CT scan from 2 years prior demonstrating duodenitis (green circle) and periduodenal inflammatory change (yellow arrow). 

CT scan from 2 years prior demonstrating duodenitis (green circle) and periduodenal inflammatory change (yellow arrow). 

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Introduction: Paraduodenal pancreatitis (PP) is an under-recognized form of focal chronic or recurrent pancreatitis. Since PP presents with non-specific symptoms and shares radiological and histopathological features with other entities, it can be challenging to diagnose. Presentation of case report: Herein, a case of a 64 year-old Caucasian mal...

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... years prior the duodenal lesion was identified when he first presented to his local hospital with symptoms of gastric out- let obstruction ( Fig. 1). At the time of presentation to our centre, computed tomography (CT) revealed narrowing at the junction of the 1st and 2nd part of the duodenum in conjunction with a cystic lesion abutting the pancreatic head (Fig. 2). Magnetic res- onance imaging (MRI) also obtained at this time revealed a 3.2 by 2.6 cm lesion between the duodenum and pancreatic head. The lesion demonstrated slightly low signal intensity on T2-weighted sequence, and low signal intensity on T1-weighted sequence with delayed enhancement. There was no evidence of common bile duct (CBD) or pancreatic duct dilatation. Based on the radiological findings, the differential diagnosis included ectopic pancreatic tis- sue, cystic gastrointestinal stromal tumor (GIST), and lymphoma. The possibility of adenocarcinoma was not completely ruled out, though felt less likely given the chronicity of both his symptoms and imaging ...

Citations

... [39][40][41][42] Chronic pancreatitis (including groove pancreatitis) has been known to cause GOO, although this adverse event is uncommon. 14,[43][44][45] Although surgery forms a primary modality for its management, other endoscopic techniques including EBD have been tried with variable success. 14,[43][44][45][46] Previous studies including ours report a dismal outcome with EBD for chronic pancreatitis-associated GOO. ...
... 14,[43][44][45] Although surgery forms a primary modality for its management, other endoscopic techniques including EBD have been tried with variable success. 14,[43][44][45][46] Previous studies including ours report a dismal outcome with EBD for chronic pancreatitis-associated GOO. 4,14,44 Adverse events of EBD include pain, bleeding, and perforation. ...
... 14,[43][44][45][46] Previous studies including ours report a dismal outcome with EBD for chronic pancreatitis-associated GOO. 4,14,44 Adverse events of EBD include pain, bleeding, and perforation. Perforation has been reported to occur in up to 8% of cases. ...
Article
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Chandigarh, India Background and Aims: Peptic ulcer disease (PUD)-related gastric outlet obstruction (GOO) is known to respond favorably to endoscopic balloon dilation (EBD). However, data on efficacy of EBD for other etiologies of benign GOO are sparse. We aimed to compare the response of EBD among different etiologies of GOO.
... Основной причиной дуоденальной непроходимости считается распространение воспаления на парадуоденальную клетчатку и стенку ДПК. Развитие декомпенсированной формы нарушения эвакуации из желудка возникает редко [34][35][36]. ...
Article
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Aim: to present modern methods of diagnosis and treatment of chronic pancreatitis for gastroenterologists, general practitioners and physicians. Chronic pancreatitis (CP) is a long-term inflammatory disease of the pancreas, manifested by irreversible morphological changes in the parenchyma and pancreatic ducts, which cause pain and/or persistent impairment of function. Current concept on the etiology of CP is reflected by the TIGAR-O classification. The criteria for establishing the diagnosis of CP include typical attacks of abdominal pain and/or clinical and laboratory signs of exocrine, endocrine insufficiency with the mandatory detection of characteristic morphological changes (calcifications in the parenchyma and pancreatic ductal stones, dilatation of the main pancreatic duct and its branches). CT, MRCP, and pancreatobiliary endosonography are recommended as the methods of choice to verify the diagnosis of CP. Conservative treatment of patients with CP is provided for symptom relief and prevention of complications. Individual cases with severe non-interactable abdominal pain, as well as a complicated course of the disease (development of ductal hypertension due to main pancreatic duct stones or strictures, obstructive jaundice caused by compression of the common bile duct, symptomatic postnecrotic cysts, portal hypertension due to compression of the portal vein or thrombosis of the splenic vein, persistent duodenal obstruction, pseudoaneurysm of the celiac trunk basin and the superior mesenteric artery) serve as an indication for endoscopic or surgical treatment. The Guidelines set out modern approaches to the diagnosis, conservative, endoscopic and surgical treatment of CP, and the prevention of its complications. Conclusion. The implementation of clinical guidelines can contribute to the timely diagnosis and improve the quality of medical care for patients with chronic pancreatitis.
... duodenum, the pancreatic head, and the common bile duct. 1 Although common clinical presentation is constituted by abdominal pain, weight loss, and jaundice, association with gastric outlet obstruction (GOO) has been reported. 2 In recent years, the introduction of lumen-apposing metal stents (LAMSs) led to the diffusion of a novel technique to manage GOO. Endoscopic ultrasound (EUS)-guided gastroenteroanastomosis (EUS-GEA) has been shown to provide long-term luminal patency without the associated morbidity of a surgical intervention. ...
Article
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Video 1Technical pitfalls in EUS-guided gastroenteroanastomosis in an 84-year-old man with gastric outlet obstruction owing to cystic paraduodenal pancreatitis.
... Gastric retention is an uncommon but not rare complication of AP featured by the delayed emptying of gastric contents and can be divided into gastric outlet obstruction (GOO) and gastric hypomotility [2]. There are a couple of factors causing this complication: (1) The pancreatic necrosis with large size can compress the surrounding gastrointestinal tract [3,4]; (2) The inflammatory ooze from the pancreas in AP can infiltrate the surrounding gastrointestinal tract and causes tract edema [5]; (3) Gastric wall cholinergic nerves and smooth muscle is invased and come into dysfunction [6]; (4) High intra-abdominal pressure inhibits the motility of gastrointestinal tract [7]. ...
... Gastric retention is an uncommon but not rare complication of AP featured by the delayed emptying of gastric contents and can be divided into gastric outlet obstruction (GOO) and gastric hypomotility [2]. There are a couple of factors causing this complication: (1) The pancreatic necrosis with large size can compress the surrounding gastrointestinal tract [3,4]; (2) The inflammatory ooze from the pancreas in AP can infiltrate the surrounding gastrointestinal tract and causes tract edema [5]; (3) Gastric wall cholinergic nerves and smooth muscle is invased and come into dysfunction [6]; (4) High intra-abdominal pressure inhibits the motility of gastrointestinal tract [7]. ...
... Previous studies reported several cases of GOO developed after 4 weeks from the onset of AP result from the compression of pancreatic pseudocyst (PP) or walled-off necrosis (WON) [3,12,13]. However, to our knowledge, GOO developed within the first 4 weeks of AP is rarely reported. ...
Article
Objective The aim of this study was to describe the clinical characteristics and management of gastric outlet obstruction following acute pancreatitis(AP). Background Gastric outlet obstruction (GOO) is not uncommon in acute pancreatitis (AP) and can occur throughout the course. However, the clinical features and related treatment of GOO is rarely reported. Methods A retrospective review of AP patients with a diagnosis of GOO from March 2017 to June 2020 was performed. The diagnosis and management of GOO, as well as the demographic characteristics and clinical outcomes of the study patients, were collected and analyzed. Results Over the three years, there were 60 AP patients developed GOO, constituting an incidence of 5.7%. Thirty-three patients (55.0%, 33/60) developed GOO in the first 4 weeks and 27 patients (45.0%, 27/60) after 4 weeks from onset. Pancreatic necrosis compression (60.6%; 20/33), gastric outlet gastrointestinal edema (27.3%, 9/33) are the main causes of early-onset GOO (≤4 weeks), while wall-off necrosis (92.6%, 25/27) is the leading cause in the late phase (>4 weeks). The management of GOO incorporates both supportive and specific treatment like gastric decompression, gastric juice reinfusion, percutaneous catheter drainage, etc. The mortality of AP patients with GOO (≤4 weeks) was 21.2% and none patients who developed GOO (>4 weeks) died. Conclusions GOO, as a gastrointestinal complication developed in AP patients, has two peak incidences in the duration of AP and needs to be paid more attention to.
... Groove pancreatitis refers to inflammation of the focal "groove" area that is defined as the narrow space surrounded by the duodenum, pancreas head and common bile duct, and in the pure type the involvement area is restricted to the groove area but in the segmental type the scarring tissue extends to the dorso-cranial portion of the pancreatic head (2). This disorder has been called by some other nomenclatures because of its eccentric area such as paraduodenal pancreatitis (9), paraduodenal wall cyst and pancreatic hamartoma of the duodenal wall. The etiology of the disease is not well understood but some possible related causes were addressed such as alcohol abuse, gastric and duodenal peptic ulcer, and congenital obstruction of the Santorini duct. ...
Article
Full-text available
Background Groove pancreatitis is a type of pancreatitis where inflammation occurs in the “groove area” which is the narrow space surrounded by the duodenum, head of the pancreas and common bile duct, where lymph nodes, blood vessels and pancreatic duct exist. Groove area inflammation causes duodenal stenosis/obstruction, narrowing of the extrahepatic biliary tree and sometimes pancreatitis. The exact etiology of the disease is not well understood but Santorini duct obstruction (congenital or acquired) may be associated with inflammation of the groove area, which is partly caused by excessive alcoholic intake or gastric/duodenal peptic ulcer in adults. Case presentation We report a very rare pediatric case of groove pancreatitis. The imaging findings were typical for groove pancreatitis and the bypass operation to release duodenal stenosis and extrahepatic biliary tree obstruction was performed instead of doing pancreaticoduodenectomy often done in adult cases. Conclusion Groove pancreatitis is a rare disorder and a pediatric case is quite rare but pediatric surgeons should keep in mind this rare disorder when we meet the case with biliary dilatation and/or duodenal stenosis.
... Complications of the heterotopic pancreas are pancreatitis of the heterotopic tissue, pseudocyst formation, abscess, endocrine dysfunction, malignant degeneration, mechanical obstruction, and bleeding [4,6,[13][14][15]. ...
Article
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Introduction: Heterotopic pancreas is a rare congenital anomaly. We report a case of esophageal heterotopic pancreas complicated by recurrent mediastinal abscess and treated by minimally invasive resection. Presentation of case: A 31-year-old woman was admitted with a history of recurrent chest pain, dysphagia, and heartburn. CT scan revealed focal confined collection in the lower mediastinum surrounding esophagus. Endoscopic ultrasound revealed a subepithelial lesion. The patient was treated by minimally invasive esophagectomy and made an uneventful postoperative recovery. Discussion: The management of subepithelial lesions would depend on their size, ability to exclude other etiologies and their associated symptoms. The patient, in this case, was obviously symptomatic and accurate differentiation from malignant etiologies could not be accurately made. Conclusion: Although pancreatic heterotopia is rare, it should be remembered in the differential diagnosis of various gastrointestinal lesions.
... A látott kép általában malignitásra negatív eredményt ad, de olykor a malignitás gyanúja is felmerül, amennyiben sejtatípia jelei azonosíthatók, valamint a sejttörmelék összetéveszthető necroticus törmelékkel. Az orsósejtekben gazdag minta lágyrész-daganat, például leiomyoma/leiomyosarcoma, gastrointestinalis stromalis tumor (GIST) lehetőségét vetheti fel [4,9,[18][19][20]. A sebészi reszekátum makroszkópos vizsgálatakor jellemző a minor papillának megfelelő területen a duodenumfal heges megvastagodása; a hegesedés gyakran ráterjed a környező pancreasfeji szövetre, komprimálhatja a ductus choledochust. ...
... A szomatosztatinanalóg kezelésnek a fájdalomra gyakorolt, noha csak rövid távon leírt kedvező hatását több szerző is említi. (A pancreasnedv-termelés csökkentése révén az intrapancreaticus nyomást befolyásolja [7,13,20,[29][30][31].) Mindazonáltal a biztonsággal nem kizárható esetleges neoplasticus folyamat miatt gyakran történik primeren részleges pancreatoduodenectomia (hagyományos vagy pylorusmegtartásos Whipple-műtét), mely a betegség progressziója vagy terápiarezisztencia miatt is szükségessé válhat. ...
Article
The paraduodenal, or groove pancreatitis is a lesser-known type of chronic pancreatitis, often mimicking malignancy, hence resulting in serious differential diagnostic challenges. Herein we report two cases of this entity. Both required analysis of the surgical specimen in order to ensure the diagnosis due to inadequate preoperative histological sampling and a vague clinical presentation. In the first case, strong suspicion of malignancy following imaging, while in the second, severe gastric outlet stenosis indicated the resection. In our report, we give a clinicopathological summary from the literature of this entity, including its epidemiology, clinical presentation and applicable diagnostic methods as well as macroscopic and microscopic pathomorphology. The pathogenesis of this disease is complex. Beside the role of alcohol, anatomic variations of the pancreatic ductal system, pancreatic islets in duodenal wall resulting from incomplete involution of dorsal pancreas, or Brunner gland hyperplasia (often observed as part of the lesion) can all play a role in the disturbance of pancreatic fluid discharge in the minor papilla area, eventually leading to this specific localised inflammation. In addition, recent investigations revealed a susceptible role of genetic polymorphism in the persistent inflammatory disorders of the pancreas. Besides summarizing the differential diagnostic aspects, we also discuss therapeutic possibilities, underlining the conservative methods, which can be used with good efficacy after a successful identification of this entity. Orv Hetil. 2019; 160(22): 873-879.
... [39][40][41][42] Chronic pancreatitis (including groove pancreatitis) has been known to cause GOO, although this adverse event is uncommon. 14,[43][44][45] Although surgery forms a primary modality for its management, other endoscopic techniques including EBD have been tried with variable success. 14,[43][44][45][46] Previous studies including ours report a dismal outcome with EBD for chronic pancreatitis-associated GOO. ...
... 14,[43][44][45] Although surgery forms a primary modality for its management, other endoscopic techniques including EBD have been tried with variable success. 14,[43][44][45][46] Previous studies including ours report a dismal outcome with EBD for chronic pancreatitis-associated GOO. 4,14,44 Adverse events of EBD include pain, bleeding, and perforation. ...
... 14,[43][44][45][46] Previous studies including ours report a dismal outcome with EBD for chronic pancreatitis-associated GOO. 4,14,44 Adverse events of EBD include pain, bleeding, and perforation. Perforation has been reported to occur in up to 8% of cases. ...
Article
Background and aims: Peptic ulcer disease (PUD)-related gastric outlet obstruction (GOO) is known to respond favorably to endoscopic balloon dilation (EBD). However, data on efficacy of EBD for other etiologies of benign GOO is sparse. We aimed to compare response of EBD among different etiologies of GOO. Methods: Records of all patients with benign GOO who underwent EBD at our tertiary care center between January 1998 to December 2017 were analyzed. Dilation was done using through-the-scope balloons. Procedural and clinical success of EBD was compared among different etiologies. Results: A total of 306 patients were evaluated, of whom, 264 (mean age - 37.89 + 17.49; males - 183, females - 81) underwent dilation. Etiologically caustic ingestion was the commonest cause of GOO (53.8%) followed by PUD (26.1%) and medication-induced (8.3%). Overall procedural and clinical success was achieved in 200 (75.7%) and 243 (92.04%) patients respectively requiring a mean (SD) of 2.55 (2.8) and 5.37 (3.9) sessions respectively. Caustic-induced GOO responded less favorably, requiring a higher number of dilation sessions and having more refractory strictures than other etiologies. Medication-induced GOO performed worse than PUD-related GOO. Of the 264 patients, 9 (3.4%) had perforation during EBD, 3 of them had a contained leak and were managed conservatively, whereas 6 patients underwent successful surgery. Conclusion: EBD is successful in a majority of patients with benign GOO, with caustic-induced GOO and medication-induced GOO being more difficult than PUD-related GOO.
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An 83-year-old man was referred to our hospital for a detailed evaluation for vomiting. Esophagogastroduodenoscopy and abdominal computed tomography showed duodenal stenosis with wall thickness. Biopsy including endoscopic ultrasound-guided fine-needle aspiration of the thickened wall showed inflammation without malignancy. During the clinical course, wall thickening of the distal bile duct appeared. Biopsy under endoscopic retrograde cholangiography showed papillary adenocarcinoma. Surgery revealed that the tumor had widely invaded the duodenal wall from the outside; therefore, only gastrojejunostomy was performed. It was hypothesized that the cholangiocarcinoma had progressed to the serosal side, disseminated in the peritoneum, infiltrated the duodenal serosa, and caused duodenal stenosis.