Melenic Stools Research Articles

Atypical endoscopic finding of colocolic intussusception: case report and literature review

Adult-onset colonic intussusception is a rarely encountered condition that leads to large intestinal obstruction with time. Patients often present with a variety of symptoms that are non-specific making it challenging to arrive at a definitive diagnosis. This is worrying as diagnostic delay could lead to a significant increase in morbidity and mortality. We wish to present and describe a case of an atypical endoscopic finding of colocolic intussusception secondary to ascending colon cancer. Sixty-seven-year-old lady was referred for 1 month's duration of passing melenic stools with mucus followed by a week's complain of hematochezia. Clinical examination and other relevant blood results were unremarkable except for iron deficiency anemia. Initial colonoscopy revealed a large mass within the splenic flexure with inconclusive biopsies. A more detailed colonoscopy repeated the following day revealed a massive, black-to-yellowish lesion within the splenic flexure with no viable mucosa seen. Colonic bezoar was initially suspected, however various endoscopic retrieval methods proved futile. Switching to a slimmer diagnostic gastroscope, the colon was carefully negotiated until a large ulcer was found within the ascending colon, adjacent to the mass' origin. An emergency CT abdomen and subsequently extended right hemicolectomy performed revealed a colocolic intussusception with sealed perforation secondary to an ascending colonic mass acting as an intussusceptum. Histopathology evaluation confirmed an ascending colon adenocarcinoma (pT2N0M0) amidst a background of extensive ischemic changes. Endoscopic descriptions of colonic intussusception are unusual given their rarity. Furthermore, these lesions can mimic a colonic bezoar as a result of fecal accretion and this can ultimately lead to false diagnostic and therapeutic decisions. In such instances, clarification with a CT scan before management decision can potentially avert unnecessary endoscopic intervention and complications.

S2277 Black Esophagus! A Devastating Sequela of Complete Heart Block

Introduction: Acute esophageal necrosis (AEN) or black esophagus is a rare condition arising due to ischemic injury of the esophagus. Usually, it involves the distal portion given its relative hypovascular nature compared to other esophageal segments. Here we highlight a patient found to have hemorrhagic shock secondary to black esophagus after initial presentation for complete heart block. Case Description/Methods: A 75-year-old female presented after a syncopal episode. She was hypotensive on arrival with EKG showing complete heart block. An emergent transvenous pacer was placed given cardiogenic shock with eventual upgrade to permanent pacer. Unfortunately, she decompensated shortly after placement of permanent pacer with new altered mentation. EKG showed an appropriately paced rhythm. Labs revealed sudden anemia with hemoglobin 6.9 g/dL down from 10.1 g/dL. Echocardiogram was negative for pericardial effusion. Pacer site was clean, dry, and intact. Initially, the etiology of her anemia was unclear given lack of overt blood loss. However, the patient began having several bouts of melenic stools with hemodynamic instability requiring vasopressor support. Medication review revealed that the patient had been started on aspirin and clopidogrel the day prior given concerns for acute coronary syndrome. An emergent bedside EGD showed diffuse circumferential panesophageal black mucosa and severely ulcerated stomach and duodenum consistent with ischemic injury. No visible vessel or active bleeding was identified. Unfortunately, the patient continued having melenic stools requiring blood transfusions. However, nuclear medicine bleeding scan could not localize the source of bleed. A goals of care discussion was held with the family who ultimately opted for hospice care. Discussion: Commonly seen as an incidental finding, black esophagus is an exceedingly rare entity with a prevalence of 0.2%. Its pathophysiology is not well understood, but thought to involve a 2-hit sequence where the initial insult predisposes to injury caused by a second insult. In our patient, her initial insult was clearly cardiogenic shock secondary to complete heart block followed by the second insult likely due to the introduction of antiplatelet agents. Unfortunately, treatment is largely supportive and prognosis is poor with mortality rates ranging from 13-35%. As such, clinicians should consider AEN as part of their differential for GI bleed given the potential for devastating consequences.

S2563 Upper GI Bleed Caused by Ampullary AVM

Introduction: GI bleed (GIB) is responsible for 1,000,000+ hospitalizations every year, and a mortality rate of 2-10%. Ampullary AVMs are an uncommon etiology of GIB and difficult from a diagnostic standpoint. We present a case of 77-year-old man presenting to emergency department (ED) with acute shortness of breath (SOB) and chest pain (CP), and dark stools for 4 days, found to have acute GIB caused by ampullary AVM. Case Description/Methods: 77-year-old white male presented to ED with acute SOB and CP. Past medical history included aortic regurgitation s/p valve replacement, atrial fibrillation s/p ablation and watchman, chronic anemia with baseline Hgb of 9, HTN, HFpEF, and ulcerative colitis s/p curative total proctocolectomy and ileostomy with modified Kock pouch procedure. Physical exam was unremarkable aside from dark-appearing ileal pouch output. He was not on anticoagulation and denied Pepto-Bismol use. Abnormal labs included Hgb/Hct of 5.1/16.4, BUN:Cr 37:1.93, and hemoccult positive stool from ileal pouch. Presenting symptoms of anemia (CP, SOB) were consistent with lab findings, concerning for GIB in setting of hemoccult positive stool. He received IV Protonix, Rocephin, and 1u pRBCs for acute blood loss anemia secondary to suspected GIB and was admitted to hospitalist. GI was consulted to do EGD, which showed active bleeding around major papilla, suggesting hemobilia. Subsequent CT A/P with contrast showed no clear etiology of bleed, so nuclear medicine bleeding scan was performed. The scan was unremarkable, and he continued to have melena, requiring 2u of pRBCs. Finally, ERCP was pursued to evaluate for potential biliary source. A normal bile duct (BD) was identified via cholangiogram, measuring 10mm without filling defect. Sphincterotomy was performed, followed by BD sweeping using a stone extraction balloon. No blood clots were noted, making hemobilia less likely. However, slow bleeding from inferior aspect of ampulla was visualized. The site was lavaged and appeared to be ampullary AVM (see Figure). Before ablation of AVM, a PD stent was placed to reduce likelihood of post-ERCP pancreatitis. Following procedure, his Hgb normalized, and he stopped having melenic stools. He continued PPI treatment outpatient and is doing well. Discussion: To our knowledge, no case of GIB caused by ampullary AVM is found in the literature. Thus, this case reports a rare finding of ampullary AVM and provides support for endoscopy as diagnostic approach in such patients.Figure 1.: Ampullary AVM.

An Unusual Complication of Endoscopic Cyanoacrylate Injection for Gastric Varix

Question: A 46-year-old man with Child A alcoholic cirrhosis had received band ligation 2 months ago for bleeding esophageal varices. An interval computed tomography scan demonstrated liver cirrhosis with multiple portosystemic collateral circulations and shunts including a large splenorenal shunt (Figure A). In this episode, he presented with melenic stool with anemic symptoms for 2 days. The initial evaluation revealed blood pressure of 92/50 mm Hg with hemoglobin level of only 6.6 g/dL. After resuscitation, an emergency endoscopic evaluation under conscious sedation demonstrated a large gastric varix type 2 (GOV2) with two white nipple signs (Figure B).

S2355 An Unusual Presentation of a Rare Cause of Lower Gastrointestinal Bleeding: Cecal Dieulafoy’s Lesion Presenting as Melena

Introduction: Dieulafoy’s lesion is characterized as a large tortuous submucosal artery projecting through a small mucosal defect with no evidence of primary mucosal ulceration or erosion. These lesions are uncommonly identified as causes of acute gastrointestinal (GI) bleeding, accounting for only 1-2% of cases. Dieulafoy’s lesions can occur throughout the entire GI tract, most commonly occurring in the stomach (72% of cases) and rarely in the lower GI tract (5% of cases). Typically, lower GI tract Dieulafoy’s lesions present as hematochezia. We report an unusual case of a cecal Dieulafoy’s lesion that presented as melena. Case Description/Methods: A 64-year-old male with a relevant past medical history of hypertension, rheumatoid arthritis (on chronic steroids) and superior vena cava thrombosis (on anticoagulation) presented with melena. The patient denied bright red blood per rectum, or any other gastrointestinal symptoms. His vital signs were stable at the time of presentation. Physical examination was unremarkable except for melenic stool on rectal exam. Labs were significant for a hemoglobin of 7.0 g/dL (prior baseline of 12.0 g/dL), AST 67 U/L, ALT 43 U/L, ALP 219 U/L, INR 1.17, and PTT 55.3 seconds. Due to evidence of persistent bleeding, three units of packed red blood cells were transfused and a pantoprazole drip was initiated with suspicion of an upper GI source of bleed. Endoscopy was performed, which showed esophagitis with no active bleeding and gastritis. A colonoscopy was then performed which revealed a solitary Dieulafoy’s lesion in the cecum. An overlaying adherent clot was dislodged to reveal the lesion. Complete hemostasis was achieved using four hemostatic clips. Post procedural course was uncomplicated and the patient’s hemoglobin remained stable. Discussion: Our case describes a cecal Dieulafoy’s lesion that presented, unusually, as melena. There have been several reports of cecal Dieulafoy’s lesion presenting as hematochezia. To our knowledge, this is the first reported case of a cecal Dieulafoy’s lesion presenting solely as melena. We aim to add to the relatively few cases of cecal Dieulafoy’s reported, and help improve the diagnostic accuracy of these type of lesions. Without timely diagnosis and treatment, Dieulafoy’s lesions have the potential to progress to life-threatening bleeding. Thankfully, with expedient diagnosis and with modern endoscopic tools, hemostasis can be achieved in up to 90% of such cases.Figure 1.: A: Bleeding cecal Dieulafoy’s lesion B: Endoscopic clip removing adherent clot and exposing visible vessel C: Hemostasis achieved with four hemostatic clips.

S2445 When Recurring Infections Mask an Atypical Presentation of Inflammatory Bowel Disease

Introduction: Pyoderma gangrenosum (PG) is an uncommon and severe extraintestinal manifestation (EIM) of inflammatory bowel disease (IBD) with head or scalp involvement being exceeding rare. About one-third of presentations can be precipitated by skin trauma or infection, otherwise known as pathergy. These ulcers develop acutely, may not correlate with IBD activity, and can predate IBD diagnosis. Here we present an atypical presentation of PG in the setting of newly-diagnosed IBD. Case description/methods: A 35-year-old male with prior diagnosis of recurrent, diffuse soft tissue infections presented for management of presumed sepsis due to soft tissue infection. Two weeks prior to presentation, patient developed painful and purulent left lower extremity ulcer followed by worsening of facial and scalp ulcerations (Fig A-C). Patient reported prior diagnosis of facial folliculitis 1 year ago triggered by a stressor event that resolved but then had recurrence 3 months prior to this encoutner. Skin biopsy was unremarkable and was managed with IV antibiotics due to suspected infection. CT abdomen and pelvis during that admission showed circumferential sigmoid and rectal wall thickening concerning for colitis, but patient did not pursue further outpatient work up. Since being discharged from prior hospitalization, the patient experienced ongoing melenic stools. Prior to hospital transfer, patient was febrile to 39.4˚C, WBC count of 33k/ul and hemoglobin of 6.1g/dl for which endoscopy was performed showing diffuse erosive gastritis. Wound cultures grew staphylococcal aureus, and he was started on IV antibiotics. Initial concerns for IBD were based on imaging, ulcer concerning for PG, and three-year history of diarrhea elicited after admission. Laboratory work up is summarized in Table 1. Sigmoidoscopy showed cobblestoning with non-bleeding mucosal ulcerations and sigmoid colon biopsies demonstrated severely active colitis (Fig D,E). Skin biopsy was concerning for PG with superimposed infection. Patient was started on steroid therapy with improvement of diarrhea and inflammatory markers. Patient was discharged on oral steroids and planned follow up for initiation of biologic therapy. Discussion: This patient received a new diagnosis of IBD almost solely based on his presenting dermatological findings. This individual initially presented with recurrent skin wounds, however, eliciting further history of recurrent diarrhea, shifted the work up beyond infectious etiologies to earlier diagnosis and treatment of PG and IBD.Table 1.: Laboratory Data Depicting Patient Hospital Course.Figure 1.: Figure A and B: An extensive, necrolytic ulceration with an irregular, violaceous and undermined borders of the left lower extremity Figure C: Diffuse ulcerated lesions of the head and scalp Figure D and E: Endoscopy image of rectosigmoid mucosa with ulcerations, congestion, erythema, granularity and loss of vascularity.

Reversal of Hepato-renal Impairment Induced by Meloxicam Paracetamol Toxicity in a Labrador Dog

An 8 years old male Labrador dog was referred to Small animal Medicine Referral Clinic, Veterinary Clinical complex, Veterinary College and Research Institute, Orathanadu for fever, anorexia, hematemesis and melenic stools. The dog on treatment with 2 ml of Meloxicam Paracetamol combination IM, along with Injection Oxytetracycline and fluid therapy for 3 days by locally and did not respond to treatment thus was referred. Clinical dullness, lethargy, respiratory distress, visible mucosal jaundice, ecchymosis on ventral abdomen was noticed. Physical examination revealed, halitosis, ulceration in the tip of the tongue, dehydration, pre scapular LN enlargement, distended abdomen, fluid thrill and splenomegaly. Hematology revealed anemia and thrombocytopenia. Biochemical analysis revealed Hyperbilirubinemia, Elevated BUN, Creatinine, AST, ALT, ALP and hypoalbuminemia. Abdominal ultrasound reveled splenomegaly, focal hyperechoic liver parenchyma, cortex echogenicity of right kidney and perirenal fluid accumulation. ECG revealed peaked T wave. Radiography revealed hepatosplenomegaly. Hemato-biochemical alteration was monitored before and after therapy. Animal was managed with fluid therapy, Acetylcysteine, Amino acid and supportives and the dog had an uneventful recovery.

An Unusual Case Report of Fatal Oral Ingestion of the Emerging “Bath Salt” Eutylone

Background: The abuse of novel psychoactive substances, such as synthetic stimulants, is increasing each year with modifications to drug scaffolds to alter pharmacokinetics or pharmacodynamics. Psychosis, cardiotoxicity, and excited delirium have been documented with intense sympathomimetic stimulants. The clinical recognition of these substances is challenging as routine blood and urine drug screening protocols do not readily detect the presence of these synthetic substances. We report an unusual case of oral ingestion of eutylone with subsequent confirmation of this substance. Case details: A 49-year old female with history of chronic cardiovascular comorbidities, type 2 diabetes, depression, and end stage renal disease was presented to Emergency Department with 2-3 week history of abdominal distention with melenic stools. She was found to have onset ascites with melena prompting GI consultation. An esophagogastroduodenoscopy was performed revealing a white crystalline material obstructing mid oesophagus. A sample was obtained and the procedure was halted due to sever hemodynamic instability. To the best of our knowledge, there are no previous reports of fatal oral ingestion of eutylone by a 49-year old with no documented history of substance abuse. Discussion: This case is concerning because eutylone is new substance that may not be detected during routine testing, is easy to obtain over the internet, and has the potential to cause mortality.

S2125 Gastroduodenal Artery Pseudoaneurysm Presenting With Bleeding Pancreatic Necrosis, Duodenal Erosion, and Melena: A Unique Case

INTRODUCTION: Melenic stools are typically indicative of gastrointestinal bleeding that may originate anywhere from the nares to cecum. Most common etiologies include gastritis, peptic ulcer disease, angioectasias, gastro-esophageal varices or malignant lesions. Here, we describe a rare case of melena caused by gastroduodenal artery (GDA) pseudoaneurysm with bleeding pancreatic necrosis and duodenal erosion. CASE DESCRIPTION/METHODS: A 58-year-old female with a history of class III obesity, chronic obstructive pulmonary disease, and recurrent pancreatitis presented with melenic stools, abdominal pain, and fatigue. Initial labs were significant for a hemoglobin of 6.0 g/dL. Computed Tomography (CT) of abdomen showed diffuse pancreatic necrosis with gas throughout the pancreas, which had progressed from imaging one month prior. Upper endoscopy was significant for erythematous duodenopathy but did not reveal any clear source of bleeding. Colonoscopy showed dark stool mixed with blood and hematin. In view of ongoing bleeding and transfusion requirements, push enteroscopy was performed showing a large blood clot and necrotic material in the duodenal bulb and second portion of the duodenum. Findings were concerning for erosion of pancreatic necrosis through the wall of the duodenum and erosion through a blood vessel resulting in active bleeding. Interventional radiology (IR) was consulted, and angiography demonstrated a GDA pseudoaneurysm which was successfully coil embolized. After the embolization, she was managed non-operatively due to her substantial co-morbid conditions. In total, she required 14 units of packed red blood cells during the hospitalization. Her bleeding resolved and she was discharged on high dose of oral proton pump inhibitors. DISCUSSION: Representing only 1.5% of visceral arterial aneurysms, GDA pseudoaneurysms very seldomly occur as a result of acute pancreatitis with necrosis. A history of recurrent pancreatitis is frequently noted. Pseudoaneurysm formation occurs due to pancreatic enzyme release and subsequent chronic inflammation, resulting in breakdown of the arterial wall and blood collection enclosed by adjacent fibrous tissue. Our case demonstrates an even rarer occurrence of erosion of the pancreatic necrosis through the wall of the duodenum, with active bleeding from the GDA pseudoaneurysm manifesting as severe gastrointestinal bleeding. Timely recognition is vital, as 40% of ruptured GDA pseudoaneurysms result in death. Management is completed through IR embolization or surgery.

S1487 Simultaneous Pancreatico-Enteric Fistulae: A Complication of Pancreatic Intraductal Papillary Mucinous Neoplasm

INTRODUCTION: Intraductal papillary mucinous neoplasms (IPMN) are mucin producing tumors which arise from epithelial cells of the pancreatic duct. They present with varying degrees of dysplasia, possess the potential for malignant transformation and require definitive surgical management. IPMNS have been reported to fistulize into the surrounding organs. We present a case in which an IPMN fistulized into both the gastric body and the duodenum. CASE DESCRIPTION/METHODS: A 67-year-old female with a PMH of CAD, HTN, CKD, aortic stenosis, sick sinus syndrome s/p AICD presented with abdominal pain and unintentional weight loss. CT scan of the abdomen revealed diffuse enlargement of the pancreas with marked dilatation of the pancreatic duct, which measured up to 3.8 cm. She underwent diagnostic ERCP/EUS at which time a bulging ampulla with classical “fish eye” appearance was identified (Figure 1). A pathology specimen was collected and the patient was diagnosed with IPMN. While awaiting surgical intervention the patient re-presented with symptomatic anemia and melenic stools, indicating UGIB. Upper endoscopy was performed, revealing a large gastropancreatic fistula along the greater curvature of the proximal gastric body with mucin protruding (Figure 2). Biopsies taken from the gastric fistulous tract and mucin specimen cytology confirmed pancreatic IPMN. The patient was not amenable to complete pancreatectomy and partial pancreatectomy was attempted.It was however aborted intraoperatively due to prominent and undisecteble pancreatic vasculature,due to copious underlying adhesions. The patient instead underwent repair of the gastropancreatic and colopancreatic fistulae with partial omentectomy, as per patient preference. Post-op course was uneventful, and the patient was discharged with outpatient follow up and plan for conservative care. DISCUSSION: Pancreatic IPMNs progress from benign neoplasms to invasive neoplasms in an average span of 5-6 years. However, both IPMNs possess potential for fistula formation into a surrounding structure as fistula formation may occur from direct invasion or secondary to inflammation.In this case, we observed the unusual presentation of a benign IPMN forming simultaneous fistulous tracts to the gastric and duodenal lumens.Figure 1.: Upper GI endoscopy showing gastric body with mucin protruding.Figure 2.: Upper GI endoscopy showing gastric body with mucin protruding.

S3458 A Tale of Two Dieulafoy’s: Massive GI Hemorrhage from Synchronous Dieulafoy Lesions

INTRODUCTION: Dieulafoy lesions (DL) are an elusive source of gastrointestinal hemorrhage accounting for 5% of all cases. They consist of large aberrant submucosal arterioles that erode through overlying epithelium. Patients present with hematemesis, melenic stools, and/or hemodynamic instability. Bleeding is from a single lesion in the stomach (64%), small intestine (20%), colon (10%), or esophagus (2%). Diagnosis is difficult in the absence of overt bleeding and repeat endoscopy is often required. Management includes epinephrine injection, thermal ablation, hemoclips, or resection. Unfortunately, recurrence can be seen in 5-10% of cases. We report an exceedingly rare case of two synchronous DL actively bleeding during one hospitalization. CASE DESCRIPTION/METHODS: A 61 year old male with ESRD, CAD status-post bypass grafting, atrial fibrillation, and heart failure status-post mitral valve replacement presented with four weeks of melena. Index endoscopy demonstrated duodenal bulb and cecal angioectasias that were ablated with snare polypectomy of four polyps. Bleeding persisted so capsule endoscopy was pursued showing fresh blood in the jejunum and distal ileum. Upper double balloon-assisted enterography (DBE) showed an actively bleeding DL in the mid-distal jejunum that was treated with APC, hemoclips and marked with India Ink. Melena and transfusion-dependent anemia persisted and repeat upper DBE showed oozing from prior DL ablation, thus retreated with APC. Bleeding continued but IR angiogram was unrevealing, so resection was pursued. Unfortunately, despite resection, video capsule, and two colonoscopies with hemoclip placement at polypectomy sites, bleeding continued. A lower DBE revealed an actively bleeding DL 50cm proximal to the ileocecal valve that was treated with APC and hemoclips. Hemostasis was achieved and the patient was discharged. DISCUSSION: Despite endoscopy and small bowel series, the source is not found in up to 5% of overt GI hemorrhages. While DL account for only 5% of GI bleeding cases, they are important due to their propensity to cause significant hemorrhage. DL are typically solitary; only two cases of synchronous DL have been reported in literature, and were isolated to the stomach or stomach and small bowel. This is an unusual case of persistent GI bleeding caused by two active small bowel DL (distal jejunum and ileum) which were synchronously bleeding during one hospital admission. As far as we know, this is the only reported case of two actively bleeding DL in the small bowel.Figure 1.: Initially identified DL in mid-distal jejunum treated with APC & hemoclips.Figure 2.: Synchronous DL 50cm from ICV.

S2082 Importance of Coronavirus Disease 2019 Screening Before Endoscopic Procedures

INTRODUCTION: Asymptomatic coronavirus disease 2019 (COVID-19) is estimated to be between 15 to 40% of all cases. This needs to be distinguished from pre-symptomatic disease as patients are asymptomatic for a while, but eventually have symptoms. Since COVID-19 patients are contagious while asymptomatic, healthcare providers are at high risk of exposure. Although mass testing may prevent healthcare worker exposure, mass testing may not be possible due to insufficient healthcare resources. To illuminate the importance of COVID-19 screening, we present a 66 year-old asymptomatic male with a COVID-19 positive screen before an esophagogastroduodenoscopy (EGD). CASE DESCRIPTION/METHODS: A 66 year-old African American non-Hispanic male with a past medical history of ischemic stroke, hypertension, and hyperlipidemia, presented to the emergency department with bright red blood per rectum and melenic stool. He denied any fever, chills, night sweats, cough, dyspnea, abdominal pain, diarrhea, nausea, or vomiting. His bleeding began one week after starting apixaban for a left internal jugular vein thrombosis. Initial laboratory was significant for a microcytic anemia (11.2 g/dL). Therefore, he was admitted for further evaluation of gastrointestinal bleed. Gastroenterology was consulted and recommended proceeding with an EGD. However, recent hospital guidelines warranted COVID-19 screening in all patients undergoing a procedure. Although the patient had asymptomatic respiratory symptoms, he tested positive for COVID-19. Therefore, endoscopy was cancelled. Once serial hemoglobin was stable, he was discharged after two days of hospitalization. DISCUSSION: Healthcare workers are at high risk of COVID-19 infection. In an observational study enrolling 1,099 Chinese patients infected with COVID-19, 3.5% were healthcare workers. Gastroenterologists are at high risk of infection as some procedures create viral aerosolization. However, pre-endoscopic and nationwide screening could decrease infection rate. South Korea successfully contained COVID-19 spread through mass testing. Although such solution could be implemented in the United States, insufficient healthcare utilization of resources including limited tests and reagent supplies are potential hurdles. We present the importance of COVID-19 screening before endoscopy. Although the long-term benefits of pre-endoscopic COVID-19 screening is not well known, pre-endoscopic screening may be an effective way to limit healthcare worker exposure.

S1411 Acute Esophageal Necrosis in a 29-Year-Old Patient With ESRD

INTRODUCTION: Acute esophageal necrosis (AEN), or Gurvits Syndrome, is a rare disorder with an incidence of about 0.001-0.2% with males having a 4:1 predilection. It is diagnosed clinically with endoscopic visualization of sharply demarcated circumferential black necrotic tissue occurring in the distal 1/3rd of the esophagus; whilst sparing the GEJ. Patients with AEN often have other comorbidities; such as vascular compromise, ESRD, DKA, malignancy, and duodenal ulcers. In 90% of cases, initial presentation includes melena, coffee ground emesis or frank hematemesis. We present a case of AEN seen in a 29-year old male with ESRD; amongst other comorbidities. CASE DESCRIPTION/METHODS: Our patient is a 29-year-old African American male with a history of ESRD on HD, HTN, and poorly-controlled T2DM who presented for sepsis secondary to non-healing diabetic foot ulcer. Vitals were significant for T 100.9, P 100, BP 168/78. Labs were significant for wbc 31.49, Na 130, K 3.1, BUN 41, Cr 9.80, CRP 21. Patient was treated for presumed osteomyelitis. During hospitalization, patient underwent HD three times per weekly schedule. On day 6, 8, and 10, he became hypotensive during his HD sessions. On day 13, he was found unresponsive and hypotensive with large melenic stool. Upon stabilization, EGD showed black necrotic esophagus spanning the entire length until GEJ. Colonoscopy was unremarkable. Conservative management with NPO, IVF, pRBC and IV PPI was done. Repeat EGD two weeks later showed patchy areas of necrosis interspersed with exudate seen throughout the esophagus improved from prior EGD. He recovered remarkably well including tolerating an oral diet. DISCUSSION: Although the exact pathophysiology is unknown, a two hit hypothesis postulates the proposed mechanism for AEN formation. An initial event precipitates a lack of blood flow causing necrosis and vulnerability to insults that precipitate bleeding at the affected site. There is eventual reversal of necrosis with normalization of the tissue. Prognosis is poor and carries a high mortality rate from 15 to 35% and is dependent upon underlying disease. Some complications include esophageal perforation, stenosis and stricture, and mediastinitis. Management of AEN involves treating underlying disease along with supportive care. Although our patient was young, he had multiple comorbidities including ESRD, vascular compromise, DM and septic shock. This led to the development of ischemia and eventually necrosis especially in vulnerable areas of distal third of the esophagus.

971 EVERY TRICK IN THE BOOK: ADVANCED MANAGEMENT OF REFRACTORY BLEEDING IN A PATIENT WITH ROUX-EN-Y GASTRIC BYPASS

A 76-year old male with a history of a Roux-en-y gastric bypass initially presented to our ED with melenic stools and hypotension. The patient underwent an upper endoscopy without a source of bleeding identified. Over the next several months the patient had multiple admissions for gastrointestinal bleeding without a source identified. The patient came back to our hospital with abdominal pain and was found to have a perforated duodenal ulcer which was successfully managed surgically. In the following months the patient again came back to our ED with bleeding. It was decided that an endoscopic examination of the excluded stomach and proximal duodenum was necessary to assess for a source of bleeding. The patient underwent an endoscopic ultrasound with a trans-remnant lumen apposing stent placement. Brisk bleeding was identified originating from an ulcer in the duodenum. Subsequently the patient underwent multiple hemostasis maneuvers, including covered metal stent placement and, eventually, an EUS-guided injection of coils and gelfoam directly into a branch of the gastroduodenal artery. Since our final intervention the patient has had no further bleeding. This case is illustrative of the vast array of therapeutic interventions that are available to endoscopists. Although intra-arterial coiling procedures are more difficult than intravenous treatments, such interventions are possible and have a potential for high impact in difficult cases.

1998 Hemostatic Spray for Secondary Hemostasis Following Endoscopic Variceal Band Ligation

INTRODUCTION: Endoscopic application of hemostatic powder for the treatment of GI bleeding has now been well-described in the literature and utilized for multiple years in clinical practice. Its use as primary and salvage therapy in upper GI bleeding has been established following its approval for non-variceal GI bleeding. Successful use has even been reported in post-variceal banding ulcers, however in very small patient numbers with comparatively less data in acute, ulcerated, post- banding bleeding occurring with simultaneous gastric and esophageal varices. CASE DESCRIPTION/METHODS: We present a case of a 57-year-old male with medical history including hepatitis C, cirrhosis, tobacco use, chronic kidney disease, duodenal ulcer, gastritis, ascites, esophageal varices, and diffuse/infiltrative hepatocellular carcinoma associated with tumor thrombus of the portal and hepatic veins who presented to the emergency department for new melenic stools. Hemoglobin was 12.4 g/dL on presentation, decreased to 10.2 g/dL by consultation at which time the melena progressed to hematochezia with an episode of hematemesis. The calculated MELD-sodium score was 19. Physical examination was pertinent for soft, distended abdomen without tenderness and no asterixis. IV ceftriaxone, pantoprazole, and octreotide were initiated. The patient received a single unit of packed red blood cells during hospitalization. EGD demonstrated large distal esophageal varices and an actively-spurting Type 1 (GOV1) gastroesophageal varix. Two bands were placed on esophageal varices and the gastric varix was banded to eradication with cessation of bleeding. Hematemesis recurred the following day and repeat EGD was performed for salvage therapy noting that prior evaluation deemed the patient non-candidate for liver transplant or TIPS procedure. Ulcerated varices were encountered at the prior banding sites with a large pool of coagulated blood in the stomach and hemostatic spray was successfully applied to each site. Hemoglobin remained stable after repeat hemostatic therapy without subsequent need for transfusion. DISCUSSION: Ordinarily, persistent bleeding following variceal banding in decompensated cirrhosis warrants TIPS consideration if a candidate and needed for rescue therapy. However, this case lends credence to the use of hemostatic spray in non-TIPS candidates for treatment of post-banding ulcerated variceal bleeding in both esophageal and gastric etiologies.

2666 Disseminated Renal Cell Carcinoma Presented as Obscure Gastrointestinal Bleeding

INTRODUCTION: Metastatic disease to the gastrointestinal tract is frequently observed in patient with known disseminated malignancies. Among those, melanoma, breast and lung cancer are commonly reported. Renal cell carcinoma (RCC) metastasis to small bowel is rare and the presentation varies from obstructive symptoms, intussusception, as well as, gastrointestinal bleeding. CASE DESCRIPTION/METHODS: A 85 years old male with medical history of pulmonary embolism on apixaban and progressive stage IV RCC despite multiple lines of therapy on lenvatinib, presented with progressive fatigue and melenic stools. Denied abdominal pain, change in bowel habits, prior episodes of bleeding, or NSAIDs use. Vital signs were unremarkable. Physical exam was pertinent for non-tender abdomen, no distention, active bowel sounds, no rebound or guarding, and a rectal exam that revealed melenic stools. Labs: Hemoglobin of 6.8 g/dL (Baseline 10.3 g/dl), electrolytes, kidney and liver function tests were unremarkable. Computerized tomography (CT) of the abdomen and pelvis revealed multiple hepatic, retroperitoneal and mesenteric metastases. He received two units of packed red blood cells with appropriate response. Apixaban was held and he was admitted for workup of gastrointestinal bleeding. Esophagogastroduodenoscopy was unrevealing, while colonoscopy showed a few non-bleeding colonic and rectal angioectasias. A subsequent capsule endoscopy demonstrated an actively bleeding jejunal lesion (Figure 1). He continued to have large melenic bowel movements, and his hemoglobin decreased to 5.5 g/dL. A computed tomography angiography showed a blush of contrast in the jejunum, near the site of a tumor implant (Figures 2 and 3). An interventional radiology embolization was performed, with successful hemostasis. DISCUSSION: One autopsy series reported that only 2 out of 44 metastatic tumors to the small intestine were duodenal implants of RCC. In recent years, however, the number of published reports of RCC small bowel metastasis has been increasing. Retrograde venous spread to the paravertebral vessels has been propose as the route of dissemination of RCC to the intestine and solitary, bulky hypervascular lesions might be diagnostic if seen on CT scan. Luminal evaluation may localize the bleeding and offer potential treatment, however, angiography with embolization is the preferred therapeutic approach for small intestine lesions. Small bowel metastases must be considered as an etiology of bleeding when patients with RCC present with melena.

2386 Shock Liver: A Complication of Gastroduodenal Artery Embolization

INTRODUCTION: PUD is the most common cause of acute upper GI bleeding. Duodenal ulcers are 4x more likely to bleed than gastric ulcers. Posterior duodenal ulcers, are more likely to erode into the gastroduodenal artery (GDA) resulting in massive bleeding requiring intervention. Liver failure is a known complication of gastroduodenal artery embolization due to inadvertent embolization of the main hepatic artery [1,2]. CASE DESCRIPTION/METHODS: A 71 year old lady presented with a hemoglobin of 5.7 g/dL with a baseline of 10.7 g/dL. She was resuscitated with pRBCs and fluids to a hemoglobin of 8.7 g/dL. EGD showed an active 3 cm bleeding ulcer at the duodenal bulb with a visible vessel and adherent clot. Hemostasis was achieved with epinephrine, two hemoclips and gold probe cautery. On POD# 5, she had two melenic stools and an acute drop in hemoglobin reaching a nadir of 6.4 g/dL which prompted a repeat EGD. An ulcerated area on the posterior wall of the bulb was bleeding, hemostasis with epinephrine and three hemoclip deployment failed. Subsequently, she underwent gastroduodenal artery coiling. During the embolization, the coil was partially protruding into the hepatic artery. Coil repositioning failed. POD# 1, AST and ALT trended up to 2814 IU/L and 1375 IU/L from a baseline of 14 IU/L and 10 IU/L on admission, respectively. INR trended up from 1.23 to 1.8, she developed encephalopathy, was diagnosed with shock liver and transferred to outside liver transplant center. DISCUSSION: Technical success rates of transcatheter arterial embolization are extremely high (>90%) while clinical success rates vary from 60%-90% [3]. This difference may be attributed to multiorgan failure, coagulopathy, and bleeding from trauma or invasive procedures [4]. A lack of understanding of the factors that influence clinical outcome also plays a role. Transcatheter therapeutic embolization has a very high rate of success and should be considered as an alternative to surgery in high-risk populations. [1,2]. Endoscopic embolization usually has a low rate of complications of rebleeding, infarction, and rarely coil migration [3,5,]. Coil migration has been described after embolization of the GDA, but infrequently been reported to be fatal. Our patient had movement of the sheath used to protect the hepatic artery and the catheter resulting in partial migration of the coils into the hepatic artery which led to shock liver. To our knowledge, few cases of coil migration inducing hepatic failure have been reported in the literature.

2358 Zieve's Syndrome: A Case of an Unusually Profound Hemolysis in the Setting of Alcoholic Liver Disease

INTRODUCTION: Zieve’s Syndrome is a cause of hemolytic anemia in alcoholic liver disease, thought to arise from altered erythrocyte metabolism (pyruvate kinase instability) and hyperlipidemia (lysolecithin may trigger hemolysis). It is an under recognized syndrome, and often times leads to patients undergoing extensive clinical work ups. CASE DESCRIPTION/METHODS: A 73-year-old male with a history of alcohol abuse presented to the emergency room for acute jaundice associated with melenic stools, and dark urine. Physical exam was notable for dry mucous membranes, scleral icterus and conjunctival pallor, No oral ulcers, rashes or petechiae were found. Initial labs included a hemoglobin of 5.5G/DL, LDH 753IU/L, and a negative Coombs test. Based on his liver function tests, his R factor was 1.6, consistent with a cholestatic pattern of injury. Through his hospital course he had a rising alkaline phosphatase as high as 226 Units/L, and total bilirubin of 11.5 MG/DL. Triglycerides were elevated (289MG/DL) compared to prior lipid study. Abdominal ultrasound revealed an echogenic liver consistent with fatty infiltration. Lab workup was negative for HFE (hemochromatosis) mutations, autoimmune hepatitis, HIV, CMV, HCV, and EBV. Prior to coming to the hospital, the patient spent time out in the woods. Given risk of tick exposure, in the setting of hemolytic anemia, he was evaluated for tick borne illness. He was started on Doxycycline, and Atovaquone to empirically cover Lyme and Babesia, as well as Piperacillin-Tazobactam while blood and urine cultures were pending. Parasite studies and blood/urine cultures returned negative. His hemolytic anemia was refractory to 8U of packed red blood cells, and 1U of fresh frozen plasma. Eventually, the patient was diagnosed with Zieve's Syndrome. DISCUSSION: Zieve’s Syndrome is characterized by a triad of alcoholic steatohepatitis, jaundice, and transient hyperlipidemia. The challenging aspect of this case lies in the fact that these findings are often seen under the constellation of other diseases, leading patients to unnecessary tests and studies. Immediate management of the syndrome is comprised of supportive care, while definitive treatment is alcohol cessation.

1605 Typhoid Fever: GI Bleed From an Ancient Disease

INTRODUCTION: Gastroenterologists periodically encounter ileocecal wall thickening in a patient with abdominal pain, fevers and gastrointestinal bleeding in an inpatient setting. A unifying diagnosis for a patient with these radiologic findings and symptoms could include inflammatory, infectious, or malignant etiologies. We present a case of a patient presenting in this way, who has found to have salmonella bacteremia as well as colonic and ileocecal valve ulcers on endoscopy. CASE DESCRIPTION/METHODS: A 51-year-old man with a past medical history notable for bladder cancer status-post BCG treatment presented with a three day history of crampy abdominal pain and fevers. He denied any diarrhea or vomiting. Exam was notable for a temperature of 102.7 and mild tenderness to palpation in lower abdomen. Admission labs were notable for normal leukocyte count and mildly elevated hepatocellular enzymes (AST 63, ALT 97). Due to his high fever, blood cultures were drawn. CT scan was notable for marked wall thickening at the ileocecal junction with enlarged regional lymph nodes. On the day after admission, he had a melenic stool and was scheduled for EGD and colonoscopy. EGD was unremarkable, but his colonoscopy was notable for two 3-5mm ulcers in the ascending colon as well as an ulcerated and inflamed ileocecal valve, which was unable to be intubated. Concern was for infectious or malignant etiology of these findings. Multiple blood cultures returned positive for Salmonella enterica with Vi antigen, shortly thereafter. He was treated with ceftriaxone and metronidazole for his bacteremia, and later transitioned to ciprofloxacin, with improvement in symptoms. Biopsies of the ulcers showed chronic active colitis. They were also notable for B and T cell clones which were concerning for lymphoma. To follow up on these concerns, he had repeat colonoscopy three weeks later which noted resolution of his ascending colon ulcerations and ileocecal valve inflammation. His terminal ileum was intubated and appeared normal. Biopsies of the ileocecal valve revealed benign colonic mucosa. After completion of antibiotic therapy, the patient denied any further symptoms. DISCUSSION: This case illustrates the importance of maintaining a broad differential in a patient with colonic inflammation on imaging and ulcerations noted on endoscopy. Also, this case highlights key features of typhoid colitis which can include GI hemorrhage with a predilection for right-sided colonic involvement.

3037 Spontaneous Cystgastrostomy From Pancreatic Pseudocyst Erosion Into Gastric Wall Resulting in Gastrointestinal Hemorrhage

INTRODUCTION: Pancreatic pseudocysts are a common complication of pancreatitis. Spontaneous erosion of a pseudocyst into adjacent organs is rare, manifesting in a variety of clinical symptoms and presentations. We present a case of spontaneous fistulization of a pancreatic pseudocyst into the stomach resulting in life-threatening bleeding. CASE DESCRIPTION/METHODS: A 60-year-old gentleman with history of type 2 diabetes mellitus, hypertension and chronic pancreatitis with known pancreatic pseudocyst presented with multiple episodes of melena associated with fatigue, weakness and epigastric pain aggravated by food intake. He denied history of peptic ulcer disease but admitted to chronic NSAID use. Physical examination revealed a pale patient with mild generalized abdominal tenderness without signs of peritonitis. Melenic stools were noted on digital rectal exam. Labs were significant for critical normocytic anemia with Hgb 6.3 g/dL. CT scan of abdomen and pelvis showed an 11.7 × 9 cm lesion in the pancreatic body with calcified rim communicating with gastric antrum. Gastrograffin swallow showed contrast transfer from stomach into the pseudocyst. A CT-Angiogram of the abdomen and pelvis failed to reveal a source of bleeding or peripancreatic pseudoaneurysms. Patient underwent EGD which showed 1 centimeter antral fistula-opening representing a spontaneous cystogastric fistula. No ulcers were found. The patient eventually underwent surgical excision of pancreatic pseudocyst, antrectomy and Billroth-II reconstruction. DISCUSSION: Pseudocysts complicate 20-40% of chronic pancreatitis. They can cause pain, bowel obstruction, infection, or hemorrhage. Treatment is indicated when cysts become symptomatic or grow beyond 5 cm. However, pseudocysts often resolve by spontaneous drainage into the pancreatic ductal system. Rarely, they can rupture into the peritoneal cavity or erode into nearby hollow organs. Bleeding can be the result of pseudocyst erosion into nearby vessels or rupture of nearby pseudoaneurysms. While involvement of gastroduodenal, splenic, hepatic and inferior pancreaticoduodenal arteries has been reported, none of these sources could be identified in this case. Treatment can take the form of direct embolization or surgical hemostasis. In summary, we have presented a case of pancreatic pseudocyst with spontaneous cystogastric fistula formation accompanied by massive upper GI bleeding eventually treated by surgical excision and Billroth-II reconstruction.