End-to-Side Splenorenal Shunt for Treatment of Portal Hypertension Sarjit S. Gill, MS; Forrest C. Eggleston, MD; Chander


Singh, MS,

Twenty-eight patients with portal hypertension were treated with splenectomy and end-to-side splenorenal shunt. Nineteen had cirrhosis and nine had portal vein thrombosis. Among the patients with cirrhosis, there was one hospital death due to recurrent bleeding in a patient in whom shunt could not be constructed and only splenectomy was done. During the follow-up period, one patient developed encephalopathy and later died of liver

failure. There were three additional deaths, one due to an unrelated cause and two due to liver failure. All the remaining patients are well and none has had recurrent bleeding. All the patients with portal vein thrombosis survived the operation and are well. None has had recurrent bleeding. Encouraged by these results, we continue to use end-to-side splenorenal shunt in all patients except small children.

variety portasystemic Even thoughcomplicating past portal hypertension,

shunts has been of 30 years for the treatment of var¬ there still iceal bleeding is debate as to which is the best type of shunt. The end-toside portacaval shunt has had the largest trial and has been the most effective in lowering portal pressure and preventing bleeding. However, because of its many side effects, particularly encephalopathy, it frequently de¬ creases the quality of life to such a degree that the patient does not derive any ultimate benefit. As a result, several other types of shunts have been tried.1-' End-to-side splenorenal shunt was one of the earliest shunts to be used. However, it has fallen into disrepute and is not commonly used despite data to prove its superi¬ ority. Because of early good results with the use of this shunt, we have continued to use it routinely in all patients having variceal bleeding, except small children. It is the purpose of this article to review our experience with this shunt during the past seven years. a



for the


Twenty-eight patients with portal hypertension were treated splenectomy and end-to-side splenorenal shunt during the past seven years. All but two had bled during the recent past and, in ten, hemorrhage was life-threatening at the time of admission or during hospitalization. In eight of these ten, tamponade with a Sengstaken-Blakemore balloon had to be employed. Two of these had recurrent bleeding on discontinuing the tamponade and, in with

them, construction of the shunt was done on an emergency basis. Complete hemogram, liver function tests, and roentgenographic

publication Sept 11, 1974. Department of Surgery, Christian Medical College and Hospital, Ludhiana, Punjab, India. Reprint requests to Department of Surgery, Christian Medical College and Hospital, Ludhiana, Punjab, India (Dr. Eggleston). Accepted

From the



examination of the upper part of the gastrointestinal tract using barium were done in all cases. Measurement of splenic pulp pres¬ sure and splenoportography were done, usually on the morning of surgery. Although varices were seen on barium swallow in only 16 patients (57%), they were demonstrated in all patients on splenoportogram. The mean splenic pulp pressure was 420 mm saline. Eighteen patients (64%) had hypersplenism. The indications for shunt were variceal bleeding in 26 and hypersplenism associated with high portal pressure and gastroesophageal varices in two.

Cirrhosis Group There were 19 patients, 12 female and seven male, in whom the of portal hypertension was cirrhosis. Most of the patients were in the third and fourth decade of life, the youngest being 17 and the oldest 61 years of age. Six patients had consumed moder¬ ate amounts of alcohol and two gave a history of jaundice. Accord¬ ing to the criteria of Child,5 ten were in group A and nine in group B. Nine patients had moderate ascites that was easily controlled preoperatively. Assessment of hepatic portal flow was made from the splenoportograms as described by Warren.17 It was normal or only slightly reduced in eight, moderately reduced in ten, and se¬ verely reduced in one. cause

Portal Vein Thrombosis


There were nine patients, eight male and one female, in whom the cause of portal hypertension was thrombosis of the portal vein. All had normal livers. Six were in their second decade, the youngest patient being 10 and the oldest 38 years of age.



We constructed a central splenorenal shunt as recommended by Clatworthy and Boles.7 The approach was made through an oblique abdominothoracic incision in the ninth intercostal space. The lesser sac was entered through the gastrosplenic omentum and the splenic artery was identified along the upper border of the pancreas and ligated. The splenic vein was identified in the hilum of the spleen and followed medially until it disappeared under the pancreas. The central end was clamped by a vascular clamp, a tie was placed peripherally, and the vein was divided. The remaining attachments of the spleen were then divided and the spleen re¬ moved. The body of the pancreas was reflected to the patient's right, providing excellent exposure to the posterior surface of the splenic vein. The many small pancreatic tributaries were carefully isolated, ligated, and divided, and the vein freed up to its con¬

fluence with the inferior mesenteric vein. Next, a transverse inci¬ sion was made in the posterior peritoneum centered over the renal hilum, and the left renal vein was isolated in its medial part. Heparin sodium (50 mg in adults and 25 mg in children) was given intravenously, the renal artery clamped, and a medial segment of the renal vein isolated between vascular clamps. An ellipse of its anterior wall was excised. The splenic vein was brought to the re¬ nal vein, avoiding torsion or kinking. Its excess length was ex-

Downloaded From: http://archsurg.jamanetwork.com/ by a University of Manitoba User on 06/19/2015

Portal Vein Thrombosis Cirrhosis Death With Cirrhosis

fi ü i






: :


' V.„





Survival, yr Fig 1.—Aortogram in patient who developed systemic hyperten¬ sion following construction of splenorenal shunt. Note left renal ar¬ tery stenosis (arrow) that resulted from injury with application of vascular clamp.

Fig 2.—Follow-up of 27 patients who survived operation and were discharged from hospital. Four deaths occurred among patients with cirrhosis. Only one patient developed encephalopathy; he sub¬ sequently died. No patient had recurrent bleeding.

cised, leaving

nie abscess in one malaria in one.

an oblique stoma that was anastomosed to the win¬ dow in the renal vein using 6-0 monofilament suture. A continuous over-and-over suturing technique was used. In children, the ante¬ rior suture line was made with interrupted sutures. Just before the final suture was tied, the clamp on the splenic vein was mo¬ mentarily released to wash out any clots and the inside of the vein was thoroughly irrigated with heparinized saline.

RESULTS A satisfactory shunt was constructed in 27 patients (96%), all of whom did well and were discharged from the hospital. In one patient with cirrhosis, only splenectomy was done because of excessive intraoperative bleeding; she bled a few days later, developed septicemia, and died. This was our only hospital mortality. The two patients in whom the shunt was done on an emergency basis did well. Tamponade was discontinued on completion of the shunt. They have not bled since. COMPLICATIONS

Complications occurred

in four patients. One patient admitted two months postoperatively complaining of headache. She was found to be hypertensive. Blood pres¬ sure was 180/120 mm Hg. An intravenous pyelogram showed no dye in the left kidney. An aortogram revealed stenosis of the left renal artery (Fig 1) and reduction in size of the left kidney. This presumably was the result of injury to the artery from the application of a vascular clamp. An attempt was made to repair the stenosis, but it was unsuccessful. Accordingly, nephrectomy was done. After nephrectomy, the inferior mesenteric vein was can¬ nulated. Pressure was 180 mm of saline compared with 350 preshunt, and the portogram revealed the shunt to be patent. She is now one year postshunt, normotensive, and has not had recurrent bleeding. Other complications were less serious, namely, subphrewas


wound infection in one, and


Follow-up information is available in all cases. Figure 2 shows the length of follow-up and the number of late deaths in the entire series. Complete hemogram and liver function studies have been done on all. Barium swallow was done in patients who had varices on this examination




Four patients have died during the follow-up period. Following an eight-week afebrile postoperative course, one patient suddenly developed fever and died after a few days. She never bled. Necropsy was not done. We believe the cause of death was probably unrelated to the oper¬

ation. One 50-year-old man with advanced cirrhosis (group B) died at home two months after surgery. A portacaval shunt had been done initially, at which time the portal vein was found to be partially thrombosed. The shunt was done after thrombectomy, but it did not stay open and the patient bled again. A splenorenal shunt was then done. He did well initially but died later, presumably of liver fail¬ ure. He did not bleed. Necropsy was not done. The third patient died of liver failure and fungal septi¬ cemia 3% years postshunt. He had alcoholic cirrhosis (group B) and had resumed drinking after the operation. He did well until the terminal illness. His shunt was found open at necropsy. The fourth patient developed encephalopathy at three years postshunt and died of liver failure one year later. This is the only patient in this series who developed


Downloaded From: http://archsurg.jamanetwork.com/ by a University of Manitoba User on 06/19/2015

The remaining 14 patients are doing well after con¬ struction of the shunt. No patient has rebled. All are working normally. They have improved considerably in health, and ascites has not recurred in any of the nine pa¬ tients in whom it was present preoperatively and has not developed in any other patient. The hemoglobin level in every patient is above 12 gm/100 ml, the mean hemoglobin level now being 13.2 gm/100 ml (preoperative, 6.2 gm/100 ml). The blood pic¬ ture has returned completely to normal in the patients who had hypersplenism before surgery. The liver func¬ tions have improved in every case. Mean serum albumin level postoperatively is 4.9 gm/100 ml as compared to a mean of 3.9 gm/100 ml preoperatively. Portal Vein Thrombosis


All nine patients in this group survived the operation and are doing extremely well. None had recurrent bleed¬






Portasystemic shunts are created most commonly for the treatment of variceal bleeding complicating portal hy¬ pertension. In patients with portal vein thrombosis, such shunts protect the patient from recurrent bleeding and cause very few side effects. However, in patients with cir¬ rhosis, the outlook is entirely different. Here, if a shunt di¬ verts large volumes of intestinal venous blood from the liver, it impairs hepatocellular function and produces en¬ cephalopathy. An ideal shunt should prevent variceal bleeding and cause no untoward effects. Recently, Warren et al1 and Britton8 listed the physiological criteria of an ideal shunt, the most important of which is that such a shunt should preserve hepatic portal flow while adequately decompressing the gastroesophageal varices. These crite¬ ria are perhaps best fulfilled by the distal splenorenal shunt, as devised by Warren et al,1 and the side-to-side splenorenal shunt with ligation of the mesenteric end of the splenic vein, as suggested by Britton.8 The end-to-side splenorenal shunt also appears to meet these criteria and is technically much easier. This latter type of shunt has been described as a small variety of side-to-side porta¬ caval shunt; however, because of its smaller size and loca¬ tion, it behaves physiologically quite differently from a standard side-to-side portacaval shunt. Since it is smaller in diameter, it is hemodynamically less effective and of¬ fers greater resistance to the flow of large volumes of blood through it. The direction of the flow of blood in the superior mesen¬ teric vein after the construction of the shunt, whether hepatopetal or hepatofugal (through the shunt), depends on the relative resistance to the flow of blood in the liver and through the shunt. In early stages of cirrhosis, the in¬ trahepatic resistance is probably lower than that through the shunt; consequently, the superior mesenteric vein flow is predominantly hepatopetal. Britton" used wedge phlebography to study six patients in whom he had done side-to-side splenorenal shunts. In none could the contrast material injected by hand be forced in a retrograde direc-

tion into the superior mesenteric vein or into the shunt, indicating that hepatopetal portal flow only was present. Since a splenorenal shunt done side-to-side is similar he¬ modynamically to one done end-to-side, the portal flow following the latter is also likely to be hepatopetal. There is indirect evidence in our series that the end-toside splenorenal shunt does not divert large amounts of superior mesenteric vein blood from the liver. As judged from the preoperative splenoportograms, hepatic portal flow was normal or only moderately reduced in all except one of our patients. These are the patients who do poorly following the construction of a shunt that diverts large amounts of blood from the liver. Yet, following the sple¬ norenal shunt, all of the patients did well; none developed hepatic failure or encephalopathy during the early postop¬ erative period. Of the three deaths due to liver failure, only one occurred during the early follow-up period. This patient had advanced cirrhosis and hepatic portal flow was already severely reduced before the construction of the shunt. The other two deaths, including the one that followed a period of encephalopathy, occurred 3!/2 and four years postshunt and appear related to progression of in¬ trinsic liver pathology rather than to diversion of portal blood. To be sure, end-to-side splenorenal shunt does create a potential channel for reversal of portal blood flow occur¬ ring as the disease in the liver advances and the intra¬ hepatic resistance increases. But, this can happen in a pa¬ tient in whom no surgical shunt has been constructed through natural portasystemic shunts and has happened in one patient in whom distal splenorenal shunt was con¬ structed by Warren.9 The major reason a splenorenal shunt is not frequently used is that it is one of the more difficult shunts to create and has the highest incidence of occlusion. The splenic and renal veins are small, thin, and fragile compared to the much wider, thicker, and stronger portal vein and inferior vena cava. However, if the splenic vein is followed cen¬ trally, it becomes thicker and wider, and a central sple¬ norenal shunt is less difficult to create and is more likely to stay open. This shunt is placed very close to the entrance of the coronary vein, thereby providing excellent decom¬ pression of gastroesophageal varices. Because of its small size, it does not lower the intestinal venous pressure to normal. This has been shown to be beneficial, as a raised intestinal venous pressure slows ammonia absorption.1" However, it does lower the pressure enough so that the varices do not bleed. Employing such a shunt, we have not had recurrent bleeding in any of our patients observed up to seven years. Linton et al1112 and Hallenbeck et al" have reported on the superiority of end-to-side splenorenal shunt over porta¬ caval shunt. From a comparative analysis of splenorenal and portacaval shunts, Linton et al11 concluded that pa¬ tients have longer, healthier, and happier lives following a splenorenal shunt than following a portacaval shunt. At the end of five years, 57% of their patients who had had splenorenal shunts were alive as opposed to 36% who had had portacaval shunts. They reported an incidence of 68%

Downloaded From: http://archsurg.jamanetwork.com/ by a University of Manitoba User on 06/19/2015


hepatic coma following portacaval shunt, as compared following splenorenal shunt. Hallenbeck et al13 re¬ ported a 25% incidence of encephalopathy following por¬ tacaval shunts, but only a 5% incidence following splenore¬ nal shunts. They also reported a better survival following splenorenal shunts than following portacaval shunts. The incidence of recurrent bleeding (19%) was the same in both shunt groups in the series reported by Linton et al11 and similar results were reported by Hallenbeck et al.13 In the series of McDermott et al,14 encephalopathy occurred twice as frequently following portacaval shunts as follow¬ ing splenorenal shunts. However, the patients in the lat¬ to 7%

ter group had better liver functions and were in better general condition. Voorhees et al,15 on the other hand,

found no statistically significant difference in the inci¬ dence of encephalopathy among the patients undergoing portacaval and splenorenal shunts. They reported a much higher incidence of probable shunt occlusion (19%) follow¬ ing splenorenal shunt than following portacaval shunt (5%). In our small series of 19 patients in whom portal hy¬ pertension was due to cirrhosis, we were able to get good results and confirm the value of the end-to-side spleno¬ renal shunt. Among patients with portal hypertension due to portal vein thrombosis, splenorenal shunt is one of the two shunts that can be constructed. These patients are mostly children. The splenic vein is of good caliber by the age of 8 years, and it is possible to construct a splenorenal shunt from this age onward. Hypersplenism is frequently associated with portal hy¬ pertension. While reduction of portal hypertension follow¬ ing a portacaval shunt frequently corrects hypersplenism, the results are not always predictable. Sometimes it per¬ sists and may even become worse.1618 Splenectomy com¬ bined with splenorenal shunt always cures hypersplenism. This was our experience. We do not believe in the use of prophylactic shunt, but if a patient with hypersplenism is found to have portal hypertension and varices on splenoportography, splenectomy is combined with a splenorenal shunt. This was done twice in this series. For variceal bleeding that cannot be controlled by con¬ servative measures, emergency portacaval shunt is gener¬ ally recommended in good-risk patients.19 However, this may not be a good shunt in a patient who is bleeding ac¬ tively and, as a result, has further impairment of his liver function as well as a lot of blood in his bowel. A splenore¬ nal shunt may be a better shunt since it does not divert as large a quantity of intestinal blood from the liver. This

shunt was used twice in these circumstances with excel¬ lent results. Thus, we see that an end-to-side splenorenal shunt has wide application among the patients with portal hyper¬ tension. We have been so pleased with its results that we now use it in every case of portal hypertension that re¬ quires a shunt for variceal bleeding, except in small children. References 1. Warren


WD, Zeppa R, Fomon JJ: Selective trans-splenic de-

of gastroesophageal varices by distal splenorenal shunt. Ann Surg 166:437-455, 1967. 2. Britton RC, Voorhees AB Jr, Price JB Jr: Selective portal decompression. Surgery 67:104-113, 1970. 3. Drapanas T: Interposition mesocaval shunt for treatment of portal hypertension. Ann Surg 176:435-448, 1972. 4. Haller JD, Glick H, Hallman GL, et al: Portal decompression by side-to-side splenorenal venous anastomosis: Results in 14 patients. Arch Surg 102:316-321, 1971. 5. Child CG III: The Liver and Portal Hypertension. Philadelphia, WB Saunders Co, 1964, p 50. 6. Warren WD, Fomon JJ, Viamonte M, et al: Preoperative assessment of portal hypertension. Ann Surg 165:999-1012, 1967. 7. Clatworthy HW Jr, Boles ET Jr: Extrahepatic portal bed block in children: Pathogenesis and treatment. Ann Surg 150:371\x=req-\ 383, 1959. 8. Britton RC: Surgical treatment of complications of portal hypertension. Ann NY Acad Sci 170:358-366, 1970. 9. Warren WD, in discussion, Jackson FC, Perrin EB, Felix WR, et al: A clinical investigation of the portacaval shunt: V. Survival analysis of the therapeutic operation. Ann Surg 174:672-701, 1971. 10. Price JB Jr, McCullough W, Peterson L, et al: Effects of portal systemic shunting on intestinal absorption in the dog and in man. Surg Gynecol Obstet 125:305-310, 1967. 11. Linton RR, Ellis DS, Geary JE: Critical comparative analysis of early and late results of splenorenal and direct portacaval shunts performed in 169 patients with portal cirrhosis. Ann Surg 154:446-459, 1961. 12. Linton RR: A splenorenal or a portacaval shunt? Surg Gynecol Obstet 121:117-118, 1965. 13. Hallenbeck GA, Wollaeger EE, Adson MA, et al: Results after portal-systemic shunts in 120 patients with cirrhosis of the liver. Surg Gynecol Obstet 116:435-442, 1963. 14. McDermott WV Jr, Barnes BA, Nardi GL, et al: Postshunt encephalopathy. Surg Gynecol Obstet 126:585-590, 1968. 15. Voorhees AB Jr, Price JB Jr, Britton RC: Portasystemic shunting procedures for portal hypertension: 26 years experience in adults with cirrhosis of the liver. Am J Surg 119:501-505,1970. 16. Tumen HJ: Hypersplenism and portal hypertension. Ann NY Acad Sci 170:332-344, 1970. 17. Liebowitz HR: Splenomegaly and hypersplenism pre- and post-portacaval shunt. NY State J Med 63:2631-2638, 1963. 18. Rousselot LM, Panke WF, Bono RF, et al: Experience with portacaval anastomosis: Analysis of 104 elective end-to-side shunts for the prevention of recurrent hemorrhage from esophagogastric varices (1952 through 1961). Am J Med 34:297-307,1963. 19. Conn HO: The prognosis and management of bleeding esophageal varices. Ann NY Acad Sci 170:345-357, 1970.

Downloaded From: http://archsurg.jamanetwork.com/ by a University of Manitoba User on 06/19/2015

End-to-side splenorenal shunt for treatment of portal hypertension.

Twenty-eight patients with portal hypertension were treated with splenectomy and end-to-side splenorenal shunt. Nineteen had cirrhosis and nine had po...
1MB Sizes 0 Downloads 0 Views