Distal Splenorenal Shunt for Management ofVariceal Bleeding in Patients with SchistosomalHepatic Fibrosis

FAROUK A. EZZAT, F.R.C.S. MOHAMED A. ALY, M.D. OSAMA 0. BAHGAT, M.D.KAREEM M. ABU-ELMAGD, M.B.B.CH. OMAR M. FATHY, M.D. ATEF A. SALAM, M.D.*IBRAHIM Y. ALY, M.D. MOHSIN H. EL-BARBARY, M.D. MICHAEL H. KUTNER, PH.D.t

The distal splenorenal shunt was performed in 60 patients withschistosomal hepatic fibrosis in whom no evidence of cirrhosiswas documented by preoperative needle and operative wedge bi-opsy. No patients have been lost to follow-up with a median of37 months (range: 17-86). The results showed low operativemortality (1.7%), high patency rate (92.5%), and low recurrentvariceal hemorrhage (6.7%). Thrombosed shunts were treatedeither by refashioning the shunt (1 patient) or splenectomy andgastric devascularization (2 patients). Initial hyperbilirubinemiaand reduction in serum albumin were found in the early post-operative period, with persistent hyperbilirubinemia in 32% ofthe patients. The 5-year survival was 88%, with liver diseaserelated mortality in only three patients. Clinical encephalopathywas detected in three patients (5.1%); only one of them was in-capacitated. These data showed that: (1) selective shunt (distalsplenorenal shunt, DSRS) is an effective surgical procedure inthe treatment of schistosomal variceal bleeding, (2) shuntthrombosis is rare and can possible be corrected if detected early,(3) schistosomal patients have a better survival and a lower in-cidence of encephalopathy after DSRS than that reported in cir-rhotics, and (4) liver biopsy should be performed for proper as-sessment of the schistosomal population especially in the geo-graphic areas where the schistosoma parasite and viral hepatitisare endemic.

B5 LEEDING ESOPHAGEAL VARICES as a complicationofportal hypertension is the most common causeof upper gastrointestinal hemorrhage in Egypt.'

It is the leading cause of death in patients with schisto-somal hepatic fibrosis and portal hypertension. Althoughthe initial bleeding episode may be fatal, patients usuallyhave multiple episodes extending over many years.2 Theeconomic impact of this disease is compounded by thefact that it affects individuals at the peak of their produc-tive life.3

From the Gastroenterology Unit, Department of Surgery,Mansoura University School of Medicine, Mansoura, Egypt

Hepatic schistosomiasis represents the prototype ofanintrahepatic presinusoidal block with normal architectureand cellular function.2'4 5 Therefore, any protection againstrecurrent variceal bleeding with maintained portal per-fusion, in such patients with good hepatic reserve couldonly improve long-term survival and quality of life.

Considerable controversy still exists regarding thechoice of a particular operative procedure for the treat-ment of portal hypertensive syndrome.6-" The presentknowledge of the hemodynamics of schistosomal portalhypertension is at best incomplete. As a result, the rec-ommendation for a surgical approach in the treatment ofthese patients has been used on personal bias or the un-proven assumption that their response to a given proce-dure is similar to those with alcoholic or posthepatiticliver disease.The objective ofthis work is to evaluate specifically the

clinical and hemodynamic responses ofschistosomal por-tal hypertensive patients to the selective distal splenorenalshunt (DSRS). Although the clinical outcome of selectiveshunt has been carefully analyzed in the cirrhotic popu-lation,'2"13 only a few scattered publications have focusedon this surgical procedure in the schistosomalpatients.'4-'7 Because data emanating from the countrieswhere schistosomiasis is endemic have suggested the co-existence of chronic active hepatitis and/or cirrhosis inpatients with hepatosplenic schistosomiasis,'8"20 our studydesign was based on accurate histological and serologicaldiagnosis of hepatic pathology.

* Professor of Surgery, Emory University School of Medicine.t Department of Biometry, Emory University School of Medicine.Supported by Peace Fellowship Program for Egypt.Reprint requests: Farouk A. Ezzat, F.R.C.S., Gastroenterology Unit,

Mansoura University Hospital, Mansoura, Egypt.Submitted for publication: March 18, 1986.

Materials and Methods

Patient Population

The study population was a consecutive series of 60patients with hepatosplenic schistosomiasis, portal hy-

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DSRS IN SCHISTOSOMAL PORTAL HYPERTENSION

pertension, and variceal bleeding, managed by distal sple-norenal shunt between February 1978 and July 1984.These patients were part of a larger total population of371 patients seen over the same time interval managed,as shown in Table 1. All patients included in this studyfulfilled the following criteria:

(1) History of at least one major episode of varicealbleeding. The minimal time interval between the last var-iceal hemorrhage and surgery was 4-6 weeks.

(2) Histological diagnosis of schistosomal hepatic fi-brosis by Tru-cutO needle and/or wedge biopsy with no

evidence of coexisting cirrhosis.(3) No symptoms or signs suggestive of encephalopa-

thy, schistosomal cor-pulmonale, and/or associatedchronic peptic ulcer.

There were 59 male and 1 female patients with a mean

(±SD) age of 36.5 ± 10 years (range: 19-62). Clinical andlaboratory assessment at presentation showed 49 Child'sclass A, 10 Child's B, and one Child's C.

Preoperative EvaluationAll patients included in the study were subjected to

stool and urine analysis, physical examination, hemato-logical studies, biochemical profile of liver and kidneyfunctions, endoscopy, intravenous pyelography, cardio-pulmonary assessment, neuropsychiatric examination,abdominal ultrasonography, and liver biopsy.

Stool and urine analyses were done for diagnosis andtreatment ofactive schistosomal infestation. Rectal biopsywas done in negative cases to exclude closed active lesions.The clinical, hematological, and biochemical exami-

nation focused on ascites, encephalopathy, platelet andwhite cell count, hematocrit, albumin, bilirubin, pro-

thrombin time, serum glutamic transaminases, and fastingplasma ammonia. In addition, renal function, fluid andelectrolyte status, and concomitant urinary or gastroin-testinal infection were assessed and managed before op-

eration.Endoscopic evaluation was done to document

esophagogastric varices and exclude any associated gastricor duodenal lesions such as chronic ulcer or malignancy.Endoscopy was done before and after DSRS under thesupervision of one endoscopist using a grading systemderived from the method of Conn and Brodoff2' as fol-lows: Grade 0-no or submucosal esophageal or gastricveins; Grade I-varices with a diameter less than 3 mm;Grade II-varices 3-5 mm in diameter; Grade III-var-ices with a diameter more than 5 mm.

Intravenous pyelography was done for every patientincluded in the study to verify the position of the leftkidney and to detect any obstructive lesions in the urinarytract. In those with obstruction, this was corrected priorto DSRS.The clinical examination of the cardiopulmonary sys-

tem included electrocardiography (ECG) and echocardi-

TABLE 1. Total Population Referred between February 1978and July 1984 with Variceal Bleeding by Disease Etiology

and Management Method

Schisto- Post-somal hepatitic* Mixed* Total

Selective shunt 60 54 36 150Splenectomy and

devascularization 15 20 15 50Total shunts 15 5 8 28Other surgical therapy

Splenectomy and coronaryvasoligation 105

Splenic artery and leftgastric ligation 15

Stappler esophageal trans-section 23

Total population 371

* Thirty per cent of these patients had chronic active hepatitis.

ography. These were mandatory in all patients to excludemoderate and severe degrees of schistosomal cor-pul-monale.The neuropsychiatric evaluation was done by the de-

partment of neurology and included neurological exam-ination and an electroencephalogram (EEG). ParsonSmith grading22 was used: grade C-mild; grade D-moderate; grade E-severe.Abdominal ultrasonography was done for the liver and

spleen to assess size and exclude any concomitant hepaticor splenic lesions such as lymphoma and malignancy.

Liver biopsy was done before operation by Tru-cutneedle in 90% of the patients.

Surgical Technique

The standard distal splenorenal shunt, as described byWarren et al.,7 was applied to all patients with interruptionof the collaterals connecting the gastrosplenic compart-ment to the portomesenteric axis. Operative time rangedfrom 4 to 5 hours. Blood loss was usually between 500-1000 ml. Temporary occlusion ofthe splenic artery duringsplenic vein dissection was helpful in minimizing bloodloss. Thickening of the splenic vein wall with degenerativeplaques was noticed in some patients but did not precludesatisfactory anastomosis. In most patients wedge biopsyfrom the liver was taken. Routine sump drainage for 12hours was done in the majority of the patients.

Longitudinal Follow-up

All patients had follow-up studies at 3, 6, and 12 monthsand every year thereafter. The median follow-up time was37 months (range: 17-86), with no patients being lost tofollow-up.

Postoperative studies included all the preoperativeclinical, biochemical, neurological, and medical assess-ments. Additionally, endoscopic evaluation was done at6 months, 1 year, and when clinically indicated. Liver

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FIG. 1. Patent shunt on a transsplenic portogram. Note the large tortuoussplenic vein with opacification of the inferior vena cava.

biopsy was repeated in patients with suspected chronicactive liver disease, especially in those with chronic hy-perbilirubinemia.

Assessment ofshunt patency. In 53 of the 60 patients,angiographic studies were done to assess patency of their

FIG. 2. Angiographic documentation of shunt patency on the venous

phase of splenic artery injection; rapid washout through the renal veinwith good visualization of the inferior vena cava.

shunt. The lack of sophisticated angiographic equipmentand technical support for routine visceral imaging earlyin the study dictated assessment of shunt patency for allpatients by:

(1) Visualization of the shunt with percutaneoustranssplenic portography (Fig. 1). A 16-18 French cath-eter-trocar set was used with a fast manual injection of50-60 ml of contrast.

(2) Reduction in the size of the spleen, which wasmeasured by the distance of its palpable margin and lowerpole from the left costal margin.

(3) Reduction by one or more endoscopic grade in thesize ofthe esophageal and gastric varnces at 6-12 months.The same endoscopist supervised preoperative and post-operative assessment.

Transsplenic portography was performed 3-6 monthsafter surgery in 42 patients. In addition, earlier spleno-portography was done in six patients to rule out suspectedshunt occlusion. Since 1984, hepatic and visceral angiog-raphy were available using the percutaneous femoral ac-cess, and the venous phase of splenic artery injection wasused to confirm shunt patency in five patients (Fig. 2).

Definitions

Operative mortality was defined as death within 30 daysof surgery or the same hospitalization.

Rebleeding was defined as at least a 2-unit blood trans-fusion requirement and/or a drop of the hematocritbelow 30%.

Encephalopathy. In this study, clinical encephalopathywas defined as either acute or chronic mental confusionclearly related by the patient or a family member, or de-tection of disorientation by a neurologist who was un-aware of the surgical status of the patient. Confusion orcoma prior to death from hepatic failure was excluded.

Subclinical encephalopathy was the combination ofhyperammonemia and abnormal EEG.

Statistical Analysis

Survival was analyzed by the Kaplan-Meier method.23Changes in the biochemical data and variceal sizes wereanalyzed using paired t-test and Sign test, respectively.

Results

Survival

The survival curve for the whole population is shownin Figure 3. The operative mortality was 1.7%. The overallsurvival currently is 86%. The causes and time of deathin the five mortalities are given in Table 2. It is importantto note that only three patients died from liver disease

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DSRS IN SCHISTOSOMAL PORTAL HYPERTENSION

1 2 3 4Years

5 6 7 8

FIG. 3. Kaplan-Meier survival plot for schistosomal patients after DSRSwith cumulative survival of 86% and standard error of 2.9%. The mean(±SD) follow-up period for these patients was 41 ± 24 months. Thepatient who died in an automobile accident is considered as censoredobservation.

related complications, two of hepatic cell failure and thethird of variceal hemorrhage.

Shunt Patency

Shunt patency was documented angiographically in 49of the 53 patients studied; giving a thrombosis rate of7.5%. Ofthe seven patients who did not have postoperativeangiography, six had a benign clinical course with reduc-tion of variceal and splenic sizes, providing indirect evi-dence of shunt patency. The time scale to thrombosis inthe four patients with angiographic evidence of shunt oc-clusion and the clinical course of these patients are givenin Table 3. It is interesting to note that one ofthese patientsdeveloped a large splenoportal collateral (Fig. 4). Follow-ing a conservative medical treatment in this patient, therewere no further bleeding episodes until he died from anautomobile accident.

Endoscopic evaluation of 55 patients before and at 6-12 months after DSRS showed a significant (p < 0.001)reduction in the size of varices. These changes are sum-marized in Table 4.

Rebleeding

Variceal rebleeding occurred in four patients for an in-cidence of6.7%. Two had documented shunt thrombosis,

TABLE 2. Deaths Following DSRS, with Time Intervaland Cause ofDeath

Time until Death(mo) Cause

I Hepatic cell failure4 Hepatic cell failure18 Complication of transsplenic portography30 Automobile accident78 Variceal hemorrhage

569TABLE 3. Patients with Documented Shunt Thrombosis

at Angiography, with Time and Clinical Course

Size ofTime Rebleeding Varices Management

5 days ++ 2++ Refashioned shuntSplenectomy and

7 days - 3+++ devascularizationSplenectomy and

10 days + 3+++ devascularization6 months - 3+++ Conservative

one had refashioning of the anastomosis, and the otherhad splenectomy and gastric devascularization (Table 3).The third died at 78 months and the status of his shuntwas never known, while the fourth had patent shunt(1.7%). The variceal bleeding in the patient with patentshunt occurred on the seventh postoperative day, re-

sponded to simple measures and did not require furthersurgery. Nonvariceal upper gastrointestinal hemorrhageoccurred in another patient 8 days after surgery becauseof postoperative pancreatitis and gastric erosions.

Ascites

Five patients developed moderate ascites in the earlypostoperative period, which was resolved with salt restric-tion and diuretics at 3 months in four patients and at 12months in one patient.

Encephalopathy

Absence of encephalopathy before surgery was a cri-terion for patient selection. Three patients (5.1%) devel-

FIG. 4. Thrombosed shunt with large splenoportal collateral on trans-splenic portogram 6 months after DSRS..

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TABLE 4. Endoscopic Changes in Variceal Size in 55 PatientsEvaluated prior to and 6-12 Months after DSRS

PreoperativePostoperative Grade

No. ofGrade* Patients 0 I II III

I 2 2II 16 11 5III 37 15 20 2 -

* Grades defined in the text.

oped clinical encephalopathy at some time during the fol-low-up period. The onset of encephalopathy was asso-

ciated with impairment of hepatocyte function, as shownby elevated serum bilirubin and fasting ammonia levels(Table 5).

Restriction of dietary protein combined with lactuloseand neomycin therapy reduced the degree of clinical en-cephalopathy with improvement in the functional capac-ity. Only one patient was unable to return to his normaldaily productivity.

Subclinical encephalopathy was detected in three pa-tients with abnormal EEG and high fasting plasma am-

monia level. They had no limitation in their daily activity.

Biochemical Data

Serum albumin, bilirubin, and prothrombin time be-fore and 1 week after operation were analyzed in most ofthe patients. For long-term results, patients were dividedinto three subsets according to the length of their last fol-low-up.

Immediate postoperative changes showed significantreduction in albumin (p < 0.01) and increase in bilirubin(p < 0.001), with no significant change in prothrombintime (Table 6). At last evaluation time, the changes forpatients in each category are given in Table 7. While sta-tistical significance can be shown for increases in bilirubinand reduction in albumin at some time points, mainte-nance ofalbumin above the mean of 3.5 g/dl and bilirubinbelow 2.5 mg/dl suggests that these changes are not ofclinical significance.The most recent biochemical profile of all patients

showed chronic hyperbilirubinemia in 19 patients (32%),with a total serum bilirubin ranging from 2 to 5.3 mg/dl

TABLE 5. Patients with Clinical Encephalopathy

FastingClinical Onset Ammonia BilirubinDegree (mo) (,ug/dl) (mg/dl) EEG

Severe 6 140 4.3 CModerate 24 110 2.3Mild 6 130 3.2 B

Normal range of plasma ammonia in our laboratory is 5-83 ,g/dl.

Ann. Surg. * November 1986

TABLE 6. Seven to Ten Day Postoperative Changes in Serum Albumin,Bilirubin, and Prothrombin Time*

Preop Postop p Value

Albumin (N = 52) 4.0 ± 0.4 3.6 ± 0.6 <0.01Bilirubin (N = 50) 1.0 ± 0.4 1.3 ± 0.7 <0.001Prothrombin time(N =52) (+sec) 1.4 ± 1.0 1.3 ± 1.0 NS

* Normal values: albumin, 3-5.2 g/dl; bilirubin, 0.2-1.2 mg/dl.

and a mean of 3.0 ± 1 mg/dl. Their preoperative totalserum bilirubin was 1 ± 0.4 mg/dl. None ofthese patientsdeveloped viral hepatitis or cirrhosis after surgery, asshown by liver biopsies and/or serological studies for viralhepatitis.

Hemodynamic Studies

The preliminary results of the preoperative imagingstudies showed some of the angiographic features asso-ciated with hepatosplenic schistosomiasis. The hepaticwedge injection showed a homogenous parenchymogramwith nondistorted hepatic veins. The splenic artery injec-tion showed a large tortuous splenic artery and huge spleen(Fig. 5). Visualization of the portal system is variable,depending on contrast dilution. but the portal vein wasusually better seen on the venous phase of splenic arteryinjection than on the superior mesenteric artery injection.

In the five patients with angiographic studies 1 yearafter DSRS, portal perfusion was maintained in all pa-tients with minimal collateral formation (Fig. 6).

Discussion

A few reports are available in the English literaturedealing with selective shunt in the schistosomal popula-tion.'4-'7 Most of these studies consist of a small serieswith incomplete and short term follow-up. Also none ofthese reports has emphasized the importance of histolog-ical diagnosis of hepatic schistosomiasis. Therefore, thepossibility of coexistence of other entities of liver diseasesuch as cirrhosis and chronic active hepatitis cannot beexcluded in such studies.

This current study represents the largest consecutiveseries of patients, with histologically proven schistosomalhepatic fibrosis, treated with selective splenorenal shunt.It is also the first clinical trial to address long-term survivalafter DSRS in this patient population.Some technical aspects of the DSRS procedure in

schistosomal patients need to be addressed. The large sizeof the spleen and the congestion in the gastrosplenopan-creatic compartment, particularly during clamping ofthesplenic vein, carry the potential for significant blood loss.Routine temporary clamping of the splenic artery priorto dissection of the splenic vein has proved to be veryhelpful in minimizing blood loss. Splenic arterial clamping

DSRS IN SCHISTOSOMAL PORTAL HYPERTENSION 571TABLE 7. Late Postoperative Changes in Serum Albumin, Bilirubin, and Prothrombin Time

Albumin (g/dl) Bilirubin (mg/dl) Prothrombin Time (+sec)

Preop Postop Preop Postop Preop Postop

12-24 months(N= 17) 4.1±0.3 3.6±0.5t 1.2±0.4 2.3±1.3* 2.0±0.9 2.8± 1.2t36-48 months (N = 10) 4.3 ± 0.4 3.8 ± 0.3* 1.1 ±0.5 1.9 ± 1.3 1.1 ± 0.6 0.9 ± 0.660-84 months (N = 13) 3.7 ± 0.5 3.8 ± 0.4 0.6 ± 0.2 1.6 ± 0.8* 1.2 ± 1.5 1.5 ± 1.3

* p < 0.01 from preop. t p < 0.05 from preop.

also facilitates dissection of the partially collapsed largesplenic vein, especially during ligation and interruptionof the pancreatic tributaries. This dissection also provedto be less complicated in schistosomal patients as com-pared to alcoholics because of the soft pancreas and min-imal splenopancreatic adhesions. One other feature thatneeds to be emphasized is the excessive tortuosity of thesplenic vein in some ofthese cases. Special care is neededin aligning the transsected splenic vein with the renal veinbecause of the increased risk of kinking the former.Splenocaval anastomosis is another option in such cases,particularly if there is excessive separation between thesplenic and left renal vein. It is important to mention thatthickening or degenerative plaques of the wall of thesplenic vein in the hilar segnent are not contraindicationsfor selective shunt.The preoperative Child's A/B classes for most of the

patients with an operative mortality of 1.7% emphasizethe good surgical risk and improved liver reserve in schis-tosomal population. This is in agreement with the findingsreported by the Brazilian investigators.'4 The reportedoperative mortality from centers where only alcoholic or

posthepatitic patients are seen is considerably higher(range: 1-16%), with liver cell failure being the primarycause of death in these series.'3'24The high patency rate of selective shunt in the schis-

tosomal patients is well documented in this series (92.5%).The large size of the splenic vein, hence the size of theshunt, the high flow rate in the hyperdynamic spleniccompartment, and the fact that it is a vein-to-vein anas-tomosis explain this high patency rate. Shunt failure ismainly due to technical errors in these cases. Postoperativepancreatitis is another factor that may lead to shuntthrombosis, although schistosomal patients seem to beless prone to this complication than is the alcoholic pop-ulation.

Because ofthe hyperdynamic circulation in the spleniccompartment ofthe schistosomal patients, thrombosis ofa selective shunt is expected to create a higher degree ofvenous congestion than in cirrhotics. These patients arethen at a higher risk of developing variceal hemorrhagein the early postoperative period. In one instance in ourseries, the patient developed splenoportal collaterals thatseemed to protect him against this complication.

Because of this increased risk of rebleeding, early rec-ognition and correction of shunt failure are strongly rec-

FIG. 5. This splenic arteriogram shows large tortuous splenic artery andhuge schistosomal spleen.

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FIG. 6. Good portal perfusion on the venous phase of SMA in a schis-tosomal patient I year after DSRS.

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ommended to prevent death from exsanguination. If theshunt cannot be salvaged, the surgeon has a choice be-tween a total shunt or splenectomy with gastric devas-cularization. However, total shunt has two major disad-vantages in this situation. First, it might fail to immedi-ately decompress the splenic compartment; second, itexposes the patient to the risk of developing disablingencephalopathy. Our preference in these cases is to dosplenectomy and gastric devascularization. It is question-able whether sclerotherapy would give lasting protectionagainst variceal bleeding in these occluded patients. How-ever, in patients with a patent shunt, sclerotherapy is avaluable technique in the control ofvariceal bleeding untilthe shunt attains its maximal decompressive effect.Our results indicate that DSRS is highly effective in

protecting against a recurrence of variceal bleeding. Onlyfour patients had variceal rebleeding (6.7%), and one ofthese four had a patent shunt (1.7%). For reasons that arenot clear to us, the Brazilian investigators reported a higherincidence ofrebleeding after selective shunt in their schis-tosomal patients.'4 They cited an incidence of 16.6% butdid not elaborate on the causes of bleeding, nor did theyspecify the functional status ofthe shunt in those patients.

Ascites was a minimal problem during the postoperativeperiod and nonexistent at the end of the first year. TheBrazilian group has reported a 10% incidence of ascitesafter DSRS in their patient population.'4 This overall in-cidence of early postoperative ascites in the schistosomalpatients compared to the cirrhotic population (10-56%)'3may be related to good liver reserve and lower sinusoidalpressure in schistosomal hepatic fibrosis.4The significant drop in albumin and increase in bili-

rubin, in both the immediate postoperative period andalso at late follow-up, reflects some degree ofparenchymalinvolvement in schistosomal hepatic fibrosis26 that be-come accentuated after DSRS. This encroachment on thehepatic reserve may be explained by impairment in theperfusion ofhepatocytes due to sinusoidal obstruction byextensive hepatic fibrosis,27-30 and deposition of collagen

FIGS. 7A and B. Kaplan-Meier survival plot for pres-ent study (schistosomal)compared to Emory series(cirrhotics). Five-year sur-

n = 60 vival is 88% in schistosomalSchistosomal Hepatic Fibrosis patients (B), 70% in nonal-

coholics, and 40) in alco-a . a a a a ~~~~~~~~holicpatients (A).

1 2 3 4 5 6 7 8Years

in the perisinusoidal (Disse) spaces.3" In addition, thepiecemeal necrosis in the periportal areas and the periph-eral nodules formed in the hepatic parenchyma under-neath the liver capsule2 may also indicate some degree ofparenchymal damage in these patients.One ofthe important findings ofthis study is the initial

and chronic rise in total serum bilirubin (32%). The initialrise can be reduced by temporary clamping ofthe splenicartery, especially during interruption ofthe splenic outflowand shunt performance (unpublished data from our cen-ter).25 Chronic hyperbilirubinemia in these patients isusally associated with reasonable serum albumin andnormal prothrombin time. Similar observations have beenmade by other investigators.'4'25 Theoretically, this hy-perbilirubinemia may be attributed to a hemolytic mech-anism as well as reduced clearance by the liver. The in-creased hemolysis can be explained by the increased tur-bulent splenic blood flow in the splenic sinusoidal bedand across the splenorenal anastomosis. Also, impairedclearance possibly may be due to hepatocellular dysfunc-tion and/or diversion of the hemolytic pigments awayfrom the liver.'4 These assumptions need further hema-tological and hemodynamic investigations.The quality of life after shunt therapy is largely deter-

mined by the presence or absence ofencephalopathy. Withthe hemodynamic and metabolic advantages of selectiveshunt, clinical encephalopathy was detected in only 5.1%of our series. The reported higher incidence (13.3%) inthe same population by the Brazilian group'4 may reflectthe broad spectrum of this syndrome with the lack ofclear-cut criteria for its diagnosis and evaluation. The on-set ofencephalopathy in our patients was associated withevidence ofimpairment in the hepatocyte functions. Thelower incidence of postselective shunt encephalopathy inthe schistosomal patients as compared to that in cirrhotics,12% in the first 5 years and up to 27% at 10 years,'3'24emphasizes the importance of underlying liver disease asa factor in the development of this complication.The interrelationship between liver pathology and sur-

Vol. 204 * No.5 DSRS IN SCHISTOSOMAL PORTAL HYPERTENSION 573vival after selective shunt has been addressed by other in-vestigators.'2'32 Our study of schistosomal patients showeda 5-year survival rate of 88% as compared to 40% in al-coholic and 70% in nonalcoholic patients'2"3 (Fig. 7).Our results substantiate the superiority ofDSRS in the

management of variceal bleeding in the schistosomalpopulation. Postshunt encephalopathy is sharply reducedas compared to total shunt operations. 433 Also, the fa-vorable 5-year survival rate after the selective shunt ascompared to the total shunts underscores the importanceofpreservation ofportal perfusion. Compared to nonshuntoperations, DSRS is a far more effective procedure in pro-tecting the patients against recurrence of variceal hem-orrhage.

In view of these findings, removal ofthe spleen shouldbe avoided in the schistosomal patients. Variceal hem-orrhage in splenectomized patients can be managed bysclerotherapy, which may not be effective in many ofthesepatients.

ConclusionThis clinical trial proves that DSRS is effective in the

management of variceal hemorrhage in schistosomal pa-tients. The operative mortality ofthe procedure was 1.7%.Recurrent variceal hemorrhage occurred in only 6.7%.Five-year survival was 88%. Ofparticular importance wasthe reduced incidence ofclinical encephalopathy of 5. 1%.This low incidence ofpostshunt encephalopathy is ofgreatvalue in allowing these patients to maintain gainful em-ployment. Until the role of sclerotherapy as a definitivemethod oftreatment is fully investigated, we consider theselective shunt as the method of choice for the treatmentof variceal hemorrhage in the schistosomal patients.

AcknowledgmentsThe authors would like to thank the Emory liver team for their guidance

in formulating this worlk The appreciation is extended to the departmentof medical illustration for their technical assistance.

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