Duct Decompression Research Articles

EUS-Guided Pancreaticoduodenostomy: A New Technique for Main Pancreatic Duct Drainage in Acute and Chronic Pancreatitis

Background: Endoscopic drainage of the main pancreatic duct (MPD) in chronic pancreatitis (CP) can lead to a decrease in ductal hypertension, resulting in pain relief. Moreover, MPD drainage can be helpful in acute pancreatitis (AP) complicated with pancreatic duct disruption (PDD), in order to decrease the leakage of pancreatic juice from the disconnected pancreatic segment. However, in case of complete MPD obstruction (CP) or complete PDD (AP), transpapillary access to the proximal MPD segment cannot be obtained and conventional endoscopic ductal drainage is not possible. In these cases, a new technique, EUS-guided pancreaticoduodenostomy (PD), can be useful. Patients and Methods: We report five patients with CP (n = 4) or AP (n = 1) who underwent EUS-guided PD in order to achieve MPD drainage. In all patients, cannulation of the proximal segment of the MPD was not possible by means of a transpapillary approach. Results: Four patients with painful CP presented severe ductal dilation above a tight distal stricture. The remaining patient had presented severe AP, complicated with complete PDD and a pancreaticocutaneous fistula secondary to a previous percutaneous collection drainage. The proximal segment of the MPD was dilated in all patients. PD was performed as follows: Under EUS-guidance, a 19 gauge needle was inserted transduodenally into the proximal, dilated MPD, after its visualization with the tip of the echo-endoscope positioned in the duodenal bulb. Contrast medium was injected, confirming correct location of the needle in the duct. The needle was then exchanged over a guidewire for a 6.5 F diathermic sheath, introduced in the pancreaticoduodenal channel using cutting current. This channel was further enlarged by balloon dilation in two patients. Finally, a pancreaticoduodenal plastic straight stent was placed. In both patients who had previous balloon dilation of the PD, a 10 F stent was placed, whereas smaller diameter stents (6 F or 7 F) were initially used in the remaining patients. These stents were replaced by 10F stents during a second procedure. No complications were recorded. All patients had initial symptom resolution (pain relief and fistula closure) and remained well during a mean follow-up of 10 months (range: 3-30) with the stent in place. Conclusions: EUS guided PD is a new method of ductal decompression in patients with CP or AP, in cases when conventional ERCP fails to obtain access to the proximal MPD. Background: Endoscopic drainage of the main pancreatic duct (MPD) in chronic pancreatitis (CP) can lead to a decrease in ductal hypertension, resulting in pain relief. Moreover, MPD drainage can be helpful in acute pancreatitis (AP) complicated with pancreatic duct disruption (PDD), in order to decrease the leakage of pancreatic juice from the disconnected pancreatic segment. However, in case of complete MPD obstruction (CP) or complete PDD (AP), transpapillary access to the proximal MPD segment cannot be obtained and conventional endoscopic ductal drainage is not possible. In these cases, a new technique, EUS-guided pancreaticoduodenostomy (PD), can be useful. Patients and Methods: We report five patients with CP (n = 4) or AP (n = 1) who underwent EUS-guided PD in order to achieve MPD drainage. In all patients, cannulation of the proximal segment of the MPD was not possible by means of a transpapillary approach. Results: Four patients with painful CP presented severe ductal dilation above a tight distal stricture. The remaining patient had presented severe AP, complicated with complete PDD and a pancreaticocutaneous fistula secondary to a previous percutaneous collection drainage. The proximal segment of the MPD was dilated in all patients. PD was performed as follows: Under EUS-guidance, a 19 gauge needle was inserted transduodenally into the proximal, dilated MPD, after its visualization with the tip of the echo-endoscope positioned in the duodenal bulb. Contrast medium was injected, confirming correct location of the needle in the duct. The needle was then exchanged over a guidewire for a 6.5 F diathermic sheath, introduced in the pancreaticoduodenal channel using cutting current. This channel was further enlarged by balloon dilation in two patients. Finally, a pancreaticoduodenal plastic straight stent was placed. In both patients who had previous balloon dilation of the PD, a 10 F stent was placed, whereas smaller diameter stents (6 F or 7 F) were initially used in the remaining patients. These stents were replaced by 10F stents during a second procedure. No complications were recorded. All patients had initial symptom resolution (pain relief and fistula closure) and remained well during a mean follow-up of 10 months (range: 3-30) with the stent in place. Conclusions: EUS guided PD is a new method of ductal decompression in patients with CP or AP, in cases when conventional ERCP fails to obtain access to the proximal MPD.

Drainage of Gallbladder Fossa Fluid Collections with Endoprosthesis Placement Under Endoscopic Ultrasound Guidance: A Preliminary Report of Two Cases

Collections of fluid in the gallbladder fossa can be detected by ultrasound in as many as 29% of patients following cholecystectomy. Traditionally, persistent collections are treated by percutaneous drainage and bile duct decompression. We present two cases of persistent gallbladder fossa fluid collections which were refractory to bile duct decompression but which were successfully drained by endoscopic ultrasound-guided endoprosthesis placement. Under endoscopic ultrasound (EUS) control, a 19-gauge needle was inserted through the duodenal wall into the gallbladder fossa fluid collection. A guide wire was coiled within the collection, and an endoprosthesis was placed over the wire. Endoprosthesis insertion was successful in both cases, resulting in rapid symptomatic and radiographic improvement. EUS-guided drainage offers a minimally invasive alternative to percutaneous treatment of persistent gallbladder fossa fluid collections following cholecystectomy.

The Efficacy of Pancreatic Stenting for Management of Pancreatic Stones

Background and Aim: Pancreatic duct stones are a common finding in obstructive chronic pancreatitis and often firmly impacted proximal to a stricture. The stones and strictures may impair the pancreatic juice flow to the duodenum, inducing ductal hypertension, which is a major cause of pain. More recently, therapeutic endoscopy and stone fragmentation by extracorporeal shockwave lithotripsy (ESWL) have been used to perform pancreatic duct drainage and clearance. Pancreatic stenting is effective for the ductal decompression, but is still controversial because of the stent occulusion or the stent-related ductal changes. Therefore, we analyzed the efficacy of pancreatic stenting after stone extraction. Patients and Methods: Thirty-one patients with symptomatic pancreatic stones have been treated with endoscopy in combination with ESWL between January 1998 and September 2003. If there were one or more severe strictures in main pancreatic duct (MPD) on endoscopic retrograde pancreatography at the end of the complete stone clearance of MPD, a 7Fr, 8.5Fr or 10Fr polyethylene stent was inserted immediately after balloon dilatation of the stricture and the papilla of Vater so that all strictures were bypassed. The inserted stent was exchanged every three months or soon after any symptoms due to occulusion, and removed after one year. On the other hand, those who had mild or no stricture in MPD were observed without stenting until any symptoms related to pancreatitis were seen. Recurrent rates of pancreatic symptoms in severe and mild/no stricture group were evaluated. Results: Twenty of 31 patients had severe stricture and stenting was successful in 19 of them. The stent had been removed in 13 of 19 patients after one year's stenting period. Recurrent pancreatic pains were seen only in 3 (23%) of 13 patients in the severe stricture group by stenting, compared with 8 (73%) of 11 patients in the mild/no stricture group (p<0.01) in the mean follow up periods of 18 months. Seven of 8 patients with recurrent pancreatic pain in mild stricture group were received stenting at the recurrence, all of whom were improved. Conclusion: Additional stenting for MPD to stone extraction is effective for the management of the pancreatic stone.

Effects of early decompression and cholecystokinin inhibition in rats with acute pancreatitis induced by bile-pancreatic-duct obstruction

Biologic data related to pancreatic regeneration and acinar-cell homeostasis after ductal decompression would be useful in clinical settings to elucidate the time at which obstructions in human biliary acute pancreatitis (AP) should be removed. Our aim was to evaluate the outcome of AP after early removal of bile-pancreatic-duct obstruction (BPDO) and to ascertain whether cholecystokinin (CCK) blockade accelerates recovery from the disease. We conducted analysis of apoptosis and cell cycle, as well as measurements of enzyme and calcium load, in acinar cells using flow cytometry to ascertain the capability of the pancreas to regain its function after AP. Male Wistar rats were subjected to AP by means of BPDO for 6 hours and 24 hours. In other groups, the BPDO was opened 24 hours after induction; 3 days and 7 days later they were killed. Half of the rats in which the BPDO was opened were administered L364,718, a CCK-receptor antagonist (0.1 mg/kg/12 hours), 30 minutes before the induction of BPDO. Plasma amylase activity, hematocrit, and pancreatic weight returned to control values after BPDO opening. The highest degree of oxidative stress was found in the pancreases of rats subjected to BPDO for 6 hours, as indicated by the decrease in pancreatic glutathione content, but it was not restored 7 days after BPDO opening. Cell-cycle distribution, as measured with propidium iodide DNA staining, showed increases in the proportion of acinar cells in S-phase from 3 days after BPDO opening in L364,718-treated and nontreated rats. Annexin V-fluorescein isothiocyanate labeling revealed deletion of acinar cells by way of apoptosis 3 days after BPDO opening. However, it may be compensated 7 days after BPDO opening because regardless of whether rats were treated with L364,718, significant increases in synthesis and mitosis were detected. Accumulation of digestive enzymes and calcium in acinar cells was found during BPDO, but this appeared to have normalized 3 days after BPDO opening and onward in both L364,718-treated and nontreated rats. In conclusion, early removal of obstruction allowed rapid cell proliferation and prevented the progression of severe alterations within acinar cells induced by BPDO. CCK blockade does not accelerate pancreatic recovery after BPDO opening.

Medical therapy for chronic pancreatitis pain.

Chronic pancreatitis should be considered in all patients with unexplained abdominal pain. Management of abdominal pain in these patients continues to pose a formidable challenge. The importance of small duct disease without radiographic abnormalities is now a well-established concept. It is meaningful to determine whether patients with chronic pancreatitis have small duct or large duct disease because this distinction has therapeutic implications. Diagnostic evaluation should begin with simple noninvasive and inexpensive tests like serum trypsinogen and fecal elastase, to be followed where appropriate by more complicated measures such as the secretin hormone stimulation test, especially in patients with suspected small duct disease. No universal causal treatment is available. Non-enteric-coated enzyme preparations are useful for treatment of pain, whereas enteric-coated enzyme preparations are preferred for steatorrhea. Octreotide is used increasingly for abdominal pain that is unresponsive to pancreatic enzyme therapy. When medical therapy for chronic pancreatitis pain has failed, endoscopic therapy, endoscopic ultrasound-guided celiac plexus block, and thoracoscopic splanchnicectomy, performed by experts, may be considered for a highly selected patient population. Surgical ductal decompression is appropriate in patients with considerable pancreatic ductal dilation. The role and efficacy of cholecystokinin-receptor antagonists, antioxidants, and antidepressant drugs remain to be defined.

Predictors of Pain Response from Pancreatic Duct Stenting in Chronic Pancreatitis

The cause of pain in chronic pancreatitis is multifactorial. Endoscopic placement of a pancreatic duct (PD) stent in this setting is based on the concept that ductal decompression reduces PD pressure, with resultant improvement in pain. To evaluate the correlation between stent patency, the pancreatogram appearance, and clinical response, researchers in Alabama prospectively evaluated the change in caliber of the PD after endoscopic stenting in 25 consecutive patients with chronic pancreatitis. Pre-ERCP pancreatograms (from 40 stent sessions) were graded as …

Prospective study of pancreatic b-cell and exocrine function following duct decompression in tropical calcific pancreatitis.

Tropical calcific pancreatitis (TCP) is a chronic, nonalcoholic pancreatitis, which is limited to developing countries. In this condition, surgical decompression of the pancreatic duct consistently leads to relief of abdominal pain. However, no data are available on the effect of such intervention on pancreatic function. The aim of the present study was to prospectively evaluate b-cell and exocrine function following ductal drainage in patients with TCP. We studied 14 consecutive TCP patients who underwent ductal decompression for abdominal pain (longitudinal pancreaticojejunostomyin 12 patients, endoscopic sphincterotomy and ductal stenting in 2 subjects). Six patients who refused similar intervention served as controls. Patients were evaluated prospectively (median follow-up 13 months) for pain score, fasting and oral glucose stimulated plasma C-peptide, serum trypsin, and fecal chymotrypsin. After intervention, 1 patient died 2 months after surgery, and 2 others were lost in follow-up. The pain score improved significantly following duct decompression (median 8.0 vs. 0, p < 0.01), while in the control group there was no change in pain score (7.0 vs. 7.0). There was no change in b-cell function after intervention (fasting plasma C-peptide [mean +/- SEM] 0.41 +/- 0.08 vs. 0.42 +/- 0.05 nmol/l; peak plasma C-peptide 2.24 +/- 0.20 vs. 2.32 +/- 0.24 nmol/l). Fecal chymotrypsin was diminished in all patients prior to intervention (1.9 +/- 0.7 U/g), and did not normalize after ductal drainage in any subject. Serum trypsin levels were variable, being elevated in 29% and diminished in 47% of subjects. All 4 subjects with elevated baseline trypsin levels had a sharp fall after intervention (1020 vs. 175 ng/ml). However, serum trypsin did not normalize after ductal drainage in any patient with a diminished baseline value. In conclusion, patients with TCP have significant reduction in abdominal pain after decompression of the main pancreatic duct. However, there is no significant change in b-cell function. A fall in elevated serum trypsin suggests that there may be relief of subclinical inflammation after intervention; however, there is no improvement in exocrine function after a follow-up of 1 year.

Effects of Acute Pancreatic Duct Obstruction on Pancreatic Perfusion: Implication of Acute Pancreatic Duct Decompression

Background: Acute pancreatitis can result in pancreatic ischaemia and necrosis. Pancreatic duct (PD) obstruction may be the first step causing ischaemia in acute pancreatitis. Nitric oxide donors can attenuate acute pancreatitis through improvement in compromised pancreatic perfusion (PP). In this study, we determined if (1) PD obstruction altered PP and (2) PD decompression or L-arginine administration reversed this change. Methods: Fifteen Australian possums were randomly assigned to two groups: Animals in group A ( n = 6) were subjected to 30 min of PD obstruction and 60 min of PD decompression. Animals in group B ( n = 9) were subjected to 120 min PD ligation and 60 min PD decompression. A subset group B ( n = 6) were subjected to intravenous L-arginine (100 μg/kg) at the end of 120 min of ligation and at the end of PD decompression. The PP (Laser Doppler fluxmetry), PD pressure and blood pressure were continuously monitored. Results: PD pressure increased from 2.9 ± 2.5 to 18.1 ± 4.9 mmHg following PD ligation. PP was reduced to 67.1% ± 4.5% ( P < 0.01) and 46.2% ± 7.5% ( P < 0.001) of baseline following 30 and 120 min of PD ligation, respectively. Following 60 min of PD decompression, PP was restored to 89.1% ± 13.4% ( P < 0.02) of the baseline in the 30-min group. However, following 120 min PD ligation, PP remained depressed. L-arginine administration after 120 min of PD ligation transiently increased PP from 46.2% ± 7.5% to 81.1% ± 8.6% ( P < 0.03) of baseline. This effect was reproduced if L-arginine was administered at the end of decompression ( P < 0.05). Conclusion: In patients with acute pancreatitis due to obstructive causes, early decompression of the PD may prevent early pancreatic ischaemia.

Surgery and Chronic Pancreatitis

It is hoped that, in this millennium, chronic pancreatitis will be diagnosed earlier in the course of the disease process. Improved axial imaging of the pancreatic duct and pancreatic parenchyma will diminish the need for other invasive tests. Surgical procedures are directed at pancreatic duct decompression or resection of the pancreas (head, body or tail) or, infrequently, total pancreatectomy. Pain relief in 75% to 90% is the general rule, with diabetes developing subsequently in as many as 33% of patients. Surgery for chronic pancreatitis is effective in correcting sequelae of pancreatic fibrosis. Endoscopic stenting of the pancreatic and bile duct is used more frequently today. Until their place is ascertained, careful performance of surgery will continue to be a mainstay of treatment.

Endoscopic therapy of chronic pancreatitis

Chronic pancreatitis is an inflammatory process characterized by destruction of pancreatic parenchyma and ductal structures with formation of fibrosis. Pain is the predominant symptom of chronic pancreatitis and its origin appears to be multifactorial. 1 Steer ML Waxman I Freedman S. Chronic pancreatitis. N Engl J Med. 1995; 332: 1482-1490 Crossref PubMed Scopus (585) Google Scholar , 2 Widdison AL Alvarez C Karanjia ND Reber HA. Experimental evidence of beneficial effects of ductal decompression in chronic pancreatitis. Endoscopy. 1991; 23: 151-154 Crossref PubMed Scopus (51) Google Scholar , 3 Karanjia ND Reber HA. The cause and management of the pain of chronic pancreatitis. Gastrointest Clin N Amer. 1990; 19: 895-904 PubMed Google Scholar , 4 Lo SK Lewis MPN Reber PU Patel A Sherman S Ashley SW Reber HA. In-vivo endoscopic trans-sphincteric measurement of pancreatic blood flow (PBF) in humans. Gastrointest Endosc. 1996; 43: 409A Abstract Full Text PDF Scopus (3) Google Scholar The multiplicity of causes of pain helps explain the mixed results achieved by current methods of therapy. Most therapeutic efforts in the treatment of chronic pancreatitis are directed toward control of symptoms. Medical therapies (dietary alterations, analgesics, nerve blocks, oral enzyme supplements, octreotide) are variably effective in relieving pain, 1 Steer ML Waxman I Freedman S. Chronic pancreatitis. N Engl J Med. 1995; 332: 1482-1490 Crossref PubMed Scopus (585) Google Scholar leaving surgical therapy as the main therapeutic option for patients who fail to improve with medical management. Early postoperative pain relief is seen in 80-90% of patients; however, pain recurs in 20-50% during long-term follow-up. 5 Bradley EL. Long-term results of pancreatojejunostomy in patients with chronic pancreatitis. Am J Surg. 1987; 153: 207-213 Abstract Full Text PDF PubMed Scopus (197) Google Scholar , 6 Malfertheiner P Buchler M. Indications for endoscopic or surgical therapy in chronic pancreatitis. Endoscopy. 1991; 23: 185-190 Crossref PubMed Scopus (26) Google Scholar Surgical drainage procedures are associated with a morbidity rate of 20-40% and an average mortality rate of 4%. 3 Karanjia ND Reber HA. The cause and management of the pain of chronic pancreatitis. Gastrointest Clin N Amer. 1990; 19: 895-904 PubMed Google Scholar While endoscopic therapy has revolutionized the approach to a variety of biliary tract disorders, it is only recently that the indications for therapeutic endoscopy have been expanded to include disorders of the pancreas. 7 Bedford RA Howerton DH Geenen JE. The current role of ERCP in the treatment of benign pancreatic disease. Endoscopy. 1994; 26: 113-119 Crossref PubMed Scopus (20) Google Scholar , 8 Kozarek RA Traverso LW. Endotherapy of chronic pancreatitis. Int J Pancreatol. 1996; 19: 93-102 PubMed Google Scholar , 9 Kaikaus RM Geenen JE. Current role of ERCP in the management of benign pancreatic disease. Endoscopy. 1996; 28: 131-137 Crossref Scopus (9) Google Scholar , 10 Sherman S Lehman GA. Endoscopic therapy of pancreatic disease. The Gastroenterologist. 1997; 5: 262-277 PubMed Google Scholar , 11 Kozarek RA Chronic pancreatitis in 1994: Is there a role for endoscopic treatment?. Endoscopy. 1994; 26: 625-628 Crossref PubMed Scopus (18) Google Scholar Although the endoscopic approach has not been compared directly to surgery, endoscopic drainage is appealing in that it may offer an alternative to surgical drainage procedures with generally less morbidity and mortality. Furthermore, endoscopic procedures do not preclude subsequent surgery, if necessary. Moreover, the outcome from reducing the intraductal pressure by endoscopic methods may be a predictor for the success of surgical drainage. 12 Huibregtse K Smits ME. Endoscopic management of diseases of the pancreas. Am J Gastroenterol. 1994; 89: S66-S77 PubMed Google Scholar

Prospective Evaluation of Morphology, Function, and Quality of Life After Extracorporeal Shockwave Lithotripsy and Endoscopic Treatment of Chronic Calcific Pancreatitis

Therapeutic endoscopy may be effective in selected patients with chronic calcific pancreatitis (CCP). We prospectively evaluated the early outcome of extracorporeal shockwave lithotripsy (ESWL) in combination with interventional endoscopy, using broad inclusion criteria. A total of 48 consecutive patients (35 male, 13 female) were recruited for ESWL and endoscopic therapy of symptomatic CCP. Symptoms, quality of life, pancreatic morphology and function were assessed before and after. Multiple stones (n = 43), strictures (n = 34), and pancreas divisum (n = 11) were found. A median of 13 ESWL sessions (range 2-74) with a median of 22,100 shockwaves (1,700-150,900) were required. Endoscopic pancreatic sphincterotomy (n = 48), stricture dilation (n = 12), and/or stenting (n = 27) were performed. After therapy, drainage of the pancreatic duct system was achieved in 36, complete stone clearance in 21 patients. Follow-up (n = 38) at 7 months (range 5-9) showed a significant decrease in pancreatic duct diameter (p < 0.001) and pain score (p < 0.0001) whereas complete pain relief was observed in 45% of cases. Several quality of life scores improved significantly. Weight gain occurred in 68% of patients. Normalization of fasting blood glucose and HbA1c levels were observed in four patients, without modifying their treatment. Improvement in pain score correlated with weight gain and decrease in pancreatic duct diameter. Nonalcoholic etiology was associated with a better chance for improvement in pain score and decrease in pancreatic duct diameter. The presence of strictures did not deteriorate the clinical outcome. Besides pain relief, ESWL in combination with interventional endoscopy resulted in pancreatic ductal decompression, weight gain, and improvement in quality of life in a considerable number of patients with advanced CCP.

Prospective evaluation of morphology, function, and quality of life after extracorporeal shockwave lithotripsy and endoscopic treatment of chronic calcific pancreatitis

OBJECTIVE: Therapeutic endoscopy may be effective in selected patients with chronic calcific pancreatitis (CCP). We prospectively evaluated the early outcome of extracorporeal shockwave lithotripsy (ESWL) in combination with interventional endoscopy, using broad inclusion criteria. METHODS: A total of 48 consecutive patients (35 male, 13 female) were recruited for ESWL and endoscopic therapy of symptomatic CCP. Symptoms, quality of life, pancreatic morphology and function were assessed before and after ESWL. RESULTS: Multiple stones (n = 43), strictures (n = 34), and pancreas divisum (n = 11) were found. A median of 13 ESWL sessions (range 2–74) with a median of 22,100 shockwaves (1,700–150,900) were required. Endoscopic pancreatic sphincterotomy (n = 48), stricture dilation (n = 12), and/or stenting (n = 27) were performed. After therapy, drainage of the pancreatic duct system was achieved in 36, complete stone clearance in 21 patients. Follow-up (n = 38) at 7 months (range 5–9) showed a significant decrease in pancreatic duct diameter ( p < 0.001) and pain score ( p < 0.0001) whereas complete pain relief was observed in 45% of cases. Several quality of life scores improved significantly. Weight gain occurred in 68% of patients. Normalization of fasting blood glucose and HbA1c levels were observed in four patients, without modifying their treatment. Improvement in pain score correlated with weight gain and decrease in pancreatic duct diameter. Nonalcoholic etiology was associated with a better chance for improvement in pain score and decrease in pancreatic duct diameter. The presence of strictures did not deteriorate the clinical outcome. CONCLUSIONS: Besides pain relief, ESWL in combination with interventional endoscopy resulted in pancreatic ductal decompression, weight gain, and improvement in quality of life in a considerable number of patients with advanced CCP.

Expandable Metal Stents for Benign Pancreatic Duct Obstruction

Among patients with advanced chronic pancreatitis and morphologically demonstrable main pancreatic duct (MPD) abnormalities who are candidates for endotherapy, about two-thirds have a MPD stricture and require stenting to achieve appropriate ductal decompression. The standard stent used in this indication is the plastic stent, which provides a median patency rate of 6 to 12 months. The requirement for stent exchange represents a limitation for the treatment of this relatively young patient population. By analogy with the biliary tract, the authors hypothesize that self-expandable metal stents might offer a long-lasting drainage of the MPD. Several years ago the authors used such stents on an experimental basis to treat patients with MPD strictures. Although routine use of self-expandable metal stents should be discouraged, the authors propose some guidelines for further technical improvement.

Update on diagnosis and management of chronic pancreatitis.

Chronic pancreatitis should be considered in all patients with unexplained abdominal pain. The importance of small duct disease without obvious radiographic abnormalities is an important new concept. It is meaningful for the clinician to define whether the patient with chronic pancreatitis has small duct or large duct disease. Diagnostic evaluations should begin with a simple, noninvasive, inexpensive test such as serum trypsinogen, to be followed by more complicated testing such as the secretin stimulation test, particularly in those patients with small duct disease. Non-enteric-coated pancreatic enzyme preparations are preferred for the treatment of pain whereas enteric-coated pancreatic enzyme preparations are the drugs of choice for treating steatorrhea. Octreotide may become an important therapy for treating abdominal pain unresponsive to pancreatic enzyme therapy. Endoscopic treatment of the pain of chronic pancreatitis should be used only in highly selected patients and may cause damage to the pancreas. Surgical ductal decompression is appropriate in selected patients.

Feline Model of Chronic Obstructive Pancreatitis: Effects of Acute Pancreatic Duct Decompression on Blood Flow and Interstitial pH

The mechanism by which duct decompression (DD) relieves pain in patients with chronic pancreatitis (CP) is unknown. CP is associated with increased tissue pressure (IP), low pancreatic microvascular blood flow (PMBF), and interstitial pH (pH(I)). The aims of this study were to examine the effects of acute DD on PMBF, increased IP, and pH(I) in cats with CP. The main pancreatic duct was partially obstructed. At 6 weeks PMBF (ml/min/100g H2 gas clearance), IP (mmHg needle electrode), and pH(I) (microelectrode) were measured before and after secretin stimulation. The duct was then opened, and the studies were repeated. PMBF normally increased with secretin stimulation (118 +/- 20 versus 271 +/- 52, P < 0.05). IP was unaltered, and pH(I) decreased as hydrogen ions produced during bicarbonate secretion were dissipated (7.41 +/- 0.01 versus 7.38 +/- 0.01, P < 0.05). In CP, basal PMBF was lower than normal (51 +/- 6 versus 118 +/- 20, P < 0.05) and decreased with stimulation (51 +/- 3.5 versus 31 +/- 3.5, P < 0.05). Basal pancreatic IP was increased (3.47 +/- 0.7 versus 0.05 +/- 0.3, P < 0.05) and increased further with secretory stimulation (3.47 +/- 0.7 versus 4.41 +/- 0.7, P < 0.05) (a compartment syndrome). The low basal pancreatic pH(I) (7.23 +/- 0.02) did not change with secretin stimulation, since bicarbonate secretion was minimal. DD decreased IP (3.66 +/- 0.5 versus 2.81 +/- 0.5, P < 0.05) and increased PMBF (50 +/- 6 versus 79 +/- 6, P < 0.05) and pH(I) (7.24 +/- 0.02 versus 7.34 +/- 0.02, P < 0.05). The normal increase in PMBF after stimulation was restored (79 +/- 6 versus 218 +/- 54, P < 0.05). pH(I) now increased with stimulation (7.34 +/- 0.002 versus 7.37 +/- 0.002, P < 0.05), perhaps due to the marked hyperaemic response. DD acutely restored basal and stimulated PMBF and IP towards normal. Basal pancreatic pH(I) also improved and reflects the underlying ischaemia.

Effects of early ductal decompression in human biliary acute pancreatitis

Pezzilli, R.; Billi, P.; Barakat, B.; Baroncini, D.; D'lmpeno, N.; Miglio, F. Author Information

Effects of early ductal decompression in human biliary acute pancreatitis.

It was recently demonstrated in experimental models that, after pancreatic outflow obstruction, serum amylase levels first increase and then progressively decline regardless of whether the obstruction was maintained or relieved. Furthermore, early decompression of the ductal biliary system may prevent the progression of the disease. This finding prompted us to look for a similar pattern in patients with obstructive acute pancreatitis due to biliary stones. Forty-two patients with biliary acute pancreatitis were prospectively studied. Twenty-one patients underwent urgent endoscopic sphincterotomy (ES), and 21 received conservative medical treatment (CMT). The two groups were comparable for sex, age, onset of pain, and severity. Serum amylase and lipase were determined in all patients on admission and 24 h later. The percentage variation of serum amylase and lipase was calculated considering, for each patient, the concentrations of the two enzymes assayed on admission and 24 h later. On admission, all patients had elevated serum concentrations of amylase (mean +/- SEM: ES, 2,560+/-473 U/L; CMT, 1,783+/-481 U/L) and lipase (ES, 3,037+/-574 U/L; CMT, 3,179+/-724 U/L). The serum amylase variation (mean +/- SEM) was -65.6+/-5.5% in the ES and -47.2.1+/-8.1% in the CMT patients. The serum lipase variation was -59.1+/-7.7 and -33.1+/-18% in the same groups, respectively. These differences were not statistically significant. Acute pancreatitis worsened in one patient in the ES group and in seven in the CMT group; this difference was statistically significant (p < 0.02). The mean length of hospitalization was 8.9 days in the ES group and 19.7 days in the CMT group (p < 0.001). Serum pancreatic enzymes determination is not useful to evaluate the results of the early decompression of biliary duct in human acute pancreatitis. Indeed, early endoscopic sphincterotomy may result in a substantial improvement in the outcome of biliary acute pancreatitis.

Effects of early ductal decompression in human biliary acute pancreatitis

Pezzilli, R.; Billi, P.; Barakat, B.; Baroncini, D.; D'lmpeno, N.; Miglio, F. Author Information

Transcystic biliary decompression after direct laparoscopic exploration of the common bile duct.

A purpose-designed transcystic common bile duct (CBD) decompression cannula is described for use as an alternative to T-tube insertion following laparoscopic direct CBD exploration. This permits safe primary closure of the choledochotomy. Following direct supraduodenal laparoscopic clearance of large common bile duct stones, the biliary decompression cannula is inserted percutaneously inside its peel-away sheet over a guide-wire into the CBD via the cystic duct. When in place, the cannula is secured to the cystic duct by two catgut extracorporeal Roeder knots and the choledochotomy is then closed. The terminal multiperforated S-shaped segment of the Cuschieri biliary decompression cannula prevents postoperative dislodgement. Transcystic decompression of the extrahepatic biliary tract using the Cuschieri cannula has been used in 12 patients who underwent laparoscopic supraduodenal CBD exploration for large or occluding stones. There was no instance of postoperative dislodgement of the cannula and all patients had effective drainage of the common bile duct (average 300 ml bile per 24 h). The procedure was uncomplicated in all but one patient who developed self-limiting leakage from the CBD suture line in the early postoperative period. The median hospital stay after surgery was 4 days, with a range of 3 to 10 days. The cystic duct decompression cannula was capped and sealed under an occlusive dressing at the time of discharge. Removal of the cannula was carried out without any complications as a day case 11-16 days after surgery. Transcystic biliary decompression is safe and effective. The experience with is use indicates that compared to T-tube drainage, transcystic decompression may accelerate recovery and reduce the hospital stay in patients following laparoscopic direct exploration of the CBD. Its insertion is less technically demanding than placing a T-tube through the choledochotomy. Transcystic decompression with complete primary closure of the CBD realizes the full benefits of the single-stage management of common bile duct calculi and permits confirmation of complete stone clearance after surgery.

Endoscopic sphincteroclasy: a useful therapeutic tool for biliary endoscopy in Billroth II gastrectomy patients.

Endoscopic exploration of the common bile duct is generally more difficult and hazardous in patients with a Billroth II gastrectomy than in patients with normal anatomy. Hydrostatic dilation of the papilla, which we term "endoscopic sphincteroclasy", provides a useful alternative to sphincterotomy in such patients. Endoscopic sphincteroclasy was carried out in five patients with a Billroth II anastomosis. There were four men and one woman, aged 58 to 90 years. One patients was cirrhotic, with impaired coagulation. Four presented with typical cholangitis, and one had pain and jaundice. The common bile duct was dilated in all five patients. Four had choledocholithiasis and one had a cholangiocarcinoma. Sphincteroclasy was carried out with balloon dilators mounted on 0.035-inch guide wires. Immediate extraction of stones was achieved in three of the four patients with choledocholithiasis. In one case, a control endoscopic retrograde cholangiopancreatography was necessary to remove residual stones, without additional dilation. Insertion of the endoprosthesis was possible without difficulty in the patient with a malignant stricture. None of the patients required a sphincterotomy. No complications were observed up to six months after the sphincteroclasy. We recommend the use of endoscopic sphincteroclasy in patients with a Billroth II gastrectomy who require endoscopic therapy, as well as in patients in need of emergency bile duct decompression who have impaired coagulation.