bluuebunny/crossref_metadata_2025 huggingface dataset:
1759 Dysphagia in Extra-Pyramidal Syndrome: A Reversible and Uncommon Presentation
Authors: Sun Haozhe , Abbas Hafsa , Jyala Abhilasha , Badipatla Kanthi Rekha , Nayudu Suresh Kumar
Published: October 2019

INTRODUCTION:

Neuroleptic medications are known to cause extrapyramidal syndrome (EPS) in individuals taking antipsychotic medications. However, dysphagia is an uncommon clinical entity presenting as EPS. We present a case of dysphagia in an individual taking Haloperidol confirmed by swallowing studies, which resolved entirely on discontinuation of Haloperidol and appropriate medical management.

CASE DESCRIPTION/METHODS:

A 22-year-old male with a history of bipolar disorder was admitted to the inpatient psychiatric unit for an episode of psychosis. He was started on oral valproic acid, oral haloperidol as well as scheduled monthly injections of Haloperidol Decanoate. One week after his discharge, he was seen in the clinic for coarse tremors and stiffness in all his extremities. It was decided to taper haloperidol and start benztropine. In two weeks, he presented to the emergency room with difficulty in swallowing (both liquids and solids) as well as worsening stiffness of all four extremities. Physical examination was significant for masked facies, bradykinesia with decreased active range of motion of both the upper and lower extremities. A computed tomography (CT) of his head, neck, and soft tissues showed no acute abnormalities. A functional swallow evaluation was performed which revealed oral decompensation for regular solid texture, marked by excessive chewing and delayed anterior to posterior transit. There was no remarkable oral residue, symptoms or signs of airway protection deficits were appreciated on assessment. Esophagogastroduodenoscopy did not reveal any structural etiology for his dysphagia. He was admitted to hospital; haloperidol was discontinued and Benztropine dose was increased. Also, he was started on diphenhydramine His symptoms were completely resolved in four days. He was discharged home in stable condition.

DISCUSSION:

Extrapyramidal symptoms (EPS) are a well-known adverse reaction from antipsychotic medications, that can range from acute dystonia, akathisia, parkinsonism to tardive dyskinesia. Dysphagia is a known but rare side effect of antipsychotic medications. Our case stresses the importance of suspecting drug-induced dysphagia in individuals on neuroleptics. Early diagnosis can decrease morbidity and hospital stay as the main stay of management of these patients is to discontinue precipitating agent and reversing physiological effects by medical management that can result in shortening disease course and better outcomes.
1771 Eosinophilic Esophagitis Presenting With Esophageal Wall Dissection
Authors: McCarron Joshua D. , Lawson Robert D.
Published: October 2019

INTRODUCTION:

Eosinophilic esophagitis (EoE) is a chronic immune/antigen-mediated, inflammatory disease with a wide spectrum of presentation from mild dysphagia to food impaction. We describe the presentation and management of a patient whose initial presentation of EoE included the rare complication of esophageal dissection.

CASE DESCRIPTION/METHODS:

A 30-year old Caucasian male presented to the emergency department after 10 days of dysphagia and odynophagia. His physical exam was normal. Initial laboratory evaluation revealed mildly elevated troponin I and leukocytosis. CT imaging with IV contrast showed an air-fluid level within the distal esophagus. EGD could only be completed with a pediatric gastroscope (5.4-mm) due to severe, diffuse narrowing of the esophagus. The entire esophagus had findings of EoE including edema, furrowing, and circumferential rings. The lumen of the proximal esophagus was 12-15 mm with acute narrowing to 7mm at 27-cm. Most notable was a 1-cm x 2-cm hole at 25-cm which communicated with a fluid-filled, granulation tissue lined space that paralleled the distal esophagus (Figure 1). Biopsies showed >50 Eos/hpf consistent with EoE. The patient was started on broad-spectrum antibiotics, IV proton pump inhibitor therapy, topical steroid and kept NPO. CT imaging with IV and gastrograffin contrast demonstrated a long segment intramural dissection with a double-barreled esophageal lumen (Figure 2). Following consultation with cardiothoracic surgery, endoscopic management was pursued. Endoscopic suturing was not attempted given severe luminal narrowing. The tissue proved too fibrotic for hemostasis clips. A through-the-scope, fully-covered self-expanding esophageal stent (FCSEMS) was deployed across the defect and a feeding tube was inserted. An elemental diet was started. Follow-up imaging showed obliteration of the false lumen by post-procedure day 9 (Figure 3). Repeat EGD one month later showed an intact lumen but with delicate-appearing granulation tissue at the location of the previous hole (Figure 4), thus another FCSEMS was placed and elemental diet was resumed with plans for repeat EGD in 4 weeks.

DISCUSSION:

Intramural esophageal dissection is a rare, potentially life-threatening complication of EoE which can be medically and endoscopically managed. “The views expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the United States Air Force, the Department of the Navy, Department of Defense, or the U.S. Government.”
1772 Novel Use of Low Dose Amitriptyline in the Prevention of Deglutition Syncope: A Case Report
Authors: Shah Ravi , Mayuga Kenneth A. , Gabbard Scott
Published: October 2019

INTRODUCTION:

Deglutition syncope is a rare entity with approximately 100 reported cases. It is a subtype of neurocardiogenic syncope triggered by deglutition secondary to organic and functional esophageal pathology. There are limited treatment options, and here we report a case of using low-dose amitriptyline (10 mg) for deglutition syncope.

CASE DESCRIPTION/METHODS:

A 58 year old male with hypertension, diabetes mellitus, and peripheral neuropathy presented to gastroenterology clinic with a diagnosis of deglutition syncope. Over the preceding year, he experienced four syncopal episodes while eating, described as lightheadedness before losing consciousness for a minute. Electroencephalogram, electrocardiogram, and echocardiography were unremarkable. Tile-table test showed reflex vasovagal syncope with systolic vasodepression (63 mm Hg) without cardioinhibition. Continuous telemetry showed sinus bradycardia (50 bpm) followed by three sinus pauses up to 4 seconds and return to normal sinus rhythm during episodes of dysphagia and lightheadedness. Evaluation for dysphagia with esophagogastroduodenoscopy (EGD) was unremarkable. Esophagram showed tertiary contractions in the mid-distal esophagus. Esophageal manometry was unremarkable for dry swallows with premature contractions possibly suggestive of distal esophageal spasm (Figure 1). Patient refused repeat EGD. A diagnosis of deglutition syncope with combined cardioinhibition and vasodepression secondary to esophageal spasm was made. Pacemaker implantation was recommended for syncopal symptoms from cardioinhibition; however, the patient declined due to potential persistence of symptoms from vasodepression. Initial recommendations of dietary changes and avoidance of triggering medications were made. Calcium channel blockers and nitrates were limited by bradycardia and hypotension. Hyoscyamine provided partial relief, but pre-syncopal symptoms persisted. Low-dose amitriptyline was initiated for the potential underling etiology of esophageal spasm. After a year, the patient reported resolution syncopal symptoms and dysphagia.

DISCUSSION:

Deglutition syncope due to cardioinhibition and vasodepression secondary to underlying esophageal spasm was diagnosed with tilt-table testing, continuous telemetry, and esophageal manometry. Amitriptyline was chosen for its anticholinergic effects and esophageal neuromodulator properties. Low-dose amitriptyline may be considered as a preventative treatment for resistant deglutition syncope.
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.
1944 BRTO for Treatment of Persistent Gastric Variceal Bleed in a Patient With HCC
Authors: Villavicencio Jaimy , Guerrero Daniela , Elkhattib Ismail
Published: October 2019

INTRODUCTION:

Gastric varices are often associated with formation of spontaneous left-sided porto-systemic shunts, which arise to relieve portal hypertension or bypass obstruction. Gastro-renal shunts are the most common (80%), followed by gastro-caval shunts. Balloon Retrograde Transvenous Obliteration remains one of the primary measures to prevent re-bleeding from gastric varices. This procedure consists of inserting a balloon into the outflow vein of a shunt, allowing injection of a sclerosant for occlusion. It has the advantage of not diverting blood to bypass the liver, but it can worsen portal pressure and increase risk for ascites or esophageal variceal bleeding.

CASE DESCRIPTION/METHODS:

67-year-old male with past medical history of untreated Hepatitis C was admitted after syncope. He also had nausea, lightheadedness and hematemesis. In the ED, his blood pressure was stable with an Hb of 9.5 mg/dL. Ceftriaxone, an octreotide drip and PPI were promptly started. 3 units of blood were transfused. Urgent endoscopy did not reveal esophageal varices, but profuse active bleeding in the fundus was seen. Attempts to control the hemorrhage were ineffective due to lack of visibility. CT scan of the abdomen showed a cirrhotic liver with a 6 cm mass in the right lobe and a large gastric varix with a gastrorenal shunt. Importantly, there was no evidence of portal or splenic vein thrombosis. Left-sided TIPS was tried, but attempts to pass from left portal vein to left hepatic vein were futile due to challenging anatomy. After multiple transfusions the patient eventually underwent successful BRTO. He had no further bleeding and was ultimately diagnosed with HCC.

DISCUSSION:

BRTO is indicated primarily for prevention of recurrent gastric variceal bleeding. It is useful in patients with elevated MELD score, right-sided heart failure or hepatic encephalopathy, who are at high risk for TIPS. Patients with gastric variceal bleeding and concomitant HCC usually have more advanced cirrhosis and lower possibility of HCC treatment. This is due to bleeding-related hepatic decompensation and overall poorer liver functional reserve. Although BRTO has its disadvantages, its ability to divert blood flow towards the liver is thought to possibly preserve hepatic function. This might make patients with HCC and gastric varices good candidates for BRTO, allowing better possibility for treatment and increased survival. Further long-term studies are needed to evaluate prognosis and complications of BRTO in these patients.
1951 Not All Diverticular Bleeds Are Colonic: A Rare Case of Zenker's Diverticulum Bleeding and Endoscopic Treatment
Authors: Henry George , Allawy Allawy , Matherly Scott , Vachhani Ravi
Published: October 2019

INTRODUCTION:

Zenker's diverticulum (ZD) is a retropharyngeal pouch formed with herniation through Killian’s triangle. The diverticulum is thought to be developed through traction & pulsion but precise mechanism is unknown. Prevalence estimated to be 0.01–0.11%; ZD is predominantly in adults age >60. ZD is associated with dysphagia, halitosis, regurgitation & cough. But very rarely associated with bleeding - only 7 cases reported in the literature. Aspirin irritation is theorized as the etiology, as all reported cases involved aspirin or other anti-platelet medication.

CASE DESCRIPTION/METHODS:

A 73 year-old male with history of obesity, GERD, former smoker, & coronary artery disease presented with hematemesis & hemoptysis. 1 week prior to onset of bleeding, he was hospitalized for STEMI requiring intubation which was traumatic with minor bleeding, & he underwent drug eluting stent placement to the left anterior descending artery. He was discharged home on aspirin & clopidogrel. Patient had awakened due to the sensation of liquid pooling in the back of his throat; he cleared this with a cough & noted the liquid to be gross blood. He then had ongoing small volume hemoptysis & hematemesis. He denied dysphagia, NSAID usage & breakthrough reflux symptoms on daily PPI. On exam, tachycardic to 120s, otherwise vitals normal; diaphoretic & pale but otherwise benign exam. Patient’s hemoglobin had decreased from 13.3 g/dL at discharge to 8.7 g/dL in the ER; also notable for blood urea nitrogen of 45 mg/dL. ENT evaluated initially due to complaint of hemoptysis & recent traumatic intubation. Laryngoscopy revealed blood pooling at the esophageal inlet; this could be cleared voluntarily by patient, but it immediately reaccumulated. Otherwise the oropharyngeal exam was normal. EGD was subsequently performed & this revealed large ZD which was filled with fresh blood. This area was lavaged & small ulcer seen at base; multiple clips were placed with successful hemostasis. Further exam of esophagus, stomach & proximal duodenum revealed no additional source. Patient’s bleeding stopped & tolerated resumption of aspirin & clopidogrel without further incident.

DISCUSSION:

ZD bleeding is an extremely rare event, so treatment modalities may not be readily familiar to most medical staff. We report the third case of ZD bleeding treated with endoscopic hemostasis; all cases have been successful & well tolerated. Traditionally, ZD bleeding has been treated surgically, but this may not be an option in certain populations or situations.
1961 Everolimus-Associated Gastric Antral Vascular Ectasia in a Patient With Advanced Breast Carcinoma
Authors: Richardson Elizabeth B. , Chen Vida , Kaufman Adam B.
Published: October 2019

INTRODUCTION:

Targeted cancer therapies have led to improvement in survival time and quality of life for patients with various cancer types, including advanced breast cancer. Everolimus is a mammalian target of rapamycin (mTOR) inhibitor approved for use in combination with exemestane for advanced hormone-receptor positive, HER2-negative breast cancer in post-menopausal women. While typically well-tolerated, a few cases of upper gastrointestinal bleeding from gastric antral vascular ectasia (GAVE) associated with everolimus have been described, primarily in oncology literature. In our patient, we present a case of gastrointestinal bleeding due to GAVE during treatment with everolimus. Given the clinical consequences of this adverse effect, gastroenterologists must maintain awareness of the associated risk of gastrointestinal hemorrhage and approach to treatment in patients treated with this agent.

CASE DESCRIPTION/METHODS:

Our patient is a 64-year-old female with stage III left breast invasive ductal carcinoma (HER2-negative, estrogen receptor positive, progesterone receptor positive). She underwent left lumpectomy, adjuvant doxorubicin and cyclophosphamide, paclitaxel, and radiation. Follow-up revealed bony metastases and right upper lobe pulmonary metastatic disease. She was initiated on exemestane and everolimus. Three weeks later, she presented with severe weakness and dyspnea. Rectal examination with dark hemoccult positive stools. Laboratory findings revealed Hgb of 6.0 g/dL. An upper endoscopy showed no source of bleeding. The patient responded to blood transfusions and Hgb stabilized. One month later, the patient represented with symptomatic anemia. A repeat upper endoscopy revealed blood with diffuse gastric antral oozing consistent with GAVE. She was treated with argon plasma coagulation (APC), and everolimus was discontinued. The patient stabilized after endoscopic therapy and was discharged after recovery.

DISCUSSION:

Gastrointestinal bleeding due to GAVE while undergoing treatment with everolimus is an uncommon event with an unknown mechanism. Review of current literature shows that few similar cases have been previously reported. Our patient responded well to therapy with APC. However, progression to life-threatening bleeding with poor response to endoscopic therapy has been described. As use of everolimus increases, we are more likely to encounter gastrointestinal bleeding due to GAVE. Clinicians should remain alert to the risk of severe bleeding and the utility of APC in these patients.
1966 Jejunal Submucosal Hemangioma as a Cause of Massive Gastrointestinal Bleeding: A Case Report
Authors: Numan Laith , Elkafrawy Ahmed A. , Tomaw Andrew , Campbell Donald R.
Published: October 2019

INTRODUCTION:

Small intestinal hemangiomas are uncommon tumors that usually present with gastrointestinal bleeding (GIB). Hemangiomas account for only 0.05% of all intestinal tumors. The most common location in the small intestine is the mid-jejunum. Diagnosis, detection, and treatment can be challenging and may require surgery.

CASE DESCRIPTION/METHODS:

An 81-year-old female presented to the emergency department with a one-week history of melena, associated with fatigue and palpitations. She denied hematemesis, hematochezia, NSAIDs use, or the use of anticoagulants or antiplatelet agents. Her vital signs were stable, and her physical examination was unremarkable except for lower limb edema. Hemoglobin was 4.7 g/dl, which was lower than her baseline of 8 g/dl. The patient was transfused to maintain her hemoglobin above 7 g/dl, and a proton pump inhibitor infusion was initiated. Esophagogastroduodenoscopy was performed, and benign-appearing and non-bleeding polyps were detected in the gastric fundus and body. Colonoscopy did not detect significant abnormalities other than moderate diverticulosis, internal hemorrhoids and old melenic liquid throughout the colon but no active bleeding. Due to continued blood transfusion requirements, a video capsule endoscopy was performed, and active bleeding was detected. Push enteroscopy was performed, and a polypoid nodule with central umbilication and red spot was detected in the proximal jejunum [Figure 1]. The lesion was biopsied, and post-biopsy bleeding developed. Hemostasis was achieved by injection of epinephrine (1:10000 concentration) and application of three hemoclips. Subsequently, the patient underwent a laparoscopic segmental jejunal resection. Histologic examination of the resected specimen demonstrated a jejunal submucosal hemangioma with surrounding hemorrhage, an organizing hematoma, and no evidence of dysplasia or malignancy.

DISCUSSION:

Submucosal hemangiomas are a rare cause of GIB. They can present with melena and severe anemia. As the most common site is mid-jejunum, it is difficult to detect submucosal hemangiomas. In this case, the lesion was detected by video capsule endoscopy and was reached by push enteroscopy. Surgery is usually required for a definitive diagnosis and definitive treatment.
1969 Splenic Artery Pseudoaneurysm Presenting as GI Bleed: A Diagnostic Conundrum
Authors: Zahir Fathima Z. , Mehta Amit , Wan David
Published: October 2019

INTRODUCTION:

The splenic artery is a common site of visceral artery pseudoaneurysms following the aorta and iliac arteries. It is a rare complication of pancreatitis (52% of cases), abdominal trauma, post-op complications and peptic ulcer disease. This report discusses a patient with recurrent pancreatitis, admitted for upper GI bleed who was found to have a SAP.

CASE DESCRIPTION/METHODS:

A 25-year-old man with history of recurrent pancreatitis complicated by pseudocyst status post cyst-gastrostomy, presents with 1 week of fatigue, dyspnea and a sensation of “fluids sloshing around” in his abdomen. He noted dark black stools, and had an episode of hematemesis. There was no blood per rectum. Hemoglobin was 6.5 and he was poorly responsive to transfusions. A CTAP revealed a 10 × 4 × 7 mm pseudoaneurysm arising off the proximal splenic artery without active arterial bleed. He was thought to have a brisk upper GI bleed, right-sided colonic bleed or a fistula between the GI tract and splenic artery. An EGD was aborted as it revealed >500cc of blood in the gastric body, after which the patient underwent emergent IR coil embolization of the SAP via the femoral artery. The patient received a total of 6 units of pRBCs, 1 unit of FFP and platelets each during his hospital course. He remained hemodynamically stable off vasopressors, with repeat hemoglobin of 8.

DISCUSSION:

Recurrent pancreatitis causes enzymatic digestion of the splenic arterial wall, leading to elastic tissue fragmentation, resulting in SAP formation. It is also hypothesized that a long-standing pseudocyst (as in the case of our patient) can induce SAP due to vascular erosion from enzymes within the pseudocyst. While ∼2.5% of cases are found incidentally, most reported cases present with abdominal pain, GI bleed, hemosuccus pancreaticus and hematemesis. A patient with recurrent pancreatitis presenting with persistent anemia or GI bleed without obvious explanation should be managed with a high clinical index of suspicion for SAP. SAPs carry a 35% risk of rupture, and must be promptly managed due to mortality rates reaching 90% if left untreated. While it is challenging to diagnose SAP that presents as GI bleed, the patient’s history of recurrent pancreatitis increases the likelihood of SAP. Once the SAP is detected via imaging, the exact location, size and risk of rupture must be communicated to perform the correct form of treatment, with an aim to prevent life-threatening bleeds, and preferably preserve the spleen for its immunologic functions.
1975 Not Your Typical GI Bleeding: Gastrointestinal Involvement in Systemic Amyloidosis
Authors: Zhang Danmei , Buffie Charlie , Martin Tracey , Wan David
Published: October 2019

INTRODUCTION:

Systemic amyloidosis is a rare disease that occurs preeminently in the elderly and can affect different kind of organ systems depending on the locality of amyloid build-up. Most typically fibril formation causes damage to the kidney and heart. Here, we report the case of a man with systemic amyloidosis and sudden onset of Hematochezia.

CASE DESCRIPTION/METHODS:

A 90 y/o male with a history of chronic heart failure due to amyloidosis of unknown origin, CAD, AFib, HTN, HLD, OSAS, peripheral vascular disease, CKD and diverticulosis presented to the ED with one episode of bright red blood per rectum and microcytic anemia. On arrival patient did not have any abdominal pain, nausea, vomiting, or diarrhea. He continued to have several bloody episodes. Rectal exam showed bright red blood with clot and hard brown Bristol 1 stool balls without blood. Initial work up including CBC, CMP, and coags was notable for Hb 9.7 g/dl, Plts 137 × 10(3)/uL, Troponin 0.19 ng/mL, PT 36.6s, and INR 2.8. The patient received IV fluids and 3 units of RBCs, blood thinners and anti-platelet medication were held, and patient was prepped for colonoscopy. Endoscopy showed diffuse, friable, patchy, hemorrhagic mucosa in the transverse colon, hepatic flexure, ascending colon, and cecum, consistent with amyloid. Diverticulosis was confirmed with no evidence of active bleeding. No endoscopic interventions were performed given minimal benefit and risk of high rebleeding.

DISCUSSION:

There are about 30 different types of amyloidosis with a varying spectrum of clinical presentation.[i] In a retrospective study 3% of patients with amyloidosis had biopsy proven involvement in the GI tract.[ii] Intestinal involvement usually presents clinically with either GI bleeding, malabsorption, protein-losing gastro-enteropathy, or chronic gastrointestinal dysmotility. Given his cardiac and abdominal history and presentation with lower GI bleeding differential diagnosis were initially drawn to diverticular bleeding versus ischemic colitis. In this case, the colonoscopy results and pre-condition of amyloidosis were attributed to be the cause of hematochezia. Biopsies were not collected given bleeding risk and low impact on further management.