Transfusion Medicine,

ABO/Rh/Antibody Screen

ABO/Rh (tube method)

Reaction scale = 0 (no reaction) to 4+ (strong reaction)

LISS low ionic strength solution, AHG anti-human globulin, CC check cells, NT not tested, RBC

red blood cell, SC screen cell

3 Cold Case 10

Recommended Reading 11

Questions

1 What is the patient’s ABO/Rh type?

2 What antibodies did you identify?

3 What antibodies cannot be ruled out?

4 Are the antibodies clinically significant? Why or why not?

5 Is there a risk of hemolytic disease of the fetus/newborn (HDFN)? Why or why not?

Answers

1 What is the patient’s ABO/Rh blood type? The patient is group A, Rh-positive

blood type Refer to Chap #1, question 1 answer for further information on ward and reverse ABO typing

for-2 What antibodies did you identify? Anti-Lea and anti-Leb (Lewis blood group) antibodies are both present

3 What antibodies cannot be ruled out? Anti-C and anti-Kpa cannot be ruled out, but are unlikely since these would react more strongly at warm temperatures

4 Are the antibodies clinically significant? Why or why not? Anti-Lea and

anti-Leb antibodies are not usually clinically significant since they are cold-reacting immunoglobulin M (IgM) antibodies (i.e., reactive at 4 °C or room temperature); they do not cause hemolytic transfusion reactions or hemolytic disease of the fetus/newborn However, warm-reacting IgG anti-Lea has been found on rare oc-casions It is not uncommon for some women who are normally Lea or Leb posi-tive to lose the Lewis antigen expression during pregnancy and develop anti-Le antibodies

5 Is there a risk of HDFN? Why or why not? The baby is not at risk for HDFN

because the Lewis antibodies are cold-reacting IgM; IgM is a pentameric ecule that is too big to cross the placenta unlike IgG which can breach the pla-cental barrier Also, Lewis antigens are not RBC antigens per se; rather, they are plasma antigens that are adsorbed to the RBC membrane but are not found on newborn RBCs until several months after birth

© Springer International Publishing Switzerland 2016

M T Friedman et al., Immunohematology and Transfusion Medicine,

pa-ABO/Rh/Antibody Screen

ABO/Rh (gel method)

Antibody screen (gel method)

Reaction scale = 0 (no reaction) to 4 + (strong reaction)

RBC red blood cell, SC screen cell

15 Recommended Reading

1 What antibodies did you identify?

2 Are the antibodies clinically significant? Why or why not?

3 How many red blood cell (RBC) units would you need to screen in order to find two compatible (i.e., negative for the corresponding antigen) units in case the patient needs blood transfusion? (Refer to the table of RBC antigen frequencies, using antigen frequencies listed under Caucasian population)

anti-is not clinically significant

3 How many RBC units would you need to screen in order to find two

com-patible (i.e., negative for the corresponding antigen) units in case the patient needs blood transfusion? (Refer to the table of RBC antigen frequencies)

Given that the frequency of Jka antigen is 77 % (Caucasian population cy), there is a 23 % chance of finding an RBC unit that is Jka antigen negative Thus, 2/0.23 = 8.69 or 9 units need to be screened in order to find 2 that are Jka

frequen-antigen negative Note that the cold autoantibody does not factor into this tion since it is not clinically significant Also note that although there is a high probability that the patient may not need blood for his knee surgery, given the ad-vanced surgical techniques used today to minimize blood loss, it is a good idea to prepare blood ahead of time for any patient who has an antibody problem since there is always the slightest chance of unexpected bleeding requiring transfusion

equa-Recommended Reading

1 Storry JR Other blood group systems and antigens In: Roback JD, Grossman BJ, Harris T, Hillyer CD, editors Technical manual 18th ed Bethesda: AABB; 2014, pp 351–2.

© Springer International Publishing Switzerland 2016

M T Friedman et al., Immunohematology and Transfusion Medicine,

DOI 10.1007/978-3-319-22342-1_5

Chapter 5

I Can “See” Clearly Now

Clinical History

A 16-year-old female with sickle cell disease now presents with aplastic crisis with

a hematocrit (Hct) of 17 % (the patient’s baseline Hct is 28 %) The patient has been transfused many times with the last red blood cell (RBC) transfusion occurring 1 month ago The patient has a known history of anti-E antibody A sample (ethylene-diaminetetraacetic acid, EDTA anticoagulant) is submitted to the blood bank for stat type and crossmatch of two RBC units

ABO/Rh/Antibody Screen

ABO/Rh (tube method)

Reaction scale = 0 (no reaction) to 4+ (strong reaction)

LISS low ionic strength solution, AHG antihuman globulin, CC check cells, NT not tested, RBC

red blood cells, SC screen cell

18 5 I Can “See” Clearly Now

Questions

1 What antibodies did you identify?

2 Are the antibodies clinically significant? Why or why not?

3 Can the weakly positive autocontrol and direct antiglobulin test (DAT) be plained? How does the Rh(c) antigen phenotype result help you?

ex-4 What antibodies would you expect to find in the eluate?

Answers

1 What antibodies did you identify? The patient has developed anti-c antibodies

in addition to anti-E, which are both identifiable on the panel This scenario often develops, as patients who develop anti-E have almost certainly been exposed to

c antigen as well (e.g., R1 (DCe) patients transfused with R2 (DcE) blood) The converse is not true; however, patients with anti-c are not likely to have been exposed to E antigen [1]

2 Are the antibodies clinically significant? Why or why not? Most Rh

antibod-ies are clinically significant since they are warm-reacting (i.e., 37°C) globulin G (IgG) antibodies capable of causing a delayed hemolytic transfusion reaction or hemolytic disease of the fetus/newborn (HDFN) After alloimmuni-zation, antibodies may persist for many years The c antigen is more immuno-genic than the E antigen Anti-c may cause a severe HDFN; anti-E usually does not cause HDFN, and when it does, it is usually mild (though severe cases have been reported) [2]

immuno-3 Can the weakly positive autocontrol and DAT be explained? How does the

Rh(c) antigen phenotype result help you? It is likely that anti-c antibody is

causing the weakly positive autocontrol and DAT From the Rh(c) phenotype (i.e., antigen typing) result, it is evident that the patient has a mixed population (i.e., mixed field) of RBCs in circulation due to the recent transfusion (1 month ago), and that the RBCs from at least one of the donor units is positive for c antigen to which the patient has newly developed alloantibodies In addition, phenotyping of the donor RBCs from tubing segments, if available (donor tubing segments are saved for a week or more after transfusion in the case of reaction), could be done to confirm c antigen-positive donor RBCs as the cause of the posi-tive autocontrol in this patient

4 What antibodies would you expect in the eluate? Anti-c antibodies are

expect-ed since they would be bound to the transfusexpect-ed c-antigen-positive donor RBCs

in the patient’s circulation Anti-E should not be bound to the patient’s RBCs since the patient should have been receiving E-antigen-negative RBCs based on the history of anti-E and, hence, would not be eluted Elution techniques release and concentrate antibodies that are bound to red cells; the resulting eluate can

be tested against a panel to confirm the specificity of the antibody coating the RBCs

Answers

20 5 I Can “See” Clearly Now

2 Leger RM The positive direct antiglobulin test and immune-mediated hemolysis In: back JD, Grossman BJ, Harris T, Hillyer CD, editors Technical manual 18th ed Bethesda: AABB;2014:425.

© Springer International Publishing Switzerland 2016

M T Friedman et al., Immunohematology and Transfusion Medicine,

15 % The patient was referred to the emergency department by her primary care physician for stat RBC transfusion of two units A type and crossmatch sample (EDTA anticoagulant) is submitted to the blood bank

ABO/Rh/Antibody Screen

ABO/Rh (tube method)

Reaction scale = 0 (no reaction) to 4 + (strong reaction)

RBC red blood cells, LISS low ionic strength solution, AHG antihuman globulin, CC check cells,

NT not tested, SC screen cell

22 6 You Really “Oughta” Get This

5HDFWLRQVFDOH QRUHDFWLRQ WRVWURQJUHDFWLRQ  LISS low ionic strength solution,

23 ABO/Rh/Antibody Screen

24 6 You Really “Oughta” Get This

5HDFWLRQVFDOH QRUHDFWLRQ WRVWURQJUHDFWLRQ LISS

25 Answers

Questions

1 What antibodies did you identify?

2 What is the significance of the autocontrol and direct antiglobulin test (DAT) in this case?

3 What is the significance of the patient’s Rh(c) phenotype, eluate panel, and toadsorption panel results?

au-4 Write the patient’s Rh phenotype using the Rh–hr (Wiener) system:

5 How would you manage this patient’s RBC transfusion needs?

6 What is the mechanism by which IV RhIg improves ITP? What is the cance of IV RhIg treatment in this case, if any?

signifi-Answers

1 What antibodies did you identify? Warm autoanti-c antibody is present.

2 What is the significance of the autocontrol and DAT in this case? In the

absence of recent transfusion (i.e., transfusion within prior 3 months), a positive autocontrol and DAT signify the presence of an autoantibody It should be noted that a positive DAT alone does not signify hemolysis; rather, a workup for hemo-lysis must be performed, including tests for markers of hemolysis (e.g., bilirubin, lactate dehydrogenase (LDH), and haptoglobin) However, clinically significant hemolysis is more likely to occur when there is C3d coating of the RBCs in addi-tion to IgG (remember that the polyspecific DAT includes reactivity for both IgG and C3d) It should also be remembered that autoimmune hemolytic anemia can occur in the absence of a positive DAT, for example, when the level of bound IgG is below detection or when IgM or IgA antibodies are involved which are not detected by typical Coombs reagent

3 What is the significance of the patient’s Rh(c) phenotype, eluate panel, and

autoadsorption panel results? The panel results show that the warm

autoan-tibody has anti-c-like specificity The eluate and autoadsorption panels help to confirm the presence of an autoantibody and rule out alloantibody presence Elu-tion is a technique that removes and concentrates IgG antibody bound to RBCs, allowing for identification of the free antibody Autoadsorption, on the other hand, uses autologous RBCs to adsorb warm autoantibodies from plasma, allow-ing for identification of any present alloantibodies left behind A major limitation

of autoadsorption is that it should not be used in a recently transfused (i.e., within prior 3 months) patient as circulating donor RBCs may adsorb out alloantibodies

in addition to autoantibodies, thus leading to a false-negative result

4 Write the patient’s Rh phenotype using the Rh–hr (Wiener) system? Given

that the patient is positive for all five of the major Rh antigens (DCcEe), the most likely phenotype is R1R2 If you do not recall Rh nomenclature, this is a good time to review the Wiener and Fisher–Race Rh nomenclature See table in Chap

#2, question 3 answer

23 ABO/Rh/Antibody Screen