Pancreatic Ascites: a Rare Complication of Distal Splenorenal Shunt
Paul M. Gekas, MD, Geneva, Illinois Parviz Nikoomanesh, MD, Baltimore, Maryland Gardner W. Smith, MD, Baltimore, Maryland
Over the past 10 years, the surgical treatment of portal hypertension has been enhanced by the development of the distal splenorenal shunt [1,2]. One of the complications of this procedure is the development of ascites [ 1,3,4], which has on occasion been chylous in nature [5,6]. Herewith we present the first reported case of pancreatic ascites secondary to a distal splenorenal shunt. Case Report The patient was a 48 year old white woman admitted with massive hematemesis. She had a long history of alcohol abuse, reportedly discontinued 7 years earlier after her first episode of gastrointestinal bleeding. Before the present admission, she had been hospitalized on 15 occasions for gastrointestinal hemorrhage; varices had been endoscopically demonstrated as the source of bleeding on three admissions. During this interval she had cirrhosis proved by liver biopsy, and she underwent umbilical vein catheterization with angiography, which suggested portal vein thrombosis. The patient never had jaundice but did have intermittent mild ascites and mild encephalopathy in conjunction with major bleeding episodes. There was progressive splenomegaly associated with hematologic hypersplenism and some mild upper abdominal discomfort. She had no history of pancreatitis. Throughout the 7 years since her first episode of bleeding, she adamantly refused both definitive angiography and surgical therapy. On the present admission the patient had both hematemesis and melena; she presented with evidence of hyFrom the Departments of Medicine and Surgery. The Baltimore City Hospitals and The Johns Hopkins Medical Institutions, Baltimore, Maryland. Reauests for reprints should be addressed to Gardner W. Smith. MD. Department of Sur$ery, The Johns Hopkins Hospital, 601 North Broadway: Baltimore, Maryland 21205.
povolemia but was not in shock. She had no jaundice, ascites, or encephalopathy. The bleeding initially responded to iced saline lavage but recurred 2 days after admission, requiring 5 units of blood and intravenous vasopressin for control. Endoscopy at this time demonstrated hemorrhage from esophageal varices. The patient then finally consented to angiography, which revealed a recanalized portal vein, partial thrombosis of the superior mesenteric vein, and a huge splenic vein measuring 3 cm in diameter but otherwise apparently normal (Figure 1). The left renal vein was normal. The patient’s condition stabilized and she consented to a distal splenorenal shunt, which was performed electively. She had no jaundice, ascites, or encephalopathy, and the results of liver function tests were only mildly abnormal, making her a Child class A candidate. The serum amylase level was normal. At operation 800 ml of clear, yellow, ascitic fluid, massive splenomegaly,. and extensive vascular adhesions were found. The splenic vein was approached through the lesser sac from the inferior border of the pancreas. It was immediately apparent that the patient had chronic pancreatitis, which had not been detected previously. Dissection of the splenic vein and of its junction with the superior mesenteric and portal veins was accordingly difficult. On completion of the dissection, thrombosis of the superior mesenteric and portal veins was confirmed, but it was thought that the splenic vein was patent, although unusually large. The left renal vein was exposed and preparations were made for the distal splenorenal shunt. However, when the splenic vein was transected, it was apparent that two thirds of its diameter was occluded by organized thrombus. Because no other alternative was available, a thrombectomy was performed and, since flow seemed adequate, the distal splenorenal anastomosis was completed. The operation was concluded by division of the right gastroepiploic and coronary veins.
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Figure 1. Preoperative venous phase splenic arteriogram demonstrating a huge spleen and a greatly enlarged splenic vein.
The patient had an uneventful postoperative course and was discharged on the 15th postoperative day. At the time of discharge she had mild ascites that seemed to be responding to a low-salt diet, spironolactone, and hydrochlorothiazide. She was also noted to have a mild elevation of serum amylase to 296 dye units (DU)/dl (normal, 40 to 200 DU/dl). One week after discharge she had no complaints, continued mild ascites, and a serum amylase level of 696 DU/ dl. However, she returned 1 week later (almost 1 month after the operation) with severe abdominal pain, tense ascites, a 10 pound weight gain in 1 week, and a serum amylase level of 1,680 DU/dl. She was readmitted and diagnostic paracentesis revealed straw-colored ascitic fluid, sterile on culture, with an amylase level of 13,800 DU/dl and a protein content of 2.7 g/dl. Other diagnostic studies disclosed an amylase/creatinine clearance ratio of greater than 10, and sonography revealed no pseudocyst of the pancreas. Angiography confirmed the patency of the distal splenorenal shunt (Figure 2). The patient was treated vigorously with total parenteral nutrition, furosemide, spironolactone, [email protected]
, acetazolamide, and cimetidine. The serum amylase level remained above 1,500 DU/dl for about 2 weeks, during which time tense ascites persisted and encephalopathy developed. The patient also developed a right pleural effusion that had an amylase level of 4,800 DU/dl and a protein content of 3.8 g/dl. She then began to show gradual improvement and was finally discharged on the 48th hospital day, free of ascites and with a normal level of serum amylase and no gastrointestinal symptoms. The patient has since been followed up for 12
Volume 139, November 1979
Figure 2. Postoperative venous phase splenic arteriogram demonstrating a patent distal splenorenal shunt.
months, during which time the serum amylase level has remained less than 100 DU/dl and she has had no evidence of diabetes, no ascites, no symptoms, and has returned to work. Comments Pancreatic ascites has only recently been commonly recognized, and before 1967 only 13 cases had been reported . It is characterized by massive ascites associated with elevated serum and fluid amylase levels, relatively normal liver function tests, and an ascitic fluid protein level usually greater than 3 g/d1 [7-91. It is generally thought to be caused by rupture of the pancreatic ductal system, usually secondary to acute alcoholic pancreatitis, and more rarely by trauma, intraductal stones, duplication cysts of the pancreatic or biliary ducts, and ampullary stenosis . This condition is commonly seen in association with a pseudocyst [8,10]. The pleural effusions often seen concomitantly with this condition have biochemical characteristics similar to those of the ascitic fluid [11,12]. The cause of pancreatic ascites in the present case could be multifactorial since the patient had a long history of alcohol abuse, chronic pancreatitis, and also surgical trauma to the pancreas. The latter factor seems the most probable cause. In the first place, the surgical dissection of the splenic vein was extremely difficult and traumatic due to the chronic pancrea-
Gekas et al
titis and splenic vein thrombosis. Secondly, the onset of pancreatic ascites 4 weeks after operation is commensurate with the temporal relation in previously reported cases of traumatic pancreatic ascites . The only diagnostic study not employed in this patient to further elucidate the problem was endoscopic retrograde cholangiopancreatography. This study is of great value for patients who require operative therapy . However, because of recent major surgery, known vascular adhesions, and severe portal hypertensibn, it was elected to avoid operation in the present patient if at all possible. This decision was somewhat reinforced by the absence of sonographic evidence of a pseudocyst. Accordingly, it was decided that endoscopic retrograde cholangiopancreatography was not indicated. The treatmeht of pancreatic ascites remains somewhat controversial, although an initial trial of medical therapy is usually recommended [7,8,14]. The basic medical principle of treatment is to decrease pancreatic secretion, which may be accomplished by totalparenteral nutrition in combination with pharmacologic agents such as anticholingeric drugs and acetazolamide [7,8,15]. Repeated paracentesis , peritoneal lavage , and low dose pancreatic irradiation  have also been employed on occasion. Medical therapy is successful in slightly less than 50 per cent of cases , but fortunately succeeded in the present case. Ascites has become recognized as a frequent complication of distal splenorenal shunt [2,3,4]. The lymph fluid is usually thought to be intestinal or hepatic in origin , although recently a few cases of chylous ascites after this operation have been reported [5,6]. Most patients respond well to medical management, but the use of a LeVeen peritoneovenous shunt has been required on occasion . Pancreatic ascites has not previously been described as a complication of this procedure. However, the management of this problem differs in some respects from the treatment of cirrhotic or chylous ascites. Thus it is recommended that any patient in whom severe ascites develops after a distal splenorenal shunt should have appropriate diagnostic studies performed to rule out pancreatic ascites before therapy is instituted.
Ascites has become recognized as a common postoperative complication of the distal splenorenal shunt. On rare occasions the ascites has been chylous in nature. The present report is the first documented case of pancreatic ascites occurring after this operation. This complication developed in the combined setting of chronic pancreatitis and surgical trauma to the pancreas. Since the management of pancreatic ascites differs from that of cirrhotic or chylous ascites, it is recommended that this diagnosis be considered whenever a patient develops severe ascites after a distal splenorenal shunt.
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