bluuebunny/crossref_metadata_2025_split huggingface dataset:
1784 Esophageal Granular Cell Tumor Treated With Cap-Assisted Endoscopic Mucosal Resection
Authors: Estifan Elias , Mohamed Abdalla , Cavanagh Yana , Grossman Matthew 
Published: October 2019

INTRODUCTION:
Granular cell tumors (GCT) are rare neoplasms that can occur throughout the body. They were first described in the tongue by Abrikossoff in 1926 and initially known as Abrikossoff tumor. Most GCTs are benign neoplasms with a schwann cell origin however they may also be locally aggressive.

CASE DESCRIPTION/METHODS:
We encountered a 38 years-old Female with no past medical history who underwent gastroscopy for non-specific abdominal pain. She was incidentally found to have a 1 cm, oval, submucosal lesion at 29 cm from the incisors (Figure 1). Endoscopic ultrasound (EUS) was pursued and revealed a hyperechoic lesion that appeared to be located within the luminal interface/superficial mucosa (Figure 2). The mass measured 8 mm in maximal thickness on EUS. Cap-assisted endoscopic mucosal resection was planned. A solution of saline and methylene blue was injected with the adequate lifting of the lesion from the underlying muscularis propria. A distally attaching cap was fitted with a snare in anticipation of endoscopic mucosal resection (EMR). The lesion and a peripheral margin (total area of 18 mm) were successfully resected and retrieved by suctioning into the cap (Figure 3). Pathology of the specimen showed a granular cell tumor with affirmative S100 and no evidence of intestinal metaplasia or dysplasia. Surveillance EGD, performed 3 months after the initial EMR, confirmed complete resection with no recurrence. Biopsies revealed benign esophageal squamous mucosa.

DISCUSSION:
Cap-assisted EMR is a valuable tool in the armamentarium of the gastroenterologist. It offers the benefits of EMR, in that this technique is able to obtain larger tissue samples compared to biopsy without the loss of a safety profile and provides the added pleasantry of a short learning curve. It is limited by the size of the cap and is unable to resect more extensive lesions en-bloc. Lesions smaller than 3 cm in diameter that is confined to mucosal or submucosal layers are the ideal candidates for this technique, as evidenced by our case.
1790 Black Esophagus or Acute Esophageal Necrosis: A Case Series and Single-Institution Experience
Authors: Ghoneim Sara , Dalal Shaman , Shah Aun , Landsman Marc , Kyprianou Annette 
Published: October 2019

INTRODUCTION:
Acute esophageal necrosis (AEN) or ‘black esophagus’ is a rare disease of the esophagus with an endoscopic prevalence of 0.02%. It generally presents with signs of upper GI bleeding including melena and hematemesis. Its pathophysiology is largely attributed to severe illness states that affect the perfusion of the esophagus. The distal esophagus being least vascular is most commonly affected. Upper endoscopy reveals circumferential black discoloration. Biopsies are taken to confirm necrosis, as well as rule out infection or pigmentation. Management is generally supportive, with endoscopic resolution seen in many cases with correction of the underlying insult.

CASE DESCRIPTION/METHODS:
Three patients with AEN were identified over the last 2 years at our institution. Two females aged 67 and 78 were admitted within the same month in 2019 with epigastric pain and coffee-ground-emesis. Both were found to be in diabetic ketoacidosis (DKA). One of them was diagnosed with CHF with reduced ejection fraction (40%). Both patients had documented T2DM and atherosclerotic disease. Laboratory findings showed elevated serum glucose and anion-gap metabolic acidosis with elevated beta-hydroxyburate. Both underwent EGD which was notable for a circumferential black esophagus that abruptly terminated at the gastro-esophageal junction (Figures 1 and 2). The third patient was a 35-year-old male with poorly-controlled T1DM (A1c 9.1%) who noticed melenic stools 2 days prior and presented with hypovolemic shock. EGD was consistent with black esophagus. Biopsy showed acute inflammatory exudates with necrotic cells and numerous fungal hyphae. He was started on micafungin for two weeks and twice daily PPI. EGD 8 weeks later showed complete resolution of initial findings (Figure 3).

DISCUSSION:
AEN is a rare cause of upper GI bleed, more commonly reported in men and in patients with underlying vasculopathies who present with severe illness. Peak incidence is in the sixth decade of life. Existing literature reports DKA as a relatively common precipitating factor. All of our patients presented with upper GI bleed secondary to AEN and were in DKA superimposed on low perfusion states due to CHF, atherosclerotic disease and sepsis respectively. Two out of three patients were females. Based on our case series, it appears that DKA, a critical illness in itself, further worsens existing low perfusion states. This can manifest as upper GI bleeding. DKA demands prompt correction, especially in patients with concomitant vasculopathy.
1792 An Unusual True Esophageal Epiphrenic Diverticulum in the Setting of Heterotopic Gastric Mucosal Patches: A Case Report
Authors: Sidhu Tahnee , Dokmak Amr , Krishnan Sandeep 
Published: October 2019

INTRODUCTION:
Esophageal diverticula (ED) are a rare structure abnormality with prevalence estimated to be between 0.06% to 4%. Esophageal epiphrenic diverticula (EED) are diverticula in the distal 10cm of the thoracic esophagus and are typically false diverticula with outpouching of only the submucosa and mucosa as the result of an esophageal motility disorder. Within ED, EED constitutes less than 10% of all esophageal diverticula, with an incidence of 1:500,000/year. Here we report a case of a true esophageal epiphrenic diverticula in the setting of heterotopic gastric mucosa patches (HGMPE) found after presentation with epigastric symptoms.

CASE DESCRIPTION/METHODS:
A 35-year-old female with a past medical history of endometriosis presented with a few months of epigastric pain, nausea, and vomiting with no response to treatment for gastroesophageal reflux disease (GERD) prompting investigation with esophagogastroduodenoscopy (EGD) which revealed a diverticulum 29cm from the incisors with normal surrounding mucosa. She returned for endoscopic ultrasound (EUS) for further evaluation with development of dysphagia with no regurgitation or halitosis. Repeat EGD prior to EUS revealed areas suggestive of ectopic gastric mucosal patches 28 cm from the incisor with a single diverticulum at the posterolateral aspect of the esophagus. Z line was at 38 cm from the incisors. EUS showed a single esophageal diverticulum from 28 to 30 cm with all 4 wall layers indicating a true diverticulum. Pathology from biopsy at the 29 cm showed cardia type mucosa with chronic inflammation without evidence of metaplasia, dysplasia, or intramucosal eosinophils significant for HGMPE.

DISCUSSION:
ED, particularly EED are a rare entity with varying clinical manifestations including dysphagia, regurgitation, weight loss, chest pain, halitosis, aspiration, and heartburn with the majority of patients being asymptomatic until the diverticula are larger than 5cm. Moreover, EED typically are false diverticula with the involvement of the mucosa and submucosa as a result of a motility disorder. The majority of true ED are located within the mid esophagus secondary to tuberculosis, histoplasmosis, and malignancy. Here, we describe a case with HGMPE resulting in a 2 cm true diverticulum within the distal third of the esophagus not identified on initial evaluation highlighting a cause for ED not previously identified in the literature and the importance for a thorough assessment of patients with esophageal disease.
1880 Failure of Withdrawal Through the Abdominal Wall - A New Percutaneous Gastrostomy Tube Placement Complication: A Case Series
Authors: Salcedo Juan , Pearlman Michelle , Barkin Jamie S. 
Published: October 2019

INTRODUCTION:
Percutaneous endoscopic gastrostomy (PEG) tubes are the preferred method for long-term nutritional support, having a success rate of 95 to 100% regardless of the technique. Common reasons for failed endoscopic gastrostomy tube placements are complete oropharyngeal or esophageal obstruction, suboptimal gastric transillumination, or deterioration in the clinical status during the procedure. Aim: present the first case series of three patients with unsuccessful PEG tube placements because of failure to withdrawal the gastrostomy tube through the abdominal wall.

CASE DESCRIPTION/METHODS:
Methods: We conducted a MEDLINE database query by combining the search terms “Gastrostomy and adverse effects”, “Gastrostomy and methods”, “Gastroscopy” and “Percutaneous Endoscopic Gastrostomy”. The resultant 408 articles were pulled from the literature. English language article titles and abstracts were screened, and the appropriate articles reviewed. No previous case reports of unsuccessful PEG placement secondary to failed withdrawal of the PEG tube through the abdominal wall. We report three cases. All clinical data were carefully reviewed. Exclusion criteria was failure of PEG placement due to other circumstances (such as inability to pass the scope, inadequate gastric transillumination on the abdominal wall, absence of endoscopic confirmation of digital imprint upon external pressure, or failed needle insertion). Results:Three patients were included (two females, one male). The average age was 62 years old (range 58 to 66 years). All of the cases presented unsuccessful PEG placement using the Flow 20 Pull® PEG tube (Cook Medical®, Winston-Salem, North Carolina). Two of the three patients had pneumoperitoneum, one with generalized peritonitis after the failed PEG attempt, requiring exploratory laparotomy.

DISCUSSION:
This is the first report of patients with unsuccessful PEG placement secondary to the inability to withdraw the gastrostomy tube through the abdominal wall. Failure was likely caused from the tangential entrapment of the PEG tube tip in the gastric wall or subcutaneous tissue. We hypothesize that this may be related to the short and blunt - shaped tip of the Flow 20 Pull® PEG tube (Cook Medical®). Endoscopists other than the authors have reported difficulty withdrawing this PEG tube through the abdominal wall (personal communication).
1882 Diagnosing Sarcoidosis From the Gastrointestinal Tract
Authors: Karim Syed S. , Singh Davinder , Prasa Jarin , Rizvon Kaleem , Mustacchia Paul 
Published: October 2019

INTRODUCTION:
Sarcoidosis is a multi-system disease with 90% occurrence in the lungs and mediastinal lymph nodes. Involvement of the gastrointestinal tract (GIT) occur in less than 1 % of cases. We illustrate a patient who presented with gastrointestinal symptoms leading to the diagnosis and multidisciplinary management of sarcoidosis.

CASE DESCRIPTION/METHODS:
61-year-old African American female with gastroesophageal reflux disease and an umbilical hernia had constipation alternating with diarrhea and vomiting associated with greasy food. Examination showed an umbilical hernia and a soft, non tender abdomen. In her stool, pathogenic parasites and clostridium difficile was negative. Serum tissue transglutaminase and IgA levels were normal. Upper endoscopy and EUS revealed a polypoid mass in the gastric antrum which was limited to the mucosa. Histology showed inflammation, crypt abscesses and non caseating granulomas. Special stains for acid fast bacilli and fungi were negative. Quantiferon gold was negative. Colonoscopy was unremarkable. Suspicion for sarcoidosis led to a CT thorax, which revealed peri-hilar lymphadenopathy. The patient was sent to pulmonology and ophthalmology. Her symptoms were tackled without steroids in a symptomatic fashion.

DISCUSSION:
When sarcoidosis affects the GIT, the stomach is the most common site and with few reported cases in the esophagus, colon and rectum. Symptoms are non-specific, such as: nausea, vomiting, diarrhea, and abdominal pain. Diagnosis depends on three factors: biopsy confirming non-caseating granuloma in the GIT, involvement in at least one additional organ, and exclusion of other common granulomatous diseases, such as Crohn’s disease, tuberculosis and fungi. Our patient had an antral non-caseating granuloma.Multiorgan involvement was demonstrated by per-hilar lymphadenopathy. Tuberculosis and fungi were ruled out with negative stains and quantiferon gold. Nearly all patients with crohn’s disease develop distal colonic involvement, and upper GIT involvement is rare when there is no disease beyond the ligament of treitz. Our patient had multiple colonoscopies negative for Crohn’s. Management is based upon severity; asymptomatic patients require no treatment and severe cases receive glucocorticoids. Our patient’s did not need any steroids since subsequent endoscopies had no further granulomas. Although rare, sarcoidosis may involve the GIT, and clinicians should begin the work up if granulomas are found and refer the patient to the appropriate departments.
1885 Cat Scratch Stomach: A Rare Endoscopic Finding
Authors: Park Connie , Dicaprio David , Swaminath Arun 
Published: October 2019

INTRODUCTION:
“Cat scratch colon” has been used in literature to describe superficial linear hemorrhagic tears in the colon that resemble scratches from a cat’s claws. These tears are rare, with a prevalence of about 0.25% and are usually found in the right colon and cecum in association with barotrauma during colonoscopy. Cases reporting these findings were associated with less compliant colons, as in collagenous colitis, diversion colitis, and colonic compression. Cat scratch findings in the stomach have been less common. Here we report the case of a young female with “cat scratch” findings in the stomach during upper endoscopy.

CASE DESCRIPTION/METHODS:
A 29-year-old female with autoimmune thyroiditis and ileocolonic Crohn’s disease presented to our clinic endorsing a 30-pound weight loss over 3 years, abdominal pain, sitophobia, nausea, and overlapping symptoms of diarrhea and constipation. She endorsed occasional ketorolac use for her menstrual symptoms. She denied vomiting, hematochezia, melena, past or current substance use, laxative use, or eating disorder. Abdomen was nontender on exam. Endoscopy initially revealed normal esophagogastroduodenal mucosa, but as the endoscope was withdrawn, several “cat scratch” lacerations were noted in the gastric fundus and cardia. Equipment was confirmed to be supplying CO2. Antral and duodenal biopsies revealed chronic gastritis and focal metaplasia, but were negative for Helicobacter pylori. Colonoscopy and colonic biopsies were normal.

DISCUSSION:
In the only other reported case of “cat scratch stomach” in a 47-year-old male with dyspepsia and otherwise unremarkable history, the authors hypothesized that air retention from the pylorus and lower esophageal sphincter led to colonic over-distention and contributed to the tears. Similarly, our findings may be sequelae of barotrauma despite sole use of CO2. Considering the patient’s nonsteroidal anti-inflammatory drug (NSAID) use and the correlation of “cat scratch colon” with collagenous colitis, collagenous gastritis may also predispose these findings, despite absence on our biopsy. The significance of these endoscopic findings is not yet clear. As such, we hope to add to the literature to help elucidate the etiology and clinical significance of these gastric tears.
1888 Colonoscopy as a Cause of Appendicitis
Authors: Adu-Gyamfi Kwabena , Adeniji Olaitan , Patri Sandeep 
Published: October 2019

INTRODUCTION:
Millions of colonoscopies are performed annually in the United States. Acute appendicitis is a rare complication of colonoscopy which many general providers may remain oblivious of. Albeit a rare entity, it can lead to patient mortality. We present a case of acute appendicitis which occurred after colonoscopy in which there was no evidence of pre-existing appendiceal disease. Increased physician awareness may help reduce delays in diagnosis and treatment.

CASE DESCRIPTION/METHODS:
A 55-year-old woman underwent a routine outpatient screening colonoscopy. She had no complaints prior to the procedure. Bowel preparation was adequate. A 6mm sessile polyp was noted in the cecum and was resected by cold snare polypectomy. The appendiceal orifice was normal in appearance. No other significant findings were noted. About 12 hours after colonoscopy, she started experiencing severe right lower quadrant abdominal pain and presented to the emergency room. Vital signs were within normal limits besides a pulse was 101 beats per minute. Right lower quadrant abdominal tenderness was noted on exam. Laboratory results noted WBC count of 12.9 x 103/ul (3.8-10.7 x 103/ul) and rest of basic labs were normal. A computed tomography (CT) scan of abdomen noted a dilated 13mm appendix with surrounding inflammatory changes in the surrounding fat and an impacted appendicolith [Figure 1] She underwent open appendectomy with findings of acute appendicitis with no signs of perforation. Post-operatively, patient recovered quickly and discharged home after 24 hours. At a one week follow up she was still recuperating well with no concerns.

DISCUSSION:
Acute appendicitis following colonoscopy has an estimated incidence of 0.038%. Different causal mechanisms proposed include fecalith impaction, barotrauma from overinsufflation of air or direct trauma to the appendiceal orifice. The majority of patients present within 24hrs of colonoscopy. Abdominopelvic CT imaging remains the most useful diagnostic modality. The majority of reported cases have required surgical management with intraoperative findings ranging from acute appendicitis to gangrenous or perforated appendicitis. It can mimic more benign conditions such as post-colonoscopy gas pain, cramping or post-polypectomy electrocoagulation syndrome. Greater provider and patient cognizance of the risk of appendicitis following colonoscopy will enhance prompt diagnosis and appropriate treatment.
1890 An Attack of Disseminated MAC
Authors: Boland Katherine , Tollivoro Ted , Nakanishi Yukihiro , Gaspard Gregory 
Published: October 2019

INTRODUCTION:
A 43-year-old woman with a past medical history of AIDS presented with a 3 month history of diarrhea, abdominal pain, and weight loss. She was noted to have pancytopenia with a profound anemia. Alkaline phosphatase was elevated with normal AST and ALT. Stool culture, C diff, shiga toxin, and stool cryptosporidium Ag were negative. Mediastinal, axillary, retroperitoneal, and inguinal lymphadenopathy were noted on CT scan with splenomegaly.

CASE DESCRIPTION/METHODS:
ID and GI were consulted who recommended initiation of azithromycin, rifabutin, and ethambutol given the high suspicion for disseminated Mycobacterium avium complex (MAC). After 12 days of hospitalization, her diarrhea had not improved, and the decision was made to perform EGD and colonoscopy. EGD demonstrated atrophic mucosa in the 2nd and 3rd portions of duodenum. Colonoscopy showed severe colitis in the ileocecal valve. The TI had multiple erythematous, hypervascular appearing lesions with the appearance of angioectasias. The pathology of the duodenal, terminal ileum, IC valve, and random colon biopsies all showed acid-fast bacilli bacteria within the macrophages. Given the endoscopy findings with blood cultures which were previously positive and eventually grew MAC, the diagnosis of disseminated MAC was confirmed. Her diarrhea gradually improved and she was restarted on HAART before discharge.

DISCUSSION:
In the post-HAART era, the incidence of diarrhea attributed to opportunistic infections has decreased1; however, the workup and evaluation for infectious diarrhea continues to be paramount. The American Society for Gastrointestinal Endoscopy recommends stool testing for pathogens as the first-line evaluation followed by endoscopy when the diarrheal illness is persistent and stool tests fail to reveal a cause in immunocompromised patients2. MAC can affect several parts of the gastrointestinal system. In one review of previously reported cases of MAC with GI involvement, endoscopy demonstrated involvement of the duodenum (76%), rectum (24%), ileum (6%), colon (4%), esophagus (4%), and jejunum (2%)3. MAC colonization of the gastrointestinal tract is important because it increases the risk of disseminated MAC with the risk of MAC bacteremia approaching 60% with in 1 year4. Our approach to this patient was to perform endoscopy only when her symptoms persisted despite treatment. This case was interesting in that duodenum, ileum, and colon were all affected. Lastly, this case was an excellent example of several classic MAC findings.
1938 A Case of Diffuse Antral and Pyloric Ulcers
Authors: Shaikh Abdullah S. , Baliss Michelle , Chatila Ahmed , Abdulla Hamza , Parupudi Sreeram 
Published: October 2019

INTRODUCTION:
Antral gastric ulcers are typically managed through endoscopic therapy, proton-pump inhibitors, and treating any underlying cause such as Helicobacter pylori. However, in the presence of multiple, deep, continuously bleeding ulcers, partial gastrectomy is a mainstay of treatment. We present a case of a patient who was found to have diffuse, deep antral and pyloric ulcers and was managed through solely interventional radiology embolization.

CASE DESCRIPTION/METHODS:
A 59 year old male patient with multiple bouts of alcoholic pancreatitis, hypertension, and chronic obstructive pulmonary disease who presented with anemia but no signs of overt GI bleeding. Patient's risk factors included NSAID use. However, CT A/P showed active bleeding with extravasation into the stomach with subsequent respiratory failure led to intubation and ICU admission. EGD showing diffuse, partially obstructing, deep antral and pyloric ulcers covering the entire antrum and pylorus not amenable to endoscopic intervention with recommendation to possibly pursue surgical intervention. Arteriograms of the celiac trunk, SMA, left gastric artery, splenic artery, common hepatic artery, and gastroduodenal artery demonstrated no active bleeding. Surgery was consulted and recommended no immediate surgical intervention, opting for interventional radiology to preform embolization if patient continues to bleed. As the patient continued to bleed, the decision was made to embolize the gastroduodenal artery. The patient did well post-procedure with stable hemoglobin with plans to follow up outpatient to determine the cause of the diffuse ulcerations.

DISCUSSION:
Diffuse, bleeding antral gastric ulcers are a consideration for antrectomy or partial gastrectomy if the lesions are not amenable to endoscopic intervention. However, in the case of our patient, interventional radiology embolized the gastroduodenal arterial, despite no active bleeding on CT angiography. The empiric embolization successfully treated the source of bleeding without need for surgical intervention. Our case helps emphasize that Interventional Radiology embolization of the gastroduodenal artery may be considered in patients with multiple actively bleeding, antral gastric ulcers who are not surgical candidates despite the lack of bleeding on CT angiography.