Non-bleeding Ulcer Research Articles

S3649 Choroidal Melanoma: A Rare Cause of Gastric/Duodenal Pigmented Macules

Introduction: Choroidal melanoma is the most common primary intraocular malignancy. Two to four percent of newly diagnosed patients have evidence of metastatic disease. Up to half of patients will develop metastatic disease. The liver is the primary site of metastasis as the tumor spreads hematogenously. Metastasis to the gastrointestinal tract is rare in ocular melanoma in contrast to cutaneous melanoma. We present a case of ocular melanoma with metastasis to the gastrointestinal (GI) tract. Case Description/Methods: An 81-year-old female with a history of choroidal melanoma of the left eye diagnosed in 2015 treated with radiotherapy presented to the hospital with fatigue and weight loss of 30 pounds over the last few months. On admission she was normotensive and afebrile. On physical exam her abdomen was distended and nontender. Labs were notable for Cr 2.3 mg/dL, AST 698 IU/L, ALT 286 IU/L, ALP 488 IU/L, Albumin 2.3 g/dL, Total bilirubin 4.9 mg/dL, WBC 13.3 K/uL, Hgb 11.7 g/dL, platelets 206 K/uL and INR 1.6. Computed tomography without contrast of the abdomen/pelvis showed lobular contour of the liver with multiple hyperdense foci scattered throughout concerning for metastases. Ultrasound with dopplers revealed portal vein thrombosis. Patient underwent endoscopy for variceal screening with no evidence of varices. However, scattered throughout the stomach were hyperpigmented macules of variable size (a, b). In her duodenum, there were additional lesions (c) and two non-bleeding ulcers with pigmented lesions. Biopsies were consistent with metastatic melanoma. Ultimately, hospice was pursued. Discussion: Choroidal melanoma metastases in the GI tract are rare. When patients with a history of melanoma, regardless of its origin, present with nonspecific symptoms, physicians should have a high suspicion for metastatic disease. Metastases are endoscopically diagnosed as pigmented or amelanotic nodules, ulcerations, macules or mass. Patients are typically treated with palliative surgery or immunotherapy. Prognosis is typically poor with a median survival rate of 4 to 6 months.Figure 1.: Endoscopic images of hyperpigmented lesions in the stomach (a, b) and duodenum (c).

S2631 The Unusual Suspect: Gastrointestinal Bleeding From an Ampullary Dieulafoy Lesion

Introduction: Dieulafoy lesions (DLs) are an unusual but important cause of acute upper gastrointestinal bleeding (UGIBs), and can be difficult to diagnose. Three fourths are found in the stomach close to the gastroesophageal junction, but have also been reported in small bowel and colon. There are only a few reported cases of ampullary DLs. We present a rare case of a recurrent UGIB from an ampullary Dieulafoy lesion and its management. Case Description/Methods: A 65-year-old male presented for type B aortic dissection requiring endovascular repair, which was complicated by type 1 endoleak. His hospital course was complex owing to sepsis, respiratory failure, and cardiac arrest. Gastroenterology was consulted on day 16 for multiple tarry bowel movements. Esophagogastroduodenoscopy (EGD) showed healing ulcers in lower esophagus. and non-bleeding ulcers in the duodenal bulb. The culprit lesion was an oozing Dieulafoy at the major papilla. Hemostasis was achieved with epinephrine injection and thermal therapy. Rebleeding occurred 5 days after the initial EGD leading to shock and cardiac arrest. Once the patient was hemodynamically stabilized, he underwent another EGD that showed copious fresh blood in stomach body as well as the second and third portions of duodenum. Active arterial spurting was noted from the superior aspect of major papilla. Given the severe hemodynamic compromise from this bleeding, we elected to clip the lesion this time, accepting the risk of pancreatitis and/or biliary obstruction. One endoclip was placed across the dorsal aspect of major papilla and closed. Persistent oozing was noted from under the clip which was arrested by applying a hot snare to the already placed endoclip and delivering thermal energy to the area pinched by the endoclip. Complete hemostasis was then achieved [Figure 1]. Liver function tests and lipase were monitored for a week and the patient did not develop pancreatitis or biliary obstruction despite placement of endoclip across the major papilla. Discussion: Ampullary DLs are extremely rare and can present a unique diagnostic and therapeutic challenge due to their anatomical location. There is currently no consensus on how to best treat ampullary DLs. Verification of the diagnosis and definitive treatment might require repeated examinations. Early and aggressive endoscopic treatment should be adopted when an ampullary DL is suspected, and patients should be closely followed up given therapeutic interventions can potentially impair biliary drainage.Figure 1.: Endoscopic images of bleeding from ampullary Dieulafoy lesion before and after endoscopic intervention.

S2678 A Case of Capecitabine-Induced Gastrointestinal Hemorrhage

Introduction: Capecitabine is a common agent utilized in adjuvant chemotherapy for breast, esophageal and colorectal cancers. Capecitabine- induced terminal ileitis or ileocolitis leading to severe gastrointestinal bleed is rare but potentially life-threatening, requiring early intervention and timely recognition of associated symptoms. We present the case of a patient with capecitabine-induced ileocolitis who presented with persistent high-grade bloody diarrhea. Case Description/Methods: A 69 year-old-man presents to ED for 1 week of watery diarrhea and 2 days of bloody stool with clots, associated with near-syncope and fall. He had a history of right hemicolectomy with ileocolonic anastomosis due to adenocarcinoma of colon, and was receiving chemotherapy with capecitabine (3 cycles) at the time of admission. Physical exam was significant for pallor, diffuse abdominal tenderness, and rectal exam positive for hematochezia. Laboratory investigations showed profound normocytic anemia (Hg 4.1 g/dl), elevated white blood cell count, hypokalemia, elevated lactate (3.7) and elevated INR (1.4). CT angiography of abdomen/pelvis showed thickening of distal ileum proximal to the ileocolic anastomosis, without frank extravasation identified. Colonoscopy revealed erythematous mucosa and multiple non-bleeding ulcers with overlying exudates around ileocolonic anastomosis and more proximally into the ileum, in addition to small caliber non-bleeding diverticula and internal hemorrhoids. Biopsies showed marked active inflammation with heavy lymphoblastic infiltrated, with eosinophils, neutrophils, as well as cryptic distortion and surface erosion. Diagnosis of capecitabine-induced ileocolitis performed based on the history and endoscopic findings. Withdrawal of capecitabine in addition to supportive care was performed, and symptoms eventually improved after a prolonged hospital course. Discussion: While few have described that persistent diarrhea and ileitis or ileocolitis are potential complications of capecitabine use, there is even more paucity of data regarding capecitabine-associated GI bleeding. The precise mechanism of capecitabine-induced GI injury is unknown; however it has been suggested that induces loss of epithelial surface secondary to acute mucosal injury through interference with crypt cell mitoses. Our case identifies a rare but critical presentation of capecitabine-associated GI toxicity, as the treatment with capecitabine should be considered more often as a cause of severe gastrointestinal bleeding.

S3064 Intestinal Post-Transplant Lymphoproliferative Disorder

Introduction: Post-transplant lymphoproliferative disease (PTLD) is a group of lymphoid disorders arising in the setting of immunosuppression following a solid organ or stem cell transplantation. PTLD impacts 2.8% of adults and 15% of children post-orthotopic liver transplant (OLT) at a median of 8 years. The small intestine, rich in B cells, is a common site for PTLD and the treatment is chemotherapy. Here, we present a case of a patient post-OLT presenting with abdominal pain, and anemia found to have small bowel PTLD resulting in jejunal perforation with eventual resolution of symptoms after surgical resection and chemotherapy. Case Description/Methods: 65-year old obese F with non-alcoholic steatohepatitis decompensated by hepatopulmonary syndrome with O2 dependence and hepatocellular carcinoma underwent an uneventful OLT (CMV +/-) with no immediate postoperative complications and resolution of the hepatopulmonary syndrome. Presented 2 months after the OLT with worsening LLQ abdominal pain and acute anemia. An EGD and colonoscopy completed shortly after admission showed evidence of gastric, duodenal, and descending colon non-bleeding ulcers that were biopsied. Pathology showed EBV+ atypical B cell proliferation concerning for large B cell lymphoma and monomorphic-PTLD. An EBV viral load obtained at that time was elevated and subsequent CT Abdomen/Pelvis showed scattered small sub-centimeter mesenteric and retroperitoneal lymph nodes. Her immunosuppression was minimized without a change in symptoms. She subsequently developed large volume haematochezia leading to shock and underwent an EGD and colonoscopy followed by a push enteroscopy that revealed multiple ulcers but no active bleeding site. Immediately after the procedure, she developed an acute abdomen due to a perforated Jejunal ulcer. Had an emergent exploratory laparotomy and jejunectomy with subsequent improvement in her anemia. She was treated with R-CHOP for PTLD with the resolution of her presenting symptoms. Discussion: PTLD, however rare, remains the commonest post-transplant malignancy. Once there is suspicion (pain, weight loss, and anemia post OLT), EGD/Colonoscopy reveals suspicious malignant-looking ulcers, and mucosa or lymph node biopsy confirms PTLD. The patient ultimately underwent treatment with 4 cycles of R-CHOP with surveillance EBV PCR and imaging with resolution of complete symptoms. Immediate treatment should be started with lowering immune suppression and chemotherapy rather than waiting for self-resolution in PTLD cases.Figure 1.: Jejunal and Gastric ulcers (seen on prior scopes as well) were found on the Push enteroscopy just prior to the perforation of the bleeding jejunal ulcer and eventual surgical resection of the jejunum that resolved her anemia.

S2585 Does Size Matter? A Case Series on Management of Duodenal Varices

Introduction: Duodenal varices (DVs) are a rare cause of life-threatening bleeding in cirrhotic patients. No standardized guidelines for their management exist. We present two cases of DV hemorrhage who were successfully managed by endoscopic variceal band ligation (EVL) and coil embolization respectively. Case Description/Methods: Case 1: A 63-year-old male with cirrhosis was admitted for upper GI bleeding and Hemoglobin (hgb) of 7.1. Endoscopy showed small to medium-sized DVs with stigmata of recent bleeding with a platelet plug in the second portion of duodenum. EVL was done with adequate decompression and no immediate bleeding. One week later, he developed recurrent hematochezia. Full GI work up including upper endoscopy, small bowel capsule and colonoscopy showed previously noted non-bleeding ulcers in the duodenum with no new active bleeding sites. Case 2: A 68-year-old male with cryptogenic cirrhosis complicated by large hepatocellular carcinoma causing portal vein obstruction was admitted for GI bleeding and hgb of 4.3. Endoscopy showed multiple large DVs with active bleeding. Successful hemostasis was achieved using three hemostatic clips but without adequate decompression. However, given the size of the varix, the patient then underwent successful percutaneous transsplenic porto-venous variceal coil embolization by interventional radiology (IR). Discussion: Variceal bleeding occurs in 25-30% of cirrhotic patients with ectopic varices accounting for 1-5% of these bleeds. DVs are uncommon but can cause massive hemorrhage with a high mortality up to 40%, due to challenges with treatment. Management options include EVL, sclerotherapy, clipping or IR guided Trans Jugular Intrahepatic Portosystemic Shunt (TIPS), Balloon-Occluded or Coil Assisted Retrograde Transvenous obliteration. One concern with EVL is the size of the DV and risk of re-bleeding. Among case reports using EVL, re-bleeding was seen only in 3/19 cases with hemostasis achieved with repeat banding in 2 out of the three cases. However, for successful band ligation, accessibility, and size of the varices to fit into the banding cap are important factors to consider. Small – medium duodenal varices (case 1) were adequately managed by EVL, however endoscopic decompression could not be completely achieved in large varices (case 2) and eventually required IR guided coil embolization. Therefore, the size and location of the duodenal varices are important factors to be considered in choosing the appropriate management modality for DVs (Figure 1).Figure 1.: A, Percutaneous transsplenic splenic venogram demonstrating large duodenal varix(white arrows) with linear endoscopically placed clip corresponding with site of hemorrhage in the vertical segment of the duodenum (black arrow). The splenic vein (white arrowhead) drains via the large varix as the main portal vein is occluded secondary to hepatic tumor; B, Percutaneous transsplenic splenic venogram demonstrating successful coil embolization of the varix (black arrowheads); C, Endoscopic view of large varices in second portion of duodenum, post hemostatic clip placement.

Small bowel hemorrhage from check point inhibitor enteritis: a case report

BackgroundThere is rising utilization of immune checkpoint inhibitors (ICI) for a growing number of metastatic malignancies. While gastrointestinal side effects of ICI are common, isolated ICI-induced enteritis leading to small bowel hemorrhage is rare.Case presentationA 71-year-old man with a previously resected right colon adenocarcinoma on atezolizumab and recently treated Clostridioides difficile presented with acute on chronic abdominal pain and non-bloody diarrhea. A CT scan revealed enteritis of the duodenum and jejunum without colitis. Initial endoscopic work-up revealed many clean-based non-bleeding duodenal ulcers to the third portion of the duodenum and normal rectosigmoid mucosa. The patient initially improved on steroids but was readmitted on day after discharge with hematochezia and hemorrhagic shock. Repeat CT showed improvement in enteritis; however, repeat push enteroscopy revealed multiple duodenal and jejunal ulcers, two with visible vessels requiring endoscopic intervention. He continued to have significant hemorrhage requiring transfusions despite IV methylprednisolone. Conventional angiogram revealed multiple sites of active extravasation, and he underwent small bowel resection and subsequent IR embolization due to persistent bleeding. He was then started on infliximab 10 mg/kg with resolution of his small bowel hemorrhage and diarrhea.ConclusionsSevere isolated ICI-enteritis is rare and can lead to clinically significant gastrointestinal hemorrhage. Patients with severe ICI-enteritis on endoscopy should be carefully monitored for steroid refractory disease for consideration of step-up therapy such as infliximab.

Occult strongyloides stercoralis infection masquerading as a drug reaction with eosinophilic pneumonia

Background: Pseudomelanosis or melanosis duodeni is seen in association with drugs, microorganisms or occasional bleeding, usually from peptic ulceration. We present a case of Strongyloides stercoralis presenting as pseudomelanosis duodeni during anemia workup after patient’s initial presentation as eosinophilic pneumonia. Case presentation: The patient is a 77 year-old female with a history of diastolic congestive heart failure, chronic kidney disease, diabetes mellitus, and hypertension who presented for evaluation of black stool. Two months earlier, in her prior admission for acute eosinophilic pneumonitis, the patient’s hematocrit was 26%. In her current admission with heme-positive dark stool on exam, the hematocrit dropped to 19%. The patient underwent esophagogastroduodenoscopy to identify the source of bleeding. The upper endoscopy revealed three non-bleeding ulcers in the gastric antrum and discoloration of the duodenal bulb and second portion of the duodenum. By histology, the duodenal biopsies showed areas of hemosiderin-laden macrophages in the lamina propria, focal helminth eggs and larvae in the crypt lumen with sizes ranging from 35-65 microns x ~20 microns. Polymerase chain reaction of the paraffin embedded tissue with 28S primer set detected Strongyloides stercoralis DNA, confirming the histologic findings. Given the confirmation of Strongyloides stercoralis, the patient’s initial presentation of eosinophilic pneumonia (Loeffler syndrome) may be a result of the parasitic infection or the successful response to steroid treatment for acute eosinophilic pneumonia caused Strongyloidiasis hyperinfection. The patient’s symptoms were improved with Ivermectin and hematocrit level increased to 28%. Conclusions: This case highlights the importance in recognition of helminth infection in the evaluation of eosinophilic pneumonia and pseudomelanosis duodeni. Keywords: Pseudomelanosis duodeni; Strongyloides stercoralis; Eosinophilic pneumonia; polymerase chain reaction.

S2146 Rare Presentation of a Bleeding Arteriovenous Malformation Within a Periampullary Duodenal Diverticulum

INTRODUCTION: The incidence of duodenal diverticula (DD) is reported between 0.16% and 23% in the literature, depending on the method of diagnosis, with more than 60% arising in the second part of the duodenum. Though typically asymptomatic, various complications including pancreatitis, diverticulitis, duodenal obstruction, and bleeding have rarely been reported in the literature. We present a case of melena that was initially thought to be due to epistaxis in the setting of a supra-therapeutic INR, and was later found to be secondary to an arteriovenous malformation (AVM) within a periampullary DD. CASE DESCRIPTION/METHODS: A 72-year-old male with a history of metastatic renal cell carcinoma status-post nephrectomy, aortic stenosis, end-stage renal disease on peritoneal dialysis, and atrial fibrillation on Coumadin presented with subacute epistaxis and melena. Abdominal exam was unremarkable, and labs were notable for a hemoglobin 7.1 g/dL, platelet 76 k/uL, sodium 121 mmol/L, and INR 4.5. Given a history of epistaxis requiring otolaryngology intervention on admission that could explain his melena, a gastroenterology consult was not at first pursued. However, 12 days into the hospitalization, he continued to have melena with blood transfusion requirements, despite no evidence of recurrent epistaxis. An EGD was then done and showed a 4-mm non-bleeding ulcer in the duodenal bulb, a bleeding 5-mm AVM in a large DD treated with argon plasma coagulation (APC) and clipping, and a bleeding AVM in the posterior duodenal bulb. Ongoing melena and persistent anemia later prompted an additional push enteroscopy, colonoscopy and capsule endoscopy, which showed no evidence of ongoing bleeding at the previously treated sites or new lesions with bleeding. To reduce the risk of rebleeding, the patient's medications were adjusted (Coumadin switched to Apixaban and his VEGF inhibitor was discontinued). DISCUSSION: Definitive treatment for bleeding arising from DD traditionally involves surgical removal, though there have been increasing reports of successful endoscopic therapy. In this case, we showed that APC and clipping of a bleeding AVM within a periampullary DD was a safe and effective approach. We also highlight the need to avoid the premature assumption that persistent melena in the setting of recent recurrent epistaxis precludes coexistent gastrointestinal bleeding.Figure 1.: Bleeding AVM within duodenal diverticulum, prior to treatment.Figure 2.: AVM within duodenal diverticulum after treatment with APC and clip.Figure 3.: A CT of the abdomen/pelvis demonstrating an air-filled diverticulum of the second portion of the duodenum.

S2872 A Case of CMV Enteritis Resulting in Severe Obscure GI Bleeding

INTRODUCTION: Small bowel (SB) bleeding accounts for less than 5% of gastrointestinal (GI) bleeds, in non-IBD patients, with an even smaller portion originating from the jejunum [1]. Locating SB bleeds poses great challenges, frequently resulting in delay in diagnosis. Although SB arteriovenous malformations (AVMs) are most common, other rare etiologies such as infectious enteritis should be considered. CASE DESCRIPTION/METHODS: A 62 year old male was diagnosed with T-cell lymphoma with EBV positivity and placed on high-dose steroids for one month. Staging CT chest, abdomen, and pelvis incidentally revealed intraperitoneal free air with concerns for a gastric wall neoplasm. EGD revealed a 4cm, deep, non-bleeding, non-perforated ulcer in the gastric body (Image 1). Two weeks after, he had painless melanotic stools, requiring multiple transfusions. Emergent arteriography of the celiac and mesenteric arteries did not identify a source of bleeding. Repeat CT imaging was negative for worsening free air. His course continued to worsen, requiring high-dose vasopressors and continued transfusions. Emergent EGD and colonoscopy were performed. EGD revealed a known, non-bleeding gastric ulcer. Colonoscopy showed bright red blood to the cecum with scattered, non-bleeding, ischemic-appearing ulcers (Image 2). Repeat celiac angiogram was performed two more times, eventually revealing active bleeding from small jejunal artery branches which were embolized. Due to concern for ongoing bleeding, surgical resection of the distal jejunum and proximal ileum was performed. Gross pathology demonstrated extensive ulcerations, with biopsies negative for malignancy (Image 3). Serum testing for Cytomegalovirus (CMV) was positive for strongly elevated quantitative levels and the patient was started on Valganciclovir. DISCUSSION: Delays in diagnosing SB bleeds are not uncommon and can frequently be fatal. Our case presents a complex diagnostic scenario where bleeding was presumed to be from the known gastric lesion, but complicated by inability to perform EGD safely with pneumoperitoneum. Ultimately, the patient’s immunocompromised state and steroids predisposed him to opportunistic infections such as CMV, resulting in bleeding ulcers in the jejunum and ileum. Upon literature review, CMV enteritis is exceedingly rare and accounts for under 5% of all CMV infections in the GI tract [2]. Though rare, CMV enteritis has been reported to cause massive hemorrhage requiring emergent surgery and is often associated with high mortality.Figure 1.: 4cm non-bleeding ulcer in the gastric body seen on the initial EGD.Figure 2.: Scattered ischemic-appearing colonic ulcers.Figure 3.: Gross specimen of resected and ulcerated jejunum.

S2209 Primary Aortoduodenal Fistula in a Native Aorta Causing Brisk Upper GI Bleeding

INTRODUCTION: Primary aortoduodenal fistula (ADF) is a rare cause of gastrointestinal bleeding and is difficult to diagnose. Computed tomographic angiography (CTA) can be used to detect primary ADF. Open surgery or endovascular aortic repair (EVAR) for ADF improves survival. CASE DESCRIPTION/METHODS: 73-year-old male with atherosclerotic, native, non-surgically altered, normal diameter aorta complicating ADF presented with massive GI bleeding. Initially at outside hospital and was evaluated for intermittent episodes of hematemesis and hematochezia for one month. Repeated endoscopy failed to identify a source of bleeding, but blood was seen within the colon. Nuclear scans and CTAs showed no sources of active bleed/fistulas. He was transferred to our facility for further evaluation. On admission, he was in shock with a significant drop in his Hgb. Repeat endoscopy revealed a non-bleeding ulcer with a large visible vessel in the 3rd portion of the duodenum (Figure 1). Given the location and size, was felt not to be amenable to endoscopic therapy. Patient bled overnight. Urgent CTA showed active intraluminal hemorrhage within the duodenum and proximal jejunum, and abnormal periaortic soft tissue concerning for ADF (Figure 2). The Patient was taken to the IR and was found to have an ADF. Vascular surgery was consulted intra-operatively and performed an EVAR with stent-graft of the infrarenal aorta. The patient’s GI bleeding resolved. DISCUSSION: Primary ADF is an abnormal communication between the infrarenal aorta and duodenum involving the 3rd part of the duodenum in 2/3rd of cases and the 4th part in 1/3rd of cases. Primary ADF is an extremely rare entity. There were 791 ADF cases reported between 1951 and 2010, including 253 cases of primary ADF and 491 cases of secondary ADF. Of the primary cases, all included the presence of AAA. Our case is a patient with brisk upper GI bleeding, without high suspicion of ADF due to his history of a native, nonenlarged, unaltered aorta. We believe the pathophysiology of this case was a weakened aortic wall and inflammation secondary to chronic atherosclerosis resulting in fistula formation to the duodenum. A timely and accurate diagnosis of primary ADF may be challenging due to insidious episodes of GI bleeding, which are frequently under-diagnosed until the occurrence of massive hemorrhage. Clinicians should keep a high index of awareness for primary ADF, especially in elderly patients with unknown etiology of brisk upper GI bleeding with or without a known AAA.Figure 1Figure 2

Endoscopic Management of Postlaparoscopic Sleeve Gastrectomy Leaks: A Single-Center Experience

Abstract Introduction Laparoscopic sleeve gastrectomy (LSG) is a commonly performed bariatric surgery. Sleeve leak is the most important complication, with an incidence of 1.9 to 2.4%. Various endoscopic approaches to LSG have been used, including self-expanding metal stents (SEMSs), glue injection, and clipping along with percutaneous drainage. This study was aimed to study the role of endotherapy in the management of post-LSG leaks. Methods This study included patients referred for endotherapy for post-LSG leak between January 2016 and December 2018. We maintained data prospectively, which included the location and type of leak, type of endotherapy, adverse events, and time for leak closure. Primary endotherapy included mega SEMS placement; if it failed, then secondary endoscopic therapy was performed. Results Seven patients (four females, with a mean age of 45.2 years) with a preoperative body mass index of mean 38.5 kg/m2 underwent endotherapy for post-LSG leaks. Two were acute, four were early, and the remaining one was late leak. Five were located proximally near gastroesophageal junction and two at the midsleeve level. In four (57.1%) patients, the leak was resolved by primary therapy. Three patients underwent secondary therapy that included overlapping SEMS placement (in one patient), SEMS replacement (in one patient), and short plastic biliary stent placement with Argon plasma coagulation (APC) to create a raw surface and induce granulation tissue. The median duration for leak closure was 12 weeks (range: 8–24 weeks). One patient who had partial distal migration underwent overlapping SEMS placement. Three patients had nonbleeding ulcers at the distal end of SEMS at removal. Conclusion Endotherapy is effective and safe for the management of post-LSG leaks. Additional endotherapy can be used if primary therapy is not successful for resolution of the leak.

A114 AMEBIC COLITIS AS A RARE CAUSE OF PSEUDOMEMBRANOUS COLITIS

Abstract Background Globally, Entamoeba histolytica results in nearly 40 million cases of amebic colitis and 50 000 deaths annually. The disease is common in Africa, Asia, and Central and South America but infection remains rare in North America, limited to travelers, immigrants, and immunocompromised hosts. The disease ranges from asymptomatic chronic colonization to dysentery and fulminant colitis. Endoscopically, the ulcerations may demonstrate the non-specific pattern of pseudomembranous colitis that is classically seen with Clostridoides difficile infection. Aims To discuss an unusual case of pseudomembranous colitis caused by Entamoeba histolytica. Methods The patient records were reviewed and a review of the literature was performed. Results A 54-year-old male with a remote history of peptic ulcer disease visiting from Guinea presented with a 3-day history of right sided abdominal cramping and intermittent bloody diarrhea. The pain was gradual in onset with moderate severity. He reported >5 episodes of blood intermixed with brown stools. He was incidentally diagnosed with hypertension and started on treatment two weeks prior. He denied recent antibiotic use and family history was unremarkable for inflammatory bowel disease (IBD) or other forms of colitis. There was no abdominal tenderness or bleeding on rectal examination. He had a stable normocytic anemia (Hgb 114), leukocytosis (13.4) with neutrophilia, and elevated C-reactive protein (43.4 mg/L). He was discharged with presumed resolving ischemic colitis. Colonoscopy showed diffuse colonic involvement with areas of patchy yellow plaques and a mix of shallow and deep non-bleeding ulcers suggestive of pseudomembranous colitis. He was discharged with empiric oral vancomycin, later discontinued following negative C. difficile toxin testing. Stool cultures and microscopy detected Entamoeba histolytica. Limited biopsies of the nodular ulcers failed to show any pathologic alterations or trophozoites. The patient was treated for luminal amebiasis with oral metronidazole and paromomycin but was lost to follow up on return to his native country. Conclusions Amebic colitis remains a rare entity in the developed world and is limited to travelers or recent immigrants from endemic areas. Diagnosis is typically difficult and may require endoscopy as its clinical course may resemble IBD or infectious colitis. Limited cases exist of fulminant amebic colitis causing pseudomembranous colitis, with even fewer cases of mild dysentery having this appearance. Despite pseudomembranous colitis being commonly associated with C. difficile infection, this pattern of mucosal injury may be seen with other enteric bacterial and protozoan infections, inflammatory conditions, or use of certain medications. In the appropriate clinical context, on exclusion of C. difficile, secondary causes such as active amebiasis should be considered. Funding Agencies None

2587 Never Too Old for Meckel's: A Unique Presentation of an Uncommon Source of Gastrointestinal Bleeding in Adults

INTRODUCTION: Meckel's diverticulum is a common gastrointestinal congenital malformation, affecting approximately 2% of the population. Related complications such as bleeding commonly occurs in the pediatric age group; although, in adults it is often missed. We present a case of recurrent obscure-overt gastrointestinal (GI) bleeding secondary to a Meckel's diverticulum which remained elusive after multiple diagnostic studies. CASE DESCRIPTION/METHODS: 30-year-old male with history of recurrent GI bleeding, presents to the outpatient GI clinic for further evaluation after being admitted to the intensive care unit (ICU) 3 weeks prior with massive hematochezia requiring several blood transfusions for a drop-in hemoglobin from 14 gm/dL to <7 gm/dL. The patient had undergone endoscopy, colonoscopy, and video capsule endoscopy (VCE) three years prior for similar symptoms without an identifiable source. A nuclear tagged red blood cell scan was performed showing bleeding in the proximal colon. CT angiography following showed contrast extravasation in the distal jejunum and ileum which was treated with gel foam. The patient had no further episodes of hematochezia and was discharged. After the clinic visit, the patient underwent a Meckel's scan which did not show ectopic gastric mucosa but revealed colonic bleeding proximal to the hepatic flexure. Ileocolonoscopy was normal. Subsequent VCE showed abnormal mucosa in the distal small bowel. He finally underwent a retrograde balloon enteroscopy which revealed a distal small bowel diverticulum with a single adjacent, nonbleeding ulcer (Figure 1). Biopsies of the ulcer showed gastric foveolar metaplasia. Based on the findings, he was referred for a small bowel resection which revealed a jejunal Meckel's diverticulum with gastric oxyntic heterotopia on histology (Figures 2 and 3). DISCUSSION: This case highlights the potential morbidity and possible mortality of Meckel's diverticulum as a source of lower GI bleeding. Recent studies have recommended against prophylactic surgical resection in the absence of certain risk factors including age less than 40, male gender, and macroscopic mucosal alteration. Given this patient's significant hematochezia, transfusion requirements, and gross peri-diverticular ulceration, we opted for small bowel resection. Meckel's diverticulum should always be included in the differential for occult or overt GI bleeding, especially in young patients when no other sources of bleeding are readily identifiable.

2024 Novel Approach for Management of Stomal Variceal Bleed

INTRODUCTION: Patients with cirrhosis are prone to developing bleeding from varices. Patients with cirrhosis and ileostomy can develop ileostomy varices. Only 5% of variceal bleeds are reported to be from an ileostomy varix. CASE DESCRIPTION/METHODS: A 51-year-old female with heart failure, hepatitis C cirrhosis, esophageal varices with recent banding, colectomy with ileostomy presented with ostomy bleeding. Examination of the ostomy revealed oozing from the ostomy site. The ostomy site was cauterized with silver nitrate which initially stopped the bleeding. Esophagoduodenoscopy demonstrated three columns of non bleeding varices, no red whale/nipple sign and two non bleeding esophageal ulcers. Later, ostomy bleeding recurred which led to an ileoscopy. A non-bleeding ulcer was noted in the ileum. As the scope was withdrawn, an osteal varix was noted and due to the manipulation of the scope, the varix started squirting blood. Manual pressure was applied and a foley was inflated in the ostomy tract for tamponade. After 15 minutes of tamponade, the scope was re-inserted which did not demonstrate active bleeding. Banding couldn't be performed as there was no room to manipulate the scope. A CTA demonstrated two varices originating from the superior mesenteric vein within the ostomy track (Figure 1). TIPS was contraindicated due to heart failure. 2cc of Sotradecol was injected into each varix for obliteration via ultrasound guidance. After the injection, ultrasound showed successful obliteration of the varices (Figure 2). There was no further bleeding during her hospital stay. DISCUSSION: Ileostomy variceal bleeding is uncommon. Bleeding from an ileostomy varix can occur as early as a year after ileostomy placement in patients with cirrhosis. Diagnosis is often missed. It is key to inspect the stoma for bleeding after removal of the appliance. Doppler ultrasound or CT/MRI can aid in the diagnosis. There are multiple strategies to treat a variceal ostomy bleed including local control (ligation, sclerotherapy, intravascular coil or glue emboliziation) and portal vein decompression (TIPS). In majority of cases, local therapy is used as first line treatment as demonstrated in our patient who was successfully treated with sclerotherapy. We'd like to highlight the possibility of ultrasound guided sclerotherapy of osteal varices if endoscopic sclerotherapy is not feasible. More research is needed to assess which treatment strategy provides the best outcome for patients coming in with ileostomy variceal bleeding.

2584 Running Into a Stone Wall: A Rare Case of Gastric Outlet Obstruction

INTRODUCTION: Bouveret syndrome is an extremely rare and serious form of gallstone ileus with an incidence of 1-3% and a surgical mortality rate approaching 15-33 percent. Treatment often involves a combination of endoscopic and surgical interventions. We present a case of gastric outlet obstruction and duodenal ulceration caused by 3 impacted gallstones, treated ultimately with surgery. CASE DESCRIPTION/METHODS: A 57-year-old male with no known medical conditions was admitted to the intensive care unit with a one-week history of epigastric pain, nausea, and dark emesis. He was tachycardic and hypotensive on arrival. On exam, the patient was diaphoretic with dark-bloody return from the nasogastric tube. Hemoglobin was 5.6 g/dL (ref: 14.0-16.8 g/dL) with a leukocytosis of 17.69 K/uL (ref: 4.0-10.8 K/uL). Liver enzymes were unremarkable. Given concerns for an upper gastrointestinal bleed, patient underwent an esophagogastroduodenoscopy showing a 3-cm non-bleeding ulcer in the duodenal bulb, a cholecystoduodenal fistula, and a large impacted gallstone in the first portion of the duodenum distal to the fistula (Figure 1). Subsequent contrast-enhanced computed tomography demonstrated significant pneumobilia and a perforated duodenal ulcer (Figure 2). Removal of the obstructing gallstone was unsuccessful despite using a Raptor grasping device, Roth net retriever, and snare. Patient subsequently underwent exploratory laparotomy with cholecystectomy, pyloric exclusion, Roux-en-Y gastrojejunostomy, and duodenal enterorrhaphy with Graham patch (Figure 3). He tolerated the procedure well and was discharged to a rehabilitation facility. DISCUSSION: Bouveret Syndrome is a rare form of gallstone ileus characterized by gastric outlet obstruction secondary to gallstone impaction within the duodenum or pylorus through a cholecystoduodenal or choledochoduodenal fistula. Prompt imaging is warranted and in patients with gallstone ileus, may reveal pneumobilia, bowel obstruction, and ectopic gallstone, also known as Rigler's triad. Enterolithotomy, gastrostomy with cholecystectomy, and fistula repair are considered the mainstay of management, but prompt gastroenterological evaluation is warranted to evaluate the possibility of mechanical extraction or stone fragmentation.

1744 Not an Ordinary Ulcer: A Case of an Aorto-Esophageal Fistula

INTRODUCTION: Hematemesis is a common manifestation of variceal and non-variceal upper gastrointestinal (GI) bleed with a broad differential. Aortoesophageal fistula (AEF) is a life-threatening and catastrophic cause of gastrointestinal bleeding, which is caused by the abnormal communication between the aorta and the esophagus. We are presenting a rare case aorto-esophageal fistula in a young patient who was found to have a benign appearing esophageal ulcer on endocscopy that subsequently was found to be an (AEF). CASE DESCRIPTION/METHODS: A 33-year-old Caucasian male presented to the hospital for fatigue, non-blood emesis and progressively worsening leg swelling. His history is significant for hypertension, seizure disorder, chronic kidney disease (due to pauci-immune glomerulonephritis), heart failure and a descending aortic transection due to an accident 12 years ago which was repair endovascularly. The patient reported usage of NSAIDs prior to admission for pain control but otherwise denied alcohol or other substance abuse. The patient was admitted for his progressive renal failure and was started on hemodialysis complicated with a DVT for which was started on warfarin. During his hospitalization, the patient had an episode of hematemesis with hemodynamic instability which prompted cessation of anticoagulation. An EGD revealed a 2-3 cm non-bleeding ulcer in the proximal esophagus. The patient had stabilized hematocrit and hemodynamics and was restarted on anticoagulation. A week later, the patient had another episode of massive hematemesis with hypotension. A chest x-ray showed widening of the aortic knob, suggested change in location of the thoracic stent. CT angiogram showed aortoesophageal fistula with a leaking pseudoaneurysm at the proximal aspect of the thoracic aortic endovascular stent. Surgery proceeded with endovascular aortic repair of thoracic pseudoaneurysm. Patient had multi-disciplinary management strategy for staged repair. DISCUSSION: AEF are classified as primary i.e. spontaneous erosion of the aortic wall into the esophagus or secondary caused by either esophageal malignancy, surgeries or foreign body. Exact incidence of the AEF is unknown. Early recognition is important to decrease mortality. Chiari et al described the triad of midthoracic pain, herald hemorrhage, and fatal hematemesis as usual presenting features. Endoscopy plays a significant role in the evaluation however it has a poor rate of detection for AEFs prompting the need of CT imaging with high clinical suspicion.

1895 “The First Burn Is the Deepest:” A Cautionary Tale in Superficial APC Therapy for Radiation Proctopathy

INTRODUCTION: Globally, prostate cancer is the most commonly diagnosed cancer in men. Radiation therapy remains a mainstay in the armamentarium in the treatment of this disease. Radiation proctopathy is a common side effect of this treatment modality with an incidence in patients treated with brachytherapy alone estimated to range from 8 to 13%, and up to 21% in combination with other modalities [2]. Radiation proctopathy typically presents with diarrhea, mucoid discharge, urgency, tenesmus, and bleeding. Argon plasma coagulation (APC) has become the primary therapeutic modality in the management of radiation injury. It is essential that physicians of all specialties (as well as others who care for these patients) be aware of the multiple complications of this therapy. More severe adverse events, notably rectal ulcers following APC therapy are not uncommon, with an incidence ranging from 3 to 16%. CASE DESCRIPTION/METHODS: A 67-year-old man with a history of prostate cancer treated with radiation therapy one year prior presented with intermittent rectal bleeding for one and a half months. A colonoscopy was performed, which revealed a small area near the dentate line characterized by slightly oozing neovascularized tissue consistent with radiation proctopathy. This area was treated with APC with good effect. Biopsies of this area revealed hyperplastic crypts, lamina propria fibrosis, and vascular ectasias compatible with radiation injury. Three months following treatment, the patient developed recurrent rectal bleeding. A flexible sigmoidoscopy revealed a deep non-bleeding ulcer in the rectum. Subsequent CT enterography and MRI of the pelvis demonstrated a deep rectal ulcer with abutment of a 1.5cm peri-prostatic abscess. The patient was followed closely over the next several months in concert with colorectal surgical colleagues, with serial imaging and subsequent resolution of the peri-prostatic abscess as well as cessation of rectal bleeding. DISCUSSION: As more patients with prostate cancer are treated with radiation therapy the incidence of radiation proctopathy is increasing. Although argon plasma coagulation has been shown to be an effective therapy for this issue, providers must consider and discuss with patients the potential complications of this otherwise effective and generally well-tolerated mode of treatment.

2004 Gastric Kaposi's Sarcoma in a Patient With Aplastic Anemia

INTRODUCTION: Gastric Kaposi’s sarcoma (KS) is rare and mostly seen in patients with acquired immunodeficiency syndrome (AIDS). We present here a case of gastric KS presenting as upper gastrointestinal bleeding in a human immunodeficiency virus (HIV) negative patient with aplastic anemia. CASE DESCRIPTION/METHODS: A 70-year-old African American male was admitted with the history of hematemesis. He had sudden onset of nausea and vomiting of blood. He denied any abdominal pain or melena. He was not taking any non-steroidal anti-inflammatory drug. He was known to have aplastic anemia, diabetes mellitus, hypertension gastroesophageal reflux disease and renal insufficiency. He was undergoing treatment with cyclosporine, prednisone and anti-thymocyte globulin for his aplastic anemia. His other medications included insulin glargine, duluglutide, amlodipine, hydrochlorothiazide famotidine, prochlorperazine, valacyclovir and eltrombopag. On admission, his pulse was 125/minute and blood pressure 85/60 mm Hg which returned to normal range with infusion of 1 liter of normal saline. He looked anxious. Abdominal examination was significant for mild epigastric tenderness to palpation. Rectal examination showed heme positive stool. Remainder of the examination was normal, including no new rashes or skin lesions. Laboratory values were significant for hemoglobin of 7.8 g/dl (baseline 8.0-9.0 g/dl), white count of 4,300/cmm and platelets of 89,000/cmm in keeping with known aplastic anemia. Patient had upper endoscopy which revealed 4 cratered sub-centimeter non-bleeding ulcers with rolled edges in the gastric body (Figures 1 and 2). The edges of the ulcers appeared to have increased vascularity. Biopsies were taken from the ulcer edges. Biopsies showed atypical mucosal spindle cell proliferation (Figure 3) with positive staining for D2-40 (endothelial cell) and human herpesvirus 8 (HHV–8) confirming the diagnosis of gastric KS. DISCUSSION: KS is a low-grade angiolymphoproliferative tumor arising from the endothelial cells lining the blood vessels or lymphatic vessels. It can develop in patients with significant immunosuppression irrespective of HIV status. Physicians should consider gastric KS in the differential diagnoses when patients with aplastic anemia on immunosuppressive medications present with upper gastrointestinal bleed and endoscopy shows gastric ulcers. Biopsy of the gastric ulcers in this situation is essential to establish the diagnosis.

3130 Unexplained Thrombocytopenia Associated to the Use of PPI in a Patient With a Bleeding Peptic Ulcer Disease

INTRODUCTION: Proton pump inhibitors (PPIs) are used to suppress acid production and to promote hemostasis, which significantly reduces the risk of rebleeding in upper gastrointestinal bleeding [1]. Accumulating evidence indicates an association between PPIs and thrombocytopenia in patients treated for upper gastrointestinal bleeds [2-4]. CASE DESCRIPTION/METHODS: A 38-year-old male with no significant past medical history presented to the hospital complaining of coffee ground emesis, hematochezia, dark stools and three episodes of syncope in the setting of daily naproxen use for one month. Vital signs revealed orthostasis without tachycardia or hypotension. Physical exam revealed a soft, non-tender, non-distended, abdomen with normoactive bowel sounds. Rectal exam was positive for melena but negative for hemorrhoids or any palpable masses. Initial laboratory workup was significant for a hemoglobin of 7.8, platelet count of 163, and BUN of 27. Intravenous (IV) PPI was administered for management of suspected bleeding PUD. The patient received packed red blood cells (PRBCs) with appropriate response to transfusion. Upper endoscopy revealed a pre-pyloric non-bleeding ulcer that was successfully treated. A significant drop in platelet count was noted on hospital day four which continued to decrease from 163 to 107. PPI route of administration was changed from IV to oral, resulting in an increase in platelet count to 116 by hospital day 7. DISCUSSION: PPIs are widely used for the treatment of PUD, GERD, Barrett esophagus, esophagitis, and gastritis. As the main medication used in the treatment of upper gastrointestinal bleeding, it is crucial to understand the effect of PPI therapy on platelets. Literature review suggests an association between thrombocytopenia and the use of PPIs [2-4]. However, further studies are needed to establish a direct association between PPIs and thrombocytopenia. In our case, thrombocytopenia was noted on hospital day 3 of PPI infusion. Route of administration of PPI was changed from IV to oral and thrombocytopenia improved steadily. Although the exact mechanism linking PPI therapy to thrombocytopenia remains unknown, it is important to be aware of this possibility. Close monitoring of platelet count is recommended upon initiation of PPI therapy.

1915 Delayed Post-Polypectomy Bleeding Case Report, Using Cold Snare Technique

INTRODUCTION: Most cases of colorectal cancer develop from colorectal polyps, therefore their early detection and removal decreases the risk of colorectal cancer death. Hot snare is the most commonly used endoscopic technique to eradicate colonic polyps with some inevitable post polypectomy bleeding. Cold snare polypectomy has been used recently because of its low risk of immediate and delayed post polypectomy bleeding. CASE DESCRIPTION/METHODS: A 66 y/o female with a history of ascending colon cancer status post right hemicolectomy presented for routine screening colonoscopy. She has a history of coronary artery disease status post stenting, systolic congestive heart failure and mechanical aortic valve for which she is on warfarin for anticoagulation. Warfarin was stopped 7 days before the procedure, without bridging. Colonoscopy showed two small polyps in the descending and sigmoid colon, and these were removed using cold snare. She was stable after colonoscopy and was discharged. Warfarin was restarted on the next day. Five days later she presented to the hospital complaining of bright red bleeding per rectum and bright red blood with stool. Hemoglobin had decreased from 11.4 (gm/dl) on the day of admission to 9.8 (gm/dl) the next day. Repeat colonoscopy was performed and a large clot was seen in the descending colon at one polypectomy site. There was no active bleeding from the clot though there was some minimal oozing with manipulation. The clot was not removed due to concerns of a large defect underneath that might bleed again. The surgery team was consulted during the procedure. Both GI and surgery teams decided not to proceed with any intervention. Another small non-bleeding ulcer in the sigmoid colon measuring 5 mm was seen and likely represent the site of previous polypectomy. She was monitored after the procedure, her symptoms and hemoglobin improved. Warfarin was restarted and discharged in stable condition. DISCUSSION: Cold snare polypectomy is being increasingly used as it is safe and efficient for small polyp removal. Newer polypectomy snares designed for cold snare polypectomy have been developed. This equipment may further decrease complications from smaller polypectomies. We present a case of rare delayed post polypectomy bleeding with the development of a large post polypectomy ulcer, even though anticoagulation was interrupted 7 days before the procedure. We used the traditional polypectomy snare. Results could have been different if the more modern cold snare polypectomy equipment used.