Recurrent Variceal Hemorrhage Successful Warren Shunt Roy
a
E.
Carlson, MD, William
K.
Following
Ehrenfeld, MD
\s=b\ Recurrent variceal hemorrhages are demonstrated following technically successful Warren shunt. Serial barium esopha-
grams show the progressive enlargement of distal esophageal varices. Results of celiac arteriograms and direct examination confirmed the patency of the distal splenorenal shunt. Hemorrhage from varices was shown by fiberoptic esophagoscopy; end-to-side portacaval anastomosis reduced portal pressure and stopped the bleeding.
(Arch Surg 111:587-589, 1976)
variceal bleeding followed a technically successful, selective, distal splenorenal (Warren) shunt.' During the two years following operation in this 35year-old man, the esophageal varices continued to enlarge, culminating in massive hemorrhage. Repeat angiography just prior to a last laparotomy and shunt procedure showed a widely patent Warren shunt and massive esophageal, gastric, and abdominal visceral varices.
Recurrent
REPORT OF A CASE A 35-year-old Yemenite man was found to have Schistosoma mansoni parasites in a stool culture in 1968. Upper gastrointes¬ tinal (GI) x-ray series and liver scans showed enlargement of the left lobe of the liver and splenomegaly. Examination of rectal biopsy specimens confirmed the diagnosis of schistosomiasis, and the patient was treated with stibophen. In June 1972 he had his first episode of hematemesis, and an upper GI x-ray series showed esophageal varices. A second episode of hematemesis occurred in September 1972. A decompressive procedure was considered at this time, but was deferred because of the patient's markedly abnormal clotting times. No ascites was
present. Accepted for publication Nov 21, 1975. From the Department of Surgery, University
of California Medical
Center, San Francisco. Reprint requests to Department of Surgery, University of California Medical Center, San Francisco, CA 94143 (Dr Ehrenfeld).
He was admitted to the University of California Medical Center, San Francisco, in November 1972 with hematemesis and melena. An upper GI x-ray series again showed varices, and gastroscopy confirmed variceal hemorrhage as the cause of the bleeding (Fig 1). Pertinent laboratory values were as follows: total bilirubin, 0.9 mg/100 ml; total protein, 5.6 gm/100 ml; albumin, 3.1 gm/100 ml; platelets, 85,000/cu mm, and prothrombin time, 15 seconds. A selective, distal splenorenal shunt was then performed without difficulty. The splenic vein was divided at its junction with the inferior mesenteric vein, and a 2-cm anastomosis was created between the distal end of the splenic vein and the side of the renal vein. The gastrocolic ligament, coronary vein, and left gastric artery were divided and ligated. Measurement of pre¬ shunt and postshunt pressures showed reduction in pressures in the splenic vein from 37 to 26.5 cm of ILO, and in the renal vein from 14.5 to 15 cm of H,0, and reduction in central venous pressure from 13 to 14 cm of H20. A liver biopsy specimen showed macronodular cirrhosis, with focal areas of granulomata with calcifications, consistent with schistosomiasis of one to two years' duration. A barium esophagram in March 1973 (Fig 2) showed continued presence of esophageal varices. A liver-spleen scan revealed a decrease in the size of the spleen. Results of liver function studies remained normal. A routine follow-up upper GI x-ray series in January 1975 showed enlargement of the esophageal varices and the appearance of gastric varices (Fig 3 and 4). Twenty-eight months postoperatively, in March 1975, the patient had massive hematemesis and hematochezia. Endoscopy showed large, bleeding esophageal and gastric varices. Arteriography showed a patent shunt with numerous variceal collaterals in the splenic hilus, gastric varices, and a patent portal vein (Fig 5 and 6). Laboratory studies showed the following levels: total bilirubin, 10 mg/100 ml; total protein, 5.5 gm/100 ml; albumin, 3.3 gm/100 ml; prothrombin time, 15.5 seconds; and platelets, 75,000/ 100 cu mm. The hemorrhage was not controlled with a Sengstaken-Blakemore tube, nor with vasopressin (Pitressin) tannate given intra¬ venously or intra-arterially. After 10 units of blood were trans¬ fused, the patient was reexplored and an end-to-side portacaval shunt was constructed. During the procedure the splenorenal shunt was seen to be patent. The coronary vein, left gastric artery, and gastrocolic ligament had been divided and ligated, and there were massive varices throughout the abdomen. Following construction of the portacaval shunt, the portal pressure decreased
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Fig 2.—Barium esophagrams obtained five months postopera¬ tively show persistence of esophageal varices.
Fig 1.—Barium swallow roentgenograms showing large esopha¬ geal varices and absence of gastric varices. Films were obtained just before distal splenorenal (Warren) shunt.
Fig 4.—Roentgenogram of barium-filled stomach, also obtained 14 months postoperatively, showing large fundal varices (A).
Fig 3—Another barium esophagram obtained 14 months postop¬ eratively shows progressive enlargement of esophageal varices.
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Fig 5.—Venous phase of selective superior mesenteric artery arteriogram showing patency of portal vein (A) and numerous visceral varices. Large gastric varices are also evident (B). This study was performed 28 months following Warren shunt and just preceding patient's final laparotomy.
Fig 6—Venous phase of selective celiac artery arteriogram showing wide patency of Warren shunt. Distal splenic vein (A) is shown emptying into left renal vein (B) and vena cava (C). This study was also done 28 months postoperatively.
from 34 to 13 cm of H,,0. A liver biopsy specimen showed postnecrotic cirrhosis with foci of piecemeal necrosis. The patient's postoperative course was marked by progressive hepatic and renal failure resulting in his death on the 34th postoperative day, without recurrent variceal bleeding.
pression of gastroesophageal varices by distal splenorenal shunt. Ann Surg
COMMENT
In two articles, Warren et al1 stated that, following selective decompression of the portal system, esophageal varices were diminished or had disappeared when patients were restudied with barium swallow roentgenograms or angiography. However, in a later report 3 he stated that 25% to 30% of patients with large esophageal varices retain roentgenographic evidence of persistent filling defects in the esophagus, which is comparable to Jackson et al's4 findings in a report on portacaval shunts. In a five-year follow-up review of 58 patients, Warren et al1 have had only two patients with recurrent upper GI hemorrhage; in neither case was it thought to be due to varices. A selective, distal splenorenal shunt was originally chosen for our patient in order to maintain portal flow to an already compromised liver. The patient was free of major variceal hemorrhage or encephalopathy for 28 months following operation. Interval upper GI x-ray series and gastroscopy showed progressive increase in size of the varices. Gastroscopy at the time of his last hemorrhage confirmed the esophageal varices as the bleeding source. Arteriography showed massive varices in the presence of a patent shunt.
166:437-454, 1967. 2. Warren WD, Galambos JT: Distal splenorenal shunt for portal hypertension. Hosp Practice 8:77-86, 1973. 3. Warren WD, Salam AA, Hutson D, et al: Selective distal splenorenal shunt: Technique and results of operation. Arch Surg 108:306-314, 1974. 4. Jackson FC, Perrin EB, Felix WR, et al: A clinical investigation of the
portacaval
shunt. V. Survival 1971.
Surg 174:672-701,
analysis of
the
therapeutic operation.
Ann
-
References 1. Warren
WD, Zeppa R, Fomon JJ, et al: Selective trans-splenic decom-
Invited Editorial Comment This article by Carlson and Ehrenfeld relative to rebleeding from esophageal varices in the presence of a patent distal spleno¬ renal shunt is extremely pertinent. The most frequently asked question concerning this operation is its efficacy in controlling bleeding. In our experience extending over a period of nine years, no patient has been readmitted for bleeding in the presence of a patent shunt. This article shows that this can happen. However, I would emphasize that the basic procedure we recommend is an operation, not just a shunt. The portal-azygos disconnection is an important part of the operation, and it serves both to decompress the volume of flow to varices and to increase flow to the liver. The efficacy of the portal-azygos disconnection procedure is empha¬ sized by the recent work of Nabseth and his associates, who deliberately omitted this maneuver. In those patients, there was both rebleeding and encephalopathy. In Fig 5, although not marked by an arrow, there is a tremen¬ dous collateral (as large as the portal vein) in the position of the coronary vein. All veins of this size should be obliterated at the time of surgery. A second interesting phenomenon is that the shunt did not fill through the superior mesenteric injection. When we have found large, unligated collaterals, there is usually visual¬ ization of the splenorenal anastomosis. This is a most informative report, and one that deserves careful study. W. Dean Warren, MD Atlanta
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a
E.
Carlson, MD, William
K.
Following
Ehrenfeld, MD
\s=b\ Recurrent variceal hemorrhages are demonstrated following technically successful Warren shunt. Serial barium esopha-
grams show the progressive enlargement of distal esophageal varices. Results of celiac arteriograms and direct examination confirmed the patency of the distal splenorenal shunt. Hemorrhage from varices was shown by fiberoptic esophagoscopy; end-to-side portacaval anastomosis reduced portal pressure and stopped the bleeding.
(Arch Surg 111:587-589, 1976)
variceal bleeding followed a technically successful, selective, distal splenorenal (Warren) shunt.' During the two years following operation in this 35year-old man, the esophageal varices continued to enlarge, culminating in massive hemorrhage. Repeat angiography just prior to a last laparotomy and shunt procedure showed a widely patent Warren shunt and massive esophageal, gastric, and abdominal visceral varices.
Recurrent
REPORT OF A CASE A 35-year-old Yemenite man was found to have Schistosoma mansoni parasites in a stool culture in 1968. Upper gastrointes¬ tinal (GI) x-ray series and liver scans showed enlargement of the left lobe of the liver and splenomegaly. Examination of rectal biopsy specimens confirmed the diagnosis of schistosomiasis, and the patient was treated with stibophen. In June 1972 he had his first episode of hematemesis, and an upper GI x-ray series showed esophageal varices. A second episode of hematemesis occurred in September 1972. A decompressive procedure was considered at this time, but was deferred because of the patient's markedly abnormal clotting times. No ascites was
present. Accepted for publication Nov 21, 1975. From the Department of Surgery, University
of California Medical
Center, San Francisco. Reprint requests to Department of Surgery, University of California Medical Center, San Francisco, CA 94143 (Dr Ehrenfeld).
He was admitted to the University of California Medical Center, San Francisco, in November 1972 with hematemesis and melena. An upper GI x-ray series again showed varices, and gastroscopy confirmed variceal hemorrhage as the cause of the bleeding (Fig 1). Pertinent laboratory values were as follows: total bilirubin, 0.9 mg/100 ml; total protein, 5.6 gm/100 ml; albumin, 3.1 gm/100 ml; platelets, 85,000/cu mm, and prothrombin time, 15 seconds. A selective, distal splenorenal shunt was then performed without difficulty. The splenic vein was divided at its junction with the inferior mesenteric vein, and a 2-cm anastomosis was created between the distal end of the splenic vein and the side of the renal vein. The gastrocolic ligament, coronary vein, and left gastric artery were divided and ligated. Measurement of pre¬ shunt and postshunt pressures showed reduction in pressures in the splenic vein from 37 to 26.5 cm of ILO, and in the renal vein from 14.5 to 15 cm of H,0, and reduction in central venous pressure from 13 to 14 cm of H20. A liver biopsy specimen showed macronodular cirrhosis, with focal areas of granulomata with calcifications, consistent with schistosomiasis of one to two years' duration. A barium esophagram in March 1973 (Fig 2) showed continued presence of esophageal varices. A liver-spleen scan revealed a decrease in the size of the spleen. Results of liver function studies remained normal. A routine follow-up upper GI x-ray series in January 1975 showed enlargement of the esophageal varices and the appearance of gastric varices (Fig 3 and 4). Twenty-eight months postoperatively, in March 1975, the patient had massive hematemesis and hematochezia. Endoscopy showed large, bleeding esophageal and gastric varices. Arteriography showed a patent shunt with numerous variceal collaterals in the splenic hilus, gastric varices, and a patent portal vein (Fig 5 and 6). Laboratory studies showed the following levels: total bilirubin, 10 mg/100 ml; total protein, 5.5 gm/100 ml; albumin, 3.3 gm/100 ml; prothrombin time, 15.5 seconds; and platelets, 75,000/ 100 cu mm. The hemorrhage was not controlled with a Sengstaken-Blakemore tube, nor with vasopressin (Pitressin) tannate given intra¬ venously or intra-arterially. After 10 units of blood were trans¬ fused, the patient was reexplored and an end-to-side portacaval shunt was constructed. During the procedure the splenorenal shunt was seen to be patent. The coronary vein, left gastric artery, and gastrocolic ligament had been divided and ligated, and there were massive varices throughout the abdomen. Following construction of the portacaval shunt, the portal pressure decreased
Downloaded From: http://archsurg.jamanetwork.com/ by a Thomas Jefferson University User on 06/16/2015
Fig 2.—Barium esophagrams obtained five months postopera¬ tively show persistence of esophageal varices.
Fig 1.—Barium swallow roentgenograms showing large esopha¬ geal varices and absence of gastric varices. Films were obtained just before distal splenorenal (Warren) shunt.
Fig 4.—Roentgenogram of barium-filled stomach, also obtained 14 months postoperatively, showing large fundal varices (A).
Fig 3—Another barium esophagram obtained 14 months postop¬ eratively shows progressive enlargement of esophageal varices.
Downloaded From: http://archsurg.jamanetwork.com/ by a Thomas Jefferson University User on 06/16/2015
Fig 5.—Venous phase of selective superior mesenteric artery arteriogram showing patency of portal vein (A) and numerous visceral varices. Large gastric varices are also evident (B). This study was performed 28 months following Warren shunt and just preceding patient's final laparotomy.
Fig 6—Venous phase of selective celiac artery arteriogram showing wide patency of Warren shunt. Distal splenic vein (A) is shown emptying into left renal vein (B) and vena cava (C). This study was also done 28 months postoperatively.
from 34 to 13 cm of H,,0. A liver biopsy specimen showed postnecrotic cirrhosis with foci of piecemeal necrosis. The patient's postoperative course was marked by progressive hepatic and renal failure resulting in his death on the 34th postoperative day, without recurrent variceal bleeding.
pression of gastroesophageal varices by distal splenorenal shunt. Ann Surg
COMMENT
In two articles, Warren et al1 stated that, following selective decompression of the portal system, esophageal varices were diminished or had disappeared when patients were restudied with barium swallow roentgenograms or angiography. However, in a later report 3 he stated that 25% to 30% of patients with large esophageal varices retain roentgenographic evidence of persistent filling defects in the esophagus, which is comparable to Jackson et al's4 findings in a report on portacaval shunts. In a five-year follow-up review of 58 patients, Warren et al1 have had only two patients with recurrent upper GI hemorrhage; in neither case was it thought to be due to varices. A selective, distal splenorenal shunt was originally chosen for our patient in order to maintain portal flow to an already compromised liver. The patient was free of major variceal hemorrhage or encephalopathy for 28 months following operation. Interval upper GI x-ray series and gastroscopy showed progressive increase in size of the varices. Gastroscopy at the time of his last hemorrhage confirmed the esophageal varices as the bleeding source. Arteriography showed massive varices in the presence of a patent shunt.
166:437-454, 1967. 2. Warren WD, Galambos JT: Distal splenorenal shunt for portal hypertension. Hosp Practice 8:77-86, 1973. 3. Warren WD, Salam AA, Hutson D, et al: Selective distal splenorenal shunt: Technique and results of operation. Arch Surg 108:306-314, 1974. 4. Jackson FC, Perrin EB, Felix WR, et al: A clinical investigation of the
portacaval
shunt. V. Survival 1971.
Surg 174:672-701,
analysis of
the
therapeutic operation.
Ann
-
References 1. Warren
WD, Zeppa R, Fomon JJ, et al: Selective trans-splenic decom-
Invited Editorial Comment This article by Carlson and Ehrenfeld relative to rebleeding from esophageal varices in the presence of a patent distal spleno¬ renal shunt is extremely pertinent. The most frequently asked question concerning this operation is its efficacy in controlling bleeding. In our experience extending over a period of nine years, no patient has been readmitted for bleeding in the presence of a patent shunt. This article shows that this can happen. However, I would emphasize that the basic procedure we recommend is an operation, not just a shunt. The portal-azygos disconnection is an important part of the operation, and it serves both to decompress the volume of flow to varices and to increase flow to the liver. The efficacy of the portal-azygos disconnection procedure is empha¬ sized by the recent work of Nabseth and his associates, who deliberately omitted this maneuver. In those patients, there was both rebleeding and encephalopathy. In Fig 5, although not marked by an arrow, there is a tremen¬ dous collateral (as large as the portal vein) in the position of the coronary vein. All veins of this size should be obliterated at the time of surgery. A second interesting phenomenon is that the shunt did not fill through the superior mesenteric injection. When we have found large, unligated collaterals, there is usually visual¬ ization of the splenorenal anastomosis. This is a most informative report, and one that deserves careful study. W. Dean Warren, MD Atlanta
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