scholarly journals S3207 Ectopic Location of Ampulla of Vater in the Duodenal Bulb Causing Pyloric Stenosis and Gastric Outlet Obstruction

2021 ◽  
Vol 116 (1) ◽  
pp. S1319-S1319
Author(s):  
Dawa Gurung ◽  
Howard Chung ◽  
Mahmoud Nassar ◽  
Mohsen Alshamam ◽  
Saphwat Eskaros ◽  
...  
Keyword(s):  
Pyloric Stenosis ◽  
Gastric Outlet Obstruction ◽  
Duodenal Bulb ◽  
Outlet Obstruction ◽  
Ampulla Of Vater

scholarly journals A clinical study of gastric outlet obstruction

2016 ◽  
Vol 4 (1) ◽  
pp. 264
Author(s):  
Suresh Clement H. ◽  
Ram Prasad Cherukumalli ◽  
Ch. Ravinder Rao
Keyword(s):  
Duodenal Ulcer ◽  
Pyloric Stenosis ◽  
Gastric Outlet Obstruction ◽  
Hypertrophic Pyloric Stenosis ◽  
Duodenal Bulb ◽  
Outlet Obstruction ◽  
Palliative Surgery ◽  
Infantile Hypertrophic Pyloric Stenosis ◽  
Age Group ◽  
Carcinoma Stomach

Background:From the standpoint of pathology, the term pyloric stenosis is usually inaccurate at least in adult patients, since the site of obstruction is rarely situated at the pylorus itself but, is more often placed immediately proximal to the spinchter where the diagnosis of carcinoma is most probable or more distally in the duodenal bulb where the cause is almost invariably a duodenal ulcer. The aim was to study infantile hypertrophic pyloric stenosis, benign peptic ulcer and gastric carcinoma and evaluation of electrolyte abnormalities in gastric outlet obstruction, to study various modalities of treatment and to assess pertaining to recovery from paralytic ileus.  Methods: This was a clinical observational study comprising of 40 cases of gastric outlet obstruction. The patients for this study have been selected from Prathima Institute of Medical Sciences, Karimnagar, Telangana, India from December 2013- November 2015. The cases were selected who were willing to undergo surgery.Results:Congenital hypertrophic pyloric stenosis (CHPS) is more common among first born male infants. Parental consanguinity is associated with increased incidence of congenital hypertrophic pyloric stenosis. CHPS is common in the age group of first 3-6 weeks of life (average 4 weeks). Males are more commonly affected with gastric outlet obstructions in adults. Cicatrized duodenal ulcer is more common in the age group of 30-40 years, while carcinoma stomach is more common in age group of 50-60 years. Vomiting and visible gastric peristalsis are the most common and constant symptom and sign of gastric outlet obstruction, more so in cases of cicatrized duodenal ulcers.Conclusions:Ramstedt’s pyloromyotomy is the gold standard treatment for CHPS. Patients with gastric outlet obstruction due to cicatrized duodenal ulcer require truncal vagotomy with posterior gastrojejunostomy. Vagotomy is optional in view of better response with drugs for APD. Antral carcinoma cases require curative or palliative surgery depending on the stage of the disease.

scholarly journals Endoscopic Diagnosis of Bouveret Syndrome

2020 ◽  
Vol 14 (3) ◽  
pp. 683-686
Author(s):  
Felix Hesse ◽  
Mohamed Abdelhafez ◽  
Christoph Schlag ◽  
Roland M. Schmid ◽  
Tobias Lahmer
Keyword(s):  
Computed Tomography ◽  
Female Patient ◽  
Gastric Outlet Obstruction ◽  
Rare Complication ◽  
Gallstone Ileus ◽  
Duodenal Bulb ◽  
Outlet Obstruction ◽  
Endoscopic Diagnosis ◽  
Endoscopic Imaging ◽  
Bouveret Syndrome

Bouveret syndrome is a form of gallstone ileus and a rare complication of chole(cysto)lithiasis. It describes gastric outlet obstruction secondary to an impacted gallstone. Here, we report a case of an 82-year-old female patient with gastric outlet obstruction and penetration of gallstones into the duodenal bulb on endoscopic imaging. Based on these findings Bouveret syndrome was diagnosed and confirmed by computed tomography.

“Burned-Out” Pyloric Stenosis: An Elusive Gastric Outlet Obstruction

Radiology ◽  
1975 ◽  
Vol 117 (2) ◽  
pp. 373-379 ◽  
Author(s):  
Leonard E. Swischuk ◽  
Kenneth R. Tyson
Keyword(s):  
Pyloric Stenosis ◽  
Gastric Outlet Obstruction ◽  
Outlet Obstruction

scholarly journals Bouveret’s syndrome: A challenging case of gastric outlet obstruction.

2020 ◽  
Vol 27 (06) ◽  
pp. 1316-1319
Author(s):  
Marrium Gul ◽  
Irfan Qadir ◽  
Muhammad Qasim Butt
Keyword(s):  
Gastric Outlet Obstruction ◽  
Epigastric Pain ◽  
Duodenal Bulb ◽  
Outlet Obstruction ◽  
Postoperative Recovery ◽  
Blood Analysis ◽  
Bouveret’S Syndrome ◽  
Endoscopic Extraction ◽  
Bilioenteric Fistula ◽  
Bouveret's Syndrome

Bouveret’s syndrome causes gastric outlet obstruction when a gallstone is impacted in the duodenum or stomach via a bilioenteric fistula. We present case of a 40-year-old female presented with epigastric pain and intractable vomiting for 2 days. Her physical examination and laboratory workup including blood analysis, amylase test and lipase test were normal. Plain abdominal X-ray did not show any signs of small bowel obstruction. A nasogastric tube was placed and drained 2.5 L of gastric contents immediately. Esophagogastroduodenoscopy showed a dilated stomach with excessive secretions and a large blackish-brown hard stone in the duodenal bulb. After failed attempt at endoscopic extraction, patient underwent laparotomy and removal of stone via duodenal incision. Subsequently, the patient exhibited a good postoperative recovery. The condition of the patient has remained stable after being followed up for one year.

The Value of Ultrasound in the Diagnosis of Congenital Hypertrophic Pyloric Stenosis

1993 ◽  
Vol 32 (5) ◽  
pp. 281-283 ◽  
Author(s):  
Marcos Kovalivker ◽  
Ilan Erez ◽  
Nina Shneider ◽  
Ernesto Glazer ◽  
Ludwig Lazar
Keyword(s):  
Pyloric Stenosis ◽  
Gastric Outlet Obstruction ◽  
Clinical Picture ◽  
Hypertrophic Pyloric Stenosis ◽  
Barium Meal ◽  
Outlet Obstruction ◽  
Sonographic Diagnosis ◽  
Congenital Hypertrophic Pyloric Stenosis ◽  
Clinically Significant ◽  
Pyloric Muscle

The charts of 103 children with a clinically and surgically confirmed diagnosis of congenital hypertrophic pyloric stenosis were retrospectively reviewed. We found a significant correlation between sonographic and surgical measurements of the muscular thickness of the pylorus ( r = .987, P<.001). In 73.7% (76 cases), the clinical picture of gastric outlet obstruction was present when the thickness of the enlarged pyloric muscle was 3.0 mm or more. In 26.3% (27 cases), the pyloric muscle was less than 3.0 mm wide. For 10 patients in whom the muscle width was less than 2.5 mm by sonography, a barium meal was necessary to confirm the diagnosis. The width of the pyloric muscle is the most important factor in the sonographic diagnosis of pyloric stenosis, and even a width of less than 3.0 mm may be associated with clinically significant obstruction.

scholarly journals A181 ENDOSCOPIC BALLOON DILATION IS EFFECTIVE AND SAFE IN THE MANAGEMENT OF NSAID-INDUCED NON-ULCERATIVE GASTRIC OUTLET OBSTRUCTION

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 48-50
Author(s):  
D R Lim ◽  
D Farina ◽  
W Huang ◽  
J Zhu
Keyword(s):  
Case Report ◽  
Pyloric Stenosis ◽  
Gastric Outlet Obstruction ◽  
Unusual Case ◽  
Surgical Intervention ◽  
Balloon Dilation ◽  
Outlet Obstruction ◽  
Gi Bleeding ◽  
Endoscopic Balloon Dilation ◽  
Endoscopic Balloon

Abstract Background We describe an unusual case of NSAID-induced gastric outlet obstruction (GOO) in the absence of malignancy or ulcers. This was successfully managed conservatively with drug withdrawal and serial endoscopic balloon dilation (EBD). Aims Case Report Methods Case Report and Literature Review Results A 58-year-old woman with 20-year history of daily Ketorolac use for osteoarthritis presented with iron deficiency anemia (IDA) of 58 g/L and post-prandial emesis for 2 months. There was no overt GI bleeding. Gastroscopy revealed severe erosive esophagitis and GOO with no ulcers. After a negative CT imaging ruled out extrinsic malignant compression, GOO was managed with EBD. Examination of the duodenum post-EBD revealed complete atrophy and scalloping. Focused biopsies reveal chronic gastritis, complete villous atrophy in the duodenum; ruled out H. Pylori, celiac disease, amyloidosis and dysplasia. EUS negative for infiltrative disease or regional adenopathy. Vitamin B12, anti-TTG I IgA, HLA DQ2/8 were normal. These findings made drug-induced enteropathy the top contender. PPI therapy was initiated and NSAID discontinued. Five serial EBD were performed over 4 months to 18mm. A pureed diet was tolerated after 2 dilations. Follow-up at 3 months showed partial recovery of enteropathy and pyloric stenosis. No adverse events were seen. The severe esophagitis was likely an erosive process secondary to reflux from GOO. Her IDA is likely multifactorial: Severe enteropathy and GOO may have led to chronic malabsorption; occult GI bleeding from erosions or ulcers that have healed may further contribute. Ketorolac could explain the enteropathy. COX-1 inhibition leads to decreased gastric cytoprotection. In rat models, COX-2 inhibition has been suggested to delay gastric healing and dysregulated immune response to food antigens in the small bowel [4–6]. NSAID-induced GOO almost always occur in the context of peptic ulcer disease [1,2]. A similar case [3] found pyloric stenosis in a 75-year old woman with esophagitis and ulcer-induced pyloric stenosis. They postulate that post ulcerative healing led to benign pyloric stenosis and explained the absence of ulcers. Historically, surgical intervention and stent placement have played a major role in the management of benign mechanical GOO. EBD has replaced surgical intervention as first line therapy [7] showing promising results beyond 3 months post EBD[8], sparing patients from surgery related morbidity. An algorithm has been suggested by us [Img 1] for the management of benign GOO. Conclusions We present an unusual case of NSAID-induced mechanical GOO and enteropathy. This case highlights these entities as rare but serious complications of chronic NSAID use. Management of benign mechanical GOO should be individualized. Prudence with prescribing NSAIDs to at risk populations is recommended. Funding Agencies None

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