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The incidence of post-sphincterotomy stenosis in group II patients with sphincter of Oddi dysfunction
0016-5107/93/3904-0496$1.00 + .10 GASTROINTESTINAL ENDOSCOPY Copyright © 1993 by the American Society for Gastrointestinal Endoscopy
The incidence of post-sphincterotomy stenosis in group II patients with sphincter of Oddi dysfunction Aram V. Manoukian, MD, MS, Michael J. Schmalz, MD, Joseph E. Geenen, MD Walter J. Hogan, MD, Rama P. Venu, MD, G. Kenneth Johnson, MD Racine, Wisconsin, and Milwaukee, Wisconsin
Patients with group II sphincter of Oddi dysfunction documented by elevated sphincter of Oddi pressure improve after endoscopic sphincterotomy. A large group II population was studied to determine the incidence of post-endoscopic sphincterotomy stenosis. Eighty-five patients (82 women and 3 men), ages 21 to 88 years (mean, 50 years), fulfilled the clinical criteria for group II sphincter of Oddi dysfunction; each had an elevated basal sphincter of Oddi pressure (>40 mm Hg), and received endoscopic sphincterotomy. These patients were observed for a mean of 7 ± 3 years. Four patients re-presented with clinical findings suggestive of recurrent sphincter of Oddi dysfunction; all were found to have a basal sphincter of Oddi pressure greater than or equal to 40 mm Hg. Symptoms re-developed within 4 months after endoscopic sphincterotomy (mean, 3.3 months). Endoscopic sphincterotomy was repeated in all four patients with one endoscopically treated complication. On 25-month mean follow-up, none of the patients had further signs or symptoms of papillary stenosis. Endoscopic sphincterotomy in patients with group II sphincter of Oddi dysfunction is associated with a low incidence of restenosis (4.7%). Repeat endoscopic sphincterotomy was found to be effective management in patients with papillary restenosis. (Gastrointest Endosc 1993;39:496-8.)
Group II sphincter of Oddi (SO) dysfunction is defined by both clinical and manometric criteria. In patients with the appropriate clinical signs and symptoms, the diagnosis is established by biliary manometry. Seventy to 91 % of patients with group II sphincter of Oddi dysfunction and elevated basal SO pressure improve after endoscopic sphincterotomy (ES).l The incidence of papillary restenosis, however, on longterm follow-up is not well established. The aim of our study, therefore, was to determine the incidence of this entity in a large population of patients with group II
Received September 2, 1992. For revision October 16, 1992. Accepted March 29, 1993. From St. Luke's Hospital, Racine, Wisconsin, and Medical College of Wisconsin, Milwaukee, Wisconsin. Reprint requests: Joseph E. Geenen, MD, 1333 College Avenue, Racine, WI 53403. 37/1/47499 496
SO dysfunction who had undergone endoscopic sphincterotomy. METHODS
We studied 85 group II patients with SO dysfunction from 1976 to 1991; 82 patients were women, and 3 were men. The patients' ages ranged from 21 to 88 years (mean, 50 years). Initially, SO dysfunction was suspected in those patients presenting with biliary-type pain following cholecystectomy. In addition to pain, one or two of the following was required to satisfy the clinical criteria of group II SO dysfunction: common bile duct (CBD) dilation greater than 12 mm, CBD drainage time greater than 45 minutes, and abnormal liver chemistries documented on at least two separate occasions (Table 1). The condition was confirmed manometrically in those patients who had a basal SO pressure greater than or equal to 40 mm Hg. SO manometry was obtained using a 3-lumen perfused catheter, the Beckman Dynagraph recorder (Beckman, Schiller Park, Ill.), and the Arndorfer pneumohydraulic infusion system (Arndorfer Medical, Milwaukee, Wis.) in the manner previously described. 2 Basal SO pressure was defined as the baseline pressure GASTROINTESTINAL ENDOSCOPY
Table 1. Definition of group II SO dysfunction Clinical criteria Biliary-type pain after cholecystectomy One or two of the following CBD dilation >12 mm CBD drainage time >45 minutes Abnormal liver function tests Manometric criteria Basal sphincter of Oddi pressure ~40 mm Hg
between phasic SO contractions minus the end expiratory duodenal pressure. An average basal SO pressure was obtained from all three recording tips on at least two successive catheter pull-throughs from the CBD into the duodenum. Basal SO pressures greater than 40 mm Hg (mean ± 2 SD) above the intraduodenal pressure were considered to be abnormal. In those patients with manometrically confirmed group II SO dysfunction, ES was carried out by the use of a tractiontype papillotome (Wilson-Cook, Winston-Salem, N. C.) in the usual well-accepted manner. The incision was determined by the length of the intraduodenal segment of bile duct and, to avoid complications, the degree of extrahepatic duct dilation. In the 85 patients, the length of the initial ES varied from 5 to 15 mm. Incision length was estimated by the papillotome measurement technique previously described. 2 Group II patients who had ES were observed for a prolonged period of time. The 85 patients studied represented all those in this category accessed by computer retrieval who fit the strict criteria mentioned. Repeat ERCP was carried out a mean of 1 year after initial ES to check for ductal dilation, CBD drainage time, and sphincterotomy patency. Liver chemistries were also obtained. In situations where sphincterotomy patency was questioned, SO manometry was performed. If patients developed symptoms during the I-year period, this evaluation was conducted at that time. Beyond 1 year, follow-up was carried out at the time of subsequent ERCP, by telephone, or at the time of an office visit. Initially, restenosis was suspected clinically by the recurrence of biliary pain and/or the development of abnormal liver chemistries. ERCP was then carried out with SO manometry as needed. ES was repeated in those patients who had an elevated basal SO pressure greater than or equal to 40 mm Hg. After ES, SO manometry and/or contrast drainage time was obtained on all patients with restenosis to assess sphincterotomy patency and sphincter ablation. In those patients with pain and normal SO manometry, it was believed their symptoms could be secondary to irritable bowel syndrome. RESULTS
Eighty-five patients had an ES for group II SO dysfunction. Those patients have been observed for a mean of 7 ± 3 years. Subsequently,4 of the 85 patients developed recurrent biliary pain and manometric evidence of papillary restenosis, with mean basal SO pressure of greater than or equal to 40 mm Hg. All of these patients VOLUME 39, NO.4, 1993
Table 2. Clinical presentation of papillary restenosis in group II SO dysfunction (four patients) Patient Pain 1
2 3 4
Yes Yes Yes Yes
Basal SO Delayed Dilated Abnormal pressure duct liver function tests drainage (mm Hg) No No No No
No No No Yes
No Yes No No
45 40 200 43
developed symptoms within 4 months of their initial ES (mean, 3.3 months). One patient had abnormal liver chemistries, and one patient had delayed CBD drainage (Table 2). Three of the four patients had a clinical picture similar to their initial presentation. After manometric confirmation of elevated basal SO pressures, repeat ES was performed on these four patients. The ES incision on repeat ERCP varied in length from 8 to 10 mm (mean, 9 mm). The initial ES in the same four patients ranged from 4 to 10 mm in length (mean, 6 mm). Previous studies have defined the intact sphincter as 4 to 6 mm in length; therefore, the initial ES is believed to have been sufficient for sphincter ablation. 3 One complication was associated with repeat ES. One patient developed bleeding after ES, which required a 2-unit blood transfusion. The bleeding was controlled rapidly with epinephrine injection and balloon tamponade. During a mean follow-up of 25 months, none of the four patients developed recurrent stenosis. All of these patients had follow-up ERCP and/or SO manometry that showed no evidence of restenosis. DISCUSSION
SO dysfunction is a clinical syndrome that is exemplified by the presence of biliary pain in primarily middle-aged women after cholecystectomy. It has been estimated that the overall frequency of this disorder is approximately 14 %.4 For many years, the definitive management of the condition was a surgical procedure. Long-term follow-up yielded good results, but the operative mortality rate ranged from 0.6 % to 6.0% .5-12 Recently, the treatment of SO dysfunction has become the purview of the biliary endoscopist.l· 13-16 In stone disease, the long-term results of sphincterotomy have been excellent in regard to the development of subsequent stenosisY In the present study, we set out to define the incidence of papillary restenosis specifically in patients with group II SO dysfunction. In SO dysfunction, controversy still exists as to what factors best predict the response to endoscopic therapy. Thatcher et a1. 16 favored ductal dilation and de497
layed bile duct drainage as the best prognosticators of a positive response to ES. The Australian group determined that neither ductal dilation nor manometry correlated with a positive predictive outcome to endoscopic therapy.l3 Neoptolemos et a1.l 5 concluded that patients with ductal dilation, delayed drainage, or abnormal biliary manometry fare better after ES. However, in these studies, differences in the clinical classification of patients and the lack of uniform diagnostic techniques make the interpretation and comparison of their results difficult. The Wisconsin group attempted to classify patients into three different categories based on clinical parameters. 1 They reported a 91 % response to ES in those patients with group II SO dysfunction who had basal SO pressures greater than or equal to 40 mm Hg. Bile duct morphology, drainage dynamics, or abnormal liver chemistries did not predict a positive response to therapy. Based on these criteria, a recent review from the Cleveland Clinic showed a 71 % to 82 % symptomatic improvement in a small group of patients with group II SO dysfunction when observed for a mean of 35 months.l8 In the current report, a large population of group II patients with SO dysfunction who had undergone ES were evaluated over long-term follow-up. The incidence of symptomatic papillary restenosis was documented by biliary manometry. Eighty-five patients were studied, and 4 patients (4.7 % of this group) were found to have papillary restenosis with elevated basal SO pressures. All patients presented with recurrent symptoms within 4 months of their initial ES. Repeat ES was performed in all patients with one endoscopically treated complication. During a mean follow-up period of 25 months, these patients have remained asymptomatic. All four have subsequently received ERCP and/or SO manometry to document sphincter ablation. In conclusion, ES in group II patients is associated with a low incidence of restenosis. In a large group of patients, less than 5 % of the group developed papillary restenosis on long-term follow-up. Repeat ES was an effective therapy for those patients.
498
REFERENCES 1. Geenen JE, Hogan WJ, Dodds WJ, Toouli J, Venu RP. The efficacy of endoscopic sphincterotomy after cholecystectomy in patients with sphincter of Oddi dysfunction. N Engl J Med 1989;320:82-7. 2. Geenen JE, Hogan WJ, Dodds WJ, Stewart ET, Arndorfer RC. Intraluminal pressure recording from the human sphincter of Oddi. Gastroenterology 1980;78:317-24. 3. Geenen JE, Toouli J, Hogan WJ, et a1. Endoscopic sphincterotomy: follow-up evaluation of effects on the sphincter of Oddi. Gastroenterology 1984;87:754-8. 4. Bar-Meir S, Halpern Z, Bardon E, Gilat T. Frequency of papillary dysfunction among cholecystectomized patients. Hepatology 1984;4:328-30. 5. Stefanini P, Carboni M, Potrassi N, DeBernardinis G, Negro P, Loriga P. Transduodenal sphincteroplasty: its use in the treatment of lithiasis and benign obstruction of the common bile duct. Am J Surg 1974;128:672-5. 6. Autio V, Porviner T. Results of surgical treatment of stenosis of the sphincter of Oddi. J Int Coll Surg 1965;44:656-9. 7. Partington PF. Twenty-three years of experience with sphincterotomy and sphincteroplasty for stenosis of the sphincter of Oddi. Surg Gynecol Obstet 1977;145:161-8. 8. Griffiths CA. Diagnosis of papillary stenosis by calibration. Am J Surg 1982;143:717-20. 9. Vossilakis JS, Manolas K, Bourdouris J. Transduodenal sphincteroplasty. Arch Surg 1979;114:181-4. 10. Peel ALG, Bourke JB, Hermon JJ, et a1. How should the common bile duct be explored? Ann R Coll Surg 1975;56:124-34. 11. Anderson TM, Pitt HA, Lonjmire WP. Experience with sphincteroplasty and sphincterotomy in pancreaticobiliary surgery. Ann Surg 1985;201:399-406. 12. Baker AR, Neoptolemos JP, Leese T, Fossard DP. Choledochoduodenostomy, transduodenal sphincterotomy and sphincterotomy for calculi of the common bile duct. Surg Gynecol Obstet 1987;184:245-51. 13. Roberts-Thomson IC, Toouli J. Is endoscopic sphincterotomy for disabling biliary-type pain after cholecystectomy effective? Gastrointest Endosc 1985;31:370-5. 14. Tanaka M, Ikeda S, Matsumoto S, Yoshimoto H, Nakayama F. Manometric diagnosis of sphincter of Oddi spasm as a cause of post cholecystectomy pain and treatment by endoscopic sphincterotomy. Ann Surg 1985;202:712-9. 15. Neoptolemos JP, Bailey IS, Carr-Locke DL. Sphincter of Oddi dysfunction: results of treatment by endoscopic sphincterotomy. Br J Surg 1988;75:454-9. 16. Thatcher BS, Sivak MV, Tedesco FJ, Vennes JA, Hutton SW, Achkar EA. Endoscopic sphincterotomy for suspected dysfunction ofthe sphincter of Oddi. Gastrointest Endosc 1987;33:91-5. 17. Hawes RH, Cotton PB, Vallone AG. Follow-up 6-11 years after duodenoscopic sphincterotomy for stones in patients with prior cholecystectomy. Gastroenterology 1990;98:1008-12. 18. Howerton D, Falk G, Achkar E, FleshIer B, Sivak M. Response to sphincterotomy in patients with type II and type III sphincter of Oddi dysfunction [Abstract]. Am J Gastroenterol 1992; 87:1286.
GASTROINTESTINAL ENDOSCOPY
The incidence of post-sphincterotomy stenosis in group II patients with sphincter of Oddi dysfunction Aram V. Manoukian, MD, MS, Michael J. Schmalz, MD, Joseph E. Geenen, MD Walter J. Hogan, MD, Rama P. Venu, MD, G. Kenneth Johnson, MD Racine, Wisconsin, and Milwaukee, Wisconsin
Patients with group II sphincter of Oddi dysfunction documented by elevated sphincter of Oddi pressure improve after endoscopic sphincterotomy. A large group II population was studied to determine the incidence of post-endoscopic sphincterotomy stenosis. Eighty-five patients (82 women and 3 men), ages 21 to 88 years (mean, 50 years), fulfilled the clinical criteria for group II sphincter of Oddi dysfunction; each had an elevated basal sphincter of Oddi pressure (>40 mm Hg), and received endoscopic sphincterotomy. These patients were observed for a mean of 7 ± 3 years. Four patients re-presented with clinical findings suggestive of recurrent sphincter of Oddi dysfunction; all were found to have a basal sphincter of Oddi pressure greater than or equal to 40 mm Hg. Symptoms re-developed within 4 months after endoscopic sphincterotomy (mean, 3.3 months). Endoscopic sphincterotomy was repeated in all four patients with one endoscopically treated complication. On 25-month mean follow-up, none of the patients had further signs or symptoms of papillary stenosis. Endoscopic sphincterotomy in patients with group II sphincter of Oddi dysfunction is associated with a low incidence of restenosis (4.7%). Repeat endoscopic sphincterotomy was found to be effective management in patients with papillary restenosis. (Gastrointest Endosc 1993;39:496-8.)
Group II sphincter of Oddi (SO) dysfunction is defined by both clinical and manometric criteria. In patients with the appropriate clinical signs and symptoms, the diagnosis is established by biliary manometry. Seventy to 91 % of patients with group II sphincter of Oddi dysfunction and elevated basal SO pressure improve after endoscopic sphincterotomy (ES).l The incidence of papillary restenosis, however, on longterm follow-up is not well established. The aim of our study, therefore, was to determine the incidence of this entity in a large population of patients with group II
Received September 2, 1992. For revision October 16, 1992. Accepted March 29, 1993. From St. Luke's Hospital, Racine, Wisconsin, and Medical College of Wisconsin, Milwaukee, Wisconsin. Reprint requests: Joseph E. Geenen, MD, 1333 College Avenue, Racine, WI 53403. 37/1/47499 496
SO dysfunction who had undergone endoscopic sphincterotomy. METHODS
We studied 85 group II patients with SO dysfunction from 1976 to 1991; 82 patients were women, and 3 were men. The patients' ages ranged from 21 to 88 years (mean, 50 years). Initially, SO dysfunction was suspected in those patients presenting with biliary-type pain following cholecystectomy. In addition to pain, one or two of the following was required to satisfy the clinical criteria of group II SO dysfunction: common bile duct (CBD) dilation greater than 12 mm, CBD drainage time greater than 45 minutes, and abnormal liver chemistries documented on at least two separate occasions (Table 1). The condition was confirmed manometrically in those patients who had a basal SO pressure greater than or equal to 40 mm Hg. SO manometry was obtained using a 3-lumen perfused catheter, the Beckman Dynagraph recorder (Beckman, Schiller Park, Ill.), and the Arndorfer pneumohydraulic infusion system (Arndorfer Medical, Milwaukee, Wis.) in the manner previously described. 2 Basal SO pressure was defined as the baseline pressure GASTROINTESTINAL ENDOSCOPY
Table 1. Definition of group II SO dysfunction Clinical criteria Biliary-type pain after cholecystectomy One or two of the following CBD dilation >12 mm CBD drainage time >45 minutes Abnormal liver function tests Manometric criteria Basal sphincter of Oddi pressure ~40 mm Hg
between phasic SO contractions minus the end expiratory duodenal pressure. An average basal SO pressure was obtained from all three recording tips on at least two successive catheter pull-throughs from the CBD into the duodenum. Basal SO pressures greater than 40 mm Hg (mean ± 2 SD) above the intraduodenal pressure were considered to be abnormal. In those patients with manometrically confirmed group II SO dysfunction, ES was carried out by the use of a tractiontype papillotome (Wilson-Cook, Winston-Salem, N. C.) in the usual well-accepted manner. The incision was determined by the length of the intraduodenal segment of bile duct and, to avoid complications, the degree of extrahepatic duct dilation. In the 85 patients, the length of the initial ES varied from 5 to 15 mm. Incision length was estimated by the papillotome measurement technique previously described. 2 Group II patients who had ES were observed for a prolonged period of time. The 85 patients studied represented all those in this category accessed by computer retrieval who fit the strict criteria mentioned. Repeat ERCP was carried out a mean of 1 year after initial ES to check for ductal dilation, CBD drainage time, and sphincterotomy patency. Liver chemistries were also obtained. In situations where sphincterotomy patency was questioned, SO manometry was performed. If patients developed symptoms during the I-year period, this evaluation was conducted at that time. Beyond 1 year, follow-up was carried out at the time of subsequent ERCP, by telephone, or at the time of an office visit. Initially, restenosis was suspected clinically by the recurrence of biliary pain and/or the development of abnormal liver chemistries. ERCP was then carried out with SO manometry as needed. ES was repeated in those patients who had an elevated basal SO pressure greater than or equal to 40 mm Hg. After ES, SO manometry and/or contrast drainage time was obtained on all patients with restenosis to assess sphincterotomy patency and sphincter ablation. In those patients with pain and normal SO manometry, it was believed their symptoms could be secondary to irritable bowel syndrome. RESULTS
Eighty-five patients had an ES for group II SO dysfunction. Those patients have been observed for a mean of 7 ± 3 years. Subsequently,4 of the 85 patients developed recurrent biliary pain and manometric evidence of papillary restenosis, with mean basal SO pressure of greater than or equal to 40 mm Hg. All of these patients VOLUME 39, NO.4, 1993
Table 2. Clinical presentation of papillary restenosis in group II SO dysfunction (four patients) Patient Pain 1
2 3 4
Yes Yes Yes Yes
Basal SO Delayed Dilated Abnormal pressure duct liver function tests drainage (mm Hg) No No No No
No No No Yes
No Yes No No
45 40 200 43
developed symptoms within 4 months of their initial ES (mean, 3.3 months). One patient had abnormal liver chemistries, and one patient had delayed CBD drainage (Table 2). Three of the four patients had a clinical picture similar to their initial presentation. After manometric confirmation of elevated basal SO pressures, repeat ES was performed on these four patients. The ES incision on repeat ERCP varied in length from 8 to 10 mm (mean, 9 mm). The initial ES in the same four patients ranged from 4 to 10 mm in length (mean, 6 mm). Previous studies have defined the intact sphincter as 4 to 6 mm in length; therefore, the initial ES is believed to have been sufficient for sphincter ablation. 3 One complication was associated with repeat ES. One patient developed bleeding after ES, which required a 2-unit blood transfusion. The bleeding was controlled rapidly with epinephrine injection and balloon tamponade. During a mean follow-up of 25 months, none of the four patients developed recurrent stenosis. All of these patients had follow-up ERCP and/or SO manometry that showed no evidence of restenosis. DISCUSSION
SO dysfunction is a clinical syndrome that is exemplified by the presence of biliary pain in primarily middle-aged women after cholecystectomy. It has been estimated that the overall frequency of this disorder is approximately 14 %.4 For many years, the definitive management of the condition was a surgical procedure. Long-term follow-up yielded good results, but the operative mortality rate ranged from 0.6 % to 6.0% .5-12 Recently, the treatment of SO dysfunction has become the purview of the biliary endoscopist.l· 13-16 In stone disease, the long-term results of sphincterotomy have been excellent in regard to the development of subsequent stenosisY In the present study, we set out to define the incidence of papillary restenosis specifically in patients with group II SO dysfunction. In SO dysfunction, controversy still exists as to what factors best predict the response to endoscopic therapy. Thatcher et a1. 16 favored ductal dilation and de497
layed bile duct drainage as the best prognosticators of a positive response to ES. The Australian group determined that neither ductal dilation nor manometry correlated with a positive predictive outcome to endoscopic therapy.l3 Neoptolemos et a1.l 5 concluded that patients with ductal dilation, delayed drainage, or abnormal biliary manometry fare better after ES. However, in these studies, differences in the clinical classification of patients and the lack of uniform diagnostic techniques make the interpretation and comparison of their results difficult. The Wisconsin group attempted to classify patients into three different categories based on clinical parameters. 1 They reported a 91 % response to ES in those patients with group II SO dysfunction who had basal SO pressures greater than or equal to 40 mm Hg. Bile duct morphology, drainage dynamics, or abnormal liver chemistries did not predict a positive response to therapy. Based on these criteria, a recent review from the Cleveland Clinic showed a 71 % to 82 % symptomatic improvement in a small group of patients with group II SO dysfunction when observed for a mean of 35 months.l8 In the current report, a large population of group II patients with SO dysfunction who had undergone ES were evaluated over long-term follow-up. The incidence of symptomatic papillary restenosis was documented by biliary manometry. Eighty-five patients were studied, and 4 patients (4.7 % of this group) were found to have papillary restenosis with elevated basal SO pressures. All patients presented with recurrent symptoms within 4 months of their initial ES. Repeat ES was performed in all patients with one endoscopically treated complication. During a mean follow-up period of 25 months, these patients have remained asymptomatic. All four have subsequently received ERCP and/or SO manometry to document sphincter ablation. In conclusion, ES in group II patients is associated with a low incidence of restenosis. In a large group of patients, less than 5 % of the group developed papillary restenosis on long-term follow-up. Repeat ES was an effective therapy for those patients.
498
REFERENCES 1. Geenen JE, Hogan WJ, Dodds WJ, Toouli J, Venu RP. The efficacy of endoscopic sphincterotomy after cholecystectomy in patients with sphincter of Oddi dysfunction. N Engl J Med 1989;320:82-7. 2. Geenen JE, Hogan WJ, Dodds WJ, Stewart ET, Arndorfer RC. Intraluminal pressure recording from the human sphincter of Oddi. Gastroenterology 1980;78:317-24. 3. Geenen JE, Toouli J, Hogan WJ, et a1. Endoscopic sphincterotomy: follow-up evaluation of effects on the sphincter of Oddi. Gastroenterology 1984;87:754-8. 4. Bar-Meir S, Halpern Z, Bardon E, Gilat T. Frequency of papillary dysfunction among cholecystectomized patients. Hepatology 1984;4:328-30. 5. Stefanini P, Carboni M, Potrassi N, DeBernardinis G, Negro P, Loriga P. Transduodenal sphincteroplasty: its use in the treatment of lithiasis and benign obstruction of the common bile duct. Am J Surg 1974;128:672-5. 6. Autio V, Porviner T. Results of surgical treatment of stenosis of the sphincter of Oddi. J Int Coll Surg 1965;44:656-9. 7. Partington PF. Twenty-three years of experience with sphincterotomy and sphincteroplasty for stenosis of the sphincter of Oddi. Surg Gynecol Obstet 1977;145:161-8. 8. Griffiths CA. Diagnosis of papillary stenosis by calibration. Am J Surg 1982;143:717-20. 9. Vossilakis JS, Manolas K, Bourdouris J. Transduodenal sphincteroplasty. Arch Surg 1979;114:181-4. 10. Peel ALG, Bourke JB, Hermon JJ, et a1. How should the common bile duct be explored? Ann R Coll Surg 1975;56:124-34. 11. Anderson TM, Pitt HA, Lonjmire WP. Experience with sphincteroplasty and sphincterotomy in pancreaticobiliary surgery. Ann Surg 1985;201:399-406. 12. Baker AR, Neoptolemos JP, Leese T, Fossard DP. Choledochoduodenostomy, transduodenal sphincterotomy and sphincterotomy for calculi of the common bile duct. Surg Gynecol Obstet 1987;184:245-51. 13. Roberts-Thomson IC, Toouli J. Is endoscopic sphincterotomy for disabling biliary-type pain after cholecystectomy effective? Gastrointest Endosc 1985;31:370-5. 14. Tanaka M, Ikeda S, Matsumoto S, Yoshimoto H, Nakayama F. Manometric diagnosis of sphincter of Oddi spasm as a cause of post cholecystectomy pain and treatment by endoscopic sphincterotomy. Ann Surg 1985;202:712-9. 15. Neoptolemos JP, Bailey IS, Carr-Locke DL. Sphincter of Oddi dysfunction: results of treatment by endoscopic sphincterotomy. Br J Surg 1988;75:454-9. 16. Thatcher BS, Sivak MV, Tedesco FJ, Vennes JA, Hutton SW, Achkar EA. Endoscopic sphincterotomy for suspected dysfunction ofthe sphincter of Oddi. Gastrointest Endosc 1987;33:91-5. 17. Hawes RH, Cotton PB, Vallone AG. Follow-up 6-11 years after duodenoscopic sphincterotomy for stones in patients with prior cholecystectomy. Gastroenterology 1990;98:1008-12. 18. Howerton D, Falk G, Achkar E, FleshIer B, Sivak M. Response to sphincterotomy in patients with type II and type III sphincter of Oddi dysfunction [Abstract]. Am J Gastroenterol 1992; 87:1286.
GASTROINTESTINAL ENDOSCOPY