bluuebunny/crossref_metadata_2025_split huggingface dataset:
1911 Acquired Double Pylorus: The Road Less Traveled
Authors: Ali Hiba , Tasleem Syed , Prasad Sanjay , Jarbrink-Sehgal Maria 
Published: October 2019

INTRODUCTION:
A double pylorus channel can be congenital or acquired. Acquired double pylorus is thought to be the result of a gastric or duodenal ulcer forming a fistula between the prepyloric antrum and the duodenal bulb. Although it is a rare endoscopic finding, seen in only 0.001%–0.4% of upper gastrointestinal endoscopies1, when acquired, it signifies peptic ulcer disease (PUD) which needs risk factor modification and treatment.

CASE DESCRIPTION/METHODS:
A 50-year-old man with alcohol use disorder, newly diagnosed alcoholic cirrhosis and recent NSAID use presented with confusion, melena and dark emesis. His physical exam was notable for hypotension (BP 86/55 mmHg), somnolence, confusion and positive asterixis. Laboratory values were remarkable for hemoglobin of 5 g/dL, BUN of 48 mmol/L, platelets of 271 × 109/L and INR of 2. Management included fluid resuscitation, blood transfusion, proton pump inhibitor and octreotide drip. Once hemodynamically stabilized, an upper endoscopy was performed revealing blood in the gastric body, two antral ulcers with visible vessels, but no endoscopic stigmata of liver disease. Adjacent to the pylorus, a slit-like channel connecting the prepyloric antrum to the duodenal bulb was noted and traversed with the endoscope. Helicobacter pylori work up revealed a positive serum antibody. Patient did well post-procedure and received Helicobacter pylori eradication treatment and counseling on alcohol cessation and NSAID avoidance.

DISCUSSION:
In contrast to congenital double pylorus which is an incidental finding, patients with acquired double pylorus often present with symptoms of PUD. In this case, likely culprits included NSAIDs and Helicobacter pylori. It should be distinguished from other similar appearing endoscopic findings such as gastric diverticulum, as risk factors for PUD need to be investigated in patients with an acquired double pylorus. While treatment with acid suppression and Helicobacter pylori eradication should be pursued, the fistula tract often persists despite treatment2. Endoscopic recognition and familiarity are key to ensure appropriate risk modification, treatment and prevention of endoscopic complications with side-viewing scopes.
1914 A Rare Complication of Interventional Radiology-Guided Arterial Embolization of Gastroduodenal Artery in the Setting of an Acute GI Bleed-Migrated Coils in the Duodenum
Authors: Kudaravalli Pujitha , Saleem Sheikh A. , Arif Muhammad Osman 
Published: October 2019

INTRODUCTION:
Interventional radiology guided (IR) embolotherapy can be lifesaving when an acute gastrointestinal (GI) bleed cannot be controlled with endoscopic therapy. However, IR embolization can lead to various complications and herein we present a complication which has been published.

CASE DESCRIPTION/METHODS:
A 91-year-old male presented to the emergency room with hemodynamically significant upper gastrointestinal bleeding manifesting as hematemesis. After medical optimization, the patient underwent an upper GI endoscopy (EGD) which showed large amount of frank blood in the duodenum interfering with the visualization and treatment of the bleeding site. Hence, the patient underwent an urgent IR guided arteriogram and embolization of the gastroduodenal artery by placement of vascular coils. An EGD was done 48 hours later which showed a giant non-bleeding cratered duodenal ulcer with a visible vessel and vascular coils partially protruding into the duodenal bulb lumen. No active bleeding was noted from the ulcer. Patient had no further evidence of bleeding post embolization and was discharged. The patient presented 3 months later with abdominal pain. CT abdomen showed multiple liver abscesses. IR-guided drainage of abscesses was performed and the culture grew Streptococcus Intermedius. MRCP, ERCP and barium enema were unremarkable. The patient was treated with prolonged course of IV antibiotics and recovered without any further issues.

DISCUSSION:
IR guided arterial embolization can be life-saving in cases where GI bleeding cannot be controlled endoscopically, however it can lead to serious complications including endovascular coil migration into GI lumen. Endovascular coil migration can occur immediately or several years later which can result in fatal bleeding and infection. Endoscopic removal of the migrated coil with hot biopsy forceps has been reported however in most cases this complication has been conservatively followed by endoscopy. The best approach to prevent and manage migrated endovascular coils in GI lumen remains unclear.
1921 A Case of Ovarian Varices Bleeding Presenting as an Obscure GI Bleed and Abdominal Pain
Authors: Khan Adil , Panghal Ritvika , Naeem Raza 
Published: October 2019

INTRODUCTION:
Upper GI bleed is one of the most common complications in cirrhotic patients with portal hypertension. However, when GI bleed cannot be found after performing endoscopy, one should consider an ectopic gastrointestinal variceal bleeding. Ectopic varices are portosystemic collaterals in locations other than the gastroesophageal region. We present you a case of 44 year old cirrhotic patient, who was seen for nausea, vomiting and abdominal pain with acute blood loss anemia. She was found to have an ectopic gastrointestinal variceal bleeding after a negative endoscopy.

CASE DESCRIPTION/METHODS:
44 years old female with past medical history of cirrhosis secondary to NASH presented to the ER with complaint of abdominal pain associated with nausea and vomiting while she was having sexual intercourse. Patient had CT Abdomen and Pelvis with IV contrast which was consistent with evidence of portal hypertension including large venous collaterals and splenomegaly. There was hyperdense ascitic fluid identified on the CT scan. On the left side of the hemiabdomen the fluid was hyperdense, suggestive of blood. But no site of bleeding could be identified on the study. Patient’s hemoglobin dropped by 2 grams in the ER. GI recommended to place NG tube and evaluate for blood contents. Gastric content via NG tube was non-bloody.IR was consulted who, after reviewing her CT scan images, noticed an unusual large IMV supplying large pelvic varices presumably as portal venous compression sites into systemic venous system. IR performed transhepatic portal access with pelvic variceal embolization. Interestingly, they did not find active bleed at the time of procedure. But, given recent history and CT findings, empiric embolization was performed of these varices. At completion, no residual pelvic varices was seen. Patient has successful sclerotherapy and coil embolization of the 2 pelvic-to-ovarian venous plexus varicosities for treatment of presumed source of variceal intraperitoneal bleeding. Patient was discharged home with stable hemoglobin.

DISCUSSION:
When GI bleed cannot be found after performing endoscopy, one should consider an ectopic gastrointestinal variceal bleeding. Out of all the variceal bleeding, 5% of them are ectopic variceal bleeds. As GI bleed with acute blood loss anemia can be fatal and outcome being time-sensitive, it is necessary to establish diagnosis early. Multi-slice computed tomography with contrast plays an important role in the early diagnosis of ectopic variceal bleed.
1929 Spots and Dots on the Skin and Stomach: Gastrointestinal Vasculitis
Authors: Viswanath Shilpa , Almouradi Tarek 
Published: October 2019

INTRODUCTION:
Immunoglobulin A (IgA) vasculitis is often seen in the pediatric population but can also be seen in the adult cohort. The classic histopathological finding in IgA vasculitis is leukocytoclastic vasculitis (LCV), which is a neutrophilic inflammation in post-capillary venules. Classic signs of LCV include palpable purpura, small vessel involvement, and less likely but also extracutaneous manifestations. We present a unique case of a gastrointestinal (GI) manifestation of LCV with angiodysplasia in the stomach and duodenum.

CASE DESCRIPTION/METHODS:
This is a 66-year-old female with a history of hypertension, chronic kidney disease stage III, hypothyroidism, a recent diagnosis of LCV (Figure 1) two weeks prior that returns to the hospital with a complaint of watery diarrhea, bright red blood per rectum, lower abdominal cramping, and nausea. Her vitals were unremarkable and her laboratory studies revealed elevated blood urea nitrogen (BUN), acute kidney injury, mild anemia, and leukocytosis. A computed tomography (CT) scan of her abdomen demonstrated extensive wall thickening, multifocal periduodenal inflammation, and diffuse ileal wall thickening (Figure 2). An esophagogastroduodenoscopy (EGD) revealed ulcerative esophagitis, helicobacter pylori negative duodenal ulcers, and multiple non bleeding angiodysplasias in the stomach and duodenum that were cauterized (Figure 3). A colonoscopy revealed a tubular adenomatous polyp that was removed. The patient’s symptoms resolved and she did not demonstrate any further bleeding. Her hemoglobin stabilized and she was able to tolerate a regular diet on discharge.

DISCUSSION:
Abdominal pain and bloody diarrhea can have a milieu of differentials. This patient clearly demonstrated a vasculitic GI manifestations with bowel wall thickening and inflammation on imaging, elevated BUN, anemia, bloody diarrhea, and a history of LCV. Having a proper suspicion and confirming this with imaging, endoscopy, and biopsy is imperative for the diagnosis. Without a thorough history and physical, undiagnosed vasculitis can lead to fatal consequences such as gastrointestinal hemorrhage, perforation, or more rarely infarction.
1935 An Unusual Cause of Post-Polypectomy Bleeding
Authors: Kaila Vishal , Desai Amit P. 
Published: October 2019

INTRODUCTION:
Myeloid sarcoma is a rare tumor characterized by a tissue mass of myeloid progenitor cells occurring outside of the bone marrow. Myeloid sarcoma can occur de novo or overlap with acute myeloid leukemia (AML). As with AML, myeloid sarcoma may also present as a blast transformation of myelodysplastic syndrome or neoplasm.

CASE DESCRIPTION/METHODS:
A 65-year-old male was transferred to our hospital for hematochezia after a cecal polypectomy. Two days prior to transfer, the patient underwent screening colonoscopy for colorectal cancer at an outside hospital. During the procedure, a large carpeted, sessile polyp was seen overlying the cecal fold. Endoscopic removal was attempted but was unsuccessful given the polyp’s location and size. Pathology from the partially removed polyp revealed a tubulovillous adenoma. His hemoglobin was 6.5 g/dL (13.0–17.0 g/dL) and white blood cell count was 70 M/μL (4.20–5.60 M/μL). Following blood transfusions and hemodynamic stabilization, repeat colonoscopy and bone marrow biopsy were performed. The polypectomy site revealed flat, polypoid ulcerated and friable tissue with multiple areas of bleeding and clot (Figure 1). Despite hemostatic clip placement and thermal therapy to treat areas of active oozing, the lesion continued to bleed. The surgical team was activated given known residual adenomatous tissue and the patient underwent a successful right hemicolectomy. Pathology of the surgical specimen showed a tubulovillous adenoma with focal high-grade dysplasia and central ulceration with fibrinous exudate and submucosal hemorrhage. In addition, there were immature myeloid cells infiltrating the submucosa underneath this polyp. Furthermore, sheets of myeloblasts, positive for CD34 and CD117, within the submucosa also formed a separate ulcerated, plaque-like, 1.0 cm mass distal to the polyp (Figure 2). Bone marrow biopsy showed a 70% cellular marrow with nearly 20% myeloblasts. The patient had both a tubulovillous adenoma with an infiltrating adjacent myeloid sarcoma.

DISCUSSION:
While myeloid sarcoma can affect any organ, they most commonly infiltrate the skin or gums. Colonic involvement is extremely rare. Treatment for myeloid sarcomas is identical to that of AML, even if there no evidence of bone marrow involvement.
1936 Levamisole Contaminated Cocaine Presenting as Gastrointestinal Ulcerations and Bleed
Authors: Williams Mary-Jane O. , Ayutyanont Napatkamon A. , Akhondi Hossein A. 
Published: October 2019

INTRODUCTION:
Levamisole is a widely used cutting agent for cocaine and it also contributes to increased quantity of cocaine. Gastrointestinal (GI) ulcers and bleed is a rare presentation of levamisole intoxication. We report a case of GI ulcers and bleed suspected to be from levamisole contaminated cocaine.

CASE DESCRIPTION/METHODS:
A 58 year old female presented with sore throat, headache, oral ulcers and multiple necrotic skin lesions following a tooth extraction. On examination, she was noted to have oral ulcers, peri-anal necrotic ulcers, finger eschars and a left lower extremity open blister. Painful violaceous purpuric patches with well-delineated dusky necrotic centers and a bright erythematous rim were also observed peri-anally. Laboratory studies revealed neutropenia, hyponatremia, acute kidney injury, positive antineutrophilic antibody, Hepatitis C, HSV 1 and 2, D-dimers, antidouble-stranded DNA antibodies, anti-neutrophil cytoplasmic antibodies, lupus anticoagulant antibodies and decreased protein S levels. Urine toxicology screen was positive for cocaine and opiates. Patient admitted to cocaine use due to pain from the extracted tooth. Computed Tomography (CT) of abdomen revealed moderate ascites and body wall edema. She was managed with intravenous fluids, pressors, antibiotics, antiviral, antifungal therapy. She also received treatment with filgastrim. Over the course of her hospital stay, she developed lower GI bleed and required multiple units of blood transfused. Endoscopy revealed a clean based gastric ulcer and multiple cecal colon ulcers which was managed with epinephrine injections.

DISCUSSION:
Levamisole is mostly absorbed from the GI tract and metabolized by the liver. Our patient presented with immune derangements and GI bleed after the use of cocaine to help with her pain from tooth extraction. Laboratory results were compatible with levamisole contamination. CT of the abdomen showed moderate ascites and anasarca similar to MRI characteristics of levamisole-induced leukoencephalopathy which show peripheral ring-type enhancement and edema around lesions. The mechanism of levamisole in the formation of GI ulcers is presumed to be related to ischemia. To our knowledge, this is the first case of levamisole-contaminated cocaine induced gastrointestinal ulceration and bleed. This case illustrates the potential for severe gastrointestinal ulcers and bleed with the use of levamisole and the value of high index of suspicion.
1937 A Deadly Diagnosis: Aortic Stent Causing Aorto-Esophageal Fistula
Authors: Kailas Shilpa D. , Kulkarni Prasad 
Published: October 2019

INTRODUCTION:
An aorto-esophageal fistula (AEF) is a rare but life-threatening cause of upper gastrointestinal bleeding caused by an abnormal communication between the esophagus and aorta. Etiologies include foreign body ingestion, malignancy, post-operative trauma, and ruptured TAA. We present the fatal case of a patient with profound anemia who suffered catastrophic consequences secondary to graft-esophageal fistula.

CASE DESCRIPTION/METHODS:
A 66-year-old male with history of percutaneous thoracic endovascular aortic repair 3 months prior presented with complaints of 2 weeks of dizziness, nausea, and intermittent dark stools. EGD/colonoscopy 2 months ago were negative for acute GI bleed. Upon evaluation, the patient was mildly tachycardic with positive orthostatic vital signs and fever of 100.4 F. Rectal exam did not demonstrate gross blood. Labs were remarkable for Hgb 6.8 with repeat 5.9, WBC 14, and BUN 14. CTA chest was done to investigate tachycardia and identified an enlarging distal aortic endoleak with stable short segment dissection. Vascular surgery was consulted but felt the endoleak was chronic. CT A/P ruled out retroperitoneal hematoma and he was treated with transfusions and beta blocker therapy. Following recurrent melena, our EGD revealed two areas concerning for aortic stent erosion into the esophagus at 34 and 36 cm from incisors with trace oozing, locating the source of hemorrhage. Vascular surgery reevaluated the patient with plan for graft removal and reconstruction of thoracic and abdominal aorta. Unfortunately, before advancing to surgery he decompensated after large volume hematemesis. Vasopressors were initiated for hemorrhagic shock but life-sustaining measures were eventually discontinued to respect family wishes. The etiology of his acute symptomatic anemia and massive hemorrhage was suspected to be graft-esophageal fistula.

DISCUSSION:
AEF is an unusual post-operative complication of prosthetic aortic repair. Secondary AEF can develop after open or endovascular repair of the aorta, occurring in 1.9% of patients post-endovascular aortic repair. Pathophysiology remains unclear but it is thought to arise from erosion of graft material into esophagus, graft infection with abscess rupture, or anastomotic pseudoaneurysm. Our case emphasizes the importance of raising clinical suspicion not only for hematemesis but for new onset fever with elevated inflammatory markers in the appropriate clinical setting as well as the need for emergent surgical intervention to avoid fatal outcomes.
1940 Acute Lower Gastrointestinal Bleeding Due to Multiple Colonic Polypoid Angiodysplasias in a Patient With Sickle Cell Disease
Authors: Mahpour Noah , Bhurwal Abhishek , Patel Anish V. 
Published: October 2019

INTRODUCTION:
In patients with Sickle Cell Disease who present with hematochezia, ischemic colitis is often identified as the precipitating etiology. Angiodysplasia in sickle cell is infrequently described as the cause of hematochezia, especially in young patients. Our case illustrates the unusual finding of hematochezia due to multiple polypoid angiodysplasias distributed in the entire colon of a young patient with sickle cell disease.

CASE DESCRIPTION/METHODS:
A 26-year-old male with sickle cell disease leading to cirrhosis decompensated by ascites presented with multiple episodes of painless hematochezia for one day. On physical examination, he was noticed to have relative hypotension, with ascites and bright red blood on rectal exam.His initial lab work noted a hemoglobin level of 4.3 g/dL and an INR of 5.3. As he presented with hematochezia and hypotension, he underwent a computed tomography (CT) scan with intravenous contrast, which showed a blush of contrast at the splenic flexure, indicating an active luminal hemorrhage (Figure 1). However, emergent mesenteric angiography was unsuccessful in detecting active bleeding, thus, embolization could not be performed. A subsequent colonoscopy revealed 11 actively bleeding polypoid angiodysplasias distributed throughout the entire colon (Figures 2 and 3), each treated with argon plasma coagulation and clipping to prevent further bleeding. The patient did not have any recurrent episodes of bleeding throughout his hospital course, and was discharged.

DISCUSSION:
We present a case of acute lower gastrointestinal bleeding due to multiple colonic polypoid angiodysplasias in a young patient with sickle cell disease, successfully treated with argon plasma coagulation therapy. Colonic angiodysplasia is commonly found in individuals older than 40 years of age, generally appearing as a fern-like flat or elevated bright-red lesion on endoscopy. The polypoid form of angiodysplasia is extremely rare, reported primarily in the sigmoid and transverse colon, and is easily identified based on its striking appearance. Polypoid angiodysplasia has rarely been described in patients less than 50 years of age, and has no known association with sickle cell disease. CT angiography is a potentially crucial non-invasive initial test, as it can possibly detect extravasation from actively hemorrhaging angiodysplasias. Successful endoscopic eradication therapies include argon plasma coagulation, electrocoagulation, and snare polypectomy.
1948 Dominant Claw Control: Role of OTSC Clip as Salvage Hemostasis Therapy
Authors: Shapira Gilad , Kumar Manoj , Fahmawi Yazan , Mizrahi Meir 
Published: October 2019

INTRODUCTION:
Upper Gastrointestinal Hemorrhage (UGIH) remains a common problem in modern day endoscopy. Etiologies of UGIH include variceal, nonvariceal, neoplastic, vascular malformation, and iatrogenic among others. Endoscopic hemostasis is typically achieved by through the scope (TTS) clips, epinephrine injections, ablation techniques, coils and glues and self-expandable stents. Despite having multiple tools for bleeding control, rebleeding risk remains high among single vessel ulcers and larger lesions. Here we present a case where traditional hemostasis methods failed, and an over-the-scope clip (OTSC) was used as salvage/rescue hemostasis therapy.

CASE DESCRIPTION/METHODS:
45-year-old asian Male with a history of cirrhosis secondary to alcohol presented with jaundice and melena with a hemoglobin of 5.9 gm/dl. EGD showed severe duodenitis. A side viewing duodenoscope showed a large, cratered duodenal bulb ulcer with a visible vessel. Epinephrine was injected and 5 hemoclips were placed. Despite this, there was still active oozing of blood. All the hemoclips were removed with snare. OTSC System was loaded onto a standard gastroscope and advanced to the lesion. Target tissue was sucked into the cap and OTSC® clip was released by turning the hand wheel. The clip closed itself and firmly anchored the tissue resulting in complete hemostasis. Proton pump inhibitors were continued and follow up endoscopy at 1 month showed healed ulcer site with clip in place.

DISCUSSION:
TTS clip can sometimes be not enough for UGI bleeding treatment especially during active bleeding, use in ulcers with a fibrotic base, or when the bleeding lesion is in a difficult-to-access anatomic location (e.g., gastric lesser curve or cardia, posterior duodenal wall). While OTSC have been well established in leaks, perforations, and fistulas, their role in UGIH is evolving. Several randomized trials comparing OTSC with conventional endoscopic hemostasis therapies are ongoing and results are awaiting, however our case reiterates that OTSC platform should be available and be part of endoscopic hemostasis armamentarium.