Efficacy of Platelet Transfusions in Immune Thrombocytopenia

JUSTINE M. CARR, M.D.

MARGOT S. KRUSKALL, M.D.
JAMES A. KAYE, M.D.*
STEPHEN H. ROBINSON, M.D.
Boston, Massachusetts

Records of 11 patients with immune thrombocytopenia (idiopathic and

quinidine-induced) were evaluated retrospectively for response to
platelet transfusion. Good post-transfusion platelet count increments
occurred on one or more occasions in seven of the 11 patients, with 13
of 31 platelet transfusions (42 percent) resulting in immediate posttransfusion increments of 20,000/mm3 or more. Next-day platelet
counts remalned elevated in association with five of these 13 transfusions. This study demonstrates that, contrary to common opinion,
platelet transfusia
can raise the platelet count in many patients with
immune thrombocytopenia, and therefore may be beneficial in actively
bleeding or high-risk patients with this disorder.
Conflicting recommendations have been made regarding the role of
platelet transfusion in the management of immune thrombocytopenia.
Because of accelerated platelet destruction in patients with idiopathic
thrombocytopenic purpura, many authors have concluded that platelet
transfusions are either useless [ 1,2] or should be reserved for lifethreatening hemorrhage [3-91. Some authors have warned that platelet
transfusions could further lower the platelet count [3, IO] or cause severe
febrile reactions [l I]. In contrast, a few have encouraged the use of
platelet transfusions in patients with so-called wet purpura (gingival
bleeding, epistaxis, guaiac-positive stools, hematuria, or menorrhagia)
[ 12,131. However, clinical studies to resolve the usefulness of platelet
transfusions in immune thrombocytopenia have not been reported, and
documentation of patient response has been limited to individual case
descriptions [ 14,151.
We noted that house officers in our hospital were administering
platelet transfusions to many patients admitted to the hospital with
immune thrombocytopenia. This report is a retrospective analysis of the
response to platelet transfusion by these patients.

From the Departments

of Medicine
and Pathology, Beth Israel
Hospital
and Harvard
Medical
School, and the Charles
A. Dana Research
Institute, Beth Israel Hospital,
Boston,
Massachusetts. Dr. Carr is the recipient
of American
Cancer Society
Physicians
Research
Training
Fellowship PRTF 7. Requests
for reprints
should be
addressed
to Dr. Justine
M. Carr, Beth Israel
Hospital,
330 Brookline
Avenue,
Boston,
Massachusetts
02215.
Manuscript
accepted
April 12,
1985.
* Current address:
Dana Farber Cancer
Institute,
Boston,
Massachusetts
02 115.

PAllENTS AND METHODS

Patient Population. Records of all patients with immune thrombocytopenia, either idiopathic or quinidine-induced, with platelet counts of less than
20,000/mm3, who were admitted to Beth Israel Hospital and received
platelet transfusions between January 1981 and July 1984 were reviewed.
The diagnosis of idiopathic thrombocytopenic purpura was made in six
patients with a history of recent-onset thrombocytopenia, absence of
splenomegaly, adequate megakaryocytes without other abnormalities on
bone marrow examination, and no evidence of disseminated intravascular
coagulation, sepsis, microangiopathic hemolytic anemia, post-transfusion
purpura, or recent use of marrow-suppressive drugs. Five of the six patients (Patients 1, and 3 to 6) had antiplatelet antibody studies performed;

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TABLE

TRANSFUSION

Clinical

Patient
1
2
3
4
5
8
Average
7
8
9
10
11

IN IMMUNE

Summary

Diagnosisof
Thrombocytopenia
Idiopathic
Idiopathic
Idiopathic
Idiopathic
Idiopathic
Idiopathic
Quinidine-induced
Quinidine-induced
Quinidine-induced
Quinidine-induced
Quinidine-induced

THROMBOCYTOPENIA-CARR

ET AL

of Patients

with immune

Age and Sex

Nadir Platelet
Count(per mm3)

82F
71F
27F
79M
43M
25M
55
88F
77F
74F
67F
70M

Thrombocytopenia

1,000
3,000
1,000
500
15,000
1,000
5,000
2,000
3,000
1,000
6,000

1,000

Bleeding*

Steroid
Therapy

Central nervous system hemorrhage?

Eljistaxis
Epistaxis
Eplstaxis
Central nervous system hemorrhagex
Epistaxis

i+
+
+
+
+

Upper gastrointestinal hemorrhage

Upper gastrointestinal hemorrhage
Epistaxis
None
Epistaxis

+
-

Average
75
2,600
* All patients also had petechiae and/or ecchymoses.
7 Subdural hematoma occurred after head trauma.
x Hemorrhage occurred in a previously undiagnosed brain stem subependymoma.

of Medicine

Volume

2.4

the immediate post-transfusion

recovery of platelets is approximately 70 percent, since 30 percent are sequestered

by the spleen [ 191.

RESULTS

Patient Population. Table I summarizes the clinical

data of the six patients with idiopathic thrombocytopenic
purpura and the five patients with quinidine purpura evaluated. Two patients in each group had serious hemorrhages during their period of thrombocytopenia, including
acute gastrointestinal bleeding requiring red cell transfusion (Patients 7 and 8) and hemorrhage into the central
nervous system (Patients 1 and 5). Six other patients had
epistaxis and petechiae; one (Patient 10) had petechiae
only.
Platelet Transfusions. All patients received a platelet
transfusion within seven hours of the admission platelet
count, and seven patients received transfusions on subsequent occasions during their hospitalization (Table I).
Platelet transfusions were given to these patients for a
variety of reasons, including frank bleeding, wet purpu;
ra, or, in some instances, as a diagnostic test, where it
was assumed that a good post-transfusion increment in
platelet count would be evidence against the diagnosis of
immune thrombocytopenia. Nineteen of the 31 platelet
transfusions were given to patients with idiopathic thrombocytopenic purpura, and 12 to patients with quinidineinduced thrombocytopenia. One or more post-transfusion
platelet counts were pet-formed after each transfusion.
Platelet transfusions were evaluated by calculating the
proportion of platelets found in the circulation after transfusion (the recovery), and the effect these platelets had on

103mm3/kg (females), and the number of platelets transJournal

afebrile, nonbleeding patient with a normal-sized spleen,

platelets transfused X 100 percent, where blood volume =

weight in kg X 72 X 103mm3/kg (males) or X 68 X

The American

or an estimate of 7.1 X lOi plateletd/unit

times the number
of units transfused for random-donor concentrates. In an

transfusion count per mm31 X blood volume)/number of

June 1986

4
3
5
1
5
1
3.2
6
2
1

fused was the precise bag count for singledonor products,

results of all tests were positive, as measured by the presence of immunoglobulin

and/or complement
on platelets
[ 16,171. The diagnosis of quinidine-induced
thrombocytopenia was made in five patients with a history of recent
quinidlne ingestion preceding
a sudden drop in platelet
count, no clinical or laboratory evidence for other causes of
acute thrombocytopenia,
and recovery of the platelet count
within 10 days of discontinuation
of the drug. Antiplatelet
antibodies were found in four of these five patients (Patients
8 to 11).
Platelet Transfusions.
Excluding transfusions given within 24 hours of a patients recovery from thrombocytopenia,
or during a septic episode in one patient, a total of 31
transfusions was evaluated. Patients received either random-donor, pooled platelet concentrates
(28 transfusions)
or singledonor
non-HLA-matched
platelets (three transfusions). Twenty-five of the 31 products were more than 24
hours old at the time of transfusion.
No febrile or other
transfusion reaction was reported.
Platelet Count increments
and Post-Transfusion
Platelet
Recoveries.
Absolute increments in platelet counts were
measured using the platelet count drawn one to five hours
after transfusion (the immediate count) and the platelet
count drawn 10 to 24 houis after transfusion (the next-day
count). Platelet counts were measured with a Coulter model
S-Plus for counts greater than 50,000/mm3, and with phase
microscopy for lower counts. In an afebrile, nonbleeding,
average-sized
adult patient with a normal-sized spleen, the
expected immediate count increment per unit of platelets
transfused is approximately
7,000/mm3 [ 181.
Post-transfusion
platelet recoveries were estimated using a formula that compares the number of platelets measurable after transfusion, using the immediate or next-day
count, with the number transfused, expressed as a percentage: Recovery = ([ post-transfirsion
count per mm3 - pre-

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Numberol
PlateletTransfusions

60

PLATELET

the patients platelet count (the increment). immediate

post-transfusion platelet increments and recoveries were
evaluable for 29 transfusions, the next-day values for 24
transfusions (Figure 1). For purposes of this analysis, a
platelet transfusion was considered successful (albeit
suboptimal) if it resulted in an increment of at least
20,000/mm3 in the platelet count or a recovery of at least
20 percent of the transfused platelets.
As shown in Figure 1, seven of the 11 patients in this
study (64 percent) received one or more successful platelet transfusions according to these criteria (four patients
with idiopathic thrombocytopenic purpura, three with
quinidine-induced thrombocytopenia). Thirteen of the 3 1
transfusions (42 percent) were associated with satisfactory immediate increments. Although platelet counts decreased rapidly thereafter, five of these 13 transfusions
(38 percent, or 16 percent of all transfusions) resulted in
persistently successful next-day increments, including
one to a patient with idiopathic thrombocytopenic purpura, and two to each of two patients with quinidine-induced
thrombocytopenia. With six transfusions, good post-transfusion increments were attained despite poor platelet
recoveries, due either to a large dose of platelets in some
transfusions (three 20-unit transfusions to Patient 7) or to
some patients small blood volumes (Patients 1 and 8). No
patient had a decrease in platelet count after platelet
transfusion. In two patients (Patients 7 and 8), successful platelet transfusions were temporally related to a
decrease or cessation of hemorrhage. In one other patient
(Patient 2), clinical improvement occurred despite a poor
post-transfusion platelet increment and recovery. In all
other patients, a clinical response either was not appreciated (Patients 1 and 5) or was not evaluable because
bleeding was minimal or absent.

TRANSFUSION

IN IMMUNE

THROMBOCYTOPENIA-CARR

ET AL

PATIENTS

Figure 1.

Post-transfusion
platelet increments (panel A)
and recoveries (panel s) using the immediate post-transfe
sion (one to five hours) platelet count (0) and the next day
( 10 to 24 hours) count (A). A single line connects counts
that refer to the same transfusion ( l -A).
Some transfu
sions were followed by only a single post-transfusion
count,
indicated by a symbol without a line. For purposes of anaiysis, an unavailable immediate post-transfusion
increment
and recovery after one transfusion to Patient 5 was as
sumed to be no lower than the next-day values, indicated by
-A.
Most transfusions consisted of 10 units of platelets.
Transfusions of other than 10 units are indicated by the
numbers in parentheses.
Points designating
successful
transfusions, as defined in the text, fall above the dashed
lines in each panel. ITP = idiopathic thrombocytopenic
purpura.

COMMENTS
The efficacy of platelet transfusion in immune thrombocytopenia is poorly documented in the literature. By chromium survival studies, both autologous and transfused platelets in idiopathic thrombocytopenic purpura have shottened survivals [20,21]. Several authors have stated,
without presenting clinical data, that little or no increase in
platelet count can be obtained in these settings [ 1,6,7,9],
although some note that hemostasis may be improved
after platelet transfusion [3,7-9,121. A few authors advocate prophylactic platelet transfusion in patients with wet
purpura due to idiopathic thrombocytopenic purpura or
quinidine-induced thrombocytopenia [ 12,131. However,
we could find only two case reports documenting satisfactory platelet count increments after transfusion in the
setting of immune thrombocytopenia, one in a patient with
idiopathic thrombocytopenic purpura [ 141 and the other in
a patient with quinidine-induced thrombocytopenia [ 151.
This study demonstrates that, contrary to what is often
taught, platelet transfusions increase the platelet count
immediately after transfusion in many patients with im-

mune thrombocytopenia, whether quinidine-induced or

idiopathic. In addition, in over one third of these successful transfusions, satisfactory platelet count elevations
are still observed the day after transfusion. The relative
success of transfusions in this retrospective study may
even have been underestimated. For example, platelet
counts may have been adversely affected by factors in
addition to immune destruction, including the age of the
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platelet product at the time of transfusion (25 of 31

platelet products were more than 24 hours old) [22],
active bleeding during the transfusion (four transfusions),
and fever at the start of the transfusion (two transfusions).
Alloimmunization to transfused platelets may also have
played a role, since some patients had been pregnant or
had received blood products in the past. In one instance
(Patient 7), the relative success of platelet transfusion
was in part due to the large dose of platelets given in
several transfusions (20 units), which allowed for higher
post-transfusion platelet count increments despite the
often poor platelet recoveries. In addition, steroid therapy
may have played a role in the good transfusion increments
(four of seven transfusions) seen in this patient with
quinidine-induced thrombocytopenia, and in all the patients with idiopathic thrombocytopenic purpura, but this
patient population is too small to allow a firm conclusion
to be drawn about this point.
Our findings point to the fallacy of using a response to
platelet transfusion as evidence against the diagnosis of
immune thrombocytopenia, since two thirds of our patients with this otherwise well-documented diagnosis had
successful post-transfusion increments at some point
in their courses. Further, an unsuccessful platelet transfusion on one occasion was not necessarily predictive of
subsequent responses to transfusion. The variable re
sponse to platelets may have been due to the effect of

steroids, a fall in drug levels in patients with quinidineinduced thrombocytopenia, or a problem specific to individual transfusion products.
Although transfusions of platelets can raise the platelet
count in many patients with immune thrombocytopenia,
this finding should not be interpreted as meaning that
platelets should be given routinely to these patients. Pro
phylactic platelet transfusions have decreased morbidity
in patients with thrombocytopenia due to conditions of
marrow failure such as leukemia [23]; however, platelet
counts of 20,000/mm3 or less in patients with immune
thrombocytopenia are associated with much shorter
bleeding times than in patients with marrow failure, contributing to a reduced risk of bleeding [24]. Most patients
with immune thrombocytopenia do not experience major
hemorrhage even though they do not receive platelet
support. In addition, platelet concentrates carry the same
risks as other blood components, including alloimmunization to both red cells and platelets and transmission of
infection. On the other hand, this study demonstrates a
rational basis for the use of platelet transfusions in patients with immune thrombocytopenia and life-threatening
hemorrhage. Whether platelet transfusion may be a useful
prophylactic therapy in patients with immune thrombocytopenia who are judged to be at high risk for bleeding
is a question that should be addressed by a prospective
study.

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