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⁎4663 Pancreatic sphincterotomy improves symptoms in patients with pancreatic sphincter hypertension persisting after biliary sphincterotomy.
*4661 DO PANCREATIC FEATURES IDENTIFIED WITH ENDOSCOPIC ULTRASOUND CORRELATE WITH SPHINCTER OF ODDI MANOMETRY IN PATIENTS WITH CLINICALLY SUSPECTED SPHINCTER OF ODDI DYSFUNCTION? AN EVALUATION OF 462 PATIENTS. Rig S. Patel, Mohammad A. Eloubeidi, Hugh E. Mulcahy, John T. Cunningham, Michael B. Wallace, Kenneth M. Payne, Neven Hadzijahic, Robert Etemad, Koji Matsuda, Brenda J. Hoffman, Peter B. Cotton, Robert H. Hawes, Med Univ of South Carolina, Charleston, SC. SOM is the accepted method for diagnosing SOD. EUS can evaluate anatomical features of the pancreas. The role of EUS in the evaluation of patients with clinically suspected SOD particularly in predicting the findings of SOM, is undefined. AIM: Evaluate if EUS assessment of the pancreas correlates with SOM in patients with clinically suspected SOD. METHOD: Patients with clinically suspected SOD who underwent EUS prior to SOM between 2/94 and 11/99 at MUSC were included for analysis. Patients with pancreas divisum, prior therapy to the major papilla, or inadequate SOM or EUS were excluded. EUS features of pancreatitis ( parenchymal : foci, strands, lobularity, cysts, and ductal : hyperechoic and irregular duct margins, calcification/stones, visible side-branches and duct dilatation) were compared with the SOM diagnosis of the biliary (BSOM) and pancreatic (PSOM) orifices. All EUS examinations were blinded to the findings at SOM. SOM was performed using a standard 5 F aspirating catheter and SOD diagnosed if the mean sphincter pressure from two leads was >40 mmHg. EUS was performed using a radial echoendoscope (Olympus UM-20, UM-130) at 7.5 MHz. RESULTS: Of 462 patients (mean age 45 yrs. range16-85yrs., M/F 137/325), 372 and 370 underwent unequivocal PSOM and BSOM respectively after EUS. Of the 176 patients with abnormal PSOM, 54% (n=95) had a total > 4 EUS features of pancreatitis; 46% (89/194) with normal PSOM had 3 or less features (p=1). Of patients with no EUS features, 48%(25/52) and 52% (27/52) had normal and abnormal PSOM respectively (p=0.55). Similarly there was no correlation between BSOM (148 abnormal) and the total number of EUS features. The number of parenchymal or ductal EUS features was unrelated to BSOM or PSOM. CONCLUSIONS 1] Neither the total number nor the number of parenchymal or ductal EUS features of pancreatitis predict the findings of SOM in patients with clinically suspected SOD. 2] A normal EUS examination (i.e. no features) does not exclude SOD. *4662 OCTREOTIDE REDUCES SPHINCTER PRESSURE IN SPHINCTER OF ODDI DYSFUNCTION: FURTHER SUPPORT FOR SELECTIVE DENERVATION OF THE SPHINCTER. Ali Fazel, S. Cy Li, Frank R. Burton, Saint Louis Univ, Saint Louis, MO. Sphincter of Oddi (SO) motility is modulated by inhibitory and excitatory neurons present in its myenteric plexus. The excitatory neurons are predominantly cholinergic while inhibitory neurons produce nitrous oxide and vasoactive intestinal peptide. Octreotide inhibits both groups of neurons. This explains the relatively equivocal effect of octreotide on the normal SO. In SOD evidence suggests a loss of inhibitory neurons while excitatory neurons remain intact. We hypothesize that octreotide can suppress this unopposed cholinergic activity resulting in relaxation of the hypertensive SO. Aim: To determine the effect of octreotide on the hypertensive SO. Methods: 38 patients presenting with recurrent abdominal pain and SOD (basal pressure >40 mm Hg) were studied. SOM was performed in standard fashion. The test group (n=19) received octreotide acetate 100 mg IV while the control group (n=19) received IV saline. Basal, phasic and duct pressure as well as phasic amplitude and frequency were recorded before and 3 minutes after the IV infusion. Changes in these parameters before and after IV infusions were compared. Results:See table. Octreotide caused a statistically significant reduction in basal and peak SO pressure as compared to saline. Conclusions:Relaxation of the hypertensive SO in response to octreotide supports the hypothesis of selective denervation and indicates a potential role for octreotide in the medical treatment of SOD. Effects of Octreotide on the Motility of the Hypertensive Sphincter of Oddi Octreotide (n=19) pre post Basal pressure 74.0 Phasic pressure 193 Amplitude 119 Frequency 6.5 Duct Pressure 12.0
± ± ± ± ±
40.0* 32* 28 2.6 5.4
50.7 168 118 8.8 11.0
± ± ± ± ±
25.2* 43* 36 2.6 6.0
Saline (n=19) pre post 59.5 196 137 6.4 15.6
± ± ± ± ±
19.9 39 30.9 2.8 6.0
60.7 197 136 7.0 16.5
± ± ± ± ±
P† 21.4 <.0001 39 <.01 31 NS 4.8 NS 5.4 NS
Data expressed as mean ± SD, *pre vs post: p<.01; †octreotide∆ vs saline∆
AB196
GASTROINTESTINAL ENDOSCOPY
*4663 PANCREATIC SPHINCTEROTOMY IMPROVES SYMPTOMS IN PATIENTS WITH PANCREATIC SPHINCTER HYPERTENSION PERSISTING AFTER BILIARY SPHINCTEROTOMY. Rig S. Patel, Mahesh S. Mokhashi, Hugh E. Mulcahy, Paul R. Tarnasky, John T. Cunningham, Kenneth M. Payne, Peter B. Cotton, Robert H. Hawes, Med Univ of South Carolina, Charleston, SC. BACKGROUND: PSH can persist after BSx. There is little information regarding the clinical symptom response to BSx and PSx in patients with PSH. AIM: Evaluate the effect of PSx on symptoms in patients with persistent PSH after prior BSx. METHODS: Patients with prior sphincter of Oddi dysfunction (SOD) treated initially with BSx and who had persistent PSH were analyzed. Clinical data were evaluated for the subsequent endoscopic therapy (if any). All patients were contacted by telephone to evaluate symptom response to their most recent endoscopic therapy. Manometry was performed with a standard perfused, aspirating catheter and SOD diagnosed if the mean pressure form two leads was ≥ 40 mmHg. Persistent PSH was documented by pancreatic manometry immediately after BSx and prior to PSx at a subsequent procedure. Patients who had normal pancreatic manometry were excluded from analysis. RESULTS: 42 patients (mean age 53 yrs, range 21-83 yrs , M:F=9/39) underwent isolated BSx in the setting of PSH. Of these 21 (50%) patients returned with persistent symptoms and underwent PSx. Patients were interviewed regarding symptom response at a mean of 39 months ( range 6.8-53months) after their most recent endoscopic intervention. Of the 21 patients who only had BSx as their most recent therapy (i.e. untreated PSH), 13 (62%) reported resolution of pain/symptoms, 6 (29%) reported improvement of symptoms and 2 (9%) reported no change in symptoms. Of the 21 patients who returned after BSx with persistent symptoms and who underwent PSx to treat PSH, 3 (14%) reported resolution of symptoms,11 (52%) reported improved symptoms, 6 (29%) reported no change and 1 (5%) reported worsening symptoms. After initial BSx, post-ERCP pancreatitis occurred in 4/21 (19%) patients who subsequently returned with symptoms, compared to 1/21 (5%) (NS) in patients who did not receive subsequent PSx. CONCLUSIONS: 1] Pancreatic sphincterotomy can improve symptoms in 66% of patients with prior biliary sphincterotomy but persistent PSH and symptoms. 2] However, a significant portion of patients (45%) with persistent PSH immediately after biliary sphincterotomy report symptom improvement without pancreatic sphincterotomy. This suggests that BSx alone may provide adequate symptom relief in some patients. Further study is needed to identify which patients with PSH would benefit from pancreatic sphincterotomy in addition to biliary sphincterotomy. *4664 SPHINCTER OF ODDI MANOMETRY AND ENDOSCOPIC SPHINCTEROTOMY IN PATIENTS WITH PANCREATITIS OF UNKNOWN ETIOLOGY: A LONG-TERM STUDY AND RESULTS IN A TERTIARY REFERRAL CENTER. William Mayoral, Gustavo Marino, Claudio R. Tombazzi, Hisham I. Sallout, Firas H. Al-Kawas, Georgetown Univ Med Ctr, Washington, DC. Sphincter of Oddi dysfunction (SOD) is responsible for 15% of PUE. Limited data is available about the benefit and long-term outcome of ES. The aim of this study was to evaluate the long-term outcome of ES in this group of patients. Methods: All SOM performed for PUE were reviewed. A total of 67 studies were identified. A basal sphincter of Oddi pressure (SOP) greater than 40mmHg was considered abnormal. Nineteen out of 67 patients (28%) with clinical pancreatitis had elevated SOP. All patients had biliary sphincter manometry (BSM). If the pressure was high, biliary sphincterotomy (BS) was performed. If BSM was normal, pancreatic sphincter manometry was performed (PSM), and if high, pancreatic sphincterotomy (PS) was performed. Initially, 18 patients had BS and 1 patient had PS. All patients were admitted overnight for observation. Further follow-up was obtained by telephone interview using a standard protocol, which included 21 variables addressing pain resolution, narcotic use, the need for hospital admissions or ER visits, and any further intervention. Results: Complete follow-up was obtained in all 19 patients. The mean follow up time was 54 months (Range 6 -126). Patients were categorized in 3 groups according to the presence or absence of pain with or without narcotics, and the recurrence or not of documented pancreatitis. Eleven patients (58%) were pain free. Four patients (23.5%) had mild pain that did not require narcotics, and four patients (21%) had pain that required narcotics on a daily basis. Four patients (21%) required a second procedure, which included a SOM. Two of them had a PS because of elevated pancreatic sphincter pressure. Extension of the original sphincterotomy was performed in the remaining two because of residual biliary sphincter pressure. Complications occurred in 4 patients (21%). Three had mild pancreatitis and one patient with prior sphincteroplasty had a duodenal perforation requiring surgery. Globally, fifteen patients (79%) felt better after the ES was performed, and 4 patients (21%) had no improvement. Conclusions: 1-SOD is frequently identified in patients with PUE. 2- Initial measurement of biliary sphincter pressure is adequate for identification and treatment of most patients with pancreatitis and SOD. 3- Isolated pancreatic sphincter dysfunction requiring PS is infrequent. 4- Further studies are required to confirm these results.
VOLUME 51, NO. 4, PART 2, 2000
± ± ± ± ±
40.0* 32* 28 2.6 5.4
50.7 168 118 8.8 11.0
± ± ± ± ±
25.2* 43* 36 2.6 6.0
Saline (n=19) pre post 59.5 196 137 6.4 15.6
± ± ± ± ±
19.9 39 30.9 2.8 6.0
60.7 197 136 7.0 16.5
± ± ± ± ±
P† 21.4 <.0001 39 <.01 31 NS 4.8 NS 5.4 NS
Data expressed as mean ± SD, *pre vs post: p<.01; †octreotide∆ vs saline∆
AB196
GASTROINTESTINAL ENDOSCOPY
*4663 PANCREATIC SPHINCTEROTOMY IMPROVES SYMPTOMS IN PATIENTS WITH PANCREATIC SPHINCTER HYPERTENSION PERSISTING AFTER BILIARY SPHINCTEROTOMY. Rig S. Patel, Mahesh S. Mokhashi, Hugh E. Mulcahy, Paul R. Tarnasky, John T. Cunningham, Kenneth M. Payne, Peter B. Cotton, Robert H. Hawes, Med Univ of South Carolina, Charleston, SC. BACKGROUND: PSH can persist after BSx. There is little information regarding the clinical symptom response to BSx and PSx in patients with PSH. AIM: Evaluate the effect of PSx on symptoms in patients with persistent PSH after prior BSx. METHODS: Patients with prior sphincter of Oddi dysfunction (SOD) treated initially with BSx and who had persistent PSH were analyzed. Clinical data were evaluated for the subsequent endoscopic therapy (if any). All patients were contacted by telephone to evaluate symptom response to their most recent endoscopic therapy. Manometry was performed with a standard perfused, aspirating catheter and SOD diagnosed if the mean pressure form two leads was ≥ 40 mmHg. Persistent PSH was documented by pancreatic manometry immediately after BSx and prior to PSx at a subsequent procedure. Patients who had normal pancreatic manometry were excluded from analysis. RESULTS: 42 patients (mean age 53 yrs, range 21-83 yrs , M:F=9/39) underwent isolated BSx in the setting of PSH. Of these 21 (50%) patients returned with persistent symptoms and underwent PSx. Patients were interviewed regarding symptom response at a mean of 39 months ( range 6.8-53months) after their most recent endoscopic intervention. Of the 21 patients who only had BSx as their most recent therapy (i.e. untreated PSH), 13 (62%) reported resolution of pain/symptoms, 6 (29%) reported improvement of symptoms and 2 (9%) reported no change in symptoms. Of the 21 patients who returned after BSx with persistent symptoms and who underwent PSx to treat PSH, 3 (14%) reported resolution of symptoms,11 (52%) reported improved symptoms, 6 (29%) reported no change and 1 (5%) reported worsening symptoms. After initial BSx, post-ERCP pancreatitis occurred in 4/21 (19%) patients who subsequently returned with symptoms, compared to 1/21 (5%) (NS) in patients who did not receive subsequent PSx. CONCLUSIONS: 1] Pancreatic sphincterotomy can improve symptoms in 66% of patients with prior biliary sphincterotomy but persistent PSH and symptoms. 2] However, a significant portion of patients (45%) with persistent PSH immediately after biliary sphincterotomy report symptom improvement without pancreatic sphincterotomy. This suggests that BSx alone may provide adequate symptom relief in some patients. Further study is needed to identify which patients with PSH would benefit from pancreatic sphincterotomy in addition to biliary sphincterotomy. *4664 SPHINCTER OF ODDI MANOMETRY AND ENDOSCOPIC SPHINCTEROTOMY IN PATIENTS WITH PANCREATITIS OF UNKNOWN ETIOLOGY: A LONG-TERM STUDY AND RESULTS IN A TERTIARY REFERRAL CENTER. William Mayoral, Gustavo Marino, Claudio R. Tombazzi, Hisham I. Sallout, Firas H. Al-Kawas, Georgetown Univ Med Ctr, Washington, DC. Sphincter of Oddi dysfunction (SOD) is responsible for 15% of PUE. Limited data is available about the benefit and long-term outcome of ES. The aim of this study was to evaluate the long-term outcome of ES in this group of patients. Methods: All SOM performed for PUE were reviewed. A total of 67 studies were identified. A basal sphincter of Oddi pressure (SOP) greater than 40mmHg was considered abnormal. Nineteen out of 67 patients (28%) with clinical pancreatitis had elevated SOP. All patients had biliary sphincter manometry (BSM). If the pressure was high, biliary sphincterotomy (BS) was performed. If BSM was normal, pancreatic sphincter manometry was performed (PSM), and if high, pancreatic sphincterotomy (PS) was performed. Initially, 18 patients had BS and 1 patient had PS. All patients were admitted overnight for observation. Further follow-up was obtained by telephone interview using a standard protocol, which included 21 variables addressing pain resolution, narcotic use, the need for hospital admissions or ER visits, and any further intervention. Results: Complete follow-up was obtained in all 19 patients. The mean follow up time was 54 months (Range 6 -126). Patients were categorized in 3 groups according to the presence or absence of pain with or without narcotics, and the recurrence or not of documented pancreatitis. Eleven patients (58%) were pain free. Four patients (23.5%) had mild pain that did not require narcotics, and four patients (21%) had pain that required narcotics on a daily basis. Four patients (21%) required a second procedure, which included a SOM. Two of them had a PS because of elevated pancreatic sphincter pressure. Extension of the original sphincterotomy was performed in the remaining two because of residual biliary sphincter pressure. Complications occurred in 4 patients (21%). Three had mild pancreatitis and one patient with prior sphincteroplasty had a duodenal perforation requiring surgery. Globally, fifteen patients (79%) felt better after the ES was performed, and 4 patients (21%) had no improvement. Conclusions: 1-SOD is frequently identified in patients with PUE. 2- Initial measurement of biliary sphincter pressure is adequate for identification and treatment of most patients with pancreatitis and SOD. 3- Isolated pancreatic sphincter dysfunction requiring PS is infrequent. 4- Further studies are required to confirm these results.
VOLUME 51, NO. 4, PART 2, 2000