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of Harmalol'". 1992.

81, 579-584

A prospective study to determine the safety of omitting the


antiglobulin crossmatch from pretransfusion testing

NANCY M. HBDDLE, PAMELA O'HosK1i JOEL SINGER. JOHN A. MCBRIDE. MAHMOUD A. M. ALI AND
JOHN G. KELTON Dgnrtments of Pathology and laboratory Medicine, McMaster University Medical
Centre, Henderson Hospital, and St Joseph's Hospital. Hamilton, Ontario, and The Canadian Red Cross
Blood Transfusion Service, Hamilton Centre

Received 19 Septemtær 1991: accepted for publication 24 March 1992

Summary. Transfusion medicine laboratories routinely per• Over the 2•year interval of the study 9128 patients were
form a series of pretransfusion serological tests Including: entered. There were 8936 patients (97-9%) with a negative
ABO grouping. Rh t.yping. and investigation of the antibody screen and 26 •9% (2404 patients} were transfused
recipient's serum to detect antibodies against blcod group a total of 10899 red cell concentrates. The antiglobulin
antigens (antibody screen), As a final check. most crossmatch performed after the transfusion indicated that 1
laboratories also IHfonn a crossmatch in which the 68 red cell concentrates (l •
recipient's serum is incubated with the donor's red cells would have been incompat-
followed by the addition of an antiglobulin reagent ible if the antiglobulin crossmatch had been performed
pretransfusion. These 168 red cell concentrates were trans-
(antiglobulin crossmatch). The need for the antiglobulin
fusai to 119 patients during 130 transfusion episodes
crossmatch when the screen is negative has
(defined as all transfusions administer«} within 24 h). Of the
questioned becaue there are few
130 transfusion episodes,
antibodies that are detected by this test. Such antibodies
(103/130) were false
are usually directed against low incidence antigens that are positive laboratory resutts. There were 27 transfusion epi-
not expressed on the screening cells and in many cases the safes where the antiglobutin crossmatch on blCN'd
clinical importance of these antibMies is uncertain. For was positive due to an IgG antibody. Even though these
these reasons. we performed a prospective study in which transfused red cell concentrates were designated Incompat-
patients requiring red cell transfusion had a group and ible by the antiglobulin crossmatch. none of the patients
screen #tformed. the antibody screen was negative the receiving this blood had clinical or serological evidence of
antiglobu-tin crossmatch was omitted. Following the haemolysis We concluded that tbe antiglobulin phase of the
transfusion of the blood. the antiglobulin crossmatch was crossmatch can be omitted from pretransfusion tesäng
gerformed to took for any potential incompatibility. All without putting patients at risk.
patients were monitored both serologically and clinically.

The primary goal of the transfusion medicine service is to expressing most red cell phenotypes screen),
provide the patient with the safest and most Finally, the donor's
blood are
product. Safety invoives the screening of blcod donors to with the recipient's serum
minimlæ the risk of transmitting infections plus the Ikrfor- in a procedure called the crossmatch (AABB, 1987). The
mance of traditional crossmatch involves an incubation phase to allow
tests to ensure blood product compaä- antibody to bind to the cells followed by an antiglobulin test
bility. To ensure compatibility of the red cell concentrates, to detect the red cell bound IgG. The antiglobulin crossmatch
several steps are taken. First* the donor and the recipient has been included in the compatibility test to detect antl-
are matched for ABO and Rh type. Second. any red cen bodiæ directed against low frequency antigens. which could
alloantibodies in the recipient's serum are detected by be present on the donor rd cells. but absent from the red cells
incubating the patient's serum with selected screening cells used in the antibody wreen. The need for this test has been
challenged and there heve tken debates
supø)lting and
Corr—pondence: Nancy Heddle. Room 2N38. McMaster Unlvenity refuting Its necessity (Issitt. 1985; International Forum.
Medicel Centre, 1200 Main Street
Hamilton. Ontario. Canada 1982). Most evidence is based on the calculation of risk
LSN determined by retrospectively reviewing Iakoratory records

579
580 Nancy M. Heddle
to determine how frequently the antiglobulin cros.smatch pected if there was no laboratory evidence of haemolysis
is g)siäve when the ant:ibody screen Is negative on the pretransfusion sample but three or more of these
& Henry. tests were positive in addition to a P81tåve direct or Indirect
1977; Spivak. 1980; Minb et
antiglobulin test on any of the post•transfusion samples,
1982: Oberman et al 1978.
1982: Taswell etal. 1981 Winn et al. 1980), The weakness of Total bilirubin wes measured on pre- and post-transfusion
this approach relates to the samples ifthe direct or indirect antiglobulin test was
study design and the negative pretransfusion but positive on one or more of the
use of latN)ratory outcome measures. which may not post-transfusion specimens.
clinically relevant. Clinical emluation. The hospital charts of every
To try end address these issues, we #rformed a transfused paåent who had a negative antibody screen but
pros#ctive study in which we omitted the antiglobulin
crwsmetch from our routine transfusion practice. The a posiäve antiglobulin crossmatch were reviewed by two
results of the study demonstrated that the omission of the physicians who were not aware of the ræults of the
antiglobulin cross-match will result In a laboratory tests. Chacts were also reviewed from a
percentage of patients randomly selected control group of
recelving blocxl that is incompatible by panents who had a negative antibody
testing. However. screen pretransfusion and a negatlve antlglobu]n cross-
when we analysed the clinical outcome in these pat}ents. we
match. The charts were analysed to look for any adverse
were unable to and an adverse impact. We also found thet
In patients with a negative antibcO screen. false positive clinical reactions
reactions in the andglobulln crossmatch ere more common to the transfusion. Other
then true positive reactions. Based on these results. we favour clinlca.l endpoints included a prolonged hospital stay due to
the deletion of the andglobulin crossmatch from routine adverse effects attributable to the transfusion. and any
compatibility testing. addit50naI transfusions that resulted from a drop in heemo-
globin due to the shortened survival of the transfused blood,
The study wes approved by the Ethics Review
MATERIALS AND METHODS
Committee ror each hospital.
Study design. The study was a I-year prospective study
performai at two Hamilton hospitals. All in-patients end
out-patients receiving RESULTS
transfusions were eligible for the
A total of 9128 patients were eligible for the study. 192
study unles.s they were under 16 years ofage or had a
petlents
positive direct antigiobulln test. A histocy of previous had a positive antlbody wreen and were
pregnancies and past transfusions were documented for all excluded from entering the study. There were 8936 patlents
patients. Patient diagnosis was categorized es surgical. who had negative antibody screen and 2404
medical. obstetråcal, heemetological. or trauma on the besis of
ofthe primary clinical problem. th<e patients were trensfuwd. This cohort represented the
Comßlibillty testing. All patients had en ABO group. Rh axal point ot the study. Some pat:ients were transfused
type. a direct anäglobulin test and three cell antibody several units of blood consecutively and/or were u•ansfused
screen performed on their blood on multiple occasions: therefore. we defined a 'transfusion' as
The three cell antib«iy all red cell concentrates given to a patient within a 24 h
screen was rprforrned using a saline antiglobulin technique period. The number of red cell concentrates given in these
(6: I, serum:cells) with a 15-45 min incubation at 37 oc 'transfusion' periods ranged from I to 40 (median — 2). The
(Leigb, 1978}, Any patient with a positive antibody screen 2404 transfusd patients with a negative andb«iy screen
was managed by antibody identification, phenotyping of ta:elved a total of 10 899 units of red cells which were given
donor units, and the #tforrnance of the antiglobulin cross- in 4215 transfusions.
match to condrm compatlbiJity before blood was transfused. The demographlc data of the study pat:ients is shown In
ABO and Rh compaUble Table r. Males comprised 40' 2% of the study group, Approxi-
was mately 39% of petients had been previously ü•ansrused
for patlents whose when entered tnto this study and 59% of the females in the
antibody screen was negative. The blood was Issued after study had a history of previous pregnancy. The reciplents of
Eerforrning en immediate spin crossmatch (6: I serum : cells) the cell transfusions were as follows: medical patients.
to confirm surgical patients,
compatiblllty. Approximately 24-48 h after heematological patients.
the blood had obstetrical patients. 6•
transfused* an antiglobulin crossmatch
and patients with trauma.
All 10 899 units of blood transfused to the patients with a
was performed using the pretransfusion sample and a retained
negaäve antitxxly screen had the antiglobulin crossmatch
—ment from the transfused donor unit. Polyspecißc antiglobulin
perforuned (using the pretransfusion spclmen) following
reagent was used for all antiglobulin tests, transfusion of the blood. The anäglobulio crossmatch pto-
Monitoring for transfusion reacåons: serological monitoring. duced positive resulb for 168 red cell concentrates {I 5%). These
were obtained from all transfusd petients et ted cell concentrates involved 130 transfilskons (some patients
approximaately 24 h a.rud 96 h post-transfuslon to look for received two or more red cell concentrates within
laboratory evidence of haemolys[s. A direct and Indlrect 24 h), adnulnlstered to 119 patients. All of these positive
antiglobulin test (three cell antibody screen) was performed on crossmatch tests were repeated and attempts were made to
all post-transfuslon blood samples collected* [n addltlon. the idenåfy the an&dles causing the incompatlbillty. Fot 79 •
following tests were rrformed on all pre- and post-transfusion
samples: plasma haemoglobin, haptoglobin, haemopexin— ofthe
resulb (
beem complex, and metheemalbumln (AH & Vanderlinden,
the result was a false
1977). Intravascular haemolysis was sus-
Safety of Omitting the Antiglobulin Crossmatch 581
Table Demographic and clinical data on patients with a
Toble II. ot transfusions in which there was a
negative andglülin crogxnatch in
screen. v.dth a negative
No. Per cent and $#cl.ßcity or the —n
causing the »ltlvity.
966 40+2
Males 143859+8
Fenales 81 True poüve follow-up
P•öents wlth a history of prior transfusion* 853 59+3 Oinlcal slgnlflcance (n—Z7}
Female with hlst«y o' prevlous pregnancyt 1

Diagnosis 841
Poentlal for red æll
Surgical 30s 12•7
1
Haematologlcal 34
146 Anti-lk'
Trauma
Obsterics 44•8 1

Medical Anti.Fy*
And-wet
Anu-C1't 1
UnidenUH* 10
DAT donor 4

Total 19

Not known to cause cell Anti-Bß 7


Transfusion history unavaltable on 580 patientx by the antiglobulin crossmatch
t Pregnancy history unavailable on 397 female patients. were reviewed for laboratory evidence of haemolysis. In
the group of 27 transfusions that were consldered to have
a true posltlve antiglobulin crossmatch, the direct
antiglobulin tat on the post-transfusion sample was
positive. A false positive was denned as a test that was initially in only four
positive in the antiglobulin crosstnetch but was negative on
repeat testing performed in duplicate. There were 27 of the
1 30 transfusions in which the positive results or the anåglo-
bulin crossmatch were considered true positive. Eight of the
27 were caused by antibodies that do not cause red cell
destruction (anti-Bg and anti-H). Nineteen were caused by
IgG anåbodies that could potentially cause red cell destruc-
tion. In 10 of the 19 the anåbodles could not be identified of
an insuffcient volume of serum in the pretransfu-Sion
sarnple but were considered significant as they were
demonstrated to
KgG. In four transfusions the positive
antiglobulin crossmatch was caused by IgG sensitizing the
donor red cells (donor red cells had a posltive direct
antiglobulin test). Pive transfusions involved ant.ltx)dies
known to cause red cell destruction, These five
were not detected during the initial antibcxly screen for the
followlng reasons: two were antibodies to low incidence
antigens (Wr and C.I') not expressed on the screening cells:
two
were weakly reactive and not dete&d by the
antibody screen (antl-Pl end anti-Jk4). The and-Pl had
thermal activity at 370C. The antl-jki fai}ed to react with the
screening cells even though one of the screening cells was
homozygous for the Jka antigen. One antibody (anti-Fy*)
was missed due to a technical error (Table II). Therefore,
(95% CI
of transfusions glven to patlents with a
negauve antibody screen had a positive antiglobulin cross-
match. This can also be expressed as 1% OT patients
transfused or one in every 333 red cell concentrates trans-
fused (Table 110.

I&ratorg follow-up
The laboratory tests that were performed on the post-
transfusion samples from all 130 transfusions involving
blood that was
Anti.Bß+H 1

Toul 8

• AnUbody thermal activity at 376C.


t Antibodies to low Incidenæ antlgens.
* weN demonstrated to IgG but there was
insumcient erum to determine

Table III. Prquency of POGltve antiglobulin crossmntcb in patients


with a negative
xreen.

Percentage with a posidve


cross•natch (95% Cl)

Patse True All peitlvee


(t.rue/fat*)

Transfusion* 0-6{0.4-08)
Patients
Unfis of blcxxi
transfused

& negative reactlon when repeetsd in duplicate.


antibody was e

t B)itive reacton in which a 8ßdfic


or the reaction was
to
IgGr
A transfusion was as all
concenü*tæ given to a
patient during 24 b perid.

casö. Two or these cases were due to weak IgG


which the laboratory was unable to identify. The remaining
two casæ involved anti-Fy• and anti-Jk'. [n all four cases the
laboratory tests for haemolysis were normal, None of these
patients
additional transfusions due to a fatl in
haemoglobin that could
with immune mediated
cell destruction.
Laboratory tests for haemolysis were reviewed for the
103 transfusions involving the false xjsitjve antiglobulin
cross-matches. One patient developed a weakly B)sltive
direct antiglobulin test 3 d
Antl•K was detected in
582 Nancy M. Heddle et al

Table 'V. Summary of patients with a positive follow-up antiglobulin and control who had
laboratory evidence of haemolysis or clinical evidence of an adveræ e&ct pod-transfusion.

Laboratory test result

Result of the retroepctlve dlnicel evidence ot


Study antLgtobuI'n cr«smetch DAT' HSt diverse

100762 True positive (anti-F*)


20108) True positive (antl-Jk')
True positive (no Identißcatlon) No
201704 me positive (no Identißcatlon)
201089 True pmitive Yes (%brile reaction)
201 Palse positive No
Patse positive No
201740 False lx•sidve No
201004 Fale xxitive Yes (febrile tcacüon)
Negative (control group} Yes (febrile reaction)
Neptlve (control group) Yes (chills, hym)tenslon)

Note. the DAT and haemolytic screen were negative in alt patlents pretransfusion.
• [hect antiglobulin test.
t Haemolytic scræn (consideral pmit.ive I' thre or more of the rollowing wEe abnormal:
haptoglobin, plasma heenwglobin. metheemalbumln, haemorxin—haem).
DAT was posiüve 3 d pwt&ansfusi0D due to transfuioe
alloimmunintion (anti-K).

the post-transfusion sample but not detected prevent alloimmunization to the D antigen (Case, 1980).
pretransfusion. This patient bad no other laboratory or There also is agræment that paoeots with red
alloanå-
clinical evldence ot haemolysis. Two patients had negative Endies. detected by the antibody screen. should receive bloui
direct antlglobuLin test. laboratory evidence ot beemolysis. that Is phenotypically compatible (AABB. 1990). However,
but no clinical evidence of an adverse effect (Table es our study demonstrated. patients with
are a
Clinical follow-up small minority (2% of patients). less is known about the
The review of the hospital charts Identified four patients who overall imprtance of some of the other minor blood group
had clinical ev#dence of an adverse reaction to the red cell antigens æpecially race blood group antigens. Indeed.
n•ansfusions. Three of the four had signs and symptoms of a increasing evidenæ suggats that IgG medj8td
febrile transfusion reaction. Two of these three cell
were destruction alone produces little morbidity. Physicians can
in the group who had a vositive antiglobulin crosmatch: one intentionally induce a mild haemolytic state by adrninister-
ing anti-D to D Ix:jsitive individuals as a treatanent of immune
was a false
thromtncytopenia with minimal or no adverse effects (Bussel
and the other was due to anti-Bg. The
third panent was in the control group. The fourth patient 1991).
In addition to ABO grouping. Rh typing and performing
with
the antibody scren. most transfusion medicine laboratories
evldence ot a transfusion reaction was also in
Incubate the patient's semm with the donor red cells. wash
the control group and had chills and hypotension. No
to remove unbound IgG, then add the antiglobulin reagent
patient with a positive antiglobulin crosxnatch due to an
(antiglobulin "osmatch} (Wilson & &senstaedti 1989). This
IgG antibody that had the potential to cause increased red test should detect any rwtential reactivity with uncommon
cell de8truction had any morbidity. None of the pat.ients enågens
had an increaæd hospital stay or required additional blood by the donor red cells that would not have
trans-fusions that could be attributable to the transfusion of detæted using the screening cell. Rationale for omitång
which was reacäve by laboratory tßting. this test includs: the low probability of a
reaction
when the antibody screen is negative: the add«l expense: the
DISCUSSION potential of false positive reactions: and dnally. the uncer-
The principle of transfusion medicine is to provide the tainty about the biological relevance of many or theæ
patient with the safest and most neded antigen—antibody interactions. Indeed. given the fact that
product. In an ever- rnany of these antibodies are IgG and have li.rnlted ability to
Increasing attempt to provide safer blood products. laborator- activate complement, and given the addence that ome IgG
ies have antibodies fail to cause red cell destrucuon. the neceslty of
more and more serological tests. There is no doubt about the antiglobulln a•osmatch is uncertain.
the importance of ensuring ABO compaObIIIty ABO The intent ot the study
mismatch«l transfusions can produæ serious end In this
sometirnes fatal adverse affects (Treacy. 1980). Rh was to try
testing. especially in young women. also is imrortant to and resolve this imm)rtant Issue. We perforrned a .2•year
related to the
prospecåve study in which two general hospitals provided
retrospective studies (Boral & Henry, 1977: Minuet al. 1982:
blood following performance ot the ABO group. Rh type. populations.
screen and immediate spin crossmatch. The imme- prospctive design of our study or differences in patient
lin test perforrned on cells collected 24 and 96 h after the All of
diate spin crossmatch was performed to the patients plus the controls had a direct anäglobu-
ABO with a true
compatibility. Following transfusion of the blood, we per- transfusion. Positive results were seen in four of the patients
anäglobulin crossmatch including those
formed the traditional antiglobulin crossmatch to identify
caugd by anti-Fy•. and anti-lk*. and two unidentiHed IgG
those units that might have been deemed 'incompatlbler by
laboratory tests, yet were administered to patients. The
Impact of omitting the antiglobulin crossmatch was analysed
in three ways. First. we looked Tor serological evidence of e
transfusion reaction by
a direct and indirect
antiglobulin test on 24 and 96 h post-transfusion specimens.
we investigated

of haemolysis including the patients for laboratory evidence


plasma haetnoglobin, the measurement of bllirubin. free

haem. and haptoglobin. methaemalbumin. haemolkxin—


Third. the charts ot patients trans-
fused with 'incompatible'
and charts from a control
group were reviewed to I(X'k for any clinical evidence of a
r•ansfusion reaction or adverse effects resulting from the
transfusion.
Over the 2 years of the study, a total of 10899 red cell
c.oncentrates were transfused and 168 (1 • 9.5% CI
were 1
testing. the majority of these positive reactions (79

• 2%) were
in the antiglobulin phase. On
reagents gave negative results). This rate of false positive falsethespecificitypositives

of(repeatcurrenttestingantiglobulinwithtwo different anäglobulin concentratesreacäons(I•2%}wereis

serologicallynotunexpectedincompatible.indeedpredictableasdefindgivenbya

patient received more n one incompatible unitof blood


Wefound that 35of the 10 899 (0'3%)transfused red cell

represent 27 ü•ansfuslons where one or more incompatible


positive antiglobulin crossmatch. In some situations a
period. These transfusions repreE11t the focal
durlng a 24 h peHod; hence. these 35 red cell concentrates
of the
units of
Tor antigens that do not cause
were transfused to a patient within a 24 h
cell destruction {anti-Bg
study (Table 11). In eight transfusions.
results, but subsequently the donor red cell units were shown
were specific
involved red cell concentrates that were positive in the
and anti-H). Four transfusions gave positive crossmatch
determined trcause sumcient patient serum was not avall-
to be reactive in the direct antiglobulin test. Ten transfusions
Therefore. in our study one in every 100 patients with a
gaveantiglobulintruepositivecrossmatchreactionbut anintheibodyantiglobullnspecificity

crossmatchcouldnot. abThlse forlaborchatoryracteriskization of the srHficlty of the alloantibody.

negatlve antibody screenishigherwas transfusthanthetd reporta3withbloodby whlchother


p. 283. American
Taswell et al. 1981 Banks. Arllngton. Va.
This represents one in every 333 units or
This difference may transfused.
Safety of Omitting the Antiglobulin Crossmatch 58 This study wag supported by a grant from the Ontario
Ministry of Health and the Medical Research Council
antibcxlies, One additional patient gave a positive
result on the 96 h post-transfusion sample: however. of Canada.
subsequently this patient was shown to have a »itive
direct antiglobulin test due to alloimmunlzaåon REFERENCES
to the transfusion (anti-
K). AABB ( 1987) Stmu*uråsfor Blood Banks Transfusion Services. 2th
The next step was to look for laboratory evidence of edn. p. 27. American Asux:iation of Bknd Banks. Arlington, Va.
haemolysls in the patients who received blood with a AABB (1990) rechnlcal Manual. 10th
antlglobulin crossmatch using a series of tests which AsmciaNon of
detect haemoglobin release and breakdown products.
The haemoty-tic screen was considered positive if three
or more of the following chemical tests were abnorrnal;
haptoglobin, plasma haemoglobin. methaemalbumin
and haemopexin-haem complex. Only two of the
patients with a positive antiglobulin crossmatch gave
positive results in these tests. However, in both cass
the positive antiglobulin crossmatch was a false
positive result. None of the patients receiving blood on
which the antiglobulin cro*smat.ch was a true positive
had chemical evidence of haemolysis nor did they have
any clinical evidence of a transfusion reaction.
The most clinically relevant endpoint was evidence
of adverse effects. The cherts of all patients who
received blood that was g'sitive in the antiglobulin
crossmatch (true and false positives) were reviewed.
Four patients were considered to have transfusion
reacttons with three
febrile
reac-
tions and one characterized chills and hypotension. None
of
these reactions involved immune mediated
cell
destruc-
tion and none of these reactions
within the group
of
patients in whom an anäbody that can cause red cell
destruction was detected. Indeed the only reacöon that
(kcurred in a patient with a true positive
antiglobulin
crossmatch was a febrile reaction in a patient who had an
anti-Bg.
The results of our study demonstrate that the
antiglobulin phase of the crossmatch can be omitted
from pretransfusion testing provided the patient has a
negative antibcx!y screen. This omission will evotd
unnecessary work. because the majority (80%) of
positive crossmatch results in this group will
false
The risk associated with
omitting the antiglobulin cros.smatch will be that some
units of blood having a true
antiglobulin test (O' 3% or 1/3 33
units)
will
transfused. However, in our study the
transfusion of thee units did not produce morbidity or
cell
haemolysis
in the recipient. Our study did not address this Issue in
children nor can our results necessarily
extrapoiated to
the
paediatric population tEcause of
differences
in
reticuloendothelial cell functlon and the risk of
alloimmuni-
zatjon.

ACKNOWLEDGMENT
584 Nancy M. Heddle et al

Alir M.A.M. & Vandedinden. B. (1977) Diagnosis of Intravascular crossmatch following nonreactive anäbody detection test: tre-
haemolysls using starch gel elæu•ophoresis. SuMinavian Journal of quency and cause. Transfusbn. 22. 107-110.
Hunutoløgu. 191 343—346. (hetman. H.A., Barn—. B.A. &
L.I. & Hen.ry, J B. ( 1977) 'Ihe typ and eræn: B.A. (1978) The
safe alternative of
and supplement In •bbreviøäng the maior croumatch in urgent or massive &nns-
surgical fusion. Transfusion. 18,
rransfusfon. 1 7, 1 37-141.
163-168, Oberman. H*A.. Barn—. B.A. & Steiner. E.A. (1982) ROE of the
Bus*å. J.B.. Grulano. J.N„ Klmb«ly. R.P„ Pabwa. S„ in testing for serologic incompatibility. Transfwion.
L.M.
Splvak, M. ( 1980) The imwctance or
(1991) Intravenous anti-D treeünent of immune
teting. Pretrans-
roic purpure: anatys18 ot emcacy. toxwty and mechanism
fusion Testing for the 80" (d by M. Treacy). pp. 133-139.
71. 1884-1893.
American Asociaeon or Blood Banks. Washlngton.
Ceæ. J. (1980) Rh
Taswell. H.P„ Motuhmen. T.L & Smith* T.R. (1981) Evaluation of
grouping from 1940 to the preent day.
the uefulneæ ofthe compatibility tBt. (Abstract). Transfusion. 21
Pretransfusion resUngfor the 80's (d. by M. Treacy). pp. 3-29.
607.
AABB. Washington. D.C.
Treacy, M. (1980) ABO grouøng—a crucial
Intematlonat Forum ( 1982) Do you think that the crosmetch with
Pretransfu-
donor rd cells can be
Sion Test."' for the 80's
when Nie serum or a petia-rt has
by M. Treacy), pp. 1—12. American
for the preænce of zed cell
A•cåation ot Blood Ranks,
with a cell
D.C.
panel? Vox Smwlnis. 43, 151-168.
Wilson, S.M. & Asmstnedt, RS. (1989} Compatlbltity
Issitt. P.D. (1985) Appåfed Bloat Group Serology. 3rd
and
pp. 91-92.
current transfusion pracuce: readts of a reglonal hospital survey.
Montgomery Scient.lfle PubUcaUons, Plorma.
IÆißh, K. (1978} The Winn. LC.. Transfusion, 29, (Suppl.). 2 IS.
of an antlglobulln-based R„ E-I&lgh, E.B. & Grumet* F.C- (1980)
screening tet for u.e in e toutlne ecteen to replace the c«mmatch. (Absüact)r
ransfusion Transfusion. 20, 651.
Canadian Journal
Medical Technology. 41, 26—31.
Mine. P.D..
A.L. & Sullivan. M.P. (1982) Incompatible

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