Selective Trans-Splenic Decompression of Gastroesophageal

Selective Trans-Splenic Decompression ofGastroesophageal Varices by Distal

Splenorenal Shunt

W. DEAN WARREN, M.D., ROBERT ZEPPA, M.D., JOHN J. FOMON, M.D.

From the Department of Surgery, University of Miami School of Medicine andJackson Memorial Hospital, Miami, Florida

LIFE-THREATENING hemorrhage is fre-quently an indication for surgical therapy.In patients with cirrhosis of the liver andesophageal varices, variceal bleeding is theleading cause of death and often contrib-utes to mortality from other sources, i.e.,hepatic failure.6 The efficiency of the porta-caval shunt in controlling hemorrhage hasbeen well documented.7 With proper selec-tion of patients, operative mortality can belowered to acceptable levels. In consider-ing the surgical treatment of bleeding dueto portal hypertension, several questionshave given cause for concern.

1. What are the long-term results ofportacaval shunts? Recent reports by Cal-low et al.,2 Conn and Lindenmuth,3 andJackson et al.12 have analyzed criticallythe results of shunt therapy in well-controlled, randomized studies. In spite ofa low operating mortality, survival figureshave not demonstrated the superiority ofthe surgical group (Fig. 1, 2). An analysisof the cause of death reveals substantialdifferences between the two modes of ther-apy (Fig. 3). The Boston and Hartfordseries were utilized in this study becausethe patient population is more representa-tive and the judgments more consistent

This work was partially supported by the U. S.Public Health Service, Grant No. HE 08411-04and NO.1 MO 1 FR00251 witb the Clinical Re-search Facility of the University of Miami Schoolof Medicine, Miami, Florida.

than in a large, national study. Followingportacaval shunt, the death rate from he-patic failure is greatly increased and com-pletely offsets the undeniable protectionafforded against fatal hemorrhage. A logi-cal explanation would be that the operativemortality accounted for the increased num-ber of deaths from hepatic failure. This isnot the case, however, as there was only

100

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FIG. 1. Comparative survival in randomized pa-tients undergoing prophylactic portacaval shunt.From Grace et al.7 Reprinted by permission ofGastroenterology.

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FIG. 2. Comparative survival in randomized pa-tients undergoing therapeutic portacaval shunt.From Jackson et al."2 Reprinted by permission ofArch. Surg.

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Cause of Death in Controlled Studies

| | |Hepatic Failure

18 8 81 Bleeding

Control S huntGroup Group

FIG. 3. Comparison of cause of death in shuntedand non-shunted patients in controlled series.2' 3

All patients reported are included (randomized,refusal, exclusion and therapeutic shunt groups).

one actual operative death in the com-

bined series; a few patients were never

well enough to leave the hospital. Thesedata indicate that portacaval shunt initi-ates or accelerates hepatic deterioration insome patients and the anticipated deathrate from hepatic failure is substantiallyincreased.

2. Would any major operative procedureaccelerate hepatic failure comparably? Al-though there is no definitive answer to thisquestion, the available evidence indicatesthat other than the acute changes incidentto operation little or no further hepaticdeterioration results from non-shuntingprocedures. Womack and his colleagues

Annals of SurgerySeptember 1967

have used non-shunting procedures rou-tinely and their most recent experience hasbeen reported by Johnson, Dart, Petersand MacFie.13 Although the operative mor-tality was high (eemergency procedureswere included) delayed hepatic death wasrarely seen and there was favorable long-term survival (Fig. 4).

In an important study, Hassab has re-ported the results of non-shunting proce-dures for bleeding esophageal varices inbilharzial cirrhosis.' Such patients mightappear to be excellent candidates for porta-caval shunt as they demonstrate largevarices and marked portal hypertensionwhile maintaining good hepatocellularfunction. However, dissatisfaction with lateresults has led him to virtually abandonportacaval shunts. In 355 patients with gas-tric devascularization and splenectomythere was only a 2.6% death rate fromhepatic failure (all immediately postopera-tive), one late case of jaundice and onepatient with encephalopathy. In "compara-ble patients" treated by portacaval shunt-ing, "jaundice and liver failure occur withincreasing frequency as time passes." This

100

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FIG. 4. Series 1 and 2 depict survival followingportacaval shunt as compared to the N.C.M.H.non-shunt series. The top curve is corrected byelimination of Grade C patients to more nearlymatch the degree of illness with the portacavalshunt patients. From Johnson et l.'1.3 Reprinted bypermission of Ann. SAurg.

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Volume 166 TRANS-SPLENIC DECOMPRESSION OF GASTROESOPHAGEAL VARICESNumber 3

has been confirmed by other experiencedsurgeons.9The detrimental effect of sudden, total,

portal deprivation with splanchnic venous

decompression is well documented.18 It haslong been known that normal dogs tolerateportacaval shunts poorly and usually diein hepatic failure within a few months. Asimilar syndrome has been observed inour laboratory with primates (spider mon-

key).5 The few cases of portacaval shuntwith normal liver and unobstructed portalvein in man have developed a similarsyndrome.'"An excellent study by Mikkelsen of non-

cirrhotic portal hypertension contains im-portant data that have received scant at-tention.14 Among the patients reported, 17had a patent portal vein, no evidence ofliver disease grossly, and excellent liverfunction. In this group, usually called "idio-pathic portal hypertension," there was

nothing to suggest liver decompensationprior to operation. Following portacavalshunt, 10 developed signs of encephalo-pathy or liver failure and five died in he-patic coma. These complications are rare

following non-shunting procedures.3. Should "non-shunting procedures" be

used routinely? Routine use of non-shuntingprocedures has been quite successful inbilharzial cirrhosis and in selected cases ofLaennec's cirrhosis.20 General applicationto a group of cirrhotics, however, leavesmuch to be desired. The chief problem ap-

pears to be bleeding, both in the imme-diate and late postoperative period. In thestudy by Johnson et al.,3 there were 22operative deaths (43%o) of which six were

due to continued bleeding. Of the surviv-ing patients, 45% had recurrent bleeding,31% required reoperation and 14% diedas a result of this complication. Encepha-lopathy was not encountered in the sur-

viving patients.The major advantages of this procedure,

in our opinion, are the maintenance of an

elevated intestinal venous pressure and

preservation of hepatopetal portal flow.However, this is offset, at least in part, bythe persistent danger of gastroesophagealhemorrhage.

Despite the superior results of non-

shunting procedures in stabilizing hepaticfunction and avoiding encephalopathy, itmust be remembered that a good func-tional result from portacaval shunt is seen

in perhaps 40-50% of cirrhotics and af-fords maximal protection from bleeding.This figure is much higher in patients withan essentially normal liver and extrahepaticthrombosis of the portal vein, as the ac-

commodation to loss of portal flow has al-ready been made. The mechanism of ad-justment to decreased portal venous flowis not clear. Deprivation of hepatopetalportal flow is tolerated much better if dueto extrahepatic portal vein obstructionrather than to that produced by portacavalshunt.'

4. Should splanchnic hypertension becompletely decompressed? Excepting thehepatic sinusoids, patent portacaval anasto-mosis abolishes the hypertensive state inthe portal venous system and in thesplanchnic capillary bed.25'6 Following a

side-to-side portacaval shunt the wedgedhepatic vein pressure may decrease butdoes not become normal. After an end-to-side anastomosis this pressure sometimesincreases. Nevertheless, control of ascitesis one advantage of the shunt procedure.22Two factors dull the lustre of such an

achievement. First, there is the total lossof portal flow to the liver which followsboth the end-to-side and side-to-side porta-caval shunt.24 26 Second, the control of as-

cites by nonoperative means has improvedremarkably and only rarely does one see

truly "resistant ascites." Hypersplenism, a

third major complication of portal hyper-tension is seldom completely relieved byreturn of portal pressure to normal. Onlyrarely is the condition severe enough tocreate a problem in management and

439

440 WARREN, ZEPPA

splenic artery ligation is a simple means

of achieving a satisfactory remission.Numerous studies have shown that a

well-compensated stable cirrhotic patient,without esophageal varices, and with no

further liver injury, may lead an essen-

tially normal life. Recently, Price et al.17have shown the increased rate of absorp-tion of ammonia and other substances fol-lowing shunt decompression of portal hy-pertension. This may partially account forthe relatively low incidence of portal sys-

temic encephalopathy seen in non-shuntedpatients with cirrhosis.

It appears that the advantage of boththe shunting and non-shunting operationscan be achieved while avoiding the dis-advantages of each. Ideally, an operationshould allow continued perfusion of he-patic parenchyma by portal flow from theintestine and yet decompress the venous

system in the gastroesophageal area. Gas-trosplenic isolation with distal splenorenalshunt seems to meet these requirements.

Experimental Demonstration of Trans-Splenic Gastric Drainage

Greyhounds of average weight 25 Kg.each were anesthetized with pentobarbitaladministered intravenously (35 mg./Kg.).Through a midline laparotomy incision thegastrosplenic vein was isolated and dividedjust proximal to its junction with the supe-

rior mesenteric vein. An anastomosis was

constructed between the gastrosplenic veinand the inferior venacava. In four dogs, a

polyethylene shunt was interposed be-tween the femoral artery and the severeddistal end of the gastric vein. Upon releaseof occlusion, pulsations were noted in veinswhich usually drain the cardia and fundusof the canine stomach.

Systemic arterial pressure was recordedcontinuously from a cannula through a

Statham transducer on a GME direct writ-ing recorder. Each animal received lac-tated Ringer's solution at the rate of 40-50ml./Kg./hr.

AND FOMON Annals of SurgerySeptember 1967

Splenic blood flow was estimated byXenon'33 clearance.29 While the details aredescribed elsewhere, a brief summary ofthe technics are presented to make theresults intelligible. Radioactive gas or liq-uid was injected either directly into thetissue or into the splenic artery. Care wastaken to insure constant geometric relation-ship between the sodium iodide crystaland the spleen. The output of the photo-multipler tube was amplified for recordingon a direct writer (Texas Instruments).The disappearance of peak radioactivity inthe spleen was recorded and blood flow/100 Gm. splenic tissue/minute was calcu-lated from the recorded disappearancecurve (average 22-28).

In two dogs, a gastrosplenic-inferiorvena cava anastomosis was performed un-der sterile conditions and the animals main-tained for three months. Prior to sacrificesplenoportography was performed.

Splenic blood flow as estimated byXenon133 clearance in two dogs with gastro-splenic-inferior vena caval anastomoses wassimilar to the intact dog (22 and 25 ml./100 Gm. spleen/min.) during occlusion ofthe femoral arterial-gastric venous shunt.Injection of the radioactive material intothe open arterio-venous shunt was fol-lowed by detection of the radioactivityover the spleen with recorded activitycurves similar to that found after injectionof the Xenon into the splenic artery in theintact dog. However, splenic blood flowwas reduced and the mechanism for thisphenomenon is by no means clear. It ispossible that reflex spasm of the splenicartery was initiated by hypertension in theshort gastric and splenogastroepiploic veins.Further studies should provide additionalinsights into this fascinating problem.

In the first two dogs used for these acutestudies, the detection of the blood contrib-uted to the spleen by the femoral arterial-gastric venous shunt was attempted by esti-mating oxygen saturation in the splenicvenous blood during both occlusion and

Volume 166 TRANS-SPLENIC DECOMPRESSIONNumber 3

release of the arteriovenous shunt. No sig-nificant differences were noted and thiswas attributed to the normal high oxygen

saturation of splenic venous blood in thisspecies (88-92%). In addition, the reduc-tion in splenic blood flow as discoveredby the later Xenon clearance studies prob-ably mitigated against finding an increasein the venous oxygen saturation.

In the two dogs allowed to survive for3 months, splenoportograms have demon-strated patent anastomoses. Histological ex-

amination of the spleen has revealed no

abnormalities.The results of these studies have pro-

vided support for the concept that thespleen may serve as an outflow tract forthe cardiac area of the stomach under thecondition of venous hypertension. On theone hand, diversion of splenic venous flowinto the systemic venous system is a simpletechnic and more important, the anasto-mosis remained widely patent at least forthree months in the dog. This venous shuntin no way effects splenic blood flow as

measured by Xenon'33 clearance nor is itassociated with histologic changes in thespleen of chronic survivors.

Further, it is clearly demonstrated thata gross arterio-venous fistula involving themajor gastric venous drainage in dogs re-

sults in some reversal of flow through theshort gastric circulation into the spleen.The detection of Xenon133 in the spleen fol-lowing injection of the material in thefemoral artery side of a femoral arterial-gastric venous shunt supports no other con-

clusion since Xenon'33 is not recirculated.

Methods and Material

All patients were assessed by clinicalevaluation based on careful history andphysical examination, laboratory determi-nations of hepatic function and the ap-

praisal of hemodynamic alterations. Thetechnics used to evaluate hepatic andsplanchnic vascular physiology included

OF GASTROESOPHAGEAL VARICES 441

estimation of total hepatic blood flow, liverscan, hepatic vein catheterization, spleno-portography or indirect portography andvisceral angiography.24

Total hepatic blood flow was estimated(EHBF) using radioactive colloidal gold.The normal K value in this laboratory is0.29 ± 0.05. In patients in whom liverblood flow is slightly reduced the value is0.23 ± 0.07. With moderate reduction inflow K is 0.19 ± 0.05 and with severe re-duction it is 0.16 ± 0.05. However, to in-terpret individual K values the amount ofextrahepatic gold uptake must be estimatedfrom the liver scan and the shape of thedisappearance curve of Au'98 must beevaluated.By hepatic vein catheterization it was

possible to determine the degree of portalhypertension and to gain indirect informa-tion concerning the amount of hepatopetalportal blood flow. With the catheterwedged in an hepatic vein the pressure isrecorded (WHV). The catheter is thenmoved into the free hepatic vein and thepressure is again recorded (FHV). By sub-tracting the latter from the former the cor-rected sinusoidal pressure (CSP) is ob-tained. A pressure between 6 and 14 mm.Hg signifies mild portal hypertension. Mod-erate hypertension exists when the pres-sure is between 15 and 20 mm. Hg. Above20 mm. Hg the hypertension is severe.With the catheter in the wedged positionradiopaque material is injected. Each veno-gram can be placed in one of four cate-gories. In Category 1 there is excellent fill-ing of the sinusoidal bed but no filling ofthe portal system. This is characteristic ofthose patients in whom portal flow to theliver is normal or only mildly restricted.In Category 4 there is hepatofugal flowthrough the portal vein and into thesplanchnic circulation. Categories 2 and 3are intermediate.

Splenoportography is usually the singlebest source for estimating portal hemody-

442 WARREN, ZEPPA AND FOMON

FIG. 5. With the transverse colon retracted up-ward and in a cephalad direction, the transversemesocolon is stretched. An incision in the peri-toneum at the root of the transverse mesocolon tothe left of the superior mesenteric vessels exposesthe inferior border of the body of the pancreas.

namics. Stage 1 represents normal or onlyslightly restricted hepatopetal portal flow.In Stage 2 portal flow to the liver is mod-erately restricted and in Stage 3 it is se-verely restricted. Total lack of opacifica-tion of the portal vein is the criterion forStage 4. At times indirect portography isused in lieu of splenoportography. Stagingis similar to that of splenoportography.

In presinusoidal hypertension and whenthe EHBF is relatively high and portalhepatic venous perfusion is decreased thehepatic artery may appear unduly large,perhaps because of compensatory hyper-trophy. In these situations there is a promi-nent liver blush on the late films of thehepatic arteriogram.

Six patients who had bled from esopha-geal varices were studied. Liver functionwas relatively good in all and hepaticportal perfusion was good. Because of themorbidity associated with sudden decreasein portal blood flow to the liver four pa-tients had a distal splenorenal shunt withgastrosplenic isolation and two had thestomach devascularized but the spleen wasleft in place.


Technic of Distal Splenorenal Shuntand Gastrosplenic Isolation

A long midline incision is made. Thetransverse colon is lifted upward and in acephalad direction. A transverse incision ismade at the root of the transverse meso-colon to the left of the mesenteric vessels(Fig. 5). The inferior border of the pan-creas is recognized readily and rotatedgently in a cephalad direction. With care-ful dissection in the retroperitoneal tissuebehind the pancreas and near its superiorborder, a short segment of splenic vein isidentified close to its junction with the infe-rior mesenteric vein. Small venous tribu-taries from the pancreas are dissected me-ticulously, doubly clamped, divided andligated. The splenic vein in this area isthen dissected circumferentially from sur-rounding tissue and a tape is placed aroundit. With gentle traction on the tape dissec-tion is continued in a distal direction untila segment of 4 to 6 cm. of the vein hasbeen freed. Care is exercised to avoid trou-blesome hemorrhage that occurs whentributaries are torn from the splenic vein 4

(Fig. 6). Next a transverse incision is madein the posterior peritoneum and the leftrenal vein is isolated as it crosses the aorta.The vein is freed of surrounding tissue in

vein

FIG. 6. The splenic vein has been identified.By careful division of pancreatic tributaries, a seg-ment of splenic vein is isolated. The usual rela-tionship of the splenic vein to the inferior mesen-teric vein (i.m.v.) is shown. During the surgicalprocedure the superior mesenteric vein (s,m,v.)is not dissected and usually is not seen.


a distal direction. Cephalad to the vein theleft renal artery is recognized and encircledwith a tape. Pressures in the renal vein(FRV) and splenic vein (FSV) are re-

corded. The splenic vein is cross clampedand the pressure on the hepatic side of thevein is measured (HOSP). The pressure

on the splenic side of the vein is then ob-tained (SOSP).The splenic vein at its junction with the

inferior mesenteric vein is doubly clamped,divided and the proximal end is oversewn.

The left renal artery is temporarily oc-

cluded and a segment of renal vein is iso-lated between vascular clamps. An incisionapproximately 2.5 cm. long is made in thesuperior aspect of the renal vein and thedistal end of the cut splenic vein is beveledappropriately. Tortion and kinking of thesplenic vein are avoided and a continuoussimple coaptation suture is used for theposterior wall of the anastomosis. Inter-rupted sutures are used for the anteriorwall. The clamps on the renal vein, splenicvein and finally the renal artery are re-

leased (Fig. 7, 8).Following completion of the distal spleno-

renal shunt the splenocolic and then thegastrocolic ligaments are divided. The gas-trosplenic ligament and the vessels cours-

FIG. 8. Upon completion of the anastomosis thesplenic vein is unkinked and without tortion evenwhen the pancreas is allowed to return to its nor-mal position.

ing through it are preserved. The greatercurvature of the stomach is lifted upward,the left gastric artery is divided, and thecoronary vein is identified, divided andobliterated with a continuous suture. Thegastrohepatic ligament is divided (Fig. 9).Pressure in the splenic vein (FSV), renalvein (FRV) and in the superior mesentericvein (HOSP) are again recorded.

pancreasref lected

I7

FIG. 7. The splenic vein has been divided andthe distal orifice has been oversewn in a mannerwhich leaves no cul de sac from which a throm-bus could propagate. The renal vein has been iso-lated and incised. Before application of vascularclamps, the renal artery, not shown, is occluded.The relationship of the inferior (i.m.v.) and supe-rior (s.m.v.) mesenteric veins is shown.

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FIG. 9. The completed operation is depicteddiagrammatically. Arrows indicate the direction ofblood flow. The distal splenorenal anastomosis hasbeen completed and the coronary vein has beenligated. The gastrocolic ligament has been dividedand the right gastroepiploic vein ligated. At thetime the gastro hepatic ligament is divided theright gastric vein is ligated. Blood from the infe-rior (i.m.v.) and superior (s.m.v.) mesentericveins continues to perfuse the liver by way of theportal vein.

443

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WARREN, ZEPPA AND FOMON Annals of SurgerySeptember 1967

...

FIG. 10. The left gastroepiploic artery (notshown) and vein are ligated and the gastrocolicligament is divided. The right gastroepiploic ar-tery (not shown) and vein are similarly ligated asare the short gastric vessels. The coronary vein isobliterated, the left gastric artery divided near itsorigin and finally the splenic artery is divided.

With increasing experience the technicof the operation has been modified. Ini-tially a long left subcostal incision was

used, the pancreas was approached byfreeing the splenic flexure of the colon andreflecting it caudad and in a medial direc-tion and the splenic vein was isolated dis-tally. The midline incision resulted in ex-

posure that was more satisfactory; butmore importantly, ascitic fluid which fre-quently has been a temporary postopera-tive problem does not dissect into tissueplanes. It is easier to identify and isolatethe splenic vein near its junction with theinferior mesenteric vein, the anastomosiscan be performed after mobilization of a

shorter vein segment and ligation of the

splenic vein at its junction with the inferiormesenteric vein leaves no cul de sac inwhich a thrombus may form and propa-gate. Exposure of the pancreas throughthe transverse mesocolon is satisfactoryand the pancreas can be mobilized, rotatedand retracted with considerable less traumato the organ.

Technic of Gastric Devascularizationwith Spleen in Situ

When a distal splenorenal shunt is notperformed devascularization of the greatercurvature of the stomach is the first stepin the procedure. The left gastroepiploicartery and vein are divided distal to theshort gastric vessels and beginning at thispoint the gastrocolic ligament is dividedclose to the stomach as far as the level ofthe pylorus. Here the right gastroepiploicartery is ligated. The short gastric vesselsare divided and the coronary vein is ob-literated in the manner previously de-scribed. The left gastric artery is ligatedand divided near its origin leaving the rightgastric artery as the sole blood supply tothe stomach. Finally the splenic artery isligated but the spleen is left in place (Fig.10).

Case ReportsCase 1. Two years prior to admission this 59-

year-old man had a cholecystectomy for chroniccholecystitis and cholelithiasis. At the time of op-eration there was perisplenitis and a liver biopsywas interpreted as "chronic portal hepatitis." Ap-proximately 1 year prior to admission the patient

TABLE 1. Laboratory TValues Prior to Operation

Pro- Bilirubin Bilirubin Alkaline TotalHg thrombin Total 1 Min. Phos- Protein Albumen

mg./ Platelet Activ- mg./ mg./ phatase SGOT mg./ mg./Case 100 ml. WBC Count ity % 100 ml. 100 ml. BU units 100 ml 100 ml

1 12 4,600 90,000 100 1.40 0.45 25.6 52 5.9 2.722 10.6 2,350 80,000 100 1.00 0.22 42 6.5 4.123 13.2 4,950 74,000 86 1.50 0.70 5.6 70 6.6 2.314 7.9 8,800 232,000 56 1.34 0.47 2.7 84 7.5 2.605 11.8 17,500 70 1.60 0.64 3.3 90 5.5 2.626 11.6 6,300 130,000 100 .30 2.9 16 6.0 3.15

444

Volume 166 TRANS-SPLENIC DECOMPRESSION OF GASTROESOPHAGEAL VARICESNumber 3 445

TABLE 2. Hemodynamic Data

Preoperative At Operationi Postoperative

Pre-Shunt Post-Shunt

CorrectedOccluded

Hepatic Splenic HepaticVeno- Pres- Veno-

CSP gram Porto- CSFP sure CSFP CFPP CSP gramEHBF mm. Cate- gram mm. mm. mm. mm. EHBF mm. Cate- Portogram

Case Au198 Hg gory Stage Hg* Hg Hg* Hg Au'98 Hg gory Stage

1 0.31 15 1 1 0 172 0.22 18 1 1 26 26 0 0.22 33 0.21 22 2 14 <0.12 15 2 1 19 27 4 8 <0.12 19 45 0.21 16 3 1 0.18 17 26 0.22 17 1 1 18 22 0.27

* Corrected free splenic vein pressure = free splenic pressure - renal vein pressure.

developed ascites which responded to medicaltherapy. Two weeks before coming to the hospitalhe had the first of two hematemeses necessitatingtransfusion with a total of 5,500 ml. of wholeblood. On admission the patient appeared com-

fortable, the abdomen was protuberant with as-

cites, the liver was not palpable, but the spleencould be felt three finger breadths below the leftcostal margin. Palmar erythema and spider angio-mata were absent. There was no peripheral edema.Liver function studies were performed (Table 1).With treatment the patient became free of ascitesand upper gastrointestinal series was interpretedas being compatible with small esophageal varices.An hiatal hernia was present. Blood flows usingradioactive colloidal gold were normal (Table 2).When scanned the liver was thought to be of nor-

mal size. The spleen was enlarged and isotope up-

take by it was high. Hepatic vein catheterizationwas carried out. The corrected sinusoidal pressure

was 15 mm. of mercury. When an hepatic veno-

gram was performed there was virtually no fillingof the portal venous system. Contrast material leftthe liver by way of the hepatic vein. Because thepatient seemed to have early portal hypertensionwith good hepatopetal portal flow operation was

not advised. Three months later the patient hada small hematemesis and tarry stools. Bleedingcontinued and a splenoportogram was performed.Despite the fact that the inferior mesenteric andcoronary veins filled and that varices were seen

there was good hepatopetal flow with a promi-nent liver blush on the late splenoportographyfilms. An emergency distal splenorenal shunt was

performed with ligation of the splenic artery andcoronary vein. Postoperatively the patient reac-

cumulated ascitic fluid which became infected. Inspite of drainage of multiple intra-abdominal ab-scesses the patient died. The shunt was patent atthe time of the second operation.

Case 2. A 65-year-old woman had been hos-pitalized 11 months previously and had cirrhosisof the liver, portal hypertension, hypersplenismand diabetes mellitus. Six weeks before the presentadmission she was admitted to a hospital becauseof gastrointestinal bleeding which was thought tobe from esophageal varices. On the day prior toadmission she again had gastrointestinal bleedingmanifested by tarry stools. The patient was alertand cooperative. Jaundice, spider angiomata,palmar erythema, ascites and peripheral edemawere absent. Both the liver and spleen were

Fic- 11. Wedged hepatic venogram, Category1. The variegated pattern in the sinusoidogram istypically present in cirrhosis. Branches of theportal vein do not fill and contrast material leavesby way of the hepatic vein


The splenic artery was selectively catheterized andradiopaque material was injected. On the venous

phase, flow was mainly towards the liver. A largecoronary vein opacified to show enormous gastro-esophageal collateral vessels (Fig. 13). The pa-

tient was operated upon and a distal splenorenalshunt was carried out. The coronary vein was

ligated and the gastrocolic ligament was divided.Postoperatively the estimated hepatic blood flowremained unchanged. On the venous phase of thepostoperative celiac arteriogram there was a largesplenic vein that connected directly to the leftrenal vein. Blood flowed from the splenic to therenal vein and into the inferior vena cava (Fig.14). That portal blood continued to perfuse theliver was evident from the venous phase of thesuperior mesentery arteriogram (Fig. 15). Duringthe brief follow up period the patient has had no

bleeding and no evidence of deterioration of liverfunction. Following a protein meal, ammonia lev-els did not rise significantly above the fastingvaltue (Fig. 25).

Case 3. Two years previous to admission this45-year-old man was seen by a physician and atentative diagnosis of cirrhosis of the liver was

made. Three weeks prior to admission the patientwas admitted to another institution because ofhematemesis. Medical treatment resulted in cessa-

tion of bleeding and the patient returned to full-time employment. The patient was well developedand well nourished. Spider angiomata were pres-ent over the trunk. There was no palmar erythemaor gynecomastia. The liver could be palpated 2cm. below the right costal margin. The spleen wasnot felt. There was no evidence of ascites or pe-

ripheral edema. Except for a platelet count of

FIG. 12. Large varices are present in the lowerone half of the esophagus.

moderately enlarged. Liver function tests were

within normal limits but there was pancytopenia(Table 1). Estimated hepatic blood flow was

K 0.22 (Table 2). Hepatic vein catheterizationwas carried out and the patient was found to havemoderate portal hypertension. As estimated fromthe hepatic venogram portal flow to the liver was

good (Fig. 11). On liver scan there was a highuptake of gold both in the bone marrow and inan enlarged spleen. Upper gastrointestinal seriesrevealed large gastroesophageal varices (Fig. 12).

FIC. 13. Indirect portography, Stage 1. On thevenous phase of the splenic artery arteriogramlarge gastroesophageal varices were opacified byway of the coronary vein. In spite of this porto-systemic collateral hepatopetal portal flow wasexcellent.

446


74,000 laboratory findings were only mildly ab-normal (Table 1). Estimated hepatic blood flowsyielded values of 0.19 and 0.23 (Table 2). He-patic vein catheterization was carried out. Thecorrected sinusoidal pressure was 22 mm. Hg. Onthe venogram contrast material left by way of thehepatic vein but a branch of the portal vein alsoopacified. A splenoportogram was performed and PVflow to the liver was only slightly decreased. Theinferior mesenteric vein filled. Short gastric veinsfilled and formed varices in the fundus of thestomach. Other collateral veins were also presentin the upper abdomen. A liver scan was inter-preted as showing increased uptake of gold bythe bone marrow and especially by the spleen.The liver appeared to be of normal size and thespleen was only slightly enlarged. A distal spleno-renal shunt was performed. Postoperatively the FiG. 15. Postoperative superior mespatient did poorly and died in hepatic coma. At ography. A superior mesenteric arteautopsy the hepatic artery and portal vein were performed. During the venous phase cpatent but there was extensive necrosis of the nation contrast material from the lelliver. A laminar thrombus was present in both the (LCV) and superior mesenteric v

flowed in an hepatopetal direction to fsplenic and renal vein but the shunt was patent. vein (PV) and its intrahepatic bran(

447

senteric angi-riogram wasof the exami-ft colic veinvein (SMV)fill the portalches.

Case 4. Siometinme in the past, this 43-year-oldNegro woman had been told that she had cirrhosisof the liver. The day prior to admission she hadvomited several cupsful of bright red blood. There

Fic. 14. Postoperative celiac angiography. Onfilms obtained during the venous phase of a celiacaxis arteriogram, contrast material filled the splenicvein (SV), entered the left renal vein (LRV)and flowed into the inferior vena cava (IVC).

had been no previous hematemesis or melena. Thepatient was well-developed and moderately obese.She appeared comfortable. The sclera were mildlyicteric, the abdomen was protuberant with no evi-dence of ascites and the liver and spleen were en-larged greatly. There was no palmar erythema orspider angiomata. On admission hemoglobin was7.7 Gm./100 ml. Liver function tests were slightlyabnormal (Table 1). The patient stopped bleed-ing spontaneously and upper gastrointestinal seriesshowed esophageal varices. Hepatic blood flowwas estimated using radioactive colloidal gold, butdisappearance curves were too low for accuratecalculation (Table 2). Liver scan showed a diffuseirregularity in the distribution of the isotopic ma-terial throughout the markedly enlarged liver.There was considerable uptake by an extremelylarge spleen as well as by the bone marrow. Atthe time of hepatic vein catheterization the cor-rected sinusoidal pressure was 15 mm. Hg. Thesinusoidogram was abnormal. Although branchesof the portal vein filled, venovenous shunts filledhepatic veins and it was by this route that thecontrast material left the liver. A splenoportogramwas performed. The coronary vein filled as didextensive collateral veins in the area of the fundusof the stomach and lower esophagus. A collateralvein, present in the right upper quadrant, wasthought to be the umbilical vein (Fig. 16). Flowto the liver was good and an excellent hepatogramwas obtained on the late films. A distal spleno-renal shunt was carried out, the coronary veinligated and the gastrohepatic, gastrocolic and

448 WARREN, ZEPPA AND FOMON

FIG. 16. Splenoportogram, Stage 1. Hepatopetalportal flow was good but contrast material filledthe coronary vein and opacified varices in the areaof the fundus and lower esophagus. A large col-lateral vein in the right upper quadrant was alsoopacified.

splenocolic ligaments were divided. Prior to theshunt, the renal vein pressure was 13 mm. Hgand the pressure in the splenic vein was 32 mm.

Hg. The occluded splenic vein pressure was 40

FIG. 17. Wedged hepatic venogram, Category4. Contrast material injected with the catheterwedged in an hepatic vein drained in a retrogradedirection and opacified the portal vein.


FIG. 18. Splenoportogram. Contrast materialleft the spleen by way of the splenic vein andflowed into the left renal vein and its tributariesand inferior vena cava. The lack of uniformity ofthe contrast material is the result of the Valsalvamaneuver carried out by the patient.

mm. Hg. Post-shunt the free renal vein pressurewas 12 mm. Hg and that of the free splenic veinwas 16 mm. Hg. The pressure in the portal veinwas 24 mm. Hg. Postoperatively the patient wasagain catheterized; the corrected sinusoidal pres-sure was 15 mm. Hg. On the hepatic venogramcontrast material flowed in a retrograde directionto fill the portal vein (Fig. 17). Postoperativeindirect portography was unsatisfactory but afunctioning shunt was present when the spleno-portogram was repeated (Fig. 18). When the gas-trointestinal series was repeated there was no evi-dence to suggest esophageal varices.

Case 5. Nine months prior to admission this40-year-old man experienced progressive increasein abdominal girth, lethargy, and weakness. Twoweeks prior to admission he vomited bright redblood. There was associated melena. He received1,000 ml. of whole blood and bleeding stoppedspontaneously. An upper gastrointestinal series wassaid to be diagnostic of esophageal varices. Oneweek later he had another small hematemesis butcontinued to have melena. He had an abdominalparacentesis and was transferred to this institu-tion. There had been no previous history of jaun-dice, hepatic coma, or other difficulty. The patientappeared to be well developed and well nourished.Spider angiomata were present over the chest andshoulders, the abdomen was distended with ascitesand there was edema of the abdominal wall, scro-tum, and lower extremities. The liver edge reachedthe umbilicus but the spleen could not be pal-pated. The hemoglobin was low and values fortotal protein and albumen were decreased (Table1). The thoracic duct and an hepatic vein werecatheterized. The corrected sinusoidal pressure was


FIc. 19. Wedged hepatic venogram, Category3. In this examination, done in the presence oftense ascites, branches of the portal vein were

well filled with cofitrast material.

16 mm. Hg and on wedged hepatic venogram

there was filling of portal vein branches (Fig. 19).With diuretics, drainage of thoracic duct lymphand replacement with albumen and plasma thepatient's weight dropped from 190 to 168 pounds.Blood flows using radioactive colloidal gold yieldedK values of 0.22, 0.21, and 0.20 (Table 2). Thepatient was discharged to be readmitted at an

elective time. Two days later he returned follow-ing a large hematemesis. Splenoportogram showedgood flow to the liver but there was filling of a

coronary vein and a left umbilical vein. Variceswere epresent in the gastroesophageal region (Fig.20). At operation the stomach was devascularized;the spleen was left in situ but the splenic arterywas ligated. Postoperatively the patient accumu-

lated ascites that was controlled with diuretics. Anhepatic vein catheterization done prior to dis-charge was similar to the preoperative examina-tion (Fig. 21).

Case 6. A 69-year-old woman was told shehad "an enlarged liver" 6 years previously. Shortlythereafter her spleen was also found to be en-

larged. Two months prior to admission the pa-

tient had two small hematemeses for the first time.

FIG. 20. Splenoportogram, Stage 1. A largecoronary vein filled with contrast material whichthen opacified gastroesophageal varices. Portalflow to the liver remained excellent.

She was not hospitalized. Ten days before admis-sion she had a large hematemesis and vomited"one and one-half quarts" of blood. Bleedingceased on medical therapy. The patient had nothad an illness that was suggestive of hepatitis buthad experienced ascites in the past. The patientappeared well developed, well nourished and was

comfortable and cooperative. The abdomen was

obese but without ascites. The liver could be pal-

FiG. 21. Wedged hepatic venogram, Category2. Fewer branches of the portal vein filled withcontrast material and some of it can be seen leav-ing the liver by way of an hepatic vein.

449


FiG. 22. Wedged hepatic venogram, Category FIG. 23b. Splenoportogram, Stage 1. On late1. A left hepatic vein was catheterized. Although films there was a dense hepatogram, evidence ofan excess of contrast material flooded the sinu- good hepatopetal portal flow.soids, hepatic venovenous shunts filled and onlyhepatic veins were opacified.

pated three finger breadths below the right costalmargin and the spleen was also readily palpable.Palnar erythema was present but there were no

spider angiomata. The values obtained by variousliver chemistry detenninations were almost normal(Table 1). On the upper gastrointestinal seriesthere were changes attributed to esophagealvarices. Estimated hepatic blood flows usingradioactive colloidal gold were carried out andyielded K values of 0.20 and 0.25 (Table 2). Aliver scan was performed. The uptake of the iso-tope in the slightly enlarged liver was diffuselyirregular. There was considerable uptake in an

enlarged spleen. Hepatic vein catheterization was

carried out. The corrected sinusoidal pressure was

17 mm. Hg. On the venogram there were hepaticvenovenous shunts that allowed all the contrastmedium to leave by way of the hepatic veins(Fig. 22). A splenoportogram was performed. The

FiG. 23a. Splenoportogram, Stage 1. The coro-nary and short gastric veins fflled and opacifiedvarices in the gastroesophageal area.

circulation was mainly hepatopetal with a very

prominent liver blush during the capillary phase.The coronary vein filled. Collaterals were presentin the gastroesophageal area which were suppliedby the short gastric veins as well as by the coro-

nary vein (Fig. 23). At operation a distal spleno-renal shunt was unsuccessful and the splenic ar-tery and vein were ligated. Distal to the shortgastric veins the greater curvature of the stomachwas devascularized. The entire lesser curvature ofthe stomach was devascularized and the coronary

vein was ligated. Postoperatively there has beenno further bleeding.

DiscussionPortacaval shunting remains the surest

way to prevent death from bleedingesophageal varices in the patient with a

patent portal vein.7' 15 The success of theprocedure, however, is markedly dimin-ished by untoward effects upon the liverand its metabolic processes.19 This hasbeen emphasized by critical studies inBoston 2, 7 and Hartford 3 which have failedto reveal a prolongation of life by suchprocedures (Fig. 1). On the other hand,there are unquestionably many patientswho tolerate a portacaval shunt with littledisability and remain free of the danger ofexsanguinating hemorrhage while leadingan essentially normal life.8' 26 One approachto this problem has been the attempt toidentify physiologic features which can beutilized to predict the response of a given

450


FIG. 24. Splenoporto-gram, Stage 4. Contrastmaterial left the spleenby way of the splenicvein (SV) and a largecaudally directed collat-eral (Col.). The leftrenal vein (LRV) andinferior vena cava (IVC)opacified by way of a

spontaneous shunt. Theportal vein was patent.

patient to a portacaval shunt.26 If such datawere available, a fraction of patients withbleeding esophageal varices (perhaps 40-50%) could be safely selected for theshunt procedure. Although preliminarydata has indicated some of the hemody-namic changes which might account foran untoward response to the operation, thereliability of such judgment has not beenestablished and the complexity of the dis-ease makes an easy definition of such pa-tients very unlikely. Even if appropriatetechnics of selection emerge in the near

future, there remains a large group forwhom a shunt procedure would likely bedetrimental. The non-shunting procedures,advocated chiefly by Dr. Womack and hisassociates at Chapel Hill, have added con-

siderably to the management of these pa-tients. However, the high incidence of re-

current bleeding, both in the immediateand late postoperative periods, has clearlydetracted from the achievements of thisoperation.13' 16, 28 Unfortunately, non-opera-tive management has not improved signifi-cantly and long-term survival is in constantjeopardy due to gastrointestinal hemor-rhage.7The major objective of this study was to

develop a form of therapy which wouldgive great protection from bleeding thannon-shunting operations while avoiding thesevere sequelae which may occur aftersudden, complete, portal venous diversion.The concept of gastrosplenic isolation, gas-tric devascularization and selective venous

tVC

7...

shunting by distal splenic vein-renal veinanastomosis was developed. The rationaleand specific objectives of this operation are

as follows:1. Selective reduction of pressure and

volume of flow through gastroesophagealveins. There are isolated cases of severe

bleeding from veins across an intestinalanastomosis, from hemorrhoidal veins, or

simply from unknown sites in the intes-tinal tract. However, fatal bleeding rarelyoccurs from venous hypertension in areas

other than the stomach and esophagus. Inour series of six patients with spontaneousreversal of flow in the portal vein, the mostadvanced stage of portal hypertension, onlyone has required surgery for bleeding.23These patients characteristically developextensive, caudally directed collateral,sparing the coronary-azygos system andhave little in the way of esophageal va-rices. Indeed, the initial idea of a distalsplenorenal shunt stemmed from such a

patient (Fig. 24). Successful decompres-sion of the gastroesophageal veins, how-ever, depends upon the volume of inflowand the capacity of the outflow tract. Thecritical outflow systems in this procedureare the short gastric and phrenosplenicveins, the connecting link between the gas-troesophageal veins and the low pressure

splenic venous system. From our initial ex-

perience, there is no doubt that the spleno-renal shunt completely decompresses thesplenic venous system. However, if there

is a large coronary vein, complete gastro-

451

LYE .

452 WARREN, ZEP

esophageal venous decompression mightnot be achieved due to the relatively lowvolume in the venous system leading fromthe gastric and esophageal veins into thesplenic bed. This is the principal reason

for the devascularization portion of the op-

erative procedure, although others havebeen impressed with its value in decreas-ing arteriovenous shunting.16 Final docu-mentation of success of this aspect of thestudy has not yet been accomplished.Radiographic examination by both splenicartery injection and conventional spleno-portography has shown diversion of splenicflow through a patent anastomosis into therenal vein and vena cava. Splenic veinpressure has returned to normal but thisdoes not necessarily correlate with that inthe esophageal veins. Visual and tactilecharacteristics of the stomach have changedmarkedly and resemble closely those seen

following a portacaval shunt. Esophagealvarices have disappeared or shown a

marked reduction in size by barium swal-low. No patient has had variceal bleedingin the brief elapsed period since operation.The ultimate criterion for success is con-

trol of bleeding over a long period of time.2. Maintain portal venous perfusion of

the liver. Hepatopetal portal flow is desir-able to maintain liver perfusion as near

normal as possible and thereby preservethe metabolic efficiency that results fromdirect delivery of the products of digestionand absorption to the hepatic cells. We are

firmly convinced that acute complete di-version of a large volume of portal flowoften results in a serious decline in hepato-cellular function. Recent studies in otherlaboratories have supported this conceptand controlled clinical observations, dis-cussed previously, strengthen the thesis.From the metabolic standpoint, the promi-nent clinical complication is portal-sys-temic encephalopathy. Although the pre-cise mechanism of development is un-

known, it is related to the metabolism ofnitrogenous substances. Undoubtedly many

'PA AND FOMON Annals of SurgerySeptember 1967

other metabolic abnormalities occur fol-lowing complete portacaval shunting butonly a few have received more than scantattention. For example, following the in-gestion of a large protein meal, the am-monia levels in portal blood are eight toten times that of arterial blood. Thereforeduring a given period portal venous per-fusion with 100 ml. of blood would deliverthe same amount of ammonia to the liverfor detoxification as would 1,000 ml. ofhepatic arterial blood. Preliminary studyindicates that a similar situation exists withother substances including amines, aminoacids, insulin, etc. Consequently, the suc-cessful preservation of portal flow to theliver, even if small in volume, can help toinsure metabolic stability.

Success in achieving this goal has beendocumented. On the venous phase of su-perior mesenteric arteriograms contrast ma-terial opacifies a patent mesenteric andportal venous system in an hepatopetal di-rection. The velocity of the flow appearsto be decreased, a predictable finding in asystem in which volume of flow is dimin-ished while hepatic resistance remains un-changed. Hepatic blood flows using Au198although of limited value in this situation,have not shown a significant change. Pre-and postoperative intrahepatic pressureswere essentially unchanged in Case 4.Of equal importance has been the dem-

onstration of the efficiency of postoperativeammonia metabolism (Fig. 25). Proteintolerance in these patients appears to befar superior to those having a portacavalshunt. Although the improvement may notbe due solely to continued portal venousflow to the liver, the efficiency of substrate(NH3) delivery must be an importantfactor.

3. Maintain continual venous hyperten-sion in the intestinal bed. We have pos-tulated that complete decompression of theportal venous system would lead to hemo-dynamic changes other than loss of portalflow to the liver. Prior to a portacaval shunt

w t s -t s-w-w s P7 -E v


PROTEIN TOLERANCE TEST50Ogm. protein orally et time zwo

500-

SOO

§ 400.a-

. 3000'0200~

- - Prteceo Shou

/\*-** DIbt SpWm-NOeol Shut

O 1 2 4 5 6 7

Time in Hours

FIG. 25. Comparison in ammonia levels. Porta-caval patients were admitted for study during thesame time period.

splanchnic viscera have similar capillarypressures. Following the shunt these or-

gans, except the liver, have a sudden fallin pressure to normal. The liver is the onlyorgan with continued outflow obstructionand its sinusoidal pressure rarely returns tonormal, frequently dropping only slightly.Under these circumstances, vasomotor con-

trol from baroreceptors should preferen-tially increase arterial flow to the low pres-

sure systems. Smith et al.21 have recentlyfound evidence of this phenomenon in dogswith portal hypertension but meaningfuldata in the cirrhotic patient is not yetavailable. Another beneficial aspect of con-

tinual intestinal hypertension has recentlybeen demonstrated by Price et al.17 In boththe experimental animal and man, the rateof absorption of ammonia was slowed byvenous hypertension and increased follow-ing portacaval shunt. This observation maypartially explain the relatively low flat pro-

tein tolerance curves of the patients havingthe limited shunting procedure. In Case 4particularly, superior mesenteric angiogra-phy was interpreted as showing a very

small volume of portal flow to the liverand at the time of wedged hepatic venog-raphy there was actual reversal of portalflow. In such a nearly balanced situation,the direction of flow varies depending uponvolume of superior mesenteric flow or re-

lated factors. In spite of this limited flow,

the protein tolerance curve was much morenearly normal than those seen followingportacaval shunt.

Clinical ApplicationAlthough it is too early to make defini-

tive statements regarding the efficacy ofthe new operative approach for control ofbleeding esophageal varices, some com-ment should be made regarding selectionof patients. In our opinion the patients inwhom the selective shunt or non-shuntingprocedure should be utilized regularly arethose in whom an high volume portal flowcontinues to perfuse the liver. Previousstudies have demonstrated the markedphysiologic alterations which follow porta-caval shunting.18, 25, 28 Clinical results indi-cate that for any given level of hepatic in-tegrity those patients who suffer the mostsevere physiologic changes are most apt toincur clinical deterioration. In addition, thefar advanced, portal hypertensive has littleportal flow to the liver and non-shunting orselective shunting procedures are not aptto preserve that flow.4 This was well dem-onstrated in Case 4, a patient in whom amoderate amount of portal flow reachedthe liver preoperatively but postoperativelythe portal circulation appears to be hepato-petal at one time and hepatofugal at an-other.High hepatopetal portal flow and bleed-

ing esophageal varices are most frequentlyencountered in the early hypertensive withsignificant splenomegaly. It has been docu-mented that massive splenomegaly cancause portal hypertension and esophagealvarices even in the absence of cirrhosis ofthe liver or of an obstructed portal vein.27In some patients the cirrhosis is relativelymild in terms of degree of hepatic destruc-tion, but the increased splanchnic volumeexceeds the ability of the hepatic vascula-ture to accommodate and portal hyperten-sion and collateral pathways result. If theprimary portosystemic collateral is thecoronary vein, esophageal varices and gas-

454 WARREN, ZEPPA AND FOMON Annals of Surgery454 WARREN, September 1967

troesophageal bleeding can occur veryearly in the evolution of the cirrhotic proc-ess. We believe this type of patient is al-most ideally suited for the new procedure.In the same category are the so-called idio-pathic portal hypertensives in whom nomajor obstruction to the portal venous sys-tem can be demonstrated and the liver ap-pears to be essentially normal. The delete-rious effects of portacaval shunting on suchpatients has been demonstrated by the ex-cellent study of Mikkelsen et al. who havedone much to clarify the etiology of thiscondition.14

Non-Shunt PatientsTwo patients in this series had a modifi-

cation of the gastric devascularization pro-cedure without the splenorenal shunt. Inone this was done because a technical errorprevented a successful anastomosis and theother was an emergent operation and alesser procedure was decided upon. Thesignificant variation from the technic ofothers is the omission of splenectomy. Wehave seen many large caudally directedcollaterals from the spleen and destructionof such relatively harmless pathways forvenous egress seems unwise (Fig. 24).Much of the morbidity and perhaps mor-tality of the conventional devascularizationoperation comes from the persistent bleed-ing from small vessels divided during thesplenectomy. In addition to a complete"porto-azygos disconnection," the splenicartery and all gastric arteries, save for theright are ligated. This combined procedureaccomplishes the immdiate control ofbleeding with a lesser operative procedure.The resulting decreased pressure in col-lateral pathways lessens the possibility ofrecurrence of varices in the gastroesopha-geal area.

SummaryCritical analysis of routine portacaval

shunt therapy for esophageal varices hasrevealed a lack of success in increasing

survival. Control of bleeding varices hasbeen excellent but an increased death ratefrom hepatic complications has negatedthis achievement. Non-shunting surgicalprocedures have proven superior in hepaticprotection, but are accompanied by a highincidence of recurrent bleeding.A new operative procedure is described

in which selective shunting is accomplishedthrough an in situ spleen and a distalsplenorenal shunt. The rationale of theprocedure is to decompress the area criti-cal for control of hemorrhage while main-taining a high pressure intestinal venoussystem and preserving portal flow to theliver.

Successful accomplishment of this goalhas been demonstrated radiographicallywith diversion of splenic flow through adistal splenorenal shunt while superiormesenteric flow continues to perfuse theliver. The proposed metabolic advantagehas been confirmed by a markedly superiorresponse to protein tolerance testing.From these preliminary studies, use of

this type of procedure seems indicated inpatients with high volume portal flow tothe liver. Typical examples are seen inearly cirrhosis with marked splenomegalyand in so-called idiopathic portal hyper-tension.

References1. Aldrete, J. S., McIlrath, D. G. and Hallen-

beck, G. A.: Effect of Portal Ligation andEck's Fistula on Hepatic Blood Flow andConcentration of Blood Ammonia. Surg.Forum, 17:363, 1966.

2. Callow A. D., Lloyd, J. B., Ishihara, A.,PonsAomenech, E., O'Hara, E. T., Chalmers,T. C. and Garceau, A. J.: Interim Experi-ence with a Controlled Study of Prophy-lactic Portacaval Shunt. Surgery, 57:123,1965.

3. Conn, H. 0. and Lindenmuth, W. W.:Prophylactic Portacaval Anastomosis in Cir-hotic Patients with Esophageal Varices. NewEng. J. Med., 272:1255, 1965.

4. Fomon, J. J. and Warren, W. D.: Unpub-lished data.

5. Garceau, A. J., Chalmers, T. C. and the Bos-ton Inter-Hospital Liver Group: The Natu-ral History of Cirrhosis: I. Survival withEsophageal Varices. New Eng. J. Med.,268:469, 1963.

Volume 166 TRANS-SPLENIC DECOMPRESSION OF GASTROESOPHAGEAL VARICES 455Number 3

6. Grace, N. D., Muench, H. and Chalmers,T. C.: The Present Status of Shunts forPortal Hypertension in Cirrhosis. Gastroent.,50:684, 1966.

7. Hallenbeck, G. A., Wolla-eger, E. E., Adson,M. A. and Gage, R. P.: Results after PortalSystemic Shunts in 120 Patients with Cir-rhosis of the Liver. Surg. Gynec. Obstet.,116:435, 1963.

8. Hassab, M. A.: Gastroesophageal Deconges-tion and Splenectomy in the Treatment ofEsophageal Varices in Bilharzial Cirrhosis:Further Studies with a Report on 355 Op-erations. Surgery, 61:169, 1967.

9. Hidayat, M. A.: Personal communication.10. Hubbard, T. B., Jr.: Carcinoma of the Head

of the Pancreas: Resection of the PortalVein and Portacaval Shunt. Ann. Surg., 147:935, 1958.

11. Jackson, F. C., Perrin, E. B., DeGradi, A. E.,Smith, A. G. and Lee, L. E.: Clinical In-vestigation of the Portacaval Shunt. Arch.Surg., 91:43, 1965.

12. Johnson, G., Jr., Dart, C. H., Peters, R. M.and MacFie, J. A.: Hemodynamic Changeswith Cirrhosis of the Liver: Control of Ar-teriovenous Shunts During Operation forEsophageal Varices. Ann. Surg., 163:692,1966.

13. Mikkelsen, W. P., Edmondson, H. A., Peters,R. L.,, Redeker, A. G. and Reynolds, T. B.:Extra- and Intrahepatic Portal Hypertensionwithout Cirrhosis (Hepatoportal Sclerosis).Ann. Surg., 162:602, 1965.

14. Orloff, M. J.: Emergency Portacaval Shunt:A Comparative Study of Shunt, Varix Liga-tion and Non-Surgical Treatment of Bleed-ing Esophageal Varices in Unselected Pa-tients with Cirrhosis. Ann. Surg. To be pub-lished.

15. Peters, R. M. and Womack, N. A.: Surgeryof Vascular Distortions in Cirrhosis of theLiver. Ann. Surg., 154:432, 1961.

16. Price, J. B., McCullough, W., Peterson, L.,Britton, R. C. and Voorhees, A. B.: In-

creased Intestinal Absorption Resulting fromPortal Systemic Shunting in the Dog andMan. Surg. Forum, 17:367, 1966.

17. Resrepo, J. E. and Warren, W. D.: LiverBlood Flow after Portacaval Shunt, HepaticArtery Ligation and 70% Hepatectomy.Ann. Surg., 156:719, 1962.

18. Smith, G. W.: Personal communication.19. Smith, G. W., Zug, R. C. and Wilson, S. K.:

Periarterial Neurectomy of the Hepatic Ar-tery: An Adjunct to Portacaval Shunt. Amer.J. Surg., 113:117, 1967.

20. Teague, F. B., Warren, W. D. and Respess,J. C.: Vascular Physiology in Portal Hyper-tension with Ascites. Ann. Surg., 163:112,1966.

21. Warren, W. D., Fomon, J. J., Viamonte, M.,Martinez, L. 0. and Kalser, M. H.: Spon-taneous Reversal of Portal Venous BloodFlow in Cirrhosis. Surg. Gynec. Obstet. (Inpress )

22. Warren, W. D., Fomon, J. J., Viamonte, M.and Zeppa, R.: The Pre-operative Assess-ment of Portal Hypertension. Ann. Surg.,165: , 1967.

23. Warren, W. D. and Muller, WV. H., Jr.: AClarification of Some Hemodynamic Changesin Cirrhosis and their Surgical Significance.Ann. Surg., 150:413, 1959.

24. Warren, W. D., Restrepo, J. E., Respess, J. C.and Muller, W. H.: The Importance ofHemodynamic Studies in Management ofPortal Hypertension. Ann. Surg., 158:387,1963.

25. Williams, R., Parsonon, A., Somers, K. andHamilton, P. J. S.: Portal Hypertension inIdiopathic Tropical Splenomegaly. Lancet,1:329, 1966.

26. Womack, N. A. and Peters, R. M.: An In-vestigation of the Relationship Between Por-tal Venous Pressure and Inferior Vena Cavaland Portal Venous Oxygen Saturations. Ann.Surg., 146:691, 1957.

27. Zeppa, R., Gollan, F. and Johnson, A. E.: Un-published data.

Book ReviewLower Extremity Amputations for Arterial Insufficiency: RICHARD WARREN, M.D.,

EUGENE E. RECORD, M.D., Boston, Little, Brown and Company, 1967, 102 pp.$12.50.

A short book on the technics of preoperative management, operation, postoperativerehabilitation, prostheses ordering, and safeguards for lower extremity amputations.Based on Warren's Procedures in Vascular Surgery and the authors' adopted methods;well illustrated by line drawings. Only brief mention is made of immediate prosthesisfitting; bibliography and index; attractively printed and bound; a good book for theresident's library.

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Selective Trans-Splenic Decompression of Gastroesophageal