Friable Mucosa Research Articles

Primary Neuroendocrine Tumor of the Ileostomy Stoma on 68Ga-DOTATATE PET/CT

A 75-year-old man presented with bleeding ileostomy stoma 20 years after total colectomy and end ileostomy for chronic ulcerative colitis. On physical examination, the stoma was mass-like and firm with friable mucosa. Wedge biopsy of the ileostomy stoma revealed well-differentiated neuroendocrine tumor (intermediate grade). Ga-DOTATATE PET/CT showed mass-like focal radiotracer uptake at the ileostomy site without radiotracer-avid lymphadenopathy or distant metastatic disease. No additional sites of neoplasm in the gastrointestinal tract were further identified by endoscopy. The diagnosis of isolated primary neuroendocrine tumor of the ileostomy stoma was confirmed, an extremely rare entity.

Severity of acute gastrointestinal graft-vs-host disease is associated with incidence of bloodstream infection after adult allogeneic hematopoietic stem cell transplantation.

Infections are the most common cause of non-relapse mortality in adult allogeneic hematopoietic stem cell transplant (allo HSCT) recipients. Acute gastrointestinal graft-vs-host disease (GI GVHD) often leads to friable mucosa as well as treatment interventions which can increase risk of infection. Our primary objective was to describe the relationship between increasing grades of acute GI GVHD and incidence of bloodstream infections (BSI). We reviewed 441 adults who underwent allo HSCT from 2011 to 2017 and were clinically diagnosed with GI GVHD, non-GI GVHD, or no GVHD based on the modified Glucksberg scale within the first 100days of transplantation. The maximum grades of acute GI GVHD and non-GI GVHD were used in the analysis. BSI was defined based on the presence of a blood culture positive for bacteria or fungi and treatment with antibiotics. The incidence of BSI within the first 180days of transplantation was estimated with the cumulative incidence method. Fine and Gray regression was used to assess association between clinical grade of acute GI GVHD and BSI risk, adjusting for grade of non-GI GVHD and for other significant baseline patient risk factors for BSI identified by multivariable analysis. Results are shown as hazard ratio (HR) and 95% confidence interval (CI). A similar analysis was conducted in 130 patients with histologic grade of acute GI GVHD. Overall BSI incidence by day 180 was 32%; gram-negative bacilli were the predominant organisms, followed by gram-positive cocci and fungi. Patients with grade 4 acute GI GVHD had higher risk of BSI as compared to patients with no GI GVHD (HR 2.98, CI 1.65-5.37, P<.001), while those with grade 3 acute GI GVHD had similar BSI risk (HR 0.89, CI 0.36-2.21, P=.81). Grade of GI GVHD had no association with risk of non-BSI. Results were similar in patients with histologic grade acute GI GVHD. Patients who developed BSI or non-BSI had significantly higher overall mortality risk compared to those without infectious complications (HR 2.52, CI 1.92-3.31, P<.001 for BSI; HR 1.60, CI 1.20-2.13, P=.001 for non-BSI). Grade 4 acute GI GVHD is associated with a higher risk of BSI, which is in turn associated with a higher risk of overall mortality in this population. Understanding the relationships between acute GI GVHD, BSI, and overall mortality can guide future treatment strategies for adult allo HSCT recipients.

An interesting pill to swallow

A 60-year-old woman presented with dysphagia and weight loss. Medical history was significant for oral and vulval lichen planus. Barium swallow and CT scanning revealed no abnormality. Oesophago-gastro-duodenoscopy demonstrated an...

225. Bloodstream Infections in Adult Allogeneic Stem Cell Transplant Recipients with Acute Gastrointestinal Graft-vs. -Host Disease within the First 180 Days Post-Transplantation

BackgroundInfections are the most common cause of non-relapse mortality in adult allogeneic stem cell transplant (allo SCT) recipients. Acute gastrointestinal graft-vs.-host disease (GI GVHD) often leads to friable mucosa and interventions increasing infectious risk. We describe the relationships between increasing grades of acute GI GVHD and incidence of bloodstream infections (BSI) at our institution.MethodsWe reviewed 441 adults who underwent allo SCT from 2011 to 2017 and were diagnosed with GI GVHD, non-GI GVHD, or no GVHD based on the Modified Glucksberg Scale within the first 100 days of transplant. The maximum grades of GI GVHD and non-GI GVHD were used in the analysis. A BSI episode constituted a blood culture positive for bacteria or fungi and antibiotic treatment. The incidence of BSI within the first 180 days of transplantation was estimated with the cumulative incidence method.ResultsOverall BSI incidence by day 180 was 32%; Gram-negative bacilli were the predominant organisms. Adjusting for grade of non-GI GVHD, patients with acute grade 4 GI GVHD had higher risk of BSI as compared with patients with no GI GVHD (HR 3.02, P < 0.001), while those with grade 3 GI GVHD had similar risk (HR 1.01, P = 0.98). Patients with grade 1 or 2 GI GVHD demonstrated lower BSI risk compared with those with no GI GVHD (HR 0.48, P = 0.015; HR 0.44, P = 0.08, respectively). Results were similar after adjusting for patient- and transplant-related risk factors for BSI. Grade of GI GVHD had no association with non-BSI risk. Patients who developed BSI or non-BSI had significantly higher overall mortality risk compared with those without infectious complications (HR 2.52, P < 0.001 for BSI; HR 1.60, P = 0.001 for non-BSI).ConclusionAcute grade 4 GI GVHD may reliably indicate higher BSI and overall mortality risk in this population. Understanding the relationships between acute GI GVHD and BSI can guide future treatment strategies for adult allo SCT recipients. Disclosures All authors: No reported disclosures.

A CASE REPORT: EOSINOPHILIC CYSTITIS PRESENTED WITH DEEP VEIN THROMBOSIS

A 76-year-old man presented with gross hematuria and reported the use of anticoagulant for deep vein thrombosis (DVT). Blood tests revealed eosinophilia and thrombocytopenia. Urine cytology revealed a class I specimen with a few eosinophils in the urine. We performed cystoscopy, which revealed bladder masses with friable mucosa diffusely throughout the bladder. Magnetic resonance imaging revealed possible invasion of the bladder muscle by the masses. We performed transurethral resection of the bladder masses, and histopathological examination revealed eosinophilic infiltration of the bladder wall stroma without cancerous tissue. Therefore, the patient was diagnosed with eosinophilic cystitis.Eosinophilia and thrombocytopenia promptly resolved, and the bladder masses disappeared following the administration of prednisolone for eosinophilic cystitis. DVT also improved without recurrence of eosinophilic cystitis.

2507 Amoebic Liver Abscess With Synchronous Proctitis—Presenting With Massive Lower Gastrointestinal Bleeding: A Case Report of a Rare Presentation of Amebiasis

INTRODUCTION: Amoebic colitis and liver abscess caused by Entamoeba histolytica is one of the most important enteropathogen, leading to 40-73 per 100,000 deaths annually worldwide.1,2 Transmission generally occurs by fecal-oral route and during male homosexual activity.3 Colonic involvement was seen in 58% patients with amoebic liver abscess, but only 7% presents with diarrhea and bleeding.4 CASE DESCRIPTION/METHODS: A 25-year-old MSM patient with newly diagnosed HIV infection had persistent low grade fever and diarrhea 3-4 times/day for 1 month. He sometimes noticed a small amount of fresh blood in the stool and had mild epigastric discomfort for 1 week. He had worsening abdominal pain, radiating to back and passed 1000 mL fresh blood per rectum. Physical examination showed fever (38.9oC), pallor and markedly enlarged liver with tenderness. Lab showed hemoglobin 6.1 g/dl, white blood cell count 25350 cell/ul (N 89%, L 4%, M 7%), total/direct bilirubin 1.8/1.1 mg/dL, SGOT/SGPT 353/111 U/L, albumin/globulin 2.7/6.6 g/dL, ALP 436 U/L. Colonoscopy showed a 3-cm hemi-circumferential ulcer covered by blood clots and exudative materials with friable mucosa at rectum (Figure 1). Biopsy was done at the ulcer. Abdominal CT showed a 15-cm rim-enhancing cystic lesion with internal septation occupying right liver lobe. Capsule disruption at segment VIII/V anterior aspect of liver was noted (Figure 2). Percutaneous drainage was done and found markedly turbid gray pus 500 ml. Histopathologic findings revealed severe active proctitis with ulcer and few trophozoites ingested red blood cells on the surface, compatible with amoebic proctitis (Figure 3a). The pus aspirated from the abscess showed Charcot Leyden crystals (Figure 3b). Serum for E. histolytica antigen and PCR were both positive. The final diagnosis was amoebic liver abscess with proctitis. The patient was treated with metronidazole for 2 months, with a decreased size of abscess on follow-up CT. No recurrent bleeding occurred. DISCUSSION: Although synchronous colonic lesions in amoebic liver abscess are present in over 50% patient, diarrhea and bleeding are uncommon, without unclear reasons. Caecum is the most commonly affected site (70%). Left sided ulcers are seen in elderly and those presenting with diarrhea. Oral or intravenous metronidazole or tinidazole leads to rapid clinical improvement of invasive amoebic colitis and liver abscess. Large abscess (&gt;7.7 cm) with abnormal liver tests were predictive of drainage intervention.

3235 Black Stomach: A Rare Clinical Entity in a Patient With Recurrent Primary Sclerosing Cholangitis With Cirrhosis

INTRODUCTION: Acute gastric necrosis is rarely encountered given the stomach's rich vascular distribution and collateral circulation. Reported causes of gastric necrosis include gastric outlet obstruction, intrathoracic herniation, ingestion of caustic substances, anorexia nervosa and bulimia, and systemic hypotension. We present a case of “black stomach” secondary to persistent shock in the setting of end-stage liver disease. CASE DESCRIPTION/METHODS: A 33-year-old female with a history of primary sclerosing cholangitis status post orthotopic liver transplant in 2017 was initially hospitalized for pneumonia complicated by worsening graft function (MELD 38). Liver biopsy confirmed recurrent PSC with cirrhosis. Her course deteriorated after developing multiple episodes of coffee-ground emesis and melena requiring pressors. Initial EGD showed mild portal hypertensive gastropathy and two, 5 mm clean-based ulcers in the gastric antrum. No esophageal varices were visualized. Despite medical therapy, her melena and hypotension continued, leading to acute renal failure requiring CVVH. Repeat EGD two days later showed an adherent clot in the gastric fundus and severe portal hypertensive gastropathy with spontaneous oozing. Despite supportive measures, she continued to have melena. A third EGD showed a large blood clot in the fundus that was unable to be removed. Friable mucosa was noted throughout, as well as a non-healing, clean-based antral ulcer. Two days later, a fourth EGD revealed mucosa in the fundus and proximal body that appeared black and diffusely necrotic with sloughing of mucosa, with normal mucosa distally. The patient was not a candidate for IR embolization, TIPS procedure or surgery. One week later, she decompensated and died of septic shock from VRE bacteremia. DISCUSSION: Our case demonstrates that persistent gastric ischemia in the setting of shock and underlying end-stage liver disease results in gastric necrosis noted endoscopically over the course of a week. It is possible that the patient's underlying decompensated graft cirrhosis predisposed her to developing segmental gastric necrosis and “black stomach” in the area supplied and drained by the left gastric vessels, which can be affected by shock and portal congestion. Despite aggressive measures and supportive care, gastric necrosis carries a high morbidity and mortality. Therefore, a high index of clinical suspicion is required to make an early diagnosis in order to guide potential therapeutic interventions in such critically ill patients.

2749 Looks Like a GI Bleed, Think Like a Gastroenterologist: A Case of Recurrent Bleeding in a Patient With Billroth II Operation

INTRODUCTION: Anastomotic gastric adenocarcinoma (GAC) following distal gastrectomy Billroth II for peptic ulcer disease (PUD) has long been recognized but remains poorly studied. CASE DESCRIPTION/METHODS: A 65-year-old male with history of PUD status post Billroth II in 1991 presented with multiple episodes of melena and abdominal pain. EGD revealed friable gastric mucosa with oozing ulcers on the gastric side of the gastrojejunal anastomosis (GJA) (Figure 1a–c) and severe bile reflux. Stomach biopsies were negative for H. pylori or other pathology. Patient was subsequently admitted four more times that year for similar symptoms, each time presenting with symptomatic anemia that resolves with therapy, and EGD showing superficial erosions near the GJA. It was suspected however, that the initial biopsies were likely taken from areas far from the actively bleeding sites. Therefore, the GI team insisted on an outpatient EGD when the patient was asymptomatic to accurately investigate the GJA. After multiple missed appointments, he had an outpatient EGD (Figure 1d) with biopsies of the friable mucosa positive for GAC, and eventually underwent Roux-en-Y gastrectomy with esophagojejunostomy. Biopsy of the mesenteric nodules confirmed the diagnosis of moderately differentiated Stage IIIA GAC. Chemoradiation therapy was initiated, but patient left against medical advice and ended up in hospice care eight months later. DISCUSSION: We present a patient with persistent bleeding ulcers and symptomatic anemia 25 years after a Billroth II procedure, who despite multiple endoscopic evaluations with stomach biopsies, was not diagnosed on time. Eventually, the correct diagnosis of Stage III primary GAC was made after an outpatient EGD with targeted biopsies of the area associated with recurrent bleeding. Given the negative biopsies, the persistent gastric ulcers were thought to be complications of Billroth II with a short limb leading to bile reflux, or due to patient’s poor compliance and follow up. However, it was recognized that the patient had a higher risk of GAC as he was 15-20 years after Billroth II, and more importantly, that the inpatient EGD biopsies were not of the actively bleeding area of interest. Our patient presented after a long asymptomatic interval with symptoms initially misinterpreted as benign. It is therefore imperative to maintain a high suspicion of gastric malignancy for these patients to encourage earlier diagnosis.

1531 Failed Fecal Microbiota Transplantation for Fulminant C. difficile Colitis With Toxic Megacolon

INTRODUCTION: Fulminant disease develops in 3-8% of patients with Clostridioides difficile infection (CDI) and may progress to toxic megacolon (TMC), the latter of which is typically managed surgically but has high mortality. Although fecal microbiota transplantation (FMT) is a well-established therapy for recurrent CDI, its utilization in cases of TMC is sparsely documented. Here we describe our experience with a patient who elected FMT over surgery and their clinical response. CASE DESCRIPTION/METHODS: A 74-year-old African-American woman with a recent perforated duodenal ulcer with surgical repair was transferred to our medical ICU (MICU) with septic shock from an initial CDI. She was previously treated with PO vancomycin, which was switched to fidaxomicin in the setting of continued diarrhea. On admission, she was afebrile with hypotension, tachycardia, and tachypnea. Labs showed leukocytosis, thrombocytopenia and an AKI. Physical exam revealed an acutely ill appearing woman with a diffusely tender, distended and tympanic abdomen. Fidaxomicin was stopped and PO/PR vancomycin and IV metronidazole were initiated. On day 3 of admission, the patient clinically deteriorated and abdominal x-ray demonstrated increased bowel distention. TMC was diagnosed and surgery was consulted. Colectomy was offered but she declined the procedure. FMT was discussed as an alternative, off-label therapy and she agreed to proceed with placement via colonoscopy. The elevated risk of perforation was deemed acceptable by the patient. Colonoscopy revealed pseudomembranes, deep ulcers, and friable mucosa. Donor stool was deployed at the hepatic flexure and the scope was carefully withdrawn. Over the 48 hours post-procedure, the patient had hemodynamic improvement and decreased pressor requirement. Her stool output decreased and abdominal exam improved. By 72 hours, however, the patient's condition again worsened and she elected palliative care and died shortly thereafter. DISCUSSION: While colectomy is standard treatment for fulminant CDI with TMC, FMT may represent a non-surgical alternative in selected cases. We describe transient, but profound, clinical improvement in patient parameters for 48 hours following FMT. The mechanism of benefit may be multifactorial, including repopulation of normal colonic flora and mechanical colonic decompression. Although our patient died, her case provides a framework for clinicians to consider this therapy and the expected response.

2525 A Case of IgA Vasculitis Diagnosed With Small Bowel Biopsy

INTRODUCTION: Immunoglobulin A (IgA) vasculitis is an immune-mediated condition that primarily targets small vessels. Presentation may vary- colicky abdominal pain, palpable purpura, acute arthritis, or nephritis. Adult annual incidence is 0.8-1.8/100,000. In adults, abdominal pain is rarely the presenting symptom. We report a case that presented with abdominal pain and was diagnosed with IgA vasculitis via duodenal biopsy. CASE DESCRIPTION/METHODS: A 60 year old male presented with acute onset severe periumbilical pain and watery diarrhea for several days. Pain was associated with vomiting and worsened after meals. Physical examination revealed marked periumbilical and right lower quadrant tenderness. Other review of systems and physical exam findings were unremarkable. Laboratory tests were remarkable for mild leukocytosis with neutrophilic predominance and elevated C-reactive protein. CT scan of the abdomen/pelvis showed significant patchy small bowel thickening with surrounding inflammatory changes. Small bowel enteroscopy showed edematous, purpuric and friable mucosa in the duodenum and proximal jejunum with stigmata of recent bleeding. Biopsies were obtained. Immunostaining for IgA was positive in the lamina propria, suspicious for small bowel IgA vasculitis. Shortly after that, he developed palpable purpura on upper and lower extremities. Punch skin biopsy confirmed IgA vasculitis. He was started on taper of systemic steroids, which lead to the resolution of skin and abdominal vasculitis within a few days. Currently, patient is in remission on rituximab maintenance therapy. DISCUSSION: In cases of abdominal involvement, IgA vasculitis has a predilection for small intestine. The classic endoscopic findings are diffuse mucosal reddening with hemorrhagic erosions and hematoma-like protrusions. Treatment is dependent on severity of vasculitis activity. For moderate to severe disease, systemic corticosteroids and analgesics are the mainstay of treatment. The diagnosis of IgA vasculitis is challenging, especially if abdominal pain precedes other manifestations. This case highlights the diagnostic value of early endoscopy in patients suspected of developing IgA vasculitis.

2109 Metastatic Crohn’s Disease: A Case of a Rare IBD-Related Entity at Initial Presentation

INTRODUCTION: Metastatic Crohn’s disease (MCD) is a rare cutaneous entity of Crohn’s disease that mandates specific histopathologic findings and exclusion of other granulomatous diseases and infectious processes for a diagnosis. Due to its heterogeneous clinical presentation, MCD poses a diagnostic challenge for providers. We present a case of MCD in a woman with previously undiagnosed Crohn’s disease at initial presentation. CASE DESCRIPTION/METHODS: A 68-year-old woman presented to the Emergency Room with an acute onset of left-sided abdominal pain. She also noted a 6-month history of watery diarrhea with up to 8 bowel movements daily, describing them as bloody with a jelly consistency. On examination a painful 8 cm ulcer within her intergluteal fold extending to the anus was observed. Other “knife-like” ulcerations were noted of the left inframammary breast, under the pannus and bilaterally in the inguinal folds. She underwent a flexible sigmoidoscopy which demonstrated edematous and friable mucosa with a cobblestone appearance extending from the descending colon to the rectum. Mucosal biopsies and serologic testing were both diagnostic of Crohn’s disease. Punch biopsy of the pannus ulcer showed non-caseating granulomas and was negative for mycobacterial or fungal organisms, confirming the rare diagnosis of MCD. The patient was treated with systemic and topical steroids with subsequent symptomatic improvement of both her Crohn’s flare-up and cutaneous ulcerative lesions. DISCUSSION: MCD is a rare dermatologic manifestation characterized by its non-caseating granulomatous histopathology in non-contiguous areas from the gastrointestinal tract. Typically the GI disease precedes the skin disease for at least six months, however the skin manifestation can be the first sign of Crohn’s disease. The diagnosis should be suspected when “knife-like” ulcerations are seen on physical exam in a patient with known or suspected Crohn’s disease. Exclusion of other granulomatous diseases that could mimic MCD is required to confirm the diagnosis. Early recognition of this disease may ultimately spare unnecessary tests or treatments.

1573 Ixekizumab-Induced Gastritis and Colitis in an Elderly Female With Plaque Psoriasis

INTRODUCTION: Psoriasis and inflammatory bowel disease (IBD) share common pathogenesis pathways including cytokine mediated inflammation. Interleukin-17 (IL-17) monoclonal antibodies such as ixekizumab have demonstrated excellent results in moderate to severe plaque psoriasis and psoriatic arthritis. Antagonism of IL-17 has been demonstrated in animal models to induce or worsen existing inflammatory colitis. We hereby present a case of ixekizumab-induced gastritis and colitis in a 63-year old Caucasian female with severe plaque psoriasis successfully treated with prednisone. CASE DESCRIPTION/METHODS: A 63-year old Caucasian female with history of severe plaque psoriasis and peptic strictures presented with severe bloody diarrhea, generalized abdominal pain, and tenesmus few weeks after receiving 3 doses of ixekizumab. She had no personal or family history of IBD. Her medications included 81-mg ASA, omeprazole, metoprolol, cetirizine and levothyroxine. She denied NSAID use. A colonscopy 2-years prior showed two tubular adenomas, and a gastroscopy 3 months prior to ixekizumab therapy was normal. Her diagnostic evaluation revealed (a) normal CBC, kidney function and liver chemistries, (b) negative stool cultures, microscopy and C. Difficile testing, (c) a gastroscopy demonstrating diffuse gastritis involving the body and antrum (d) a flexible sigmoidoscopy demonstrating a diffuse area of atrophic, eroded and friable mucosa with contact bleeding and thickened mucosal folds in the recto-sigmoid colon. Gastric and colonic biopsies demonstrated focal mucosal erosions with architectural distortion concerning for a drug induced gastritis and colitis. H. Pylori testing was negative. Ixekizumab was discontinued and treatment with IV steroids was started. Symptom resolution was noted by day five of therapy and she was converted to an oral steroid taper. DISCUSSION: The temporal association, the histology and the improvement with discontinuation of the medication strongly support the diagnosis of a drug induced colitis. This case is unique in the sense that it is the first in the literature to report ixekizumab-induced gastritis and colitis. Whether the patient will require long-term immunosuppression and will manifest later with IBD is to be observed. Despite the rarity of colitis associated with IL-17 inhibitors, counseling patients on this severe adverse effect is integral to the discussion between specialists and their patients prior to initiating therapy.

2535 Localized AL-Type Intestinal Amyloidosis Presenting as Refractory Iron Deficiency Anemia and Right Lower Quadrant Abdominal Pain

INTRODUCTION: Amyloidosis is characterized by extracellular deposition of abnormally folded proteins creating insoluble fibrils, which disrupt tissue structure and function. Amyloidosis can be either systemic or localized. Localized amyloidosis is defined by the production of precursor proteins in the same location as amyloid deposition. We present a case of biopsy-proven localized AL intestinal amyloidosis. CASE DESCRIPTION/METHODS: A 91-year-old female with a past medical history significant for hypertension and iron deficiency anemia not improving with oral iron presented with progressively worsening dyspnea on minimal exertion, with diffuse weakness and fatigue. She denied any NSAID use. Hemoglobin on admission was 3.8 g/dL, improving to 6.4 g/dL after transfusion of 3 units of packed red blood cells. Upper endoscopy showed very friable mucosa with contact bleeding in the duodenum, along with patchy areas of abnormal mucosa in the 2nd portion (Figure 1). Duodenal biopsies were consistent with amyloidosis based on Congo red and crystal violet stains. Liquid chromatography tandem mass spectrometry was performed on peptides extracted from the specimen and indicated AL (lambda)-type amyloid deposition. Cardiac MRI showed no evidence of infiltrative heart disease or amyloid deposition. Bone survey showed no lytic lesion, and a marrow biopsy showed no morphologic evidence of plasma cell neoplasm with normal karyotype. Urine immunofixation electrophoresis showed no abnormalities. Urine and serum protein electrophoresis showed no monoclonal protein. With no evidence of systemic amyloidosis, diagnosis of localized intestinal amyloidosis was made. No systemic therapy was indicated. Patient was treated with IV iron transfusions. At a subsequent admission, she presented with subacute right lower quadrant pain. CT abdomen/pelvis with oral and intravenous contrast showed thickening of the distal small bowel with shouldering (Figure 2). Lesion was presumed to be secondary to intestinal amyloidosis. Patient refused further invasive interventions. DISCUSSION: Localized AL-type intestinal amyloidosis is rarely diagnosed. Common symptoms are non-specific and can include erosion, ulceration, bleeding, malabsorption, intractable diarrhea, obstruction or ischemia. This patient presented with recurrent symptomatic iron deficiency anemia refractory to oral iron repletion. Intestinal amyloidosis should be considered in similar presentations.

1413 Twelve-Year-Old Male With Esophageal Dysphagia: A Diagnostic Dilemma!

INTRODUCTION: Esophageal dysphagia is defined as any difficulty or abnormality of swallowing with delay in transit of solids or liquids in the esophageal phase. We present an interesting case of a young male evaluated for esophageal dysphagia and failure to thrive who was, after an extensive workup, found to have an esophageal duplication cyst. CASE DESCRIPTION/METHODS: A 12-year-old male was transferred from a local hospital with a 4-week history of sub-sternal pain, worsening dysphagia, odynophagia, a sensation of “food stuck in his chest” and an 8-pound weight loss. He was seen by his primary physician and started on ranitidine for possible gastrointestinal reflux disease (GERD) without improvement in his symptoms. He was admitted a week later due to worsening symptoms, new onset nausea, non-bloody, non-bilious vomiting and a fever (102.5 F). Due to persistent symptoms, an upper gastrointestinal series with contrast was performed, which was concerning for an esophageal diverticulum, an esophageal manometry and ultimately, esophagogastroduodenoscopy (EGD). An EGD revealed congested and friable mucosa throughout the esophagus, and a large opening in the posterior aspect of the middle esophagus. Due to inability to intubate this opening with a regular size endoscope, a neonatal upper endoscope was used. The opening was intubated, and the esophageal cyst was visualized (Video 1). Histology revealed normal basal thickness, papillary congestion and focal hemorrhage in the proximal esophagus. Due to parental preference, the patient was referred to another institution for a second opinion, where patient received fenestration of the cyst and is doing well. DISCUSSION: Esophageal duplication cysts are congenital abnormalities that arise during embryologic development and uncommonly present as dysphagia in an adolescent. Within the GI tract, only 2% arise from the esophagus. Duplication cysts often present as a diagnostic dilemma and thus, a high index of suspicion is needed. If a patient is not responding to standard therapy for esophageal dysphagia or has recurrent respiratory symptoms/infections, it may be necessary to pursue imaging or an endoscopic procedure. Alarm signs indicating a need for advanced diagnostics include failure to thrive, iron deficiency anemia, hematemesis, hemoptysis, weight loss or unresponsiveness to medical therapy. Larger multicenter prospective trials are needed to evaluate the utility of endoscopic ultrasound in both diagnostic and therapeutic management of esophageal duplication cysts.

1778 Too Stubborn to Contract: A Case of End Stage Achalasia Presenting as a Sigmoid Esophagus

INTRODUCTION: Sigmoid esophagus is a form of end stage achalasia characterized by massive dilatation and tortuosity of the esophagus. It is associated with poor response to conventional treatment and poses a significant challenge in the management. We present a case of an elderly female with achalasia who presented with sigmoid esophagus and was not considered a surgical candidate due to comorbidities. CASE DESCRIPTION/METHODS: An 84-year-old female with medical history of achalasia, colon cancer, heart failure and end-stage renal disease, admitted for aspiration pneumonia and respiratory failure requiring mechanical ventilation. Her achalasia was diagnosed three years prior to the presentation and was treated with botulinum toxin injection multiple times. Physical exam showed copious secretions in the oral cavity. Laboratory data showed leukocytosis. Chest CT showed a markedly dilated and tortuous esophagus with 10.2 cm diameter in maximum dimension. Upper endoscopy revealed a dilated and patulous lower esophagus with a tight gastroesophageal junction without any obstructing mass. A large amount of food was noted in the entire esophagus which was removed by a Roth net. Achalasia was considered end stage and the patient was deemed not a candidate for surgical treatment of achalasia in view of the comorbidities. A percutaneous gastrostomy tube was placed. DISCUSSION: Achalasia is an esophageal motility disorder characterized by esophageal aperistalsis and failure of the lower esophageal sphincter to relax during deglutition. Sigmoid esophagus is a severe form of achalasia characterized by a tortuous and massively dilated esophagus more than 6 cm that resembles sigmoid colon. Despite the treatment by the conventional methods like surgical myotomy, pneumatic dilation or botulinum toxin, 5% of the patients may develop an end stage achalasia. Dysphagia, regurgitation and recurrent aspiration pneumonia are the main clinical features. Imaging and esophagogram show dilated esophagus. Endoscopy shows tortuous dilated lumen and friable mucosa with food debris. Manometry is usually not needed to diagnose sigmoid esophagus as the esophagogram and endoscopy are diagnostic. Whereas, Heller’s myotomy is the treatment of choice in achalasia, it is regarded inadequate for the treatment of sigmoid esophagus due to operative difficulty, and esophagectomy is considered as the most appropriate option. However, the esophagectomy is associated with 5-10 % mortality and is not an option for patients with multiple comorbidities.

2087 Severe CMV Proctitis as the Initial Presentation of Ulcerative Proctitis

INTRODUCTION: CMV colitis is seen in patients with IBD on long term immunosuppressive therapy; studies show the rate of seropositivity in IBD patients is the same as the general population (∼70%). Due to this there is a concern for reactivation when long term immunosuppressive therapy is initiated. Here we present the case of a patient who presented with CMV colitis prior to initiation of any therapy or diagnosis of IBD; CMV colitis in immunocompetent patients remains fairly rare. CASE DESCRIPTION/METHODS: A 30-year-old male with a history of EoE and PUD presented with seven days of painful hematochezia and constipation; he denied any fevers, however did have chills and cold sweats. He had no history of IVDA, intranasal drug use, anal sex, or risky sexual behaviors. His EoE symptoms were well controlled on PPI. Temperature was 103.2 F, he was tachycardic and tachypneic on presentation. CT revealed fecalization of the small bowel, significant stool burden, and rectal stool ball. He was started on lubiprostone and a bowel regimen with PEG-3350, he passed stool with significant decrease in abdominal distention, however he continued to have rectal pain and hematochezia. Colonoscopy was performed and showed diffuse severe inflammation with erythematous, granular, and friable mucosa in the rectum. He was started on rectal mesalamine and corticosteroid therapy. Biopsies returned showing CMV associated severe ulcerative proctitis without evidence of dysplasia. He was then started on ganciclovir and PICC was placed for 2 weeks of treatment. Repeat HIV and HIV viral load testing were done, both returning negative. On follow up in clinic he reported good control of his symptoms with oral and rectal mesalamine. Flexible sigmoidoscopy showed a rectal scar and significantly improved inflammation, biopsy revealed ulcerative proctitis. DISCUSSION: CMV colitis has been commonly associated with UC patients on immunosuppressive therapy. An increasing body of literature shows the presence of colonic CMV infection in patients with UC on therapy has been associated with decreased response to steroids and other immunosuppressive therapies. Prognosis is poor unless the infection is promptly identified and anti-viral therapy is started. It still remains a rare entity in immunocompetent patients. This raises the question if CMV testing should be done prior to initiation of immunosuppressive therapy in these patients and if CMV testing should be done regularly in patients with refractive UC flares.

2673 Acute Hemorrhagic Gastritis During Treatment With PD-1 Inhibitor Nivolumab for Stage IV Endometrial Cancer

INTRODUCTION: PD-1 inhibitors block immune checkpoints and activate the immune system. They show benefit in treating many advanced cancers, but are also associated with various immune-related adverse effects, including inflammatory diseases of the gastrointestinal (GI) tract. We present a rare side effect of hemorrhagic gastritis. CASE DESCRIPTION/METHODS: A 53-year-old woman with Lynch syndrome and metastatic endometrial cancer presented to our office after two weeks of epigastric abdominal pain associated with nausea and vomiting. Her primary care provider had prescribed pantoprazole and ondansetron and obtained an abdominal ultrasound, which was normal. She had been treated with nivolumab for stage IV endometrial cancer for the preceding three years, and had no evidence of disease after two years of treatment. Sucralfate was prescribed, and an upper endoscopy was scheduled. This showed white plaques in the esophagus and a severely hyperemic stomach with friable mucosa. Stomach biopsies revealed diffusely eroded gastric mucosa with marked acute and chronic inflammation, crypt abscesses, and increased intraepithelial lymphocytes with crypt degeneration and dropout. Esophageal biopsies showed mildly reactive squamous mucosa with scattered intraepithelial lymphocytes and rare eosinophils. Stains for fungal organisms, CMV, HSV, EBV, and H. pylori were negative. Nivolumab-induced acute hemorrhagic gastritis was suspected. After two weeks of prednisone 1 mg/kg daily, her symptoms did not improve. The dose was increased to 2 mg/kg and her symptoms significantly improved within one week. She was then slowly tapered off prednisone without recurrence of her symptoms at three month follow-up. She continues off nivolumab with no plans to resume further treatment by her oncologist. DISCUSSION: Immune checkpoint inhibitors are novel anti-cancer agents with increasingly widespread applications. They are associated with immune-mediated adverse effects, including inflammation of the GI tract. The diagnosis is made through pathologic and endoscopic features in the appropriate clinical context. Standard treatment is prednisone starting at 1 mg/kg, which can be increased to 2 mg/kg, and the immune checkpoint inhibitor should be discontinued. Infliximab may be considered if the disease does not respond to initial therapy. As immune checkpoint inhibitors become more common, it will be important to consider hemorrhagic gastritis in patients on such a medication who present with acute epigastric pain, nausea, and vomiting.

3129 Management of a Massive Peptic Ulcer Bleed With Over-the-Scope Clip

INTRODUCTION: Actively bleeding ulcers located in the posterior duodenal bulb are often difficult to manage with conventional endoscopic treatment. We present a case of a successful use of over-the-scope-clip (OTSC) of a spurting artery after failing multiple standard endoscopic therapies. CASE DESCRIPTION/METHODS: A 60 year-old man with a history of myocardial infarction in 2014 on aspirin and plavix presented with pre-syncopal symptoms and five episodes of melena that started one day prior to admission. The patient denied prior use of anticoagulants and history of gastrointestinal bleeding. Upon presentation, his vitals were stable and initial lab values were as follows: hemoglobin 9.8 g/dL (baseline 15 g/dL), platelet count 342 K/uL, INR 1.2, and BUN 29 mg/dL. He was started on an intravenous proton pump inhibitor. An esophagogastroduodenoscopy showed multiple large cratered ulcers measuring 1-2.5 cm involving most of the duodenal bulb. There was evidence of active bleedingfrom a spurting pulsatile vessel along the posteroinferior wall at the apex of the duodenal bulbnear the sweep (Figure 1). Initial attemptsat hemostasis wereunsuccessful despite injection of 1:10,000 solution of epinephrine andthe use of thehemostatic spray. The use of a coagulation forceps was unsuccessful as well. Given the location of the vessel and mucosal friability, the lesion was not amenable to through the scope clipping. Hemostasis was finally achieved after successful placement of a 12 mm OTSC (Figure 2). In addition, the area was retreated with the remainder of the hemostatic spray (Figure 3). The patient was transferred to the medical intensive care unit where overnight, the hemoglobin decreased from 8.2 g/dL to 7.2 g/dL without overt evidence of bleeding. The patient underwent angiography which did not reveal any active extravasation and empiric coil embolization of the gastroduodenal artery was performed. DISCUSSION: We present a case of a massive peptic ulcer bleed that was difficult to manage with standard treatment based on the large size and posterior bulb location. OTSC is commonly used for severe recurrent bleeding but its role during the index endoscopy is still unclear. OTSC should be considered as a potential first line therapy in bleeding lesions at high risk of standard endoscopic treatment failure.

2734 Immunotherapy-Mediated Hemorrhagic Gastritis After Ipilimumab and Nivolumab Therapy

INTRODUCTION: Combined checkpoint inhibitor immunotherapy with ipilimumab (anti-cytotoxic T-lymphocyte antigen 4 antibody) and nivolumab (anti-programmed cell death receptor 1 antibody) has greatly advanced the treatment of multiple malignancies but is associated with increased immune-related toxicities. Gastrointestinal toxicity is one of the most frequent adverse effects, and while lower GI tract toxicity, such as anti-CTLA-4-mediated colitis, is well known, severe toxicity of the upper GI tract is rare and not well described. We report a case of severe hemorrhagic gastritis in a patient after initiation of ipilimumab and nivolumab therapy for metastatic renal cell carcinoma. CASE DESCRIPTION/METHODS: A 70-year-old man with history of metastatic renal cell carcinoma and recent immune-related myocarditis initially presented with myasthenic weakness after receiving single doses of ipilimumab and nivolumab 5 weeks prior. His presentation was most consistent with seronegative, immune-mediated myasthenia gravis-like syndrome. He was treated with intravenous steroids and plasmapheresis. After 9 days of steroid therapy, he developed large volume melena requiring 4 units of blood despite twice-daily proton pump inhibitor therapy. Endoscopic evaluation revealed diffuse, severe inflammation with hemorrhage characterized by adherent blood and erythematous, friable gastric mucosa in the body, antrum, and prepyloric regions. Hemostatic spray was applied as a temporizing measure to control bleeding. Biopsy specimens demonstrated neutrophilic microabscesses with intraglandular apoptotic bodies, increased lymphocytes and scattered neutrophils in lamina propria, and reactive mucosal features. These findings were compatible with checkpoint inhibitor-induced acute gastritis. Immunohistochemical stains for H. pylori and cytomegalovirus were negative. Despite immunosuppressive therapy with high dose steroids, mycophenalate mofetil, and trial of infliximab, he continued to decline with ongoing anemia and progressive weakness. He was transitioned to comfort measures and died soon afterward. DISCUSSION: To our knowledge, this is the first reported case of severe hemorrhagic, non-infectious gastritis as a rare complication of immunotherapy with ipilimumab and nivolumab. Physicians should be aware that checkpoint inhibitor-induced toxicity of the upper GI tract can occur early after initiation of therapy and have a severe, refractory course. Management includes exclusion of infectious process and immunosuppressive therapy.

1917 Fatal Gastrointestinal Hemorrhage Secondary to Rare Aortoesophageal Fistula in a Patient With Esophageal Adenocarcinoma

INTRODUCTION: Aortoesophageal fistula (AEF) is a rare cause of upper gastrointestinal bleeding which is associated with extremely high mortality despite timely intervention. We present a fatal case of gastrointestinal hemorrhage from AEF in a patient with esophageal adenocarcinoma who had recently undergone esophageal stent placement and chemoradiation therapy. CASE DESCRIPTION/METHODS: A 77 year-old Caucasian man with a past medical history of cirrhosis and TNM stage IIIA hepatocellular carcinoma, status post Yttrium-90 radioembolization in April 2017, presented with progressive dysphagia in January 2018. Patient underwent esophagogastroduodenoscopy (EGD) revealing a partially obstructing, non-bleeding mass at the gastroesophageal (GE) junction (Figure 1) and placement of an esophageal stent. Dysphagia improved post stent placement. Biopsy was consistent with primary adenocarcinoma of the esophagus. He received concurrent chemoradiation therapy with paclitaxel and carboplatin. In April 2018, patient presented to the emergency department with presyncope, hematemesis and epigastric pain. He was hyptotensive with a blood pressure of 88/56 mm Hg and anemic with a hemoglobin of 7.6 g/dL. Repeat EGD was performed with unintentional migration of stent into stomach, revealing friable and ulcerated mucosa in the lower esophagus (Figure 2). Retrieval of the dislodged stent caused the ulcerated mucosa to bleed. Hemostatic clip could not adhere to inflamed mucosa and a stent was placed to minimize bleeding. Interventional radiology was consulted. Fluoroscopy revealed presence of a small aortoesophageal fistula at the site of active bleeding (Figure 3). Hemostasis was achieved with coil embolization. Unfortunately, a few hours later, patient had a recurrence of massive re-bleed and expired. DISCUSSION: Esophageal malignancy is one of the primary causes of AEF. Thoracic radiation as a standalone cause has also been documented in non-esophageal malignancies. Several reports also document that aortic grafts and esophageal stents increase the risk of AEF development in patients who undergo radiation. This case adds to the growing literature that presence of esophageal stent and subsequent radiation compounds risk of AEF development in patients with esophageal tumors. Further studies are warranted for risk stratification. Such patients presenting with hematemesis and syncope need immediate AEF evaluation and emergent intervention.