Yellow Arrow Research Articles

S1948 Toxic Megacolon as a Potential Complication Associated With COVID-19

Introduction: Coronavirus-2019 (COVID-19) presents with a wide spectrum of clinical manifestations and can affect various organ systems. Common gastrointestinal symptoms of the virus include diarrhea, nausea, and vomiting. Toxic megacolon, however, has not been cited in medical literature to be a side effect of the virus. We present a case of toxic megacolon that progressed in the setting of active COVID-19 infection. Case description/methods: A 62 year old, Hispanic male with a past medical history of hypertension, hyperlipidemia, Insulin dependent type 2 diabetes mellitus and COPD presented to the emergency room with a chief complaint of acute dyspnea with hypoxemia. Initial chest x-ray demonstrated extensive interstitial and alveolar airspace opacities suspicious for COVID-19 pneumonia. A COVID-19 PCR test was positive and the patient was admitted for acute hypoxic respiratory failure. The patient was given Tocilizumab for COVID-19, however, his oxygen requirement continued to increase on heated high flow nasal cannula. On day 10 of admission, the patient began to have about ten, loose, watery bowel movements a day. An abdominal x-ray revealed large bowel gas with dilation and a peak bowel diameter of 16.3 cm. This was confirmed with a computed tomography abdomen and pelvis with and without contrast. He then developed a fever of 101.3 degrees Fahrenheit, tachycardia in the 120s, hypotension, and a leukocytosis of 29,100 confirming the diagnosis of toxic megacolon. Testing for clostridium difficile (C diff) toxin was negative x2. He did not have a known history of inflammatory bowel disease, occupational exposures, HIV, recent medication use that may cause toxic megacolon, or recent travel prior to his hospitalization. Pre-emptive treatment of C. diff was initiated without resolution of his symptoms. The patient had a cardiopulmonary arrest soon after and his family requested cessation of CPR. Discussion: Both the short and long-term manifestations of COVID-19 have not been well-studied given the unexpected progression of the pandemic. Although GI symptoms are well known to be associated with the virus, toxic megacolon is not. This case report aims to emphasize the importance of appropriate abdominal imaging if GI symptoms begin to manifest with COVID-19. Early diagnosis will allow early symptomatic treatment as well as early surgical evaluation to decrease the likelihood of perforation.Figure 1.: Endoscopic findings and histology of colon. (a, b) Colonoscopy images demonstrating moderate inflammation with altered vascularity, erosions, friability and aphthous ulcerations. (c, d). H&E staining of colon demonstrated focal active colitis (yellow arrow) with cryptitis and abscess formation (red arrow). There were no architectural changes to suggest inflammatory bowel disease.

S3094 An Uncommon Urologic Cause of Gastric Outlet Obstruction

Introduction: Gastrointestinal (GI) malignancies are a common cause of gastric outlet obstruction (GOO). However, the etiologic contribution of non-GI malignancies to GOO is rarely described in literature. Herein, we present a case of urothelial carcinoma of the right ureter causing GOO. Case Description/Methods: An 84-year-old woman presented with 2 months of nausea, vomiting, bloating, and abdominal pain. She had a history of urothelial carcinoma of the bladder 12 years ago, for which she underwent transurethral bladder resection and was thought to be in remission. CT with IV contrast showed GOO, severe right-sided hydronephrosis, and thickening of the mid right ureter. Upper GI series demonstrated 20 X 7 mm duodenal stenosis in the second portion of the duodenum. EGD and EUS showed duodenal deformity causing GOO, without evidence of luminal or pancreatobiliary malignancy. Duodenal biopsies were normal. In the absence of an intrinsic GI cause for GOO, urologic evaluation was then conducted. A nephrostomy tube was placed to relieve right sided hydronephrosis. This did not translate into clinical improvement of GOO and temporal parenteral nutrition was required. Cytologic evaluations of urine samples were negative for malignancy. Ureteroscopy then revealed a sessile tumor at the right mid ureter and final biopsies were consistent with high-grade invasive urothelial carcinoma. The patient underwent palliative surgical gastrojejunostomy to relieve GOO. The right ureteral cancer was invading the duodenum, causing GOO. No GI malignancy was found at the time of surgery. Discussion: GOO is rarely caused by urologic malignancies, and urologic malignancies uncommonly present with GOO. To our knowledge, this is the fourth case reporting ureteral cancer as a cause of GOO. Although rare, urothelial cancer should be recognized as a cause of GOO. This should be suspected when images reveal severe hydronephrosis and when EGD/EUS do not find GI-related etiology. Ureteral cancer can cause GOO due to severe hydronephrosis or direct duodenal invasion. Since the right ureter passes behind the second part of the duodenum in the retroperitoneum, GOO more often occurs when the right urothelial system is involved. When severe hydronephrosis is present, a nephrostomy tube may suffice to relieve GOO. When a nephrostomy tube is ineffective, direct duodenal invasion should be suspected, and palliative interventions are then necessary to relieve GOO.Figure 1.: a. Axial CT image of the upper abdomen. The two open (blue) arrows indicate visualized portions of the distended stomach. The solid (yellow) arrow shows severe hydronephrosis. b. Upper GI image. The solid yellow arrow shows the obstructed proximal duodenum. Note that contrast flows freely from the stomach into the anastomosed limb (solid white arrow) status post diverting jejunostomy c. Microscopic examination of the right ureter biopsy reveals invasive urothelial carcinoma with high grade nuclei.

S2172 Dysphagia Lusoria: A Rare Case of Aberrant Right Subclavian Artery Causing Esophageal Compression

Introduction: Dysphagia lusoria is a rare disorder found in only a small percentage of individuals with an anomalous right subclavian artery causing extrinsic compression of the esophagus. Diagnosis often requires a comprehensive evaluation of dysphagia and a high index of suspicion. We present a case of dysphagia lusoria followed by a review of the pathogenesis, clinical presentation, and management of this rare condition. Case Description/Methods: A 36-year-old female was admitted to our hospital with severe sepsis secondary to a UTI. During her hospitalization, she complained of progressive dysphagia to solids for approximately 6 months. She reported intermittent globus sensation and reflux for many years. An upper endoscopy was performed and revealed a pulsatile narrowing of the proximal esophagus. Gastric and esophageal biopsies were negative. CT angiogram identified possible extrinsic esophageal compression by an aberrant right subclavian artery (ARSA). High-resolution manometry demonstrated impression at the level of the upper esophagus with an increased pressure band likely due to the ARSA. Overall impedance to solids and liquids was normal and no underlying dysmotility was identified. A diagnosis of dysphagia lusoria was made based on these findings. Unfortunately, dietary modifications and maximal medical therapy proved ineffective. Due to the severity of her symptoms, surgical repair of the aberrant vessel was ultimately recommended. Discussion: Involution of the fourth vascular arch during embryogenesis leads to the formation of the ARSA from the persisting dorsal aortic arch distal to the left subclavian artery. Because the vessel most commonly crosses between the esophagus and vertebral column, retroesophageal compression can occur. However, dysphagia lusoria is an exceedingly rare cause of dysphagia in adults. A thorough evaluation of dysphagia with endoscopic, radiologic, and manometric testing is necessary to rule out other potential etiologies before the diagnosis can be made. Patients often complain of solid-food dysphagia (most common), regurgitation, postprandial bloating, chest pain, and coughing. Treatment strategies depend on the severity of symptoms, response to conservative therapies, and candidacy for surgical intervention. Mild symptoms can often be managed using a combination of dietary and lifestyle modifications and medical therapy. Surgical evaluation for repair of the aberrant vessel is indicated for severe or refractory symptoms.Figure 1.: Figure A. Upper endoscopy demonstrating extrinsic compression of the proximal esophagus. The narrowed segment was measured at 18 cm from the incisors and had a pulsatile appearance. Figures B & C. Computed tomography angiogram of the chest (axial and coronal cuts) demonstrating the aberrant right subclavian artery (yellow arrows) with its origin from the distal aortic arch. Figure D. High-resolution manometry study demonstrating impression with an increased pressure band in the upper to mid esophagus caused by the aberrant right subclavian artery. Overall impedance to solids and liquids was within normal limits (90% complete clearance of liquid bolus swallows) with normal esophageal motility (9/10 swallows had normal contraction pattern with a mean DCI of 3127 mmHg-s-cm).

S3109 Gastric Mucosal Necrosis Due to Mucormycosis in COVID-19 Patient

Introduction: COVID-19 patients, especially severely ill have a higher probability of suffering from invasive mycoses. That was noticed in our practice, and reported in literature.1 Our review of the literature found only one case of COVID-19 related gastric mucormycosis. Here we present a second one. Case Description/Methods: 71-year-old male with Hx of T2DM who presented with shortness of breath, dry cough and fever of 5 days and tested positive for COVID-19. He was admitted for AHRF, given remdesivir and dexamethasone for 2 days and discharged home to continue 10 days course of dexamethasone. Over the course of 1-week, patient's symptoms continued to progress, and he was brought again for shortness of breath and altered mental status. In ED, patient was febrile, hypoxic and was admitted for AHRF due to SARS-Cov-2 pneumonia with possible superimposed bacterial pneumonia. He was intubated and started on pressors, empirical antibiotics, dexamethasone and remdesivir to finish another 10-day course of the latter 2. He remained intubated with multiple failed weaning attempts, and after 2 weeks, tracheostomy tube was placed, and decision was made to proceed with PEG tube placement. Endoscopic mucosal examination was suggestive of diffuse proximal gastric mucosal necrosis sparing the antrum and distal body. PEG placement was cancelled and gastric biopsies histopathology showed invasive fungal disease consistent with Mucormycosis. The patient was started on liposomal amphotericin B and isavuconazonium. After a multidisciplinary discussion, the patient was deemed as a very high risk for gastrectomy and hence surgical intervention was deferred. MRI brain and sinuses showed no signs of invasive fungal disease. 3 weeks after the diagnosis of gastric Mucormycosis he was discharged on antifungals but unfortunately, he expired a few days after discharge. Discussion: In a recent systemic review, they found that 101 cases of mucormycosis in patients with COVID-19 have been reported, of which one of them was gastrointestinal. Pre-existing DM was present in 80% of cases and corticosteroid intake was recorded in 76.3% of cases. Mucormycosis involving nose and sinuses 88.9% was most common followed by rhino-orbital 56.7%. Only one case with gastric Mucormycosis was purported, the patient presented with melena during his stay and unfortunately died in seven days. Clinicians should have a high level of suspicion for concomitant fungal infections in patients with COVID-19 to allow for prompt diagnosis and early intervention.Figure 1.: a. Axial CT image of the upper abdomen. The two open (blue) arrows indicate visualized portions of the distended stomach. The solid (yellow) arrow shows severe hydronephrosis. b. Upper GI image. The solid yellow arrow shows the obstructed proximal duodenum. Note that contrast flows freely from the stomach into the anastomosed limb (solid white arrow) status post diverting jejunostomy c. Microscopic examination of the right ureter biopsy reveals invasive urothelial carcinoma with high grade nuclei.

S2610 Perihepatic Biloma: A Rare Complication After Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Introduction: Transjugular intrahepatic portosystemic shunt (TIPS) is a minimally invasive procedure and an effective therapeutic option for managing portal hypertension complications. Biliary complications after TIPS are uncommon. Here we present a case of recurrent perihepatic biloma in a woman who underwent TIPS. Case Description/Methods: A 40-year-old woman was admitted for epigastric abdominal pain for five days. She reported taking oral contraceptive pills (OCPs) for one month before presentation. She had epigastric tenderness on examination and normocytic anemia (Hgb 10 g/L) on admission labs. CT scan of the abdomen showed a large thrombus in the main portal vein extending into the right and left portal venous branches. The patient was started on heparin drip and underwent TIPS with thrombectomy. Hypercoagulability workup was unremarkable. The post-procedure course was complicated by elevation of alkaline phosphatase (552 U/L), AST (293 U/L), and ALT (324 U/L). Abdomen MRI showed patent TIPS and persistent complete thrombosis of all intrahepatic portal venous branches. She underwent repeat thrombolysis. However, liver enzymes continued to rise, and a repeat MRI showed intrahepatic biloma at the mid aspect of TIPS (Figure 1A, B). IR-guided drainage of the biloma was performed. The hospital course was complicated by fever and leukocytosis. A follow-up CT scan showed a 13 cm complex fluid collection at the dome of the liver (Figure 2A). She underwent drainage of the new collection and received IV Cefoxotin with an interval decrease in the collection size (Figure 2B). Fever resolved, and liver enzymes normalized. Discussion: Bilomas are either intra- or extrahepatic collections of bile that can occur spontaneously, or as a result of trauma to the biliary tree, including iatrogenic injury. Bilomas are usually asymptomatic but may present with abdominal pain due to symptomatic bile peritonitis or secondary bacterial infection leading to abscess formation and sepsis. A biloma may wall off or may continue to have active bile leakage. CT intravenous cholangiography, MRI with gadolinium, and Tc99 scintigraphy can identify bile leak. Differential diagnoses include hepatic cyst and hematoma, liver abscess, loculated ascites, and postoperative fluid collections, including seroma and lymphocele. Treatment options include endoscopic drainage, IR guided, or surgical drainage with bile leak repair.Figure 1.: 1A, and 1B: MRI coronal T2W, MRI axial T2W and MRI coronal post contrast, respectively, showing intrahepatic biloma (white arrow) abutting a portion of the TIPS (yellow arrow) with upstream intrahepatic biliary ductal dilatation (blue arrow). 2A and 2B: CT coronal image demonstrates a new peri-hepatic collection surrounding the hepatic dome (black arrow) and interval placement of a percutaneous drainage catheter and decrease in size of the peri-hepatic collection (black arrow).

S2285 A Rare Cause of Upper Gastrointestinal Bleeding: Sarcina ventriculi

Introduction: Sarcina ventriculi is a gram-positive anaerobic coccus that thrives in acidic environments and uses carbohydrate fermentation as its sole source of energy. The organism was first observed in gastric contents in 1842 after a patient presented with months of bloating, nausea, and emesis. Additional investigation revealed that the bacteria was most commonly identified in patients with delayed gastric emptying or gastric outlet obstruction. Sarcina ventriculi has been implicated in cases of gastric ulcer, emphysematous gastritis, and peritonitis following gastric perforation as well as gastric adenocarcinoma and pancreatic adenocarcinoma. Case Description/Methods: A 68-year-old woman with a history of acid reflux, type 2 diabetes, hypertension and cardiomyopathy presented with hematemesis for one day. She was hemodynamically resuscitated and given an intravenous proton pump inhibitor. Esophagogastroduodenoscopy (EGD) demonstrated a large area of deeply erythematous mucosa with well-defined margins involving a large amount of the gastric fundus and proximal body. Within this area was a 2-3 cm irregular non-bleeding necrotic ulcer in the gastric body suggestive of malignancy (Figure 1A). Multiple biopsies were taken from the ulcer edge and erythematous mucosa. Pathology was significant for erosive gastropathy with superficial erosion and reactive changes as well as ulcer pathology with mucosal necrosis and erosion. Interestingly, there were scattered intraluminal microorganisms characteristic of Sarcina ventriculi (Figure 1B). Based on the few available case reports, the patient was treated with one week of metronidazole, ciprofloxacin, sucralfate, and pantoprazole. The patient is scheduled for repeat EGD to follow up in one month. Discussion: A review of the literature revealed that the initial presenting symptom of Sarcina ventriculi as hematemesis is exceedingly rare. Endoscopic evaluation in this case revealed a unique well-defined margin between normal and abnormal mucosa that, to our knowledge, is not previously characterized. There is no consensus regarding the best therapeutic agents or treatment duration. Further evaluation and documentation of resolution or persistence of Sarcina ventriculi in this case is pending completion of antibiotics and repeat EGD. These results may contribute to establishing an appropriate treatment regimen for future cases. The organism’s association with serious pathology make its identification and treatment clinically significant.Figure 1.: A) A 2-3 cm irregular non-bleeding necrotic ulcer in the gastric body and B) Necroinflammatory debris (black arrows) and admixed Sarcina ventriculi organisms arranged in tetrads (yellow arrows), 1000x H&E.

S1676 The Great Escape: The Rare Type V Mirizzi Syndrome

Introduction: Mirizzi syndrome is a rare complication of chronic gallstone disease, defined as the obstruction of the common bile duct (CBD) or common hepatic duct (CHD) secondary to compression from gallstone impaction Hartmann’s pouch. It is categorized based on the presence and degree of cholecystobiliary fistula formation; however resultant cholocystoenteric fistulas are rare. We discuss the case of a patient who presented to the outpatient clinic with evidence of painless jaundice and on further evaluation, was found to have type Vb Mirizzi syndrome. Case Description/Methods: A 44-year-old male currently on suboxone for previous opioid use disorder presented for evaluation of painless jaundice. He denied fevers, chills, abdominal pain, nausea, or vomiting. Laboratory investigations noted AST 65 IU/L, ALT 46 IU/L, ALP 347 IU/L, total bilirubin 16.9 mg/dL (direct bilirubin 13 mg/dL), albumin 3.4 g/dL, INR 1.1, negative viral serologies and acetaminophen level < 5 mcg/mL. CT abdomen with contrast showed pneumobilia, smooth hepatic contour, and splenomegaly [Figure 1A]. Endoscopic retrograde cholangiopancreatography (ERCP) showed spontaneous air in the biliary tree with bile emanating from a fistulous tract in the duodenal bulb [Figure 1B]. Contrast dye injection filled up the gallbladder thus confirming the presence of cholecystoduodenal fistula. Cholangiogram demonstrated an obstruction in the mid-CBD caused by a 22 mm stone in the gallbladder, protruding into the bile duct [Figure 1C]. The bile duct was stented and the patient underwent open cholecystectomy with CBD stone removal and repair, along with cholecsytoduodenal fistula disconnection and closure. Discussion: Mirizzi syndrome is uncommon with an incidence of < 1% per year. While previously classified as type I (extrinsic compression of the CHD or CBD without a cholecystobiliary fistula) or type II-IV (including a cholecystobiliary fistula), more recently, an extended classification has introduced type V Mirizzi syndrome encompassing types I-IV with the concomitant identification of a cholecystoenteric fistula. It is further subclassified as type Va and Vb (i.e., without and with gallstone ileus, respectively). Given that it encompasses the other subtypes, the treatment option primarily depends on the obstructing biliary lesion type. It is crucial to carefully evaluate and correctly identify patients' chronic gallstone disease complications as they can affect further endoscopic and surgical management.Figure 1.: Figure 1A: CT abdomen with contrast showing pneumobilia (red arrows); Figure 1B: Fistulous tract noted in the duodenal bulb on direct visualization (yellow arrow); Figure 1C: Cholangiogram demonstrating an obstruction in the mid common bile duct consistent with a large, approximately 22 mm bile duct stone in the gallbladder, protruding into the bile duct (red circle).

S1960 Acute Pseudomembranous Colitis, Microangiopathic Hemolytic Anemia, and Renal Injury After Pericardiectomy

Introduction: Acute colonic ischemia following surgery is usually a result of colonic hypoperfusion, particularly in watershed regions; however, it is critical to maintain a broad differential diagnosis for alternate etiologies. Case description/methods: A 57-year-old man with lupus on hydroxychloroquine and prednisone underwent elective pericardiectomy for medically refractory constrictive pericarditis. On post-operative day (POD) 3, he developed abdominal pain, nausea, and non-bloody diarrhea. Hematochezia started on POD 4. Computed tomography showed rectosigmoid thickening and perirectal fat stranding (Figure 1A). Sigmoidoscopy revealed edematous, ulcerated, and discolored mucosa from the anal verge to 30 cm proximally that abruptly normalized thereafter (Figure 1B). Sigmoid histology showed lamina propria hemorrhage with crypt withering and focal pseudomembranes (Figure 1C). Clostridioides difficile testing was negative. Colonic ischemia was favored. Given persistent leukocytosis and low fevers, antibiotics were started. From POD 4 to 8, platelets dropped from 142 to 11 × 109/L, and creatinine rose from 1.1 to 2.0 mg/dL (Figure 2). On POD 6, labs showed lactate dehydrogenase 1,107 U/L, indirect bilirubin 2.7 mg/dL, and undetectable haptoglobin, with hemoglobin dropping from 14.0 to 12.9 g/dL from POD 7 to 8. Peripheral smear on POD 8 showed schistocytes (Figure 3). Serum ADAMTS-13, complement levels, and heparin-induced thrombocytopenia panels were normal. Stool PCR detected shiga-toxin producing E. coli and shiga toxin 2, and stool cultures did not grow the 0157:H7 E. coli strain. Antibiotics were stopped due to the diagnosis of shiga-toxin induced hemolytic uremic syndrome (ST-HUS). The hemolysis, thrombocytopenia, and renal injury resolved after one week of supportive measures. Discussion: Infection by shiga-toxin producing E. coli (STEC), especially with shiga toxin 2 (which disrupts protein synthesis, causing apoptosis), presents with hemorrhagic colitis in 80% of cases and ST-HUS in up to 15% of cases. STEC is often acquired from contaminated food/ water. In this case, a hamburger from an external vendor was the suspected source. After a 3-day incubation period, STEC classically presents with abdominal pain and non-bloody diarrhea, followed by bloody diarrhea 1-3 days later. If it occurs, ST-HUS presents 1-2 weeks later from thrombotic microangiopathy. Antibiotics are linked to shiga toxin production by the encoding bacteriophage in the STEC chromosome.Figure 1.: Acute pseudomembranous colitis. A) Rectosigmoid wall thickening (green arrow) and perirectal fat stranding. B) Rectosigmoid colon was edematous, cyanotic, ulcerated, with luminal narrowing by flexible sigmoidoscopy. There was an abrupt transition to normal sigmoid mucosa at 30 cm from anal verge (not shown). C) Pathologic specimens from sigmoid colon showed crypt withering (blue arrow), lamina propria hemorrhage (orange arrow), and pseudomembrane (yellow arrow).Figure 2.: Clinical course of shiga-toxin induced hemolytic uremic syndrome (ST-HUS). Non-bloody diarrhea started on POD 3, followed by bloody diarrhea on POD 4. The patient’s thrombotic microangiopathy, signified by reduction in platelets and renal injury, began 3-4 days later, illustrating the characteristic delay from diarrhea onset and thrombotic microangiopathy in ST-HUS.Figure 3.: Peripheral smear. Peripheral smear was notable for schistocytes (blue arrow), suggestive of hemolysis, and markedly diminished number of platelets (green arrow). The combination of these features was consistent with thrombotic microangiopathy.

S2679 An Unusual Suspect for Cholestatic Liver Injury

Introduction: Vanishing Bile Duct Syndrome (VBDS) and idiopathic cholestasis (IC) have been associated with lymphoma in rare cases. In VBDS, the defining feature on liver biopsy is ductopenia, while in IC there is canalicular cholestasis and mixed inflammatory changes. Existing literature reports a few cases of paraneoplastic cholestasis with pathological features of either VBDS or IC. We describe an unique case of severe cholestasis as the presenting sign of Hodgkin’s lymphoma in the absence of bile duct loss or inflammatory changes. Case Description/Methods: 60-year-old man with no past medical history presented to the ED with increasing fatigue and jaundice that started five months earlier. He underwent cholecystectomy and intraoperative liver biopsy four months earlier which showed bland lobular cholestasis and mild lobular injury with no fibrosis, inflammatory changes, abnormal lymphocytic infiltration, or evidence of bile duct loss. An MRI/MRCP 6 weeks before presentation showed multiple small hepatic cysts and no biliary obstruction or ductal dilatation. Ursodiol 14 mg/kg/d was started 2 weeks later but he developed hypotension and presented to the ED. In the ED, vital signs were normal. Physical exam showed jaundice and hepatomegaly. Labs revealed ALP 1002 U/L, AST 81 U/L, ALT 90 U/L, total bilirubin 10.8 mg/dL, and direct bilirubin 8.1 mg/dL. Further work up showed negative AMA, ANA, ASMA and vasculitis serologies, normal ceruloplasmin, and negative viral studies including hepatitis A, B, C, HSV, CMV, HIV and COVID-19. EBV PCR was 69,697 copies/mL with positive IgG suggestive of reactivation of previous infection. Lyme and Ehrlichia serologies were negative. Repeat MRI/MRCP showed normal bile ducts but extensive retroperitoneal lymphadenopathy. Lymph node core needle biopsy revealed classic Hodgkin’s lymphoma. He was started on chemotherapy and liver enzymes improved. Discussion: Hodgkin’s lymphoma can present with cholestatic liver injury as shown in our patient who was on no medications and had no other identifiable causes of cholestasis. In the existing literature, VBDS and IC have been described as the pathological features for these patients where either ductopenia or canalicular cholestasis and mixed inflammatory changes are seen. Our case is unique because our patient had neither of these features. Bland cholestasis associated with lymphoma should be kept in the differential in someone with otherwise unexplained cholestatic liver injury.Figure 1.: Panel A: High power view of liver biopsy (200x, H&E). Yellow-green bile can be seen in dilated canaliculi. There is no significant lobular inflammation, steatosis, or other alterations. Panel B: High power view of liver biopsy (400x, H&E). Pale yellow-green watery bile can be seen in dilated canaliculi (yellow arrows). There is no significant lobular inflammation, steatosis, or other alterations. Panel C: High power view of lymph node (200x, H&E). The lymph node shows loss of normal architecture with replacement by fibrosis and an atypical lymphohistiocytic infiltrate. Scattered large cells with irregular nuclear contours and hyperchromasia are seen suggestive of Hodgkin cells. Panel D: Immunoperoxidase studies show the Hodgkin Reed-Sternberg (HRS) cells are positive for CD15 and CD30. PAX-5 is weakly expressed in the large cells in comparison to the background small B cells. CD20 stains background small B cells but is negative in the HRS cells. The immunophenotype is consistent with classic Hodgkin lymphoma.

S2198 Are Migrated Variceal Coils Amenable to Endoscopic Treatment?

Introduction: Embolization coil migration into the gastrointestinal tract is an extremely rare complication. Several case reports have described coil migration into the gastrointestinal tract after treatment of gastric varices, splenic artery pseudoaneurysm, and post-liver transplant. There is no standard of care for migrated coils, and treatment has ranged from conservative management to surgical/endoscopic removal. We report a rare case of coil migration into the stomach after direct intrahepatic portosystemic shunt (DIPS) and variceal coiling of gastric varices. Case Description/Methods: A 61-year-old man admitted with 3-week onset of epigastric pain. He has history of NASH cirrhosis complicated by bleeding esophageal and gastric varices status post coiling and embolization with DIPS in 2016. Pain was exacerbated by certain positions, and improved in the left lateral decubitus position. Pain was not related to food intake. Vitals were stable and labs were unremarkable at presentation.CT scan of abdomen and pelvis with IV contrast showed possible foreign body in the gastric lumen (Figure 1A). EGD showed migration of previous variceal coils into the gastric lumen, particularly around in the fundus and cardia (Figures 1B-C). Venogram was obtained to asses anatomy and coil location. This demonstrated complete occlusion of the previously embolized gastric varices. After the venogram, EGD was completed with successful removal of visibly migrated coils using small biopsy forceps (Figure 1D). No bleeding or complications occurred after the procedure. Although subsequent imaging showed remaining coils, there were significantly less compared to admission. The patient had intermittent resolution of his abdominal pain, but was readmitted several times afterwards for EGD removal of remaining coils. Discussion: Although etiology is unclear, the mechanism of variceal coil migration is likely related to fistula formation and inflammation within the gastric wall. In this case we attempted treatment endoscopically with removal of variceal coils with biopsy forceps. Successful removal of visualized coils alleviated abdominal pain, though it was temporary. An alternative treatment would be surgical intervention, however given risk of decompensation of cirrhosis and complications, it would be as a last resort. In the setting of successfully embolized vessels, we believe it is safe for endoscopic retrieval of the gastric coils in symptomatic patients.Figure 1.: (A) CT abdomen and pelvis showing metallic foreign body (red arrow) - coil migration from previous embolization. (B-D) Endoscopic images showing coils (yellow arrow) from previous IR intervention found in stomach fundus and cardia status post removal using small biopsy forceps.

S2969 Abdominal Pain: A Silent and Unlikely Cause

Introduction: While diverticulosis is commonly found in the large intestine it is a rare disease found in the small intestine accounting for only 0.06-1.3% of cases. Although most cases are asymptomatic, roughly 30-40%, it is crucial that it is on the differential of acute abdominal pain as it can be life threatening and potentially require surgical management. Case Description/Methods: On initial visit to the emergency room a 61 year old Hispanic male was found to have a perforated jejunal diverticula on Computed Tomography (CT) scan after initially presenting with left upper quadrant abdominal pain. He had a past medical history of hypertension and Helicobacter pylori (H. Pylori) gastritis found on esophagogastroduodenoscopy (EGD) in 2019. His past surgical history was significant for an exploratory laparotomy 25 years ago secondary to a gunshot wound in his right upper quadrant. The pain initially began in his left upper quadrant and progressed to diffuse abdominal pain. He was hemodynamically stable, afebrile and saturating well on room air. A CT scan was performed in the emergency department which displayed a perforated duodenal ulcer at the distal 3rd/4th segment of the duodenum with small surrounding retroperitoneal air and mild fat stranding. He was admitted under the surgery department and taken to the operating room. Upon dissection of the duodenum, approximately 5cm from the ligament of Treitz, a microperforation was seen which was consistent with a mesenteric jejunal diverticulum. Discussion: Jejunal Diverticulosis is a rare phenomena that can lead to life threatening complications. As most cases are asymptomatic and often miss diagnosed it is imperative that physicians consider it as a differential when the diagnosis of abdominal pain or acute abdomen is presented.Figure 1.: What was thought to be a perforated duodenal ulcer and a thin wisp of contrast adjacent to three extraluminal foci of gas, denoted by the yellow arrow, which turned out to be a perforated jejunal diverticula visualized during surgery.

Selected Articles from This Issue

Radium-223 dichloride is a radiopharmaceutical used to treat cancer that has metastasized to the bones, and whose effects are derived from both direct action of radiation on tumor cells as well as bystander effects caused by irradiation of both tumor and non-tumor cells in the bone microenvironment. Here, Canter and colleagues quantify the biological effects derived from both of these mechanisms of action. Direct effects from alpha particle irradiation (yellow arrows in the image at left) contribute to biological changes detected histologically in disseminated tumor cells and osteocytes within the range of the alpha particles. Bystander effects also contribute to biological changes in tumor cells beyond the range of the alpha particles emitted from the endosteal surface of the bone. These radiation-induced bystander effects can arise from tumor cells (white outlined arrow) and marrow cells (pink outlined arrow) within the range of alpha particles, and from bone cells (brown outlined arrow). The data suggest that bystander effects in the bone environment likely contribute to growth delay of disseminated tumor cells in bone marrow.Regulation of cancer stemness has emerged as a key tumor-intrinsic property underlying disease progression and therap. resistance. Recently, gain-of-function (GOF) mutations in p53 have been shown to promote increased stemness characteristics, but the mechanism for this is not well understood. Here, Ghatak and colleagues identify the microRNA miR-324-5p as the key effector of GOF mutant p53 that controls this phenomenon in non–small cell lung cancer (NSCLC) cells. GOF p53 isoforms expressed in NSCLC cells caused upregulation of c-Myc, which bound to and activated transcription of miR-324. The authors demonstrate that expression of CUEDC2—the direct target of miR-324-5p in this context—was ablated in cells expressing GOF p53 isoforms, and the loss of CUEDC2 expression was associated with activation of NF-κB and increased expression of stemness markers. CUEDC2 downregulation was further shown to be characteristic of human tumors bearing GOF p53 mutations. The authors conclude that TP53 mutations coupled with high miR-324-5p expression is associated with worse prognosis in lung cancer patients. Taken together, the data identify miR-324-5p as a novel epigenetic regulator of stemness properties in NSCLC.Balanced MDM2:p53 expression maintains proper cell cycle progression, whereas aberrant p53 activity is associated with developmental defects and pathologic states. Here, Mohibi and colleagues demonstrate that the RNA binding protein Zfp871 is a direct transcriptional target of p53 in vivo. Zfp871 functions to provoke a negative feedback loop regulating p53 activation by binding to the 3′UTR of MDM2 mRNA and stabilizing it. This interaction increases MDM2 expression and, by consequence, promotes degradation of p53. Mice deficient in Zfp871 were prone to early death, and heterozygous mice experienced a shortened lifespan and prominent steatohepatitis. The early death seen in Zfp871-KO mice, however, was ameliorated by ablation of Trp53. Gene expression analyses unveiled that p53 hyperactivation caused by Zfp871 loss was associated with alterations in lipid metabolism and inflammatory signaling as well as key developmental pathways. While the precise mechanism underlying the control of these pathways is yet to be determined, the data clearly demonstrate that precise control of p53 expression and activity—in part through the novel Zfp871-MDM2-p53 axis—is required to prevent the onset of pathologic conditions.Micro-metastatic lesions in the bone are often latent and can persist undetected for years in a quiescent state. However, the mechanisms by which rapidly proliferating tumor cells suddenly become quiescent upon metastasis are poorly defined. Here, Shupp and colleagues demonstrate that soluble signals from the bone metastatic microenvironment may play a key role in regulating this process. In particular, small extracellular vesicles (sEV) released by osteoblasts in proximity to breast cancer cells were shown to harbor factors such as miR-148a-3p, which had implications for breast cancer cell biology. Among other effects, the uptake of these sEV by metastatic breast cancer cells resulted in disruptions of both ERK1/2 signaling and cell cycle progression, thereby slowing cancer cell proliferation and contributing toward their latency. Taken together, the data elucidate a novel mechanism by which stromal cells influence cancer cell progression in the metastatic niche and underscore the importance of extracellular vesicles in mediating tumor–stromal cell interactions.

S3118 Through Thick and Thick: An Unusual Presentation of Gastric Amyloidosis

Introduction: GI amyloidosis (GIA) is relatively rare constitutes 3% to 8% of patients with systemic amyloidosis. A mere 1% of primary gastric amyloidosis were found to be symptomatic. We elaborate on an unusual presentation of GIA where nausea and vomiting were the only symptoms. Case Description/Methods: A 55-year-old male presents with nausea and vomiting for the past 3 weeks, found to have acute normocytic anemia (hemoglobin 6.1), leukocytosis (16K/mm3), and acute renal failure. Upper endoscopy revealed diffuse gastric wall thickening and subsequent endoscopic ultrasound revealed diffuse gastric wall thickening up to deep mucosa, up to 1.1cm in the cardia, fundus, body, and antrum. Biopsies revealed pale eosinophilic material, orangeophilic on congo red stain, and apple green birefringent on polarization microscopy consistent with AL (kappa)-type amyloidosis. Bone marrow biopsy showed hypercellular bone marrow (60%) with 6% plasma cells, chemotherapy with cyclophosphamide plus daratumumab was initiated. Free light chain levels improved to 50% within 1 month and he continues therapy for hematologic remission. Discussion: GIA is defined as the presence of GI symptoms with direct tissue biopsy with positive staining of amyloid by Congo red. Those with AL amyloidosis have median survival times of 15.84 months for those without GIA, and 7.95 months for those with GIA. Our patient with nonspecific symptoms, had lab and endoscopic evaluation; biopsy is necessary to clinch such a diagnosis.Figure 1.: Image 1: CT image demonstrating gastric mass (red arrow). Image 2: Endoscopy image demonstrating gastric mass (yellow arrow). Image 3: H&E stain of gastric mass demonstrating smooth muscle cells. Image 4: Positive smooth muscle actin stain.

S2032 Dysphagia Lusoria: A Rare Case of Progressive Dysphagia

Introduction: Deviations from the classic anatomic configuration of the aortic arch are common. An aberrant right subclavian artery is one known anatomic variant that rarely causes symptoms. Here we describe a case in which a patient presents with progressive dysphagia and is found to have retroesophageal compression due to aberrant right subclavian artery and anterior cervical osteophytes. Case Description/Methods: A 61-year-old female with a medical history of invasive ductal carcinoma of the left breast reports with dysphagia and odynophagia for one year. Initially her symptoms began with solids, but then progressed to liquids. Patient underwent CT soft tissue neck which showed an aberrant right subclavian artery compressing the posterior aspect of the esophagus near the level of the thoracic inlet as well as cervical anterior osteophytes leading to compression of the esophagus at the upper cervical aspect. She underwent barium Esophagram which also showed indentation in the posterior esophagus which was later directly confirmed by EGD. At this time, patient has been referred to vascular surgery for further management. Discussion: Aberrant right subclavian artery, or arteria lusoria, is one of the most common abnormalities of the aortic arch. The aortic arch usually branches off into the left subclavian artery, the left common carotid artery, and the brachiocephalic artery which further branches into the right common carotid and right subclavian artery. When arteria lusoria is present, the brachiocephalic artery is absent, and the right common carotid artery and right subclavian artery originate directly from the aortic arch with the latter having a distal left sided origin. Rarely, this anatomic variant can lead to compression of the esophagus and produce a condition known as dysphagia lusoria which was first described by Dr. David Bayford in 1787 in a woman with long term dysphagia after autopsy, thus it is also known as Bayford-Autenrieth dysphagia. Most patients present with symptoms in middle age or older, with mechanisms such as increased tracheal rigidity and elongation of the aorta theorized. In the case of our patient, anterior cervical osteophytes development may have contributed to symptom onset. A variety of surgical approaches for arteria lusoria are available with surgical or endovascular approaches available.Figure 1.: Imaging of our patient with dysphagia. A) Axial and B) Sagittal images of the CT soft tissue of the neck showing aberrant origin of right subclavian artery (blue bold arrow) with abnormal course behind the esophagus (red curved arrow). C) Barium esophagograms performed demonstrated extrinsic impression upon the cervical esophagus posteriorly (yellow bold arrow) causing dysphagia.

A peer-to-peer logic environment to validate flashing yellow arrow decision support system

The flashing yellow arrow (FYA) signal display creates an opportunity to enhance the left-turn phase with a variable mode that can be changed on demand. This research develops an integrated general purpose data collection module that time stamps detector and phase state changes within a National Electrical Manufacturers Association (NEMA) actuated traffic signal controller to provide recommendations for the flashing yellow arrow left-turn mode on a cycle-by-cycle basis. 115 left-turn approaches at 38 intersections with locations across the State of Florida were analyzed totaling 1370 h of video data processed including off-peak and peak conditions. Video data extraction was an essential step in developing the gap thresholds for the permissive left-turn. Actual intersection field data were obtained through loop detector mapping to the controller in the lab in real-time mode using a peer-to-peer logic environment. A custom communications software was developed to retrieve instantaneous channel input data, synchronize opposing through green phase, analyze traffic information, provide the algorithm decision, and generate a real-time log recording the events to determine whether it would be optimal to switch the red arrow to a flashing yellow arrow. The algorithm determines the time interval between the successive arrivals of vehicles and computes the corresponding headway for each lane by cycle on a second-by-second basis. Peer-to-peer logic is a necessary step to verify and validate new traffic concepts prior to field-testing and offers the advantage of acquiring and analyzing real-time traffic data coupled with video feed with the benefit of a safe environment.

Ultrafine PdRu Nanoparticles Immobilized in Metal–Organic Frameworks for Efficient Fluorophenol Hydrodefluorination under Mild Aqueous Conditions

Ultrafine PdRu Nanoparticles Immobilized in Metal–Organic Frameworks for Efficient Fluorophenol Hydrodefluorination under Mild Aqueous Conditions

トリカブト中毒に対し血液吸着（direct hemoperfusion: DHP）が有効であった1例(A case of aconite poisoning treated with direct hemoperfusion (DHP))

要旨トリカブト中毒は比較的稀な自然毒中毒であり，難治性不整脈を呈し重症化するリスクも高い。しかし特異的な治療はなく対症療法や呼吸循環管理が主とされ，血液浄化療法の効果も明らかではない。今回我々は，トリカブト中毒に対し血液吸着（direct hemoperfusion: DHP）が有効であったと思われる1例を経験したので報告する。症例は80歳の男性。自殺目的に自身で調合したトリカブト粉末を服用し，不整脈（心室頻拍）と意識障害を来して前医救急搬送され，専門的治療目的に当院転送となった。来院時は多源性の心室性期外収縮（premature ventricular contraction: PVC）が頻発し血行動態不安定であり，人工呼吸管理下にアミオダロン持続投与を開始しつつDHPを行った。その結果PVCは徐々に減少し，DHP終了時には洞調律に安定，血行動態も回復した。トリカブトの主成分であるアコニチン，メサコニチン，ヒパコニチンの血中濃度は来院時それぞれ3.95ng/mL，5.22ng/mL，1.42ng/mLであったが，DHP終了時には0.29ng/mL，0.86ng/mL，0.28ng/mLと著明に低下しており，DHPの効果と考えられた。第2病日に抜管し，以降安定して経過。精神科の介入を経て第13病日退院となった。トリカブト中毒に対するDHPにより臨床症状の改善と良好な転帰を得られ，積極的に施行を考慮すべきと思われる。

Bilateral Optic Disc Edema in Multisystem Inflammatory Syndrome in Children Associated With COVID-19.

Bilateral Optic Disc Edema in Multisystem Inflammatory Syndrome in Children Associated With COVID-19.

Dermoscopy-An Aid in the Diagnosis of Mycetoma.

A 45-year-old farmer consulted for a gradually increasing swelling over right leg. Examination revealed hard swelling with multiple discharging sinuses over right foot. Many pin-point hypopigmented macules arranged in a schematic pattern were seen, corresponding to the site of administration of indigenous medication [Figure 1]. Dermoscopic examination using DermLite™ DL3-3Gen under contact polarized mode from one of the active sinus revealed small black grains, surrounded by bluish white veil suggestive of deeper fungal colonies [Figure 2a]. White structureless area around the openings corresponding to dermal fibrosis was seen[Figure 2b]. Skin punch biopsy from the lesion demonstrated periodic-acid-schiff positive, pigmented fungal colonies over a background of granulation tissue [Figure 3].Figure 1: Diffuse woody hard swelling over dorsum of right foot with multiple discharging sinusesFigure 2: a. Dermoscopy of the sinus opening shows multiple small black grains. b. The sinuses are surrounded by bluish white veil (Red arrow). Crust surrounding the sinus opening can be seen (Yellow arrow) Structureless pink-white areas related to the underlying fibrosis was seen surrounding to the lesion (Star). (DL3 dermoscope, polarized mode 10x)Figure 3: Histopathology shows pigmented fungal colony comprising of radiating hyphae of eumycetoma, showing splendor hoeppli phenomenon and surrounded by dense neutrophilic infiltrate. (PAS stain, 10x)Mycetoma is a granulomatous infection that can be caused by bacteria (actinomycotic mycetoma) or fungi (eumycotic mycetoma). Grains represent the hallmark of mycetoma and color of grains is often suggestive of the probable causative agent. However, diagnostic facilities are often limited and inaccessible to many patients affected by this neglected tropical disease.[1] Dermoscopy is an easy, quick, and noninvasive tool, which can be helpful in visualizing minute grains and ascertain the type of mycetoma.[1] Black colored granules are highly suggestive of eumycotic mycetoma and its visualization by dermoscopy can help in early institution of definitive treatment. The dermoscopic images can also be stored and transferred electronically and an expert opinion sought through teledermoscopy.[2] Dermoscopy has been explored in the diagnosis of many pigmentary disorders, granulomatous infective diseases like leprosy and sporotrichosis.[34] The current report reinstitutes the importance of dermoscopy in diagnosis of dermatological disorders with clinico-dermoscopic-pathological correlation.[2] Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Calcium signaling induces a partial EMT.

Epithelial plasticity, or epithelial-to-mesenchymal transition (EMT), is a well-recognized form of cellular plasticity, which endows tumor cells with invasive properties and alters their sensitivity to various agents, thus representing a major challenge to cancer therapy. It is increasingly accepted that carcinoma cells exist along a continuum of hybrid epithelial-mesenchymal (E-M) states and that cells exhibiting such partial EMT (P-EMT) states have greater metastatic competence than those characterized by either extreme (E or M). We described recently a P-EMT program operating invivo by which carcinoma cells lose their epithelial state through post-translational programs. Here, we investigate the underlying mechanisms and report that prolonged calcium signaling induces a P-EMT characterized by the internalization of membrane-associated E-cadherin (ECAD) and other epithelial proteins as well as an increase in cellular migration and invasion. Signaling through Gαq-associated G-protein-coupled receptors (GPCRs) recapitulates these effects, which operate through the downstream activation of calmodulin-Camk2b signaling. These results implicate calcium signaling as a trigger for the acquisition of hybrid/partial epithelial-mesenchymal states in carcinoma cells.