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Vox Sang 1990;59:123-124 0042-9007/90/0592-0123 $2.7510

Post-Transfusion Thrombocytopenia: Its Duration in Splenic and

Asplenic Individuals
S. Hart, D . Bareford, N . Smith, A. MacWhannel, E. Lanchbury, B. Boughton
Departments of Haematology and Nuclear Medicine, Queen Elizabeth and Dudley Road Hospitals, Birmingham,

Previous work in our department showed that after blood transfusion, the platelet count often falls to levels which are
clinically significant. The probable site of platelet sequestration was identified as the spleen, and post-transfusion
thrombocytopenia was prevented by blood filters which remove microaggregate debris from the donor blood [l, 21. Since
the duration of the thrombocytopenia has not been investigated, the purpose of the present study was to establish the rate
of onset and duration of post-transfusion thrombocytopenia following packed red blood cell transfusions. In addition, the
effect of spleen size, patients' diagnosis and post-transfusion history were examined. These observations provide in-
teresting new data on the mechanisms involved in this phenomenon.

lkenty-eight patients were studied (chronic lymphocyt-
ic leukaemia: 5 , myeloma: 4, myelodysplastic syndrome: 4,
myelofibrosis: 4, haemophilia: 1, aplastic anaemia: 2, acute
lymphoblastic leukaemia: 1, and sickle cell disease: 7).
They were monitored before and after transfusion of 2 4
units of SAG-M packed red cells (Travenol Laboratories,
Thetford, UK). Transfusions were completed within 24 h
and 7 of the patients were studied again during a second
identical transfusion 4-6 weeks after the first. Platelet
counting was undertaken on a Coulter S -t4 immediately
prior to transfusion and 24,48, 72 and 96 h thereafter. All
patients received blood through a standard 170-pm clot
screen blood administration set (A 100, Avon Medical Ltd.,
Redditch, UK). Isotope spleen scans were performed using
'Tc tin colloid and a CGR Gammatone gamma camera in
the anterior and posterior positions. The images reflect
splenic macrophage activity. The patients were classified as
asplenic if there was no palpable spleen and no image on
spleen scan. Those spleens which imaged with 99Tc were
classified normal or enlarged according to the findings on
clinical examination. Changes in platelet counts were com-
pared with starting values using Student's t test. All values
are expresses as mean f 1SD.
Six of the 7 patients with sickle cell disease were shown
by spleen scan to be asplenic. One patient with sickle cell
diesease and 14 of the other patients had normal-sized
spleens. The 7 remaining patients had clinically enlarged
spleens. Figure 1 shows that the patients with normal or
enlarged spleens experienced a statistically significant de-
cline in platelet count from 161k 13 ( x 109/1) at time 0 to
151k 12 at 24h, 132 k 11at 48 h and 99 k 10 at 72h. By96h,
the platelet counts in most of the patients had returned to
pre-transfusion levels. There was no significant difference
between the patients with normal or enlarged spleens (data
not shown).
Figure 2 shows that the post-transfusion platelet counts
in 6 asplenic patients with sickle cell disease did not signif-
icantly decrease. In a further patient with sickle cell disease
and a normal spleen scan, the platelat count ( x 109/1)fell
from 445 to 355 at 24 h, and to 330 at 72 h.
Apart from the sickle cell disease patients, there was no
correlation between diagnosis and the degree of post-trans-
fusional thrombocytopenia. Three patients who were fe-
brile prior to transfusion or who became febrile during
blood transfusion did not show a greater reduction in plate-
let counts, and the number of previous blood transfusions
did not correlate with the post-transfusion platelet count
response.
In the patients with normal or enlarged spleens, tran-
fused with 2-4 units of unfiltered packed red cells, the
platelet counts fell by 38% over 72 h. This confirms and
extends previous works which showed that microaggre-
gates in donor blood can cause post-transfusion thrombocy-
topenia [l-31. In the present study, the mean fall in platelets
was only 6% at 24 h after transfusion, compared to 18 and
38% at 48 and 72 h, respectively. In addition, the sickle cell
124
Fig.1. Platelet counts before and after transfusion in 21 patients
with normal or enlarged spleens 0-96 h after blood transfusion (mean
f 1 SD). The asterisks indicate results which are statistically different
from the initial values (p<O.Ol).
patients who received similar numbers of transfused blood
units did not show any decline in their platelet counts.
These observations confirm that post-transfusion thrombo-
cytopenia is not a dilutional effect and suggest that patients
who are already thrombocytopenic and who receive unfil-
tered blood transfusions should be monitored for 3-4 days
after transfusion.
Adults with sickle cell disease show progressive splenic
atrophy [4]; spleen scans in our 7 sickle cell disease patients
confirmed this in 6 of them. None of the 6 asplenic patients
demonstrated a lower platelet count after transfusion,
whereas the one with normal spleen size responded in the
same way as the 21 other patients with normal or enlarged
spleens. It is interesting to note that splenomegaly did not
enhance the post-transfusional platelet response, but these
cases had spleens infiltrated with malignant lymphoid or
myeloid cells and it is likely that the residual macrophage-
phagocyte elements were not increased. The spleen was
shown previously to sequester platelets in patients exhib-
iting post-transfusion thrombocytopenia [2] and the pre-
sent study confirms that the spleen plays a highly significant
role. The other mechanisms underlying post-transfusion
thrombocytopenia remain unclear, but the lack of correla-
tion with the patients’ transfusion history or febrile trans-
fusion reactions would suggest that it does not involve pla-
telet alloimmunisation.
Hart/Bareford/Smith/MacWhannel/Lanchbury/Boughton
Fig.2. Platelet counts before and after transfusion in 6 asplenic
patients with sickle cell disease 0-96 h after blood transfusion (mean
f1SD). The asterisk indicates a result which is statistically different
from the initial value (p<O.Ol).
In conclusion, post-transfusion thrombocytopenia has a
longer time course than was first expected, and the spleen
does play an important role. Patients who are already
thrombocytopenic should therefore be monitored for 3-4
days after blood transfusions, or microaggregate filters
should be used to prevent the development of this poten-
tially serious phenomenon.
References
1 Lim S, Boughton BJ, Bareford D: Thrombocytopenia following
routine blood transfusion: Microaggregate blood filters prevent
worsening thrombocytopenia in patients with low platelets counts.
Vox Sang 1989;56:4&41.
2 Bareford D, Chandler ST, Hawker RJ, Jackson N, Smith M,
Boughton BJ: Splenic platelet sequestration following routine
blood transfusion is reduced by filtered/washed blood products. Br
J Haematol 1987;67:177-180.
3 Schifano J, Galligan B, Ernst P, Bernvil S: Deleterious effects of
transfused red cell products on platelet counts in thrombocytopenic
patients. Proc Am Ass Blood Banks 1988, S27.
4 Sargeant GR: Sickle Cell Disease. Oxford, Oxford University
Press, 1985, pp 109-117.
Dr. B. J. Boughton
Department of Haematology
Queen Elizabeth Hospital
Birmingham B15 2TH (UK)