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Pancreatic ascites: Management by caudal pancreatectomy and side-to-side pancreaticojejunostomy
Pancreatic Ascites: Management by Caudal Pancreatectomy And Side-to-Side Pancreaticojejunostomy
Frank C. Sparks, MD,* New Canaan, Connecticut Joel B. Levine, MD,+ Farmington, Connecticut E. Marvin Henken, MD,* Farmington, Connecticut
Pancreatic ascites usually occurs in patients with chronic alcoholic pancreatitis and is postulated to arise when pancreatic juice leaks from either a ruptured pseudocyst or disrupted major pancreatic duct [I]. An initial trial of pancreatic rest and total parenteral nutrition is indicated and results in spontaneous resolution of ascites in a significant number of cases [&2]. If the patient fails to respond to this treatment, endoscopic retrograde cholangiopancreatography is indicated to identify pseudocysts, to precisely locate the site of pancreatic duct disruption, and to identify any calculi that may be present [3]. Surgical treatment is effective in 65 to 80 per cent of patients and consists of partial pancreatectomy or internal drainage of a leaking pseudocyst or ruptured pancreatic duct by a defunctionalized Roux-en-Y jejunostomy, or both [2]. We recently treated a patient with pancreatic ascites and a chronic pain syndrome secondary to chronic alcoholic pancreatitis in whom pre- and intraoperative pancreatography failed to demonstrate the expected pseudocyst or site of pancreatic duct disruption. The ductal system was diffusely abnormal, with proximal duct of Wirsung dilatation and obstruction due to both stricture and pancreatic calculi. The distal duct was markedly ectatic and stenosed in a pattern characteristic of advanced chronic pancreatitis. Both the ascites and the patient’s chronic pain were successfully managed by caudal pancreatectomy and side-to-side pancreaticojejunostomy. To our knowledge this operative approach has not been previously described with such a clinical presentation. From the Departments of Surgery,’ Medicine,+ and Radiology,s University of Connecticut Health Center, Farmington. Connecticut. Reprint requests should be addressed to Frank C. Sparks, MD, 1 Colonial Court, New Canaan, Connecticut 06840.
Volume 136, November 1979
Case Report A 39 year old man with a long history of chronic alcoholic pancreatitis was transferred to the University of Connecticut Health Center on December 15, 1977 with a diagnosis of pancreatic ascites of 1 month’s duration. Physical examination showed a cachectic man weighing 60.43 kg (133 pounds) whose abdomen contained massive ascites: The amylase level in serum was 2,275 Somogyi units (Su)/lOO ml (normal less than 180), in ascites 29,750 Su/lOO ml, and in urine 43,000 Su/lOO ml. The rate of amylase/ creatinine clearance was 4.9 per cent. Serum albumin level was 2.0 g/100 ml. Endoscopic retrograde cholangiopancreatography demonstrated multiple irregularly dilated branched ducts within the head of the pancreas, containing numerous calculi. Ductal disruption was not demonstrated. The patient was treated first with an elemental diet and then with total parenteral nutrition and diuretics. His ascites cleared and he was discharged on January 16, 1978 weighing 56.81 kg (125 pounds), eating an unrestricted diet, and free of pain. He was readmitted on January 29,1978 with acute abdominal pain and sudden recurrence of ascites. Examination of the abdomen showed diffuse tenderness and rebound. Because the findings suggested an acute abdominal catastrophe, exploratory laparotomy was performed. Five liters of ascites was removed. The pancreas was firm and scarred. Pancreatography was not performed, but no gross pancreatic duct disruption, pancreatic abscess, pseudocyst, or fat necrosis was noted. Postoperatively the patient was treated with total parenteral nutrition. Ascites and hyperamylasemia persisted despite conservative therapy. By February 28, 1978 the patient’s nutritional status had improved markedly and operation was performed, beginning with cholecystectomy and operative cholangiography, which showed no stones in the common duct. Frozen section biopsy of the caudal tip of the pancreas showed chronic pancreatitis with almost complete replacement by fibrous tissue. Operative pancreatography was performed by way of the tail of the pancreas (Figure 1). The duct was alter-
713
Sparks et al
Figure 7. Operating room pancreaiogram performed with the catheter in the tail of the pancreas. The main duct Is segmentally strictured and dilated with prominent secondary branches. hlote the signtficant dilatation of the midduct (arrows).
nately strictured and dilated. A caudal pancreatectomy was performed. The pancreatic duct was then opened to within 1 cm of the duodenum, transecting the anterior pancreaticoduodenal artery in order to remove numerous calculi. A longitudinal side-to-side pancreaticojejunostomy with a Roux-en-Y anastomosis was performed (Figure 2). The patient had an uneventful postoperative course and was discharged on March 15,1978 on a low-fat diet. He was readmitted June 15,1978 with a history of four to six bowel movements a day. He had no further abdominal pain and a good appetite, and had continued to drink alcohol. On examination he had no ascites. Fasting glucose was 82 mg/dl, serum amylase 120 Su/dl, and serum album& 3.3 g/dl. The stool contained 16 g/24 hours of total lipids (normal less than 7) and 4.1 g/24 hours of nitrogen. Viokase@ was prescribed and the patient was discharged. He subsequently gained 5 pounds and now has three bowel movements a day. Comments
Pancreatic ascites occurs when pancreatic duct disruption is not localized by surrounding tissue, allowing pancreatic secretions to escape freely into the peritoneal cavity. Although pancreatic ascites usually does not cause peritoneal irritation, it may present as an acute abdominal catastrophe that requires urgent operative intervention [2], as it did in our patient’s second admission. Chronic pancreatic ascites has been treated by various methods, including nonoperative management with bowel rest, elemental diet, or total parenteral nutrition [I], peritoneal lavage [4], external drainage [I], resection of a pseudocyst with [2,5] and without [5] a Roux-en-Y jejunostomy to the distal pancreatic duct, sphincteroplasty [4], drainage of the pseudocyst or ruptured pancreatic duct, or both, by a Roux-en-Y jejunostomy [I], Puestow procedure [5], caudal pancreatectomy with [6,7] and without [3] 714
Figure 2. Side-to-side pancreaticojejunostomy with caudal pancreatectomy.
distal end-to-side Roux-en-Y jejunostomy, cystgastrostomy [1,2], thoracic duct drainage [8], and irradiation [9]. The choice of surgical procedure must be individualized to fit the underlying pathophysiology. An underlying principle is that procedures that relieve pancreatic obstruction will control ascites. The alternatives are multiple and the choice is based on demonstration of a specific site of duct rupture or, more commonly, the presence of a pseudocyst. Such pseudocysts were present in 45 of 73 patients reported on by Donowitz et al 111.In 15 to 30 per cent of patients a pseudocyst or disrupted duct cannot be demonstrated either pre- or intraoperatively [1,2,4]. In such cases decompression of the main duct is recommended [5]. The operative mortality rate is 6 to 22 per cent [1,2], and a major postoperative problem has been the recurrence of ascites, presumably due to failure to identify the leak or to breakdown of the anastomotic site [I]. Our patient with recurrent pancreatic ascites and chronic calcific pancreatitis had neither a pseudocyst nor a demonstrable site of duct rupture. Side-to-side pancreaticojejunostomy is a procedure designed to relieve pancreatic duct obstruction and control ascites. Caudal pancreatectomy alone is effective in treating the pain syndrome in chronic pancreatitis, especially when the ductal changes are most marked in the body and tail of the pancreas [lo], as they were in our patient. The combination of these two procedures, first described for the treatment of chronic pancreatitis with calculi [Ill, has relieved our patient of both pain and ascites. Pancreatic ascites is an interesting presentation of a complication of chronic pancreatitis. We suggest that attention should be directed to the management The Americen Journal 01 Surgery
Pancreatic
of the underlying disease. Even when a pseudocyst or duct disruption is evident, patients with chronic pancreatic ascites may additionally benefit from procedures directed at correcting coexisting complications of their chronic pancreatitis, namely obstruction from strictures and calculi, or areas of severe fibrosis, Summary A patient with pancreatic ascites is presented who had neither a pseudocyst nor demonstrable pancreatic duct disruption, despite the presence of both calculi and strictures in a dilated duct of Wirsung. Concurrently, the patient exhibited intractable abdominal pain characteristic of end-stage chronic alcoholic pancreatitis. The pancreatic ascites responded only briefly to nonoperative management with hyperalimentation. Side-to-side pancreticojejunostomy with caudal pancreatectomy relieved the patient of both pain and ascites, suggesting that this more direct approach may be worthy of consideration in patients with similar findings.
Volume 138, November 1979
Ascites
References 1. Donowitz M, Kerstein MD, Spiro HM: Pancreatic ascites. Medicine (Baltimore) 53: 183. 1974. 2. Smith RB ill, Warren WD, Rivard AA Jr, Amerson JR: Pancreatic ascites: diagnosis and management with particular reference to surgical technics. Ann Surg 177: 538, 1973. 3. Levine JB, Warshaw AL, Falchuk KR, Schapiro RH: The value of endoscopic retrograde pancreatography in the management of pancreatic ascites. Surgery 81: 360, 1977. 4. Paloyan D, Skinner DB: Clinical significance of pancreatic ascites. Am JSurg 132: 114, 1976. 5. Cameron JL, Brawiey RK, Bender HW, Zuidema GD: The treatment of pancreatic ascites. Ann Surg 170: 668, 1969. 6. Carneiro Chaves FJZ, Amarante M Jr, Domingues WS, Lopes C: Pancreatic ascites: calcification as a clue to diagnosis. Am J Gastroenterol67: 253, 1977. 7. Schindler SC, Schaefer JW, Hull D, Griffen WO: Chronic pancreatic ascites. Gasrroenferology 59: 453, 1970. 8. Dreiling DA: The lymphatics, pancreatic ascites and pancreatic inflammatory disease. Am J Gastroenterol53: 119, 1970. 9. Kavin H, Sobel JD, Dembo AJ: Pancreatic ascites treated by irradiation of pancreas. Br Med J 2: 502, 197 1. 10. Frey CF, Child CG, Frey W: Pancreatectomy for chronic pancreatitis. Ann Surg 184: 403, 1976. 11. Sato T, Kakazaki G, Saitoh Y, Maki T: Side-to-side pancreaticojejunostomy with caudal pancreatectomy for treatment of chronic pancreatitis with calculi. Arch Surg 96: 892, 1968.
715
Frank C. Sparks, MD,* New Canaan, Connecticut Joel B. Levine, MD,+ Farmington, Connecticut E. Marvin Henken, MD,* Farmington, Connecticut
Pancreatic ascites usually occurs in patients with chronic alcoholic pancreatitis and is postulated to arise when pancreatic juice leaks from either a ruptured pseudocyst or disrupted major pancreatic duct [I]. An initial trial of pancreatic rest and total parenteral nutrition is indicated and results in spontaneous resolution of ascites in a significant number of cases [&2]. If the patient fails to respond to this treatment, endoscopic retrograde cholangiopancreatography is indicated to identify pseudocysts, to precisely locate the site of pancreatic duct disruption, and to identify any calculi that may be present [3]. Surgical treatment is effective in 65 to 80 per cent of patients and consists of partial pancreatectomy or internal drainage of a leaking pseudocyst or ruptured pancreatic duct by a defunctionalized Roux-en-Y jejunostomy, or both [2]. We recently treated a patient with pancreatic ascites and a chronic pain syndrome secondary to chronic alcoholic pancreatitis in whom pre- and intraoperative pancreatography failed to demonstrate the expected pseudocyst or site of pancreatic duct disruption. The ductal system was diffusely abnormal, with proximal duct of Wirsung dilatation and obstruction due to both stricture and pancreatic calculi. The distal duct was markedly ectatic and stenosed in a pattern characteristic of advanced chronic pancreatitis. Both the ascites and the patient’s chronic pain were successfully managed by caudal pancreatectomy and side-to-side pancreaticojejunostomy. To our knowledge this operative approach has not been previously described with such a clinical presentation. From the Departments of Surgery,’ Medicine,+ and Radiology,s University of Connecticut Health Center, Farmington. Connecticut. Reprint requests should be addressed to Frank C. Sparks, MD, 1 Colonial Court, New Canaan, Connecticut 06840.
Volume 136, November 1979
Case Report A 39 year old man with a long history of chronic alcoholic pancreatitis was transferred to the University of Connecticut Health Center on December 15, 1977 with a diagnosis of pancreatic ascites of 1 month’s duration. Physical examination showed a cachectic man weighing 60.43 kg (133 pounds) whose abdomen contained massive ascites: The amylase level in serum was 2,275 Somogyi units (Su)/lOO ml (normal less than 180), in ascites 29,750 Su/lOO ml, and in urine 43,000 Su/lOO ml. The rate of amylase/ creatinine clearance was 4.9 per cent. Serum albumin level was 2.0 g/100 ml. Endoscopic retrograde cholangiopancreatography demonstrated multiple irregularly dilated branched ducts within the head of the pancreas, containing numerous calculi. Ductal disruption was not demonstrated. The patient was treated first with an elemental diet and then with total parenteral nutrition and diuretics. His ascites cleared and he was discharged on January 16, 1978 weighing 56.81 kg (125 pounds), eating an unrestricted diet, and free of pain. He was readmitted on January 29,1978 with acute abdominal pain and sudden recurrence of ascites. Examination of the abdomen showed diffuse tenderness and rebound. Because the findings suggested an acute abdominal catastrophe, exploratory laparotomy was performed. Five liters of ascites was removed. The pancreas was firm and scarred. Pancreatography was not performed, but no gross pancreatic duct disruption, pancreatic abscess, pseudocyst, or fat necrosis was noted. Postoperatively the patient was treated with total parenteral nutrition. Ascites and hyperamylasemia persisted despite conservative therapy. By February 28, 1978 the patient’s nutritional status had improved markedly and operation was performed, beginning with cholecystectomy and operative cholangiography, which showed no stones in the common duct. Frozen section biopsy of the caudal tip of the pancreas showed chronic pancreatitis with almost complete replacement by fibrous tissue. Operative pancreatography was performed by way of the tail of the pancreas (Figure 1). The duct was alter-
713
Sparks et al
Figure 7. Operating room pancreaiogram performed with the catheter in the tail of the pancreas. The main duct Is segmentally strictured and dilated with prominent secondary branches. hlote the signtficant dilatation of the midduct (arrows).
nately strictured and dilated. A caudal pancreatectomy was performed. The pancreatic duct was then opened to within 1 cm of the duodenum, transecting the anterior pancreaticoduodenal artery in order to remove numerous calculi. A longitudinal side-to-side pancreaticojejunostomy with a Roux-en-Y anastomosis was performed (Figure 2). The patient had an uneventful postoperative course and was discharged on March 15,1978 on a low-fat diet. He was readmitted June 15,1978 with a history of four to six bowel movements a day. He had no further abdominal pain and a good appetite, and had continued to drink alcohol. On examination he had no ascites. Fasting glucose was 82 mg/dl, serum amylase 120 Su/dl, and serum album& 3.3 g/dl. The stool contained 16 g/24 hours of total lipids (normal less than 7) and 4.1 g/24 hours of nitrogen. Viokase@ was prescribed and the patient was discharged. He subsequently gained 5 pounds and now has three bowel movements a day. Comments
Pancreatic ascites occurs when pancreatic duct disruption is not localized by surrounding tissue, allowing pancreatic secretions to escape freely into the peritoneal cavity. Although pancreatic ascites usually does not cause peritoneal irritation, it may present as an acute abdominal catastrophe that requires urgent operative intervention [2], as it did in our patient’s second admission. Chronic pancreatic ascites has been treated by various methods, including nonoperative management with bowel rest, elemental diet, or total parenteral nutrition [I], peritoneal lavage [4], external drainage [I], resection of a pseudocyst with [2,5] and without [5] a Roux-en-Y jejunostomy to the distal pancreatic duct, sphincteroplasty [4], drainage of the pseudocyst or ruptured pancreatic duct, or both, by a Roux-en-Y jejunostomy [I], Puestow procedure [5], caudal pancreatectomy with [6,7] and without [3] 714
Figure 2. Side-to-side pancreaticojejunostomy with caudal pancreatectomy.
distal end-to-side Roux-en-Y jejunostomy, cystgastrostomy [1,2], thoracic duct drainage [8], and irradiation [9]. The choice of surgical procedure must be individualized to fit the underlying pathophysiology. An underlying principle is that procedures that relieve pancreatic obstruction will control ascites. The alternatives are multiple and the choice is based on demonstration of a specific site of duct rupture or, more commonly, the presence of a pseudocyst. Such pseudocysts were present in 45 of 73 patients reported on by Donowitz et al 111.In 15 to 30 per cent of patients a pseudocyst or disrupted duct cannot be demonstrated either pre- or intraoperatively [1,2,4]. In such cases decompression of the main duct is recommended [5]. The operative mortality rate is 6 to 22 per cent [1,2], and a major postoperative problem has been the recurrence of ascites, presumably due to failure to identify the leak or to breakdown of the anastomotic site [I]. Our patient with recurrent pancreatic ascites and chronic calcific pancreatitis had neither a pseudocyst nor a demonstrable site of duct rupture. Side-to-side pancreaticojejunostomy is a procedure designed to relieve pancreatic duct obstruction and control ascites. Caudal pancreatectomy alone is effective in treating the pain syndrome in chronic pancreatitis, especially when the ductal changes are most marked in the body and tail of the pancreas [lo], as they were in our patient. The combination of these two procedures, first described for the treatment of chronic pancreatitis with calculi [Ill, has relieved our patient of both pain and ascites. Pancreatic ascites is an interesting presentation of a complication of chronic pancreatitis. We suggest that attention should be directed to the management The Americen Journal 01 Surgery
Pancreatic
of the underlying disease. Even when a pseudocyst or duct disruption is evident, patients with chronic pancreatic ascites may additionally benefit from procedures directed at correcting coexisting complications of their chronic pancreatitis, namely obstruction from strictures and calculi, or areas of severe fibrosis, Summary A patient with pancreatic ascites is presented who had neither a pseudocyst nor demonstrable pancreatic duct disruption, despite the presence of both calculi and strictures in a dilated duct of Wirsung. Concurrently, the patient exhibited intractable abdominal pain characteristic of end-stage chronic alcoholic pancreatitis. The pancreatic ascites responded only briefly to nonoperative management with hyperalimentation. Side-to-side pancreticojejunostomy with caudal pancreatectomy relieved the patient of both pain and ascites, suggesting that this more direct approach may be worthy of consideration in patients with similar findings.
Volume 138, November 1979
Ascites
References 1. Donowitz M, Kerstein MD, Spiro HM: Pancreatic ascites. Medicine (Baltimore) 53: 183. 1974. 2. Smith RB ill, Warren WD, Rivard AA Jr, Amerson JR: Pancreatic ascites: diagnosis and management with particular reference to surgical technics. Ann Surg 177: 538, 1973. 3. Levine JB, Warshaw AL, Falchuk KR, Schapiro RH: The value of endoscopic retrograde pancreatography in the management of pancreatic ascites. Surgery 81: 360, 1977. 4. Paloyan D, Skinner DB: Clinical significance of pancreatic ascites. Am JSurg 132: 114, 1976. 5. Cameron JL, Brawiey RK, Bender HW, Zuidema GD: The treatment of pancreatic ascites. Ann Surg 170: 668, 1969. 6. Carneiro Chaves FJZ, Amarante M Jr, Domingues WS, Lopes C: Pancreatic ascites: calcification as a clue to diagnosis. Am J Gastroenterol67: 253, 1977. 7. Schindler SC, Schaefer JW, Hull D, Griffen WO: Chronic pancreatic ascites. Gasrroenferology 59: 453, 1970. 8. Dreiling DA: The lymphatics, pancreatic ascites and pancreatic inflammatory disease. Am J Gastroenterol53: 119, 1970. 9. Kavin H, Sobel JD, Dembo AJ: Pancreatic ascites treated by irradiation of pancreas. Br Med J 2: 502, 197 1. 10. Frey CF, Child CG, Frey W: Pancreatectomy for chronic pancreatitis. Ann Surg 184: 403, 1976. 11. Sato T, Kakazaki G, Saitoh Y, Maki T: Side-to-side pancreaticojejunostomy with caudal pancreatectomy for treatment of chronic pancreatitis with calculi. Arch Surg 96: 892, 1968.
715