Patent Accessory Pancreatic Duct Research Articles

Minor papilla endotherapy in patients with ventral duct obstruction: identification and management

Pancreatic duct (PD) cannulation via the major papilla may be compromised by downstream obstruction of the ventral PD from a stone or stricture. In patients with a patent accessory PD, cannulation of the minor papilla permits stenting or stone removal upstream of the ventral PD obstruction. Data on this technique are limited. University of Colorado Hospital and Maine Medical Center endoscopy databases were queried for ERCPs with minor papilla cannulation. Technical success was defined as deep cannulation of the minor papilla. Minor papilla endotherapy included sphincterotomy, stricture dilation, stenting, or stone treatment. Clinical improvement was designated as >50% reduction in pain or narcotic analgesia. Follow-up was obtained by chart review and telephone contact. Over a 22-year period, 464 patients had minor papilla cannulation. Congenital and incomplete pancreas divisum were excluded, and 64 patients met study criteria. Technical success was achieved in 58 of 64 patients (91%). In patients with stones, 25 of 34 (74%) had clearance using endoscopic techniques. Median follow-up was 15.5 months. Twelve of 28 patients (43%) on chronic narcotic regimens reported a reduction in narcotic use by >50%, and 32 of 44 patients (73%) reached for discussion noted improved abdominal pain by >50%. Thirteen patients required surgery for symptom control. In this multicenter experience, 15% of patients undergoing minor papilla cannulation had acquired a ventral PD obstruction. Access via the minor papilla to the upstream main PD for endotherapy and clinical improvement was achieved in most patients. Increased and early recognition of these intensive therapeutic options may enhance treatment options for this complex group of patients.

Su1706 Minor Papilla Endotherapy (MPE) in Patients Without Pancreas Divisum: Identification and Management

Cannulation of the pancreatic duct (PD) via the major papilla may be compromised by downstream obstruction of the ventral portion of the PD from a stone or stricture. Cannulation of the minor papilla in patients with patent accessory PD in communication with the PD upstream of the level of ventral PD obstruction permits stenting or stone removal. Data on this technique is limited.

Patency of accessory pancreatic duct and its relation with duodenal inter papillary distance

A patent accessory pancreatic duct (APD), which acts as a safety valve, may prevent complications of endoscopic retrograde cholangiopancreatography. The interpapillary distance is probably the easiest parameter to assess the probability of APD patency. In previous studies, the patency of APD was correlated with other morphometric parameters of the accessory duct. The present study assessed the frequency of APD patency among south Indian adult cadavers of both sexes, and correlated it with the interpapillary distance. Duodeno-pancreas specimens collected from 100 cadavers with no recorded diseases of biliary pancreatic tree were studied by routine dissection method and dye injection technique. APD had a patent communication with the duodenum in 46 specimens, and was more frequent in men. The distance between the two duodenal papillae varied from 1.6-3 cm; 98% of the patent APD specimens had an interpapillary distance of ≥2 cm. We postulate that an duodenal interpapillary distance ≥2 cm suggests patency of APD.

DOES A PATENT ACCESSORY PANCREATIC DUCT PREVENT ACUTE PANCREATITIS?

The role of the accessory pancreatic duct (APD) in pancreatic pathophysiology has been unclear. We previously examined the patency of the APD in 291 control cases who had a normal pancreatogram in the head of the pancreas by dye-injection endoscopic retrograde pancreatography (ERP). APD patency was 43% and was closely related with the shape of the terminal portion of the APD. The present study aimed to clarify the clinical implications of a patent APD. Based on the underlying data, the patency rate of the APD was estimated from the terminal shape of the APD on ERP in 167 patients with acute pancreatitis. In patients with acute pancreatitis, stick-type APD, spindle-type APD, and cudgel-type APD, which showed a high patency, were rare, and branch-type APD and halfway-type or no APD, which showed quite low patency, were frequent in acute pancreatitis patients. Accordingly, the estimated patency of the APD in acute pancreatitis patients was only 21%. There was no significant relationship between the estimated APD patency and etiology or severity of acute pancreatitis. The terminal shapes of the APD with low patency were frequent in acute pancreatitis patients, and estimated APD patency was only 21% in acute pancreatitis. A patent APD may function as a second drainage system to reduce the pressure in the main pancreatic duct and prevent acute pancreatitis.

A Patent Accessory Pancreatic Duct Prevents Pancreatitis following Endoscopic Retrograde Cholangiopancreatography

Background/Aim: Pancreatitis is the most common and feared complication of endoscopic retrograde cholangiopancreatography (ERCP). We previously examined patency of the accessory pancreatic duct (APD) by dye injection endoscopic retrograde pancreatography (ERP). APD patency was found in 43% of 291 control cases who had no particular changes in the head of the pancreas compared to only 6% in patients with acute pancreatitis. APD patency was closely related with the shape of the terminal portion of the APD. This study aimed to clarify whether patency of the APD prevents post-ERCP pancreatitis. Methods:We examined retrospectively the terminal shape of the APD by ERP in 34 patients with post-ERCP pancreatitis. Based on these data, patency of the APD was estimated from its terminal shape in patients with post-ERCP pancreatitis. Results: The stick-type APD (p < 0.01), which indicated high patency, was less frequent, and the branch-type APD (p < 0.01) and halfway-type APD, or no APD (p < 0.01), which showed quite low patency, were more frequent in patients with post-ERCP pancreatitis compared with controls. Accordingly, the estimated patency of the APD in post-ERCP pancreatitis patients was only 16%, which was significantly lower than the 43% in controls. There was no significant relationship between the estimated APD patency and the severity of post-ERCP pancreatitis. Conclusions: The estimated APD patency was significantly lower in patients with post-ERCP pancreatitis. A patent APD may function as a second drainage system to reduce the pressure in the main pancreatic duct and prevent post-ERCP pancreatitis.

Clinical implications of accessory pancreatic duct

The accessory pancreatic duct (APD) is the main drainage duct of the dorsal pancreatic bud in the embryo, entering the duodenum at the minor duodenal papilla (MIP). With the growth, the duct of the dorsal bud undergoes varying degrees of atrophy at the duodenal end. Patency of the APD in 291 control cases was 43% as determined by dye-injection endoscopic retrograde pancreatography. Patency of the APD in 46 patients with acute pancreatitis was only 17%, which was significantly lower than in control cases (P < 0.01). The terminal shape of the APD was correlated with APD patency. Based on the data about correlation between the terminal shape of the APD and its patency, the estimated APD patency in 167 patients with acute pancreatitis was 21%, which was significantly lower than in control cases (P < 0.01). A patent APD may function as a second drainage system for the main pancreatic duct to reduce the pressure in the main pancreatic duct and prevent acute pancreatitis. Pancreatographic findings of 91 patients with pancreaticobiliary maljunction (PBM) were divided into a normal duct group (80 patients) and a dorsal pancreatic duct (DPD) dominant group (11 patients). While 48 patients (60%) with biliary carcinoma (gallbladder carcinoma, n = 42; bile duct carcinoma, n = 6) were identified in PBM with a normal pancreatic duct system, only two cases of gallbladder carcinoma (18%) occurred in DPD-dominant patients (P < 0.05). Concentration of amylase in the bile of DPD dominance was significantly lower than that of normal pancreatic duct system (75 403.5 ± 82 015.4 IU/L vs 278 157.0 ± 207 395.0 IU/L, P < 0.05). In PBM with DPD dominance, most pancreatic juice in the upper DPD is drained into the duodenum via the MIP, and reflux of pancreatic juice to the biliary tract might be reduced, resulting in less frequency of associated biliary carcinoma.

Clinical significance of the minor duodenal papilla and accessory pancreatic duct.

The accessory pancreatic duct (APD) is the main drainage duct of the dorsal pancreatic bud in the embryo, entering the duodenum at the minor duodenal papilla (MIP). As development progresses, the duct of the dorsal bud undergoes varying degrees of atrophy at the duodenal end. In cases of patent APD, smooth-muscle fiber bundles derived from the duodenal proper muscular tunics surround the APD. The APD shows long and short patterns on pancreatography, and ductal fusion in the two types appears to differ embryologically. Patency of the APD in control cases, as determined by dye-injection endoscopic retrograde pancreatography, was 43%. Patency of the APD may depend on duct caliber, course, and terminal shape of the APD. A patent APD may prevent acute pancreatitis by reducing the pressure in the main pancreatic duct. Pancreas divisum is a common anatomical anomaly in which the ventral and dorsal pancreatic ducts do not unite embryologically. As the majority of exocrine flow is routed through the MIP in individuals with pancreas divisum, interrelationships between poor function of the MIP and increased flow of pancreatic juice caused by alcohol or diet may increase dorsal pancreatic duct pressure and lead to the development of pancreatitis. Wire-guided minor sphincterotomy, followed by dorsal duct stenting, is recommended for acute recurrent pancreatitis associated with pancreas divisum.

Patency of the accessory pancreatic duct evaluated by dye‐injection endoscopic retrograde pancreatography: Methods and clinical implication

The accessory pancreatic duct (APD) is sometimes developmentally obliterated near the duodenum. We evaluated patency of the APD by dye‐injection endoscopic retrograde pancreatography (ERP). We injected 2–3 mL contrast medium containing indigocarmine into the main pancreatic duct (MPD) via a selectively cannulated endoscopic catheter. Patency of the APD was evaluated by observing the excretion of dye from the minor duodenal papilla. Of the 291 control cases studied, 43% demonstrated a patent APD. Patency of the APD in patients with acute pancreatitis was only 17%, significantly lower than that of controls (P &lt; 0.01). Mean caliber of patent APD was 1.6 ± 0.5 mm, significantly greater than the 1.1 ± 0.5 mm of non‐patent APD (P &lt; 0.01). Regarding the terminal shape of the APD, spindle‐ and cudgel‐type APD were frequently patent (93% and 88%, respectively, (P &lt; 0.01). With respect to APD course, long‐type APD showed most frequent patency (75%, P &lt; 0.01). Dye‐injection ERP represents a simple and definitive method for examining APD function. A patent APD may prevent acute pancreatitis by reducing pressure in the MPD. Patency of the APD might be dependent on duct caliber, course, and terminal shape.

Patent Accessory Pancreatic Duct Prevent Post-ERCP pancreatitis

Background/Aims: Pancreatitis is the most important complication of ERCP. Moreover, efforts to understand its pathogenesis and to identify ways to reduce the frequency and severity of this complication have shown no convincing benefit to date. Although very complex factors are involved in the development of post-ERCP pancreatitis, mechanical injury to the papilla causing papillary edema and restriction of pancreatic juice flow, and hydrostatic injury from over-injection are the most common causes. We have prospectively examined patency of the accessory pancreatic duct (APD) by dye-injection ERP. We examined the role of the APD in vivo, and proposed a new way to prevent post-ERCP pancreatitis. Methods: During ERP, 2 or 3 ml of contrast medium containing indigo carmine was injected through a catheter in the main pancreatic duct (MPD) with usual pressure in 443 cases. Dye excretion from the minor papilla was then observed endoscopically. Results: Of 312 controls, patency of the APD was observed in 43%, whereas in 51 patients with acute pancreatitis, only 8 (16%) had a patent APD (p<0.01). In particular, patency of the APD was seen in only one of 17 patients with acute biliary pancreatitis. Patency of the APD showed a close relationship to the course and terminal shape of the APD. The long-type APD, which joined the MPD at its neck portion and ran straight from the upper dorsal pancreatic duct, was more frequently patent than the short-type APD which joined the MPD near its first inferior branch and followed a descending course (75.5% patency vs. 36.0%, p<0.01). Regarding terminal shape of the APD, patency of the cudgel (89.2%) and spindle type (92.0%) was more frequent than of the branch type (5.9%) or saccular type (16.7%) (p<0.01). According to the above findings, we retrospectively examined patency of the APD in 25 patients with acute pancreatitis after diagnostic ERP (6500 cases). Patency of the APD was estimated at only 8% (2/25). Furthermore, 3 cases showing acute pancreatitis after stone extraction with endoscopic balloon dilatation, exhibited nonpatent APD. Conclusions: A patent APD may prevent acute pancreatitis by lowering the pressure in the MPD. During ERCP, in cases with short type APD or APD with branch or saccular terminal shape, endoscopists should be more cautious and never persist when selective cannulation is difficult, or alternatively consider prophylactic pancreatic stenting.

Relationship Between the Radiological Anatomy and Patency of the Accessory Pancreatic Duct: Dye-Injection ERP Study

Background/Aims: The accessory pancreatic duct (APD) exhibits several appearances on pancreatography, and sometimes is developmentally obliterated near the duodenum. We evaluated patency of the APD by dye-injection ERP to determine whether patency was related to duct course and shape, and size and location of the minor duodenal papilla (MIP). Methods: After routine ERP, we injected 2-3 ml of contrast material containing indigo carmine into the pancreatic duct via an endoscopic catheter and observed its secretion from the MIP endoscopically in 233 patients. Size of the MIP and distance from the orifice of the major duodenal papilla (MAP) to the apex of the MIP were measured endoscopically with measuring forceps. Maximum diameter of the APD and the length of the main pancreatic duct from its orifice to the junction with the APD were measured. Results: Patency of the APD was 48.5% (113/233). Size of the MIP varied considerably from 3 to 6 mm, but showed no correlation with patency. Six of 13 patients with chronic pancreatitis had the MIP larger than 6 mm, but only one was patent. The MIP was patent in 9 out of 10 patients (90%) when it was within 1.5 cm from the MAP. Frequency of a patent MIP was 17 out of 35 (48%) when it existed 1.5 to 2.0 cm from the MAP, and 33 out of 65 (51%) when the distance was more than 2.0 cm. The caliber of a patent APD was 1.6 +/- 0.6 mm, which was significantly larger than the caliber (1.1+/-0.4 mm) of a nonpatent APD (p<0.01). The length of the MPD from its orifice to the junction with a patent APD was 32.8+/-12.6 mm, which was significantly longer than the length to junction with nonpatent APD (22.6+/-8.2 mm)(p<0.01). The APD was classified according to duct course into long type which formed a straight line and joined the MPD at the neck portion of the pancreas, and short type which joined the MPD near the MAP and sometimes ran a descending course. Patency in the long type (75.5%) was significantly grater than in the short type (34.0%)(p<0.01). In the terminal shape of the APD, patency was most frequently observed in the spindle type (91.7%) and cudgel type (89.9%), and less frequent in the branch type (5.9%). In cases where the terminal APD had a cudgel configuration, the MIP was larger than in cases where the duct had a stick shape. Conclusions: Patency of the APD might be dependent on duct caliber, course, and terminal shape of the duct, and location of the MIP.

4623 Closure of the accessory pancreatic duct is the risk factor for post-diagnostic ercp pancreatitis.

Background: Acute pancreatitis is the most common complication of ERCP. Many risk factors such as direct mechanical trauma, hydrostatic forces, chemical effects of contrast agent injected under pressure, and microbial contamination for post-diagnostic ERCP pancreatitis have been reported. However, whether patency of the accessory pancreatic duct (APD) influences post-diagnostic ERCP pancreatitis is unknown. Aim: To evaluate the closure of the APD and several other risk factors for post-diagnostic ERCP pancreatitis. Patients and Methods: This study was conducted on 536 patients from 836 consecutive ERCPs over the past seven years. Serum pancreatic enzymes (amylase, lipase, elastase-1, trypsin, pancreatic secretary trypsin inhibitor {PSTI}) and neutrophil counts were evaluated at pre- , 5, 24, 48 and 72 hours after ERCP. Percent of increase compared with pre- ERCP value also estimated respectively. The severity of pancreatitis was classified into three groups (severe, moderate, or mild) according to the established criteria. By multivariate analysis, twelve factors: age, gender, cannulation frequency, bile duct cannulations, pancreatic contrast injections, closure of the APD, pre-ERCP values of serum pancreatic enzymes and neutrophil counts were evaluated. Results: Overall, 14/536 (2.6%) patients developed pancreatitis; 6 mild, 6 moderate, 2 severe. Patency of APD was significantly lower in the pancreatitis group than that in the non-pancreatitis group (pancreatitis vs. non-pancreatitis: 2/14, 14.3% vs. 173/522, 33.1%, respectively). The rate of pancreatitis was significantly higher in the closed APD group than in the patent APD group and two cases with severe pancreatitis were documented only in the closed APD group (closed vs. patent: 12/246, 4.9% vs. 2/175, 1.1% and 2 severe, 5 moderate, 5 mild vs.1 moderate, 1 mild). In the non-pancreatitis group, serum pancreatic enzyme values at pre-ERCP were similar between closed and patent APD groups, whereas the percent increases at 24 and 48 hours after the procedure in the closed group were higher than those in the patent group. By multivariate analysis, the significant risk factors were: female sex, cannulation frequency, closure of APD, bile duct cannulations, and pancreatic contrast injections. Conclusion: Closure of APD also carries a high risk of developing post-diagnostic ERCP pancreatitis. The appropriate use of this new prognostic indicator may provide a significant benefit in the early diagnosis of post-ERCP pancreatitis.

Patency of the accessory pancreatic duct in relation to its course and shape: a dye-injection endoscopic retrograde pancreatography study

Objective: The accessory pancreatic duct (APD) exhibits several appearances on pancreatography. We examined the patency of the APD by dye-injection endoscopic retrograde pancreatography (ERP), and studied the relationship between patency and duct course and shape. Methods: There were 213 patients with satisfactory imaging of the entire normal APD who also underwent dye-injection ERP. The length and maximum diameter of the APD and the length of the main pancreatic duct (MPD) from its orifice to the junction with the APD were measured. Results: The caliber of the patent APD was 1.6 ± 0.6 mm. This was significantly larger than the caliber (1.1 ± 0.4 mm) of the nonpatent APD ( p < 0.01). The length of the MPD from its orifice to the junction with the patent APD was 32.7 ± 12.5 mm. This was significantly longer than the length to the junction with the nonpatent APD (22.5 ± 8.1 mm) ( p < 0.01). The APD was classified according to duct course: long type, intermediate type, short type, or ansa type. Patency was most common in the long type APD (74.5%). The terminal shape of the APD was also used to classify the ducts: stick type, branch type, saccular type, cudgel type, or spindle type. Patency was most frequently observed in the spindle and cudgel type ducts. Conclusions: Patency of the APD might be dependent on duct caliber, course, and terminal shape of the duct.

Patency of the accessory pancreatic duct in relation to its course and shape: a dye-injection endoscopic retrograde pancreatography study.

The accessory pancreatic duct (APD) exhibits several appearances on pancreatography. We examined the patency of the APD by dye-injection endoscopic retrograde pancreatography (ERP), and studied the relationship between patency and duct course and shape. There were 213 patients with satisfactory imaging of the entire normal APD who also underwent dye-injection ERP. The length and maximum diameter of the APD and the length of the main pancreatic duct (MPD) from its orifice to the junction with the APD were measured. The caliber of the patent APD was 1.6 +/- 0.6 mm. This was significantly larger than the caliber (1.1 +/- 0.4 mm) of the nonpatent APD (p < 0.01). The length of the MPD from its orifice to the junction with the patent APD was 32.7 +/- 12.5 mm. This was significantly longer than the length to the junction with the nonpatent APD (22.5 +/- 8.1 mm) (p < 0.01). The APD was classified according to duct course: long type, intermediate type, short type, or ansa type. Patency was most common in the long type APD (74.5%). The terminal shape of the APD was also used to classify the ducts: stick type, branch type, saccular type, cudgel type, or spindle type. Patency was most frequently observed in the spindle and cudgel type ducts. Patency of the APD might be dependent on duct caliber, course, and terminal shape of the duct.

Patency of the human accessory pancreatic duct as determined by dye-injection endoscopic retrograde pancreatography.

The accessory pancreatic duct (APD) is the smaller and less constant pancreatic duct. The patency of the APD was investigated clinically in an effort to determine its role in pancreatic pathophysiology. Dye-injection endoscopic retrograde pancreatography (ERP) was performed in 190 cases. In the patients who exhibited filling of the fine branches of the ducts on ERP, contrast medium with indigo carmine was injected into the major duodenal papilla. The patency of the APD was determined by observing the excretion of the dye from the minor duodenal papilla. Of the 123 control cases studied, 41% had a patent APD. According to the shape of the terminal portion of the APD on accessory pancreatogram, it was classified as either the stick type (n = 63), branch type (n = 15), saccular type (n = 15), spindle type (n = 11), or cudgel type (n = 8). In these groups, 49, 0, 27, 82, and 87% of the APD were patent, respectively. The patency of the APD in the patients with acute pancreatitis was 6% (1 of 17). The difference in patency between this group and the control group was significant (p < 0.01). The patency of the APD varies with the shape of the terminal portion of the APD. A patent APD may prevent acute pancreatitis by lowering the pressure in the main pancreatic ducts.