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Pancreatic Pseudocysts At Atypical Locations- Endoscopic Management
Abstracts
M1388 Pancreatographic Investigation of Embryology of Incomplete Pancreas Divisum Terumi Kamisawa, Hitoshi Nakajima, Naoto Egawa, Kouji Tsuruta, Atsutake Okamoto
M1390 Pancreatic Pseudocysts At Atypical Locations- Endoscopic Management Deepak K. Bhasin, Surinder S. Rana, Mohit Nanda, Saroj K. Sinha, Birinder Nagi
Aims: Incomplete pancreas divisum (PD) has inadequate communication between the ventral and dorsal pancreatic ducts. This study aimed to confirm the embryology of branch fusion between the ventral and dorsal pancreatic ducts. Methods: We analyzed anatomy of pancreatic duct system in 41 cases of incomplete PD and 118 control cases. Incomplete PD was divided into 3 types: Type 1 incomplete PD (n Z 16) was characterized by tapering of the fused portion and presence of branches of the ventral pancreatic duct toward the dorsal pancreatic duct and the others displayed a branch running toward the ventral pancreatic duct in roundabout (Type 2, n Z 10) or short way (Type 3, n Z 15). Results: Length of the entire ventral pancreatic duct (c) in Type 1 incomplete PD was longer than in controls (p ! 0.05), which implies the embryological mechanism of extreme end of an upper branch of the ventral duct fuses with the dorsal pancreatic duct in Type 1. In controls, long inferior branches from Santorini’s duct were observed in 88 cases and length of Santorini’s duct from orifice to the first long inferior branch (b) was similar to lengths in Type 1 and 3, and to length of the entirety of Santorini’s duct (a) in Type 2. Length of the entirety of Santorini’s duct (a) was significantly shorter in Type 2 (p ! 0.01) and Type 3 (p ! 0.05) than in controls. A long inferior branch from the ventral pancreatic duct was observed in 81 control cases and length of the ventral pancreatic duct from orifice to the inferior branch (d) was similar to lengths in Type 1 and Type 3, and to length of the ventral pancreatic duct from orifice to junction with the communicating branch (e) in Type 2. No long inferior branches from the ventral pancreatic duct were detected in Type 2. These facts suggest embryological fusion between the long inferior branch from the dorsal pancreatic duct and the inferior branch from the ventral pancreatic duct in Type 2. Diameter of the communicating branch (z) was bigger than that of the ventral pancreatic duct (y) in 6 cases of Type 3 implies fusion of the lower branch of the dorsal pancreatic duct with the ventral pancreatic duct in Type 3. Conclusions: Embryological mechanism of incomplete PD was confirmed by measurement of pancreatograms.
Endoscopic drainage of single abdominal pancreatic pseudocyst is well reported. Data is scarce on endoscopic management of pseudocyst at atypical locations. Aim: To study efficacy of endoscopic transpapillary nasopancreatic drain placement alone in management of pancreatic pseudocyst at atypical locations. Methods: Over 4 years, 9 patients (19-50 years, 7 M) with symptomatic pseudocysts at atypical locations communicating with pancreatic duct as visualized on endoscopic retrograde pancreatography (ERP), were treated by attempted endoscopic transpapillary nasopancreatic drain placement.An informed consent was obtained, intravenous midazolam and hyoscine butyl bromide administered and ERP performed. Pancreatic duct selectively cannulated and pancreatogram obtained. A 5F/7F nasopancreatic drain (NPD) was placed across/near site of pancreatic duct disruption over a 0.025/0.035 inch hydrophilic guide wire through major or minor papilla. Therapeutic success was defined as symptomatic improvement with radiological resolution on computed tomography (CT) scan and healing of ductal disruption. Therapeutic failure was defined as persistence of pseudocyst at eight weeks after NPD placement or need for surgical or radiological intervention. Results: All 9 patients had abdominal pain on presentation. Other symptoms were early satiety (3), abdominal lump (2), fever (1) and jaundice (1). Eight patients had underlying chronic pancreatitis (Alcohol-4 [associated pancreas divisum: 1], Idiopathic-4 [associated pancreas divisum: 1]) and one patient had pseudocyst as sequelae of gall stone pancreatitis. Size of pseudocysts ranged from 2 to 13 cms. Location of pseudocysts was: mediastinal (3), intrahepatic (3), and intrasplenic (3). On ERP, all patients had partial disruption of pancreatic duct and NPD could be placed across disruption in 8/9 (88.8%) patients. The site of ductal disruption was head, body and tail in 1(11%), 5 (55.5%) and 3 (33.3%) patients respectively. In one patient, in whom deep cannulation of pancreatic duct could not be achieved because of stricture in head region, only pancreatic sphincterotomy was performed and pseudocyst resolved at 6 weeks. One patient developed fever, 5 days after procedure that was successfully treated by antibiotics. NPD got blocked in 1 patient 12 days after procedure and it was successfully opened by aspiration. Pseudocysts resolved in all patients in 4-8 weeks with no recurrence on follow up of 5-52 months. Conclusion: Pancreatic pseudocysts with ductal communication at atypical locations can be effectively treated with endoscopic transpapillary nasopancreatic drain placement, especially when ductal disruption can be bridged.
M1389 Resolved Acute Relapsing Pancreatitis: Seven Treated Patients with Santoriniceles Michael Gluck, Richard A. Kozarek Background: Determining the etiology of acute relapsing pancreatitis frequently results in multiple studies and when therapy is undertaken, limited success. In patients with ‘‘Santoriniceles,’’ a focal dilatation of the dorsal pancreatic duct at the minor ampulla, minor papilla sphincterotomy (ES) can result in cure of symptoms in most patients. We report our tertiary pancreatic center’s case series of seven patients with Santoriniceles. Methods: A chart review of patients with relapsing pacreatitis over 10 years identified 7 patients with appropriate anatomical features. Duration of symptoms, treatment modalities, and response to endoscopic therapy were recorded for those patients. Results: Seven patients (6F, 1M) with a mean age of 68.7 years were identified whose minor ampulla was dilated 7 mm or greater. Prior to diagnosis at our institution either by ERCP or MRCP, all patients had undergone at least one previous ERCP. Symptoms duration ranged from 1 to 13 years with a median of 3 years. All patients had dorsal duct dilation of greater than 4 mm. Six had pancreas divisum and one had imcomplete pancreas divisum. Needle knife (NN) ES of the minor ampulla was utilized in 2 patients, traction ES in 5 patients. There was one mild post-ERCP pancreatitis. Six patients had resolution of acute episodes of relapsing pancreatitis. One patient developed pancreatitis 5 years later, treated with balloon dilation. Conclusion: In our series, patients with Santoriniceles were predominately female who had symptoms for more than 2 years and whose diagnosis was elusive until definitive ERCP or MRCP. Endoscopic sphincterotomy was effective in resolving symptoms of acute pancreatits with minimal post procedure complications. Median Mean duration of age Sex symptoms
Mean diameter of ampulla
68.7 years
8.5 mm 3.3 5.5 mm SD 0.5 SD
6F, 3.0 years 1M
Mean dorsal duct Treatment Mean size modality follow up 2 NN, 4 4.6 years traction ES 2.9 SD
AB246 GASTROINTESTINAL ENDOSCOPY Volume 65, No. 5 : 2007
M1391 Pancreatic Ductal Abnormalities By Secretin-MRCP in Asymptomatic Subjects with Chronic Pancreatic Hyperenzymemia Alberto Mariani, Benedetto Mangiavillano, Antonella Giussani, Simona Curioni, Elena G. Spinapolice, Pier Alberto Testoni Background: An increase of serum pancreatic enzymes in asymtomatic subjects is considered a benign idiopathic biochemical abnormality because associated with a normal pancreatic morphology so that it is called ‘‘chronic nonpathological pancreatic hyperenzymemia’’ (CNPH). Aim: To evaluated pancreatic ductal morphology by secretin enhanced MRCP in asymptomatic subjects with CNPH. Patients and Methods: 20 subjects with CNPH were studied and compared with 15 age-matched subjects with non-pancreatic hyperamylasemia (CNNPHA). Transabdominal pancreatic ultrasonography and fecal chymotripsin or elastase-1 determination were normal in all cases. Secretin-MRCP (s-MRCP) evaluated: pancreatic duct morphology, main pancreatic duct (MPD) distensibility, suspected sphincter of Oddi dysfunction (SOD) and grading of the duodenal filling. Results: In the 15 subjects with non-pancreatic hyperenzymemia, s-MRCP detected only two abnormalities (in one subject a small pancreatic cyst and in another one parenchymal heterogeneity) and in 20 with pancreatic hyperenzymemia the following pancreatic abnormalities: side branches dilation in three cases (15%), small cysts in two (10%), focal MPD dilation in two (10%), irregular MPD contour in six (30%) and suspected SOD in three (15%). According to s-MRCP, subjects with asymptomatic chronic pancreatic hyperenzymemia had diagnosis of early chronic pancreatitis in 6 cases (30%). Conclusions: Asymptomatic subjects with chronic pancreatic hyperenzymemia can have pancreatic ductal abnormalities.
www.giejournal.org
M1388 Pancreatographic Investigation of Embryology of Incomplete Pancreas Divisum Terumi Kamisawa, Hitoshi Nakajima, Naoto Egawa, Kouji Tsuruta, Atsutake Okamoto
M1390 Pancreatic Pseudocysts At Atypical Locations- Endoscopic Management Deepak K. Bhasin, Surinder S. Rana, Mohit Nanda, Saroj K. Sinha, Birinder Nagi
Aims: Incomplete pancreas divisum (PD) has inadequate communication between the ventral and dorsal pancreatic ducts. This study aimed to confirm the embryology of branch fusion between the ventral and dorsal pancreatic ducts. Methods: We analyzed anatomy of pancreatic duct system in 41 cases of incomplete PD and 118 control cases. Incomplete PD was divided into 3 types: Type 1 incomplete PD (n Z 16) was characterized by tapering of the fused portion and presence of branches of the ventral pancreatic duct toward the dorsal pancreatic duct and the others displayed a branch running toward the ventral pancreatic duct in roundabout (Type 2, n Z 10) or short way (Type 3, n Z 15). Results: Length of the entire ventral pancreatic duct (c) in Type 1 incomplete PD was longer than in controls (p ! 0.05), which implies the embryological mechanism of extreme end of an upper branch of the ventral duct fuses with the dorsal pancreatic duct in Type 1. In controls, long inferior branches from Santorini’s duct were observed in 88 cases and length of Santorini’s duct from orifice to the first long inferior branch (b) was similar to lengths in Type 1 and 3, and to length of the entirety of Santorini’s duct (a) in Type 2. Length of the entirety of Santorini’s duct (a) was significantly shorter in Type 2 (p ! 0.01) and Type 3 (p ! 0.05) than in controls. A long inferior branch from the ventral pancreatic duct was observed in 81 control cases and length of the ventral pancreatic duct from orifice to the inferior branch (d) was similar to lengths in Type 1 and Type 3, and to length of the ventral pancreatic duct from orifice to junction with the communicating branch (e) in Type 2. No long inferior branches from the ventral pancreatic duct were detected in Type 2. These facts suggest embryological fusion between the long inferior branch from the dorsal pancreatic duct and the inferior branch from the ventral pancreatic duct in Type 2. Diameter of the communicating branch (z) was bigger than that of the ventral pancreatic duct (y) in 6 cases of Type 3 implies fusion of the lower branch of the dorsal pancreatic duct with the ventral pancreatic duct in Type 3. Conclusions: Embryological mechanism of incomplete PD was confirmed by measurement of pancreatograms.
Endoscopic drainage of single abdominal pancreatic pseudocyst is well reported. Data is scarce on endoscopic management of pseudocyst at atypical locations. Aim: To study efficacy of endoscopic transpapillary nasopancreatic drain placement alone in management of pancreatic pseudocyst at atypical locations. Methods: Over 4 years, 9 patients (19-50 years, 7 M) with symptomatic pseudocysts at atypical locations communicating with pancreatic duct as visualized on endoscopic retrograde pancreatography (ERP), were treated by attempted endoscopic transpapillary nasopancreatic drain placement.An informed consent was obtained, intravenous midazolam and hyoscine butyl bromide administered and ERP performed. Pancreatic duct selectively cannulated and pancreatogram obtained. A 5F/7F nasopancreatic drain (NPD) was placed across/near site of pancreatic duct disruption over a 0.025/0.035 inch hydrophilic guide wire through major or minor papilla. Therapeutic success was defined as symptomatic improvement with radiological resolution on computed tomography (CT) scan and healing of ductal disruption. Therapeutic failure was defined as persistence of pseudocyst at eight weeks after NPD placement or need for surgical or radiological intervention. Results: All 9 patients had abdominal pain on presentation. Other symptoms were early satiety (3), abdominal lump (2), fever (1) and jaundice (1). Eight patients had underlying chronic pancreatitis (Alcohol-4 [associated pancreas divisum: 1], Idiopathic-4 [associated pancreas divisum: 1]) and one patient had pseudocyst as sequelae of gall stone pancreatitis. Size of pseudocysts ranged from 2 to 13 cms. Location of pseudocysts was: mediastinal (3), intrahepatic (3), and intrasplenic (3). On ERP, all patients had partial disruption of pancreatic duct and NPD could be placed across disruption in 8/9 (88.8%) patients. The site of ductal disruption was head, body and tail in 1(11%), 5 (55.5%) and 3 (33.3%) patients respectively. In one patient, in whom deep cannulation of pancreatic duct could not be achieved because of stricture in head region, only pancreatic sphincterotomy was performed and pseudocyst resolved at 6 weeks. One patient developed fever, 5 days after procedure that was successfully treated by antibiotics. NPD got blocked in 1 patient 12 days after procedure and it was successfully opened by aspiration. Pseudocysts resolved in all patients in 4-8 weeks with no recurrence on follow up of 5-52 months. Conclusion: Pancreatic pseudocysts with ductal communication at atypical locations can be effectively treated with endoscopic transpapillary nasopancreatic drain placement, especially when ductal disruption can be bridged.
M1389 Resolved Acute Relapsing Pancreatitis: Seven Treated Patients with Santoriniceles Michael Gluck, Richard A. Kozarek Background: Determining the etiology of acute relapsing pancreatitis frequently results in multiple studies and when therapy is undertaken, limited success. In patients with ‘‘Santoriniceles,’’ a focal dilatation of the dorsal pancreatic duct at the minor ampulla, minor papilla sphincterotomy (ES) can result in cure of symptoms in most patients. We report our tertiary pancreatic center’s case series of seven patients with Santoriniceles. Methods: A chart review of patients with relapsing pacreatitis over 10 years identified 7 patients with appropriate anatomical features. Duration of symptoms, treatment modalities, and response to endoscopic therapy were recorded for those patients. Results: Seven patients (6F, 1M) with a mean age of 68.7 years were identified whose minor ampulla was dilated 7 mm or greater. Prior to diagnosis at our institution either by ERCP or MRCP, all patients had undergone at least one previous ERCP. Symptoms duration ranged from 1 to 13 years with a median of 3 years. All patients had dorsal duct dilation of greater than 4 mm. Six had pancreas divisum and one had imcomplete pancreas divisum. Needle knife (NN) ES of the minor ampulla was utilized in 2 patients, traction ES in 5 patients. There was one mild post-ERCP pancreatitis. Six patients had resolution of acute episodes of relapsing pancreatitis. One patient developed pancreatitis 5 years later, treated with balloon dilation. Conclusion: In our series, patients with Santoriniceles were predominately female who had symptoms for more than 2 years and whose diagnosis was elusive until definitive ERCP or MRCP. Endoscopic sphincterotomy was effective in resolving symptoms of acute pancreatits with minimal post procedure complications. Median Mean duration of age Sex symptoms
Mean diameter of ampulla
68.7 years
8.5 mm 3.3 5.5 mm SD 0.5 SD
6F, 3.0 years 1M
Mean dorsal duct Treatment Mean size modality follow up 2 NN, 4 4.6 years traction ES 2.9 SD
AB246 GASTROINTESTINAL ENDOSCOPY Volume 65, No. 5 : 2007
M1391 Pancreatic Ductal Abnormalities By Secretin-MRCP in Asymptomatic Subjects with Chronic Pancreatic Hyperenzymemia Alberto Mariani, Benedetto Mangiavillano, Antonella Giussani, Simona Curioni, Elena G. Spinapolice, Pier Alberto Testoni Background: An increase of serum pancreatic enzymes in asymtomatic subjects is considered a benign idiopathic biochemical abnormality because associated with a normal pancreatic morphology so that it is called ‘‘chronic nonpathological pancreatic hyperenzymemia’’ (CNPH). Aim: To evaluated pancreatic ductal morphology by secretin enhanced MRCP in asymptomatic subjects with CNPH. Patients and Methods: 20 subjects with CNPH were studied and compared with 15 age-matched subjects with non-pancreatic hyperamylasemia (CNNPHA). Transabdominal pancreatic ultrasonography and fecal chymotripsin or elastase-1 determination were normal in all cases. Secretin-MRCP (s-MRCP) evaluated: pancreatic duct morphology, main pancreatic duct (MPD) distensibility, suspected sphincter of Oddi dysfunction (SOD) and grading of the duodenal filling. Results: In the 15 subjects with non-pancreatic hyperenzymemia, s-MRCP detected only two abnormalities (in one subject a small pancreatic cyst and in another one parenchymal heterogeneity) and in 20 with pancreatic hyperenzymemia the following pancreatic abnormalities: side branches dilation in three cases (15%), small cysts in two (10%), focal MPD dilation in two (10%), irregular MPD contour in six (30%) and suspected SOD in three (15%). According to s-MRCP, subjects with asymptomatic chronic pancreatic hyperenzymemia had diagnosis of early chronic pancreatitis in 6 cases (30%). Conclusions: Asymptomatic subjects with chronic pancreatic hyperenzymemia can have pancreatic ductal abnormalities.
www.giejournal.org