ORIGINAL ARTICLE
Splenectomy and ligation of the left gastric vein inschistosomiasis mansoni: the effect on esophageal varicealpressure measured by a non-invasive techniqueCláudio Moura Lacerda, Wilson Freire,1 Paulo Sérgio Vieira de Melo, Heloisa Ramos Lacerda1 andGustavo Carvalho
General Surgery Division, University Hospital Oswaldo Cruz (UHOC), University of Pernambuco (UPE)
1Internal Medicine, Federal University of Pernambuco-UFPE, Recife, Brazil(Received for publication on February 15, 2002)

Abstract. The treatment of choice, in the Northeast of Brazil, of patients with a history of upper GI
bleeding from ruptured esophageal varices (EV) and with hepatosplenomegaly secondary to schistosomiasis (HSS), is splenectomy and left gastric vein ligation (SLGL). However, the effect of this procedure on the EV pressure, the parameter that best correlates to re-bleeding risk, has not yet beenevaluated. With the introduction of a minimally invasive technique to measure the EV pressure, it has
become possible to assess the effect of this surgery without an increased risk to the patient. SLGL wasperformed in twenty two patients with a history of HSS and upper GI Bleeding secondary to esophageal varices. The non-invasive endoscopic pneumatic balloon was used to measure the EV pressure
before surgery and the results were then compared with measurements made between ﬁve and eightdays post-operatively. The pre-operative EV pressure ranged from 20.0 mmHg to 28.7 mmHg (mean24.35 B/C 2.36 mmHg), with no correlation between the pressure and the calibre of the varices. In thepost-operative period, a signiﬁcant decrease in EV pressure was observed, ranging from 14.6 mmHgto 21.5 mmHg (mean 17.29 B/C 1.75 mmHg, p H 0.001). These results support the use of SLGL inpatients with HSS and a history of variceal bleeding. The operation results in, at least for the short term
and in the majority of cases, a reduction in the EV pressure, and therefore a reduced risk of repeating
upper GI Bleeding. (Keio J Med 51 (2): 89–92, June 2002)
Key words: splenectomy, left gastric vein, schistosomiasis mansoni

renal-splenic anastamosis resulted in re-bleeding rates
similar to those observed in some patients that had undergone splenectomy with azygo-portal disconnection(SAPD), but with greater rates of encephalopathy
and late mortality.3 These results conﬁrmed the belief
that shunts are contra-indicated in schistosomiasis
patients.4,5
In 1991, we performed an angiographic and pressure
study of the effect of the splenectomy with esophageal
variceal ligation (SEVL) on the portal hemodynamics
of these patients.6,7 It was found that the intervention
caused a signiﬁcant reduction in the diameter of theIntroduction
Since 1992, both of the University Hospitals ofRecife, Brazil, have used splenectomy with left gastricvein ligation (SLGL) as the treatment of choice inpatients with schistosomiasis mansoni and a history ofesophageal variceal bleeding. This simple technique,which has a low morbidity and mortality, has a pathophysiological basis to its use.1 The use of portosystemic
shunts in patients with HSS was affected by the resultsof the prospective randomised trial conducted in 1989
by Raia et al.2 This study demonstrated that distal

Reprint request to: Dr. Gustavo Carvalho, Cirurgia Geral & Videolaparoscopia, Av Domingos Ferreira, 2766, Recife–PE–BRAZIL (PostalCode 51020-030), telephone 55(81) 3465-7866, email: gc@elogica.com.brThis article is based on a study ﬁrst reported in Cláudio Moura Lacerda, Wilson Freire, Paulo Sérgio Vieira de Melo, Heloisa Ramos Lacerda,
Gustavo Carvalho: Esplenectomia e ligadura da veia gástrica esquerda na esquistossomose mansônica: efeito sobre a pressão das varizes deesôfago aferida por técnica não-invasiva. [The role of splenectomy and ligature of the left gastric vein on the esophageal variceal pressure
measured by a non-invasive technique in mansonic shistosomotic patients.] Rev Col Bras Cir 1999; 26: 15–19 (in Portuguese)89

90

Lacerda CM, et al: Splenectomy and ligation of the left gastric veinportal vein, an increase in the diameter of the hepaticartery and a slight increase in mean sinusoidal pressure.
In addition, in some cases, post-operatively, a large partof the portal blood ﬂow was deviated via the left gastricvein into the azygos system. As a result, the liver became arterialised and the sinusoidal pressure increased
markedly, a process similar to a porto-caval anastamosiswith poor long-term prognosis. The same process wasobserved in patients undergoing SAPD, where the disconnection is performed tangentially to the stomach,because the branches of the left gastric vein that drain
into the azygos system were left intact. To avoid theseeffects, after removal of the spleen the origin of the left
gastric vein was ligated, without ligating the esophageal
varices. This procedure was replaced with endoscopic
sclerotherapy when deemed necessary.
However, a proper evaluation of the effect of splenectomy and ligation of the left gastric vein on EV pressure, the parameter that correlates best to re-bleedingrisk, was necessary. The introduction of the non-invasiveendoscopic balloon by Gertsch in 1993 has made thispossible.8 The objective of this study is to evaluate theeffect of SLGL on EV pressure in patients with schistosomiasis and a history of upper GI bleeding secondary to esophageal varices.
Patients and Methods
In a prospective study, 22 patients between the agesof 29 and 79 with a mean age of 51.45 years were evaluated. Thirteen patients were female and nine weremale. All patients had HSS and a history of ruptured
esophageal varices, without associated hepatic disease.
All patients were classiﬁed as A-class according toChild-Pugh’s score.
The endoscopic and manometric technique describedby Gertsch in 1993 was used.9 The inﬂatable transparent balloon was ﬁxed to the endoscope and lubricated.
Upon introduction into the stomach the balloon wasgently inﬂated and deﬂated several times. It was thenpulled back up into the distal esophagus, at which point
the variceal calibre was measured using the transverselines on the balloon, that were 5 mm apart, as reference
points. Then the balloon was progressively inﬂated untilthe varix began to collapse. The manoeuvre was repeated several times until the exact moment when thevarix began to collapse could be clearly detected, atwhich point the pressure from the interior of the balloon was transmitted to the manometer and registeredon the polygraph. The procedure was repeated 4 times,
obtaining 4 pressure curves, and an arithmetic mean ofthese values was then calculated for each case.
The 22 pre-operative endoscopic evaluations wereobtained in the week before the surgical intervention,and the post-operative evaluations were performed be-tween the 5th and the 8th day post-op. Two patients
did not undergo to post-operative endoscopy. The ﬁrst
refused, and the second had died on the 4th day due tohemorrhagic complications. The same endoscopist carried out all the evaluations. In the statistical analysis
comparing the pressure values before and after surgery,the paired student t-test was used.
A standard splenectomy was performed on all thepatients, followed by ligation of the left gastric vein at
its origin, close to the portal vein. Hepatic biopsy wastaken conﬁrming that only Symmers periportal ﬁbrosis
was present, in all cases.
Results
The 42 pre- and post-operative endoscopic andmanometric examinations were performed, as describedabove, without any complications. Other than the usual
discomfort that accompanies a regular endoscopy, thepatients had no additional complaints.
SLGL was carried out in accordance with the technique standardized in our Department. The spleen wasvoluminous, in the majority of cases, with an in vitro
weight ranging from 380 g to 1,750 g, with a mean of
877:64 þ= 374:17 g. The left gastric vein was easily
identiﬁed in all cases, with its calibre ranging from 6
to 18 mm, with a mean of 9.0 mm. The oldest patientin the group, 71 years old, was found to have chroniccholecystitis at operation. After performing SLGL, acholecystectomy was carried out. The surgery proved
to be very difﬁcult, with signiﬁcant blood loss as resultof adhesions, portal hypertension and coagulopathy.
The patient developed a hemoperitoneum and despite
re-operation, succumbed on the 4th post-operative day.
The remaining cases all responded well to the surgery
and were discharged from hospital between the 6th and10th post-operative days.
Table 1 shows a summary of the variceal diametermeasured in the pre- and post-operative period. In four
patients there was a reduction in variceal diameter compared with the pre-operative measurement. In the remaining patients there was no change in the size ofthe varices. Table 2 compares variceal pressures measured in the pre- and post-operative period. In the postoperative period, a signiﬁcant reduction in EV pressures
was found (p < 0:001, t ¼ 13:9). There was no correlation between the diameter of the varices and their pressures.
Discussion
Two problems limit the classical techniques in theevaluation of portal system pressure. First, there is noconsistent correlation between mesurements obtained
at mesenteric, splenic, portal or sinusoidal levels andKeio J Med 2002; 51 (2): 89–92

91

Table 1 Comparison of Esophageal Variceal Diameter Evaluatedbefore and after Splenectomy and Left Gastric Vein Ligation –According to Palmer’s Classiﬁcation

Table 2 Comparison of Esophageal Variceal Pressures Measured
before and after Splenectomy and Left Gastric Vein Ligation (mmHg)
Case

Case

Pre-Op

01
02
03
04
05
06
07
08
09
10
11
12
13
14
15
16
17
18
19
20
21
22

L
L
M
M
L
L
L
M
L
L
M
L
L
L
L
M
L
L
L
M
L
M

L
L
M
S
L
L
L
*M
L
S
L
L
L
L
*
L
L
L
M
L
S

S-small (d < 4 mm)
M-medium (4 mm–6 mm)
L-large (d > 6 mm)*-Not available

S-0
M-7
L-15

S-3
M-3
L-14
Diameter Reduction-4(20%)

EV pressure

Reduction

Pos-Opthe risk of variceal rupture. Second, the invasive character of these techniques conveys a signiﬁcant morbidity.
The concept that the absence of valves throughout
the portal system results in a uniform pressure in all of
its tributaries does not apply to esophageal varices,where resistance that is exerted by the gastroesophageal
wall affects variceal pressure. As this resistance increases so does the pressure gradient between theportal system and the varices, conveying a degree ofprotection from upper GI bleeding. It is the pressure
gradient, which varies according to individual anatomical and functional characteristics, that explains the lackof correlation between the portal pressure and risk ofupper GI bleeding. It also explains how certain drugs, byconstricting the distal esophageal sphincter, can reduce
variceal pressure and limit upper GI bleeding in cirrhotic patients.10–12
Studies that have evaluated EV pressure by different
methods have shown that it is a sensitive and reliable
parameter in predicting upper GI bleeding.9,13,14 Of
the different methods that have been evaluated, the inﬂatable balloon was superior in terms of cost, simplicity
and precision. As an additional advantage, the tech-

Pre-OpPos-OpAbsolute (mmHg)

Relative (%)

01
02
03
04
05
06
07
09
10
11
12
13
14
15
17
18
19
20
21
22

25.0
23.5
20.0
25.5
25.7
28.7
28.5
24.6
25.5
24.5
21.5
23.3
24.3
24.0
20.3
27.3
24.5
21.5
23.5
25.5

18.5
16.2
16.5
18.3
18.2
19.5
21.5
17.8
17.7
14.4
16.1
19.5
17.3
17.2
17.0
14.6
15.3
17.0
15.6
17.7

6.5
7.3
3.5
7.2
7.5
9.2
7.0
6.8
7.8
1.1
5.4
3.8
7.0
6.8
3.3
12.7
9.2
4.5
7.9
7.8

26.0
31.0
17.5
28.2
29.1
32.0
24.6
27.6
30.6
41.2
25.1
16.3
28.8
28.3
16.2
46.5
37.5
20.9
33.6
30.5

nMin
Max
X
SD

20
20.0
28.7
24.36
2.36

20
20
14.4
3.3
21.5
12.7
17.29
7.06
1.73
2.29
t ¼ 13.9 p < 0.001

20
16.2
46.5
28.57
7.72

Table 3 Comparison of Mean Pressures Obtained from DifferentAuthors, in Patients with Hepatic Cirrhosis, Compared with the Mean
Pressure Obtained from this Study in Carriers of Schistosomiasis
MansoniAuthor
Kleber et al. (13)
Rigau et al. (9)Gertsch et al. (8)Nevens et al. (14)Lacerda et al.

Disease

NXSD

cirrhosis
cirrhosis
cirrhosis
cirrhosis
Shistosomiasis

40
47
29
15
22

17.6
15.70
20.39
16.50
24.35

–
2.80
–
3.20
2.22

nique allows a more precise evaluation of the size of thevarices, using the transverse markings on the surface ofthe bolloon.
Table 3 shows a comparison of average EV pressures
measured in cirrhotic patients from several authors,with the EV pressures obtained from this study in schistosomiasis patients. These pressures are relatively low,suggesting that patients with HSS tolerate EV pressuresthat are high, which can be explained using the Law ofLaplace.
With the introduction of a minimally invasive tech-

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Lacerda CM, et al: Splenectomy and ligation of the left gastric veinnique to measure the EV pressure, it has become possible to assess the effect of this surgery without an increased risk to the patient EV wall tension. According
to the Law of Laplace, the tension in a vessel can be
expressed by the following formula:
T ¼ ðp1  p2Þ  r=t
Where p1 ¼ intra-variceal pressure, p2 ¼ external pressure, r ¼ radius and t ¼ thickness of the vessel wall.
In the case of esophageal varices, p2 corresponds tothe pressure exerted by the distal esophageal sphincter.
Given that patients with HSS have a better nutritional
state and consequently connective tissue state than thatof cirrhotic patients, it is fair to assume that the thickness of the esophageal varices would be greater, andthat the pressure of the distal sphincter would also
be greater in patients with HSS than cirrhotic patients.
As a result, despite high intra-variceal pressures, thetension remains relatively low and explains how thesepatients are able to tolerate the higher pressures.
In this study, four patients had a signiﬁcantly reduced
variceal diameter after SLGL, suggesting that diameter
reduction does not occur rapidly after surgery. Variceal
diameter is not, therefore, a sensitive indicator in theevaluation of therapeutic modalities that interfere withportal hemodynamics.
On the other hand, EV pressure was reduced in
all cases by, on average, 28.57% (from 24.36 mmHg
to 17.29 mmHg), a difference that was statistically signiﬁcant (p < 0:001). In addition, it was noticed, thatin 19 of the 20 cases studied in both the pre- and postoperative period, the EV pressure dropped to levels
lower than the lowest value registered in the preoperative period (20 mmHg), suggesting that the intervention is, in fact, effective in the control of upper GI
bleeding.
The EV pressure did not drop in any of the cases tolevels lower than 14 mmHg, a favourable result when
considering that an excessive drop in portal pressure,which would cause reduced portal blood ﬂow, is not
physiological. It can be asserted, with a certain degreeof conviction, that the ideal portal pressure in a patientwith established schistosomotic hepatosplenomegaly is
the highest possible pressure that does not cause upper
GI bleeding.
The results of this study support the idea behind thesplenectomy and left gastric vein ligation in patientswith HSS and a history of upper GI bleeding due toesophageal varices. The intervention resulted in, at leastin the short term and in the majority of cases, a reduction in the esophageal variceal pressure to levels com-patible with hepatic function preservation and low riskof upper GI bleeding relapse.
References
1. Lacerda CM, Ramos H, Raia S, Kelner S: Pathophysiology ofportal hypertension in shistosomiasis and effect of splenectomy
and ligature of esophageal varices. Acta Cirug Bras 1993; 8: 113–
117 (in Portuguese)
2. Raia S, Mies S, Alﬁeri Junior F: Portal hypertension in mansonicschistosomiasis. World J Surg 1991; 15: 176–187
3. Strauss E: Portal hypertension in schistosomiasis: analysis ofthe clinical eveolution endoscopic and laboratory data in a randomized trial comprising three types of operation. RibeirãoPreto, 1989. Thesis (Docõncia Livre) – Faculdade de Medicinade Ribeirão Preto da Universidade de São Paulo (in Portuguese)
4. Kelner S: Evaluation of splenectomy and intra-esophageal ligature of varices in mansonic schistosomiasis. Recife, 1965. Thesis(Cátedra de Cirurgia) – Faculdade de Medicina da Universidade
Federal de Pernambuco (in Portuguese)
5. Kelner S, Ferreira, PR, Dantas A, et al: Ligature of esophageal
varices in portal hypertension caused by schistosomiasis: a 25year follow-up. Rev Col Bras Cir 1982; 9: 140–146 (in Portuguese)
6. Lacerda CM: Angiographic and pressoric changes determined bysplenectomy and ligature of esophageal varices in mansonicschistosomiasis, São Paulo, 1991. Thesis (Doutoramento) Faculdade de Medicina da Universidade de São Paulo (in Portuguese)
7. Lacerda CM, RAMOS H: Angiographic features of schistosomotic portal hypertension. In: Esophageal varices of mansonicschistosomiasis. Kelner S, Silveira M. Recife. Editora Universitßria, 1997 (in Portuguese)
8. Gertsch P, Fischer G, Kleber G, Wheatley AM, Geigenberger G,Sauerbruch T: Manometry of esophageal varices: comparison ofan endoscopic balloon technique with needle puncture. Gastroenterology 1993; 105: 1159–1166
9. Rigau J, Bosch J, Bordas JM, Navasa M, Mastai R, Kravetz D,Bruix J, Feu F, Rodes J: Endoscopic measurement of varicealpressure in cirrhosis: correlation with portal pressure and variceal hemorrhage. Gastroenterology 1989; 96: 873–880
10. Saraya A, Sarin SK: Effects of intravenous nitroglycerin andmetoclopramide on intravariceal pressure: a double-blind,randomized study. Am J Gastroenterol 1993; 88: 1850–1853
11. Stanciu C, Cijevschi C, Stan M, Sandulescu E: Endoscopic intravascular esophageal pressure measurements in cirrhotic patients:response to metoclopramide. Hepatogastroenterology 1993; 40:
173–175
12. Gupta IP, Sharma MP: Control of variceal bleed by constricting
esophageal sphincter with metoclopramide. Am J Gastroenterol
1990; 85: 474
13. Kleber G, Sauerbruch T, Fischer G, Paumgartner G: Pressureof intraoesophageal varices assessed by ﬁne needle puncture:
its relation to endoscopic signs and severity of liver disease inpatients with cirrhosis. Gut 1989; 30: 228–232
14. Nevens F, Sprengers D, Feu F, Bosch J, Fevery J: Measurementof variceal pressure with an endoscopic pressure sensitive gauge:
validation and effect of propranolol therapy in chronic conditions. J Hepatol 1996; 24: 66–73