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Pancreatic-pleural fistula: the role of ERCP in diagnosis and treatment
ERCP in diagnosis and treatment of pancreatic-pleural fistula
Pancreatic-pleural fistula: the role of ERCP in diagnosis and treatment Bassem Y. Safadi, MD, Jeffrey M. Marks, MD
Pleural effusion can develop in the setting of acute pancreatitis. The incidence varies from 3% to 17%, and up to 50% if CT is used for screening.1,2 The effusions are most commonly small, left-sided and thought to be lymphatic or sympathetic in origin. Pancreatic-pleural fistula, however, results from pancreatic duct disruption or pancreatic pseudocyst extension into the pleural cavity. This is an uncommon entity. It usually presents as a large, recurrent pleural effusion in the setting of chronic pancreatitis.3,4 We present a case of pancreaticpleural fistula where the diagnosis was confirmed by ERCP and treatment accomplished by transpapillary pancreatic duct stent placement. CASE REPORT A 54-year-old man with a long history of alcohol abuse presented with a 3-day history of abdominal pain, nausea and anorexia. A week prior to the onset of these symptoms he had been discharged from another hospital following a 2-week admission for acute pancreatitis. The patient reported 30-pound weight loss during the previous 2 months. On admission he was noted to have a large right pleural effusion. A thoracentesis performed on admission revealed a pleural fluid amylase level greater than 24,000 IU/L, lipase greater than 40,000 From the Department of Surgery, Mt. Sinai Medical Center, and the Department of Surgery, Case Western Reserve University, School of Medicine, Cleveland, Ohio. Reprint requests: Jeffrey M. Marks, MD, 6770 Mayfield Rd., No. 222, Mayfield Hts., OH 44124. Copyright © 2000 by the American Society for Gastrointestinal Endoscopy 0016-5107/2000/$12.00 + 0 37/4/102857 VOLUME 51, NO. 2, 2000
B Safadi, J Marks
IU/L and a protein concentration of 3.8 gm/dL. Initial blood tests (normal values in parentheses) showed a serum amylase of 1438 IU/L (30-110), lipase 8515 IU/L (114-286), alkaline phosphatase 172 IU/L (50-136), gamma glutamyl transferase 67 IU/L, bilirubin (conjugated/unconjugated) 0.3/0 mg/dL (0.0-0.3/0.0-1.1), and albumin 2.5 mg/dL (3.4-4.8). CT of the abdomen demonstrated the large right pleural effusion but no evidence of a pancreatic pseudocyst. US of the right upper quadrant revealed a loculated fluid collection anterior to the right lobe of the liver. The pancreatic duct was noted to be significantly dilated at 6 mm in the body and tail. The head of the pancreas was abnormal with the appearance of calcifications and some hypoechoic areas that were thought to be consistent with acute pancreatitis. The patient was given nothing by mouth and total parenteral nutrition was started. Three days following his admission, the pleural effusion recurred. At ERCP, the pancreatic duct was dilated throughout its course, with a small collection of contrast in the area of the head of the pancreas representing a pseudocyst. The fistulous tract to the right pleural cavity arose from the area of the head of the pancreas (Fig. 1). A 6F, 5 cm long Geenan stent (Wilson-Cook, Winston-Salem, N.C.) was placed in the pancreatic duct, bridging the site of leakage. A right-sided chest tube was placed for pleural drainage. Treatment with somatostatin (octreotide acetate; SANDOZ, East Hanover, N.J.) 50 µg subcutaneously three times a day was initiated. The chest tube was removed 4 days later because there was no significant drainage. The patient began taking a clear liquid diet 10 days after ERCP, which was advanced to a low fat diet. Six weeks later, a chest x-ray showed no recurrence of the effusion. The patient was eating and felt good. His serum albumin rose to 3.7 mg/dL. ERCP demonstrated no leak from the pancreatic duct. The stent was replaced with a 7F, 5 cm long Geenan stent that was removed 9 weeks later. At 10 months follow-up, the patient was doing well with no recurrence of the effusion. GASTROINTESTINAL ENDOSCOPY
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ERCP in diagnosis and treatment of pancreatic-pleural fistula
Figure 1. Retrograde cholangiopancreatogram demonstrating a dilated pancreatic duct (small white arrows), a pseudocyst in the head of the pancreas (black arrow), and a large fistulous tract between the pancreatic duct and the right pleural cavity (large white arrows).
DISCUSSION Pleural effusions resulting from internal pancreatic fistulae are typically large and have a tendency to recur. This is in contrast to sympathetic effusions that occur in the setting of acute pancreatitis and tend to be small and self-limited.1,4,5 Internal pancreatic fistulae arise as a result of disruption of the pancreatic ductal system. If the disruption occurs anteriorly and is not walled off, a pancreatic-peritoneal fistula will develop that will manifest with ascites. If the disruption develops posteriorly, the pancreatic secretions will flow into the retroperitoneum and may dissect through the aortic or esophageal hiatus into the mediastinum and present as a mediastinal pseudocyst. If the pancreatic secretions dissect into the pleural space from the mediastinum or a diaphragmatic defect, then a pancreatic-pleural fistula will develop.3,6 Pancreatic-pleural fistula is not a common entity. Rockey and Cello,5 in 1990, reported 7 patients with pancreatic-pleural fistula and reviewed 89 additional cases identified in English language publications since 1965. Uchiyama et al.7 reviewed 113 cases reported in Japanese language publications between 1972 and 1989. Common features were identified in both reports. The majority of cases occurred in men with chronic alcoholism. Half of these patients, however, had no previous history of pancreatitis. Trauma was a less common cause, having been a feature in 0% to
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5% of cases. Pancreatic pseudocyst was found in 69% to 77% of patients. The clinical manifestation was often misleading and contributed to a delay in diagnosis in many patients. The average duration of symptoms was 5.6 weeks in the review of Rockey and Cello.5 Pulmonary symptoms were more common than abdominal symptoms and were usually the presenting complaint, with dyspnea being the most common. Weight loss and malabsorption were also common. Most pleural effusions were left sided and tended to be large and recurrent. The diagnosis was suggested by the findings on thoracentesis of an exudative aspirate with markedly elevated amylase and lipase levels. The median pleural amylase level in the review by Rockey and Cello5 was 18,450 IU/L (range 1,830 to 164,187 IU/L), whereas the mean value in that by Uchiyama et al.7 was 63,960 IU/L (range 5,050 to 214,500 IU/L). Serum amylase was mildly elevated in most cases and was thought to be partly secondary to resorption of amylase from the pleural surfaces.5,7 The differential diagnosis of amylase-rich pleural effusion includes acute pancreatitis, lung carcinoma, metastatic carcinoma, pneumonia, esophageal perforation, lymphoma, leukemia, liver cirrhosis, hydronephrosis, and pulmonary tuberculosis.8 The diagnosis can be confirmed with ERCP, although it may not always demonstrate the fistulous tract.4,7 CT is valuable in the diagnosis, identifying other associated abnormalities such as pancreatic pseudocysts. Occasionally, CT can demonstrate the fistulous tract, especially if obtained immediately after ERCP.9 Pancreatic-pleural fistula and pancreatic ascites share a common pathophysiology and are labeled as internal pancreatic fistulae.6 The therapeutic approach in both entities is similar. The initial mode of therapy consists of hyperalimentation, bowel rest, and repeated thoracenteses or paracentesis. The success rate with this approach is around 40% to 60%.5,6,10 Recently octreotide, a long-acting somatostatin analogue, has been introduced in the management of pancreatic fistulae, including internal fistulae.11-15 In patients who do not respond to conservative therapy initially, a delay in therapeutic intervention increases morbidity and mortality.6 These data are derived from surgical studies in which the time frame recommended for a trial of nonoperative therapy is around 3 weeks.10 The mortality rate associated with operative treatment has been reported to range from 0% to 12%.10 A new role for ERCP in the management of internal pancreatic fistulae has emerged with reports of successful treatment by insertion of stents into the pancreatic duct.16-19 This occurred concurrently
VOLUME 51, NO. 2, 2000
ERCP in diagnosis and treatment of pancreatic-pleural fistula
with the use of pancreatic duct stents for treatment of various other pancreatic duct disorders such as external pancreatic fistulae, pancreatic pseudocyst and chronic pancreatitis.20-23 Because there is usually a disruption of the main pancreatic duct, the stent should be placed so as to bridge the site of disruption.16 Of probably greater importance, the stent should decrease intraductal pressure by bypassing either the sphincter of Oddi or any stricture in the duct.20,21 In the few cases reported, the stents used were either 5F or 7F and were kept in place for 4 to 12 weeks. Follow-up intervals have ranged from 9 to 30 months with no recurrences.16,18,19 The response following stent placement is usually dramatic, as in our case, and patients can quickly resume oral intake, typically a low fat diet.20 Therefore, complications related to nonoperative therapy including malnutrition, those associated with total parenteral nutrition, central venous catheter infections, and deep vein thrombosis can be reduced using this approach. Data are currently lacking on the longterm consequences of pancreatic duct stent placement; therefore failure of this form of therapy should be an indication for surgery.24
B Safadi, J Marks
9.
10. 11.
12.
13.
14.
15.
16.
17. 18.
REFERENCES 1. Lankisch PG, Droge M, Becher R. Pleural effusions: a new negative prognostic parameter for acute pancreatitis. Am J Gastroenterol 1994;89:1849-51. 2. Gumaste V, Singh V, Dave P. Significance of pleural effusion in patients with acute pancreatitis. Am J Gastroenterol 1992;87:871-4. 3. Anderson WJ, Skinner DB, Zuidema GD, Cameron JL. Chronic pancreatic pleural effusions. Surg Gynecol Obstet 1973;137:827-30. 4. Burgess NA, Moore HE, Williams JO, Lewis MH. A review of pancreatico-pleural fistula in pancreatitis and its management. HPB Surg 1992;5:79-86. 5. Rockey DC, Cello JP. Pancreaticopleural fistula: report of 7 patients and review of the literature. Medicine 1990;69:332-44. 6. Cameron JL. Chronic pancreatic ascites and pancreatic pleural effusions. Gastroenterology 1978;74:134-40. 7. Uchiyama T, Suzuki T, Adachi A, Hiraki S, Iizuka N. Pancreatic pleural effusion: case report and review of 113 cases in Japan. Am J Gastroenterol 1992;87:387-91. 8. Joseph J, Viney S, Beck P, Strange C, Sahn SA, Basran GS. A prospective study of amylase-rich pleural effusions with spe-
VOLUME 51, NO. 2, 2000
19.
20.
21.
22.
23.
24.
cial reference to amylase isoenzyme analysis. Chest 1992; 102:1455-9. Lee DH, Shin DH, Kim TH, Park SS, Park KN, Lee JH. Mediastinal pancreatic pseudocyst with recurrent pleural effusion: demonstration by endoscopic retrograde cholangiopancreatogram and subsequent computed tomography scan. J Clin Gastroenterol 1992;14:68-71. Lipsett PA, Cameron JL. Internal pancreatic fistula. Am J Surg 1992;163:216-20. Prinz RA, Pickleman J, Hoffman JP. Treatment of pancreatic fistulas with a somatostatin analogue. Am J Surg 1988;155: 36-42. Ridgeway MG, Stabile BE. Surgical management and treatment of pancreatic fistulas. Surg Clin North Am 1996;76: 1159-73. Parekh D, Segal I. Pancreatic ascites and effusion: risk factors for failure of conservative therapy and the role of octreotide. Arch Surg 1992;127:707-12. Poddar U, Kochhar R, Singh A, Nagi B, Singh K. Pancreaticopleural fistula: successful treatment with octreotide. Indian J Gastroenterol 1995;14:145-6. Donnelly PK, Watkin EM. Acute hemorrhagic pancreaticopleural effusion treated with somatostatin analogue SMS 201-995. Respir Med 1990;84:507-8. Saeed ZA, Ramirez FC, Hepps KS. Endoscopic stent placement for internal and external pancreatic fistulas. Gastroenterology 1993;105:1213-7. Kozarek RA, Jiranek GC, Traverso LW. Endoscopic treatment of pancreatic ascites. Am J Surg 1994;168:223-6. Kochhar R, Goenka MK, Nagi B, Singh K. Pancreatic ascites and pleural effusion treated by endoscopic pancreatic stent placement. Indian J Gastroenterol 1995;14:106-7. Iglesias JI, Cobb J, Levey J, Rosiello RA. Recurrent left pleural effusion in a 44 year-old woman with a history of alcohol abuse. Chest 1996;110:547-9. Kozarek RA. Endoscopic therapy of complete and partial pancreatic duct disruptions. Gastrointest Endosc Clin N Am 1998;8:39-53. Kozarek RA, Ball TF, Patterson DF, Raltz SL, Traverso LW, Ryan JA, Thirlby RC. Transpapillary stenting for pancreaticocutaneous fistulas. J Gastrointest Surg 1997;1:357-61. Ponchon T, Bory RM, Hedelius F, Roubein LD, Paliard P, Napoleon B, et al. Endoscopic stenting for pain relief in chronic pancreatitis: results of a standardized protocol. Gastrointest Endosc 1995;42:452-6. Binmoeller KF, Seifert H, Walter A, Soehendra N. Transpapillary and transmural drainage of pancreatic pseudocysts. Gastrointest Endosc 1995;42:219-24. Alvarez C, Robert M, Sherman S, Reber HA. Histologic changes after stenting of the pancreatic duct. Arch Surg 1994;129:765-8.
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215
Pancreatic-pleural fistula: the role of ERCP in diagnosis and treatment Bassem Y. Safadi, MD, Jeffrey M. Marks, MD
Pleural effusion can develop in the setting of acute pancreatitis. The incidence varies from 3% to 17%, and up to 50% if CT is used for screening.1,2 The effusions are most commonly small, left-sided and thought to be lymphatic or sympathetic in origin. Pancreatic-pleural fistula, however, results from pancreatic duct disruption or pancreatic pseudocyst extension into the pleural cavity. This is an uncommon entity. It usually presents as a large, recurrent pleural effusion in the setting of chronic pancreatitis.3,4 We present a case of pancreaticpleural fistula where the diagnosis was confirmed by ERCP and treatment accomplished by transpapillary pancreatic duct stent placement. CASE REPORT A 54-year-old man with a long history of alcohol abuse presented with a 3-day history of abdominal pain, nausea and anorexia. A week prior to the onset of these symptoms he had been discharged from another hospital following a 2-week admission for acute pancreatitis. The patient reported 30-pound weight loss during the previous 2 months. On admission he was noted to have a large right pleural effusion. A thoracentesis performed on admission revealed a pleural fluid amylase level greater than 24,000 IU/L, lipase greater than 40,000 From the Department of Surgery, Mt. Sinai Medical Center, and the Department of Surgery, Case Western Reserve University, School of Medicine, Cleveland, Ohio. Reprint requests: Jeffrey M. Marks, MD, 6770 Mayfield Rd., No. 222, Mayfield Hts., OH 44124. Copyright © 2000 by the American Society for Gastrointestinal Endoscopy 0016-5107/2000/$12.00 + 0 37/4/102857 VOLUME 51, NO. 2, 2000
B Safadi, J Marks
IU/L and a protein concentration of 3.8 gm/dL. Initial blood tests (normal values in parentheses) showed a serum amylase of 1438 IU/L (30-110), lipase 8515 IU/L (114-286), alkaline phosphatase 172 IU/L (50-136), gamma glutamyl transferase 67 IU/L, bilirubin (conjugated/unconjugated) 0.3/0 mg/dL (0.0-0.3/0.0-1.1), and albumin 2.5 mg/dL (3.4-4.8). CT of the abdomen demonstrated the large right pleural effusion but no evidence of a pancreatic pseudocyst. US of the right upper quadrant revealed a loculated fluid collection anterior to the right lobe of the liver. The pancreatic duct was noted to be significantly dilated at 6 mm in the body and tail. The head of the pancreas was abnormal with the appearance of calcifications and some hypoechoic areas that were thought to be consistent with acute pancreatitis. The patient was given nothing by mouth and total parenteral nutrition was started. Three days following his admission, the pleural effusion recurred. At ERCP, the pancreatic duct was dilated throughout its course, with a small collection of contrast in the area of the head of the pancreas representing a pseudocyst. The fistulous tract to the right pleural cavity arose from the area of the head of the pancreas (Fig. 1). A 6F, 5 cm long Geenan stent (Wilson-Cook, Winston-Salem, N.C.) was placed in the pancreatic duct, bridging the site of leakage. A right-sided chest tube was placed for pleural drainage. Treatment with somatostatin (octreotide acetate; SANDOZ, East Hanover, N.J.) 50 µg subcutaneously three times a day was initiated. The chest tube was removed 4 days later because there was no significant drainage. The patient began taking a clear liquid diet 10 days after ERCP, which was advanced to a low fat diet. Six weeks later, a chest x-ray showed no recurrence of the effusion. The patient was eating and felt good. His serum albumin rose to 3.7 mg/dL. ERCP demonstrated no leak from the pancreatic duct. The stent was replaced with a 7F, 5 cm long Geenan stent that was removed 9 weeks later. At 10 months follow-up, the patient was doing well with no recurrence of the effusion. GASTROINTESTINAL ENDOSCOPY
213
B Safadi, J Marks
ERCP in diagnosis and treatment of pancreatic-pleural fistula
Figure 1. Retrograde cholangiopancreatogram demonstrating a dilated pancreatic duct (small white arrows), a pseudocyst in the head of the pancreas (black arrow), and a large fistulous tract between the pancreatic duct and the right pleural cavity (large white arrows).
DISCUSSION Pleural effusions resulting from internal pancreatic fistulae are typically large and have a tendency to recur. This is in contrast to sympathetic effusions that occur in the setting of acute pancreatitis and tend to be small and self-limited.1,4,5 Internal pancreatic fistulae arise as a result of disruption of the pancreatic ductal system. If the disruption occurs anteriorly and is not walled off, a pancreatic-peritoneal fistula will develop that will manifest with ascites. If the disruption develops posteriorly, the pancreatic secretions will flow into the retroperitoneum and may dissect through the aortic or esophageal hiatus into the mediastinum and present as a mediastinal pseudocyst. If the pancreatic secretions dissect into the pleural space from the mediastinum or a diaphragmatic defect, then a pancreatic-pleural fistula will develop.3,6 Pancreatic-pleural fistula is not a common entity. Rockey and Cello,5 in 1990, reported 7 patients with pancreatic-pleural fistula and reviewed 89 additional cases identified in English language publications since 1965. Uchiyama et al.7 reviewed 113 cases reported in Japanese language publications between 1972 and 1989. Common features were identified in both reports. The majority of cases occurred in men with chronic alcoholism. Half of these patients, however, had no previous history of pancreatitis. Trauma was a less common cause, having been a feature in 0% to
214
GASTROINTESTINAL ENDOSCOPY
5% of cases. Pancreatic pseudocyst was found in 69% to 77% of patients. The clinical manifestation was often misleading and contributed to a delay in diagnosis in many patients. The average duration of symptoms was 5.6 weeks in the review of Rockey and Cello.5 Pulmonary symptoms were more common than abdominal symptoms and were usually the presenting complaint, with dyspnea being the most common. Weight loss and malabsorption were also common. Most pleural effusions were left sided and tended to be large and recurrent. The diagnosis was suggested by the findings on thoracentesis of an exudative aspirate with markedly elevated amylase and lipase levels. The median pleural amylase level in the review by Rockey and Cello5 was 18,450 IU/L (range 1,830 to 164,187 IU/L), whereas the mean value in that by Uchiyama et al.7 was 63,960 IU/L (range 5,050 to 214,500 IU/L). Serum amylase was mildly elevated in most cases and was thought to be partly secondary to resorption of amylase from the pleural surfaces.5,7 The differential diagnosis of amylase-rich pleural effusion includes acute pancreatitis, lung carcinoma, metastatic carcinoma, pneumonia, esophageal perforation, lymphoma, leukemia, liver cirrhosis, hydronephrosis, and pulmonary tuberculosis.8 The diagnosis can be confirmed with ERCP, although it may not always demonstrate the fistulous tract.4,7 CT is valuable in the diagnosis, identifying other associated abnormalities such as pancreatic pseudocysts. Occasionally, CT can demonstrate the fistulous tract, especially if obtained immediately after ERCP.9 Pancreatic-pleural fistula and pancreatic ascites share a common pathophysiology and are labeled as internal pancreatic fistulae.6 The therapeutic approach in both entities is similar. The initial mode of therapy consists of hyperalimentation, bowel rest, and repeated thoracenteses or paracentesis. The success rate with this approach is around 40% to 60%.5,6,10 Recently octreotide, a long-acting somatostatin analogue, has been introduced in the management of pancreatic fistulae, including internal fistulae.11-15 In patients who do not respond to conservative therapy initially, a delay in therapeutic intervention increases morbidity and mortality.6 These data are derived from surgical studies in which the time frame recommended for a trial of nonoperative therapy is around 3 weeks.10 The mortality rate associated with operative treatment has been reported to range from 0% to 12%.10 A new role for ERCP in the management of internal pancreatic fistulae has emerged with reports of successful treatment by insertion of stents into the pancreatic duct.16-19 This occurred concurrently
VOLUME 51, NO. 2, 2000
ERCP in diagnosis and treatment of pancreatic-pleural fistula
with the use of pancreatic duct stents for treatment of various other pancreatic duct disorders such as external pancreatic fistulae, pancreatic pseudocyst and chronic pancreatitis.20-23 Because there is usually a disruption of the main pancreatic duct, the stent should be placed so as to bridge the site of disruption.16 Of probably greater importance, the stent should decrease intraductal pressure by bypassing either the sphincter of Oddi or any stricture in the duct.20,21 In the few cases reported, the stents used were either 5F or 7F and were kept in place for 4 to 12 weeks. Follow-up intervals have ranged from 9 to 30 months with no recurrences.16,18,19 The response following stent placement is usually dramatic, as in our case, and patients can quickly resume oral intake, typically a low fat diet.20 Therefore, complications related to nonoperative therapy including malnutrition, those associated with total parenteral nutrition, central venous catheter infections, and deep vein thrombosis can be reduced using this approach. Data are currently lacking on the longterm consequences of pancreatic duct stent placement; therefore failure of this form of therapy should be an indication for surgery.24
B Safadi, J Marks
9.
10. 11.
12.
13.
14.
15.
16.
17. 18.
REFERENCES 1. Lankisch PG, Droge M, Becher R. Pleural effusions: a new negative prognostic parameter for acute pancreatitis. Am J Gastroenterol 1994;89:1849-51. 2. Gumaste V, Singh V, Dave P. Significance of pleural effusion in patients with acute pancreatitis. Am J Gastroenterol 1992;87:871-4. 3. Anderson WJ, Skinner DB, Zuidema GD, Cameron JL. Chronic pancreatic pleural effusions. Surg Gynecol Obstet 1973;137:827-30. 4. Burgess NA, Moore HE, Williams JO, Lewis MH. A review of pancreatico-pleural fistula in pancreatitis and its management. HPB Surg 1992;5:79-86. 5. Rockey DC, Cello JP. Pancreaticopleural fistula: report of 7 patients and review of the literature. Medicine 1990;69:332-44. 6. Cameron JL. Chronic pancreatic ascites and pancreatic pleural effusions. Gastroenterology 1978;74:134-40. 7. Uchiyama T, Suzuki T, Adachi A, Hiraki S, Iizuka N. Pancreatic pleural effusion: case report and review of 113 cases in Japan. Am J Gastroenterol 1992;87:387-91. 8. Joseph J, Viney S, Beck P, Strange C, Sahn SA, Basran GS. A prospective study of amylase-rich pleural effusions with spe-
VOLUME 51, NO. 2, 2000
19.
20.
21.
22.
23.
24.
cial reference to amylase isoenzyme analysis. Chest 1992; 102:1455-9. Lee DH, Shin DH, Kim TH, Park SS, Park KN, Lee JH. Mediastinal pancreatic pseudocyst with recurrent pleural effusion: demonstration by endoscopic retrograde cholangiopancreatogram and subsequent computed tomography scan. J Clin Gastroenterol 1992;14:68-71. Lipsett PA, Cameron JL. Internal pancreatic fistula. Am J Surg 1992;163:216-20. Prinz RA, Pickleman J, Hoffman JP. Treatment of pancreatic fistulas with a somatostatin analogue. Am J Surg 1988;155: 36-42. Ridgeway MG, Stabile BE. Surgical management and treatment of pancreatic fistulas. Surg Clin North Am 1996;76: 1159-73. Parekh D, Segal I. Pancreatic ascites and effusion: risk factors for failure of conservative therapy and the role of octreotide. Arch Surg 1992;127:707-12. Poddar U, Kochhar R, Singh A, Nagi B, Singh K. Pancreaticopleural fistula: successful treatment with octreotide. Indian J Gastroenterol 1995;14:145-6. Donnelly PK, Watkin EM. Acute hemorrhagic pancreaticopleural effusion treated with somatostatin analogue SMS 201-995. Respir Med 1990;84:507-8. Saeed ZA, Ramirez FC, Hepps KS. Endoscopic stent placement for internal and external pancreatic fistulas. Gastroenterology 1993;105:1213-7. Kozarek RA, Jiranek GC, Traverso LW. Endoscopic treatment of pancreatic ascites. Am J Surg 1994;168:223-6. Kochhar R, Goenka MK, Nagi B, Singh K. Pancreatic ascites and pleural effusion treated by endoscopic pancreatic stent placement. Indian J Gastroenterol 1995;14:106-7. Iglesias JI, Cobb J, Levey J, Rosiello RA. Recurrent left pleural effusion in a 44 year-old woman with a history of alcohol abuse. Chest 1996;110:547-9. Kozarek RA. Endoscopic therapy of complete and partial pancreatic duct disruptions. Gastrointest Endosc Clin N Am 1998;8:39-53. Kozarek RA, Ball TF, Patterson DF, Raltz SL, Traverso LW, Ryan JA, Thirlby RC. Transpapillary stenting for pancreaticocutaneous fistulas. J Gastrointest Surg 1997;1:357-61. Ponchon T, Bory RM, Hedelius F, Roubein LD, Paliard P, Napoleon B, et al. Endoscopic stenting for pain relief in chronic pancreatitis: results of a standardized protocol. Gastrointest Endosc 1995;42:452-6. Binmoeller KF, Seifert H, Walter A, Soehendra N. Transpapillary and transmural drainage of pancreatic pseudocysts. Gastrointest Endosc 1995;42:219-24. Alvarez C, Robert M, Sherman S, Reber HA. Histologic changes after stenting of the pancreatic duct. Arch Surg 1994;129:765-8.
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