Hiperspenisme 2
Hiperspenisme 2
Abstract
Objectives: To determine the occurrence of hypersplenism among patients with splenomegaly, to study its aetiology, and correlate
its severity with the degree of splenomegaly; and to study the response to splenectomy in patients with hypersplenism.
Design of study: A prospective study of adult patients of splenomegaly admitted over a period of ten months.
Setting: Medical wards of a large teaching hospital in South India.
Subjects: 100 adult patients.
Results: One hundred adult patients with splenomegaly were studied. Hypersplenism was observed in 28 patients. The causes of
hypersplenism in them were non-cirrhotic portal fibrosis (9, i.e., 32.2%), cirrhosis of liver (8, i.e., 28.6%), hyper-reactive malarial
splenomegaly (HMS) (7, i.e., 25%) and chronic hepatitis (2, i.e., 7.1%); and a small number of patients formed an idiopathic group
(2, i.e., 7.1%). Though the prevalence of hypersplenism increased with increasing spleen size (p < 0.0001), there was no significant
correlation between splenic size and severity of hypersplenism. Splenectomy, performed in sixteen such patients with
hypersplenism, besides resulting in improvement in cell count of all three haematopoietic cell lines, caused transient leucocytosis
and thrombocytosis in 16 (100%) and 5 (31.25%) patients respectively.
Conclusions: Hypersplenism may be observed in about one-fourth of patients with splenomegaly. Congestive splenomegaly due
to hepatic cause is likely to be the major cause in our setting. All definite cases of hypersplenism are likely to respond to splenectomy,
even with an overresponse in some instances.
Key words: Splenomegaly, Non-cirrhotic portal fibrosis, Hyperreactive malarial splenomegaly, Cirrhosis of liver.
Introduction
Unravelling the cause of splenomegaly in a given case is
often a difficult but fascinating experience. The incidence
and aetiology of splenomegaly is highly dependent on
the geographic locale.
The concept of hypersplenism among patients with
splenomegaly has been known since the eighteenth
century. The criteria to diagnose hypersplenism include
splenomegaly, a peripheral blood picture of anaemia,
neutropenia, and thrombocytopenia (either singly or in
combination), a cellular bone marrow, and significant
improvement in peripheral blood picture following
splenectomy1.
There are very few systematic and planned studies on
hypersplenism.
Findings on palpation
0.
1.
2.
3.
4.
5.
292
Result
There were 38 men and 62 women among 100 patients
of splenomegaly. The male to female ratio was 1:1.6. Of
these 100 patients, 31, 26, and 25 patients were in the
age groups of 20 - 29, 30 - 39, and 12 - 19 years
respectively.
Among 100 patients with splenomegaly, the spleen
size was Hacketts class 1, 2, 3, 4, and 5 in 17%, 31%,
28%, 15%, and 9% patients respectively. The aetiology
of splenomegaly in these patients were as shown in
Table I.
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October-December, 2005
Number of patients
(n = 100)
Malaria
22
11
Enteric fever
Cirrhosis of liver
Lymphoma
Acute leukemia
Idiopathic
Infective endocarditis
Heart failure
Haemolytic anemia
Prolymphocytic leukemia
Chronic hepatitis
Hypereosinophilic syndrome
Budd-Chiari syndrome
Table II: Malarial serology in patients with hyperreactive malarial splenomegaly (HMS) (n = 7).
Patient
Antibody titre
Before treatment
After treatment
Myelodysplastic syndrome
1.
1 : 128
1 : 64
2.
1 : 256
3.
1 : 256
1 : 64
4.
1 : 512
1 : 128
5.
1 : 128
1 : 64
6.
1 : 64
7.
1 : 128
1 : 64
Geometric
Mean titre
1 : 172
1 : 73.48
Hypersplenism
Hypersplenism was found in 28 of these patients of
splenomegaly. The causes of hypersplenism in these
patients were as follows:
1.
2.
3.
4.
5.
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293
Table III: Correlation of various degrees of splenomegaly with haematological parameters in patients with
hypersplenism (n = 28).
I
II
III
IV
(1)
(2)
(11)
(11)
(3)
4.200
3.500
8.045
5.955
3800
2100
2981
135000
52000
72090
(No. of patients)
Hb (gm/dl)
TLC (/mm3)
Platelet (/mm )
3
Correlation co-efficient
p value
6.167
+ 0.247
0.450
2663
2100
- 0.164
0.203
96727
50333
- 0.029
0.440
Effect of splenectomy
15
14
13
12
11
10
9
8
7
6
5
4
3
2
1
0
10.36
7.5
0.16
10.89
11.16
10.88
10.9
1.66
1.66
1.7
1.66
Day 3
Day 5
Day 7
Month 1
10.35
1.48
10.9
1.6
0.0
Pre-op
Day 1
Month 2
Month 3
Time
Fig. 1: Response of haemoglobin to splenectomy (n = 16).
294
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October-December, 2005
200
168
114
150
158
134
46
123
35
32
100
50
0
26
80
28
71
1.66
13
Pre-op
Day 1
Day 3
Day 5
Day 7
Month 1
Month 2
62
1.66
Month 3
Time
Fig. 2: Response of WBC (n = 16).
400
375
322
300
300
282
241
196
208
268
68
180
225
48
200
134
100
80
71
32
0
Pre-op
Day 1
Day 3
Day 5
Day 7
Month 1
Month 2
Month 3
Time
Fig. 3: Response of platelets to splenectomy (n = 16).
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295
Discussion
Hypersplenism was observed in 28 of 100 patients with
splenomegaly. Majority (60.7%) of them had splenomegaly
of congestive origin, i.e., due to NCPF and cirrhosis of liver.
Robert O Reilly also found liver disorder as a major cause of
hypersplenism (10 of 35 patients, i.e., 28.6 %) in their series6.
Improvement in all three cell lines occurred in all the 16
(100%) patients who underwent splenectomy in our series
and this was maintained in all of those who were followedup for three months. However, the results of previous
studies on effect of splenectomy, though good, have not
been so overwhelming. Duckett et al reported a positive
response to splenectomy in 88% of their 118 patients with
hypersplenism7 and Letoquart observed a positive
response in 94% of 47 patients8. Both the studies, however,
included many patients with haemoglobinopathies and
haematological malignancies like chronic myeloid
leukemia (CML) and chronic lymphatic leukemia (CLL), in
whom the diagnosis of hypersplenism itself could have
been difficult due to underlying disease.
All our 16 (100%) patients developed leucocytosis
following splenectomy and five patients (31.25%)
developed thrombocytosis. However, both leucocytosis
and thrombocytosis gradually subsided. Our observation
is similar to that of an earlier study by Hirsh et al on 49
splenectomised patients where no thrombotic
complication was observed in any of the patients despite
high platelet count, unless they had persistent anaemia9.
They postulated that anaemia stimulates thrombopoiesis,
and persistent anaemia resulted in various thrombotic
complications in five of their patients. Another study on
post-splenectomy thrombocytosis on 318 patients
revealed thrombocytosis in 75% of the patients after
splenectomy 10 . Nine patients only developed
thromboembolic complications, and four of them had
some underlying malignancy. Thus, it appears some
additional factor contributes to post-splenectomy
thrombotic complications.
Of late, alternatives to splenectomy have been suggested
for hypersplenism. These include splenic embolisation to
296
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