Clinical Vignettes/Case Reports - Biliary&sol ...

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[98]

Table 1. CT based assessment of Common bile duct diameter in different age groups

Age Group

[96B] Figure 2.

however there has been no significant change in the inpatient mortality rates. These trends may reflect improvement in the outpatient management of CP patients and increase in overall cost of healthcare, but further studies are needed to confirm this association.

No of patients

Mean CBD diameter

Standard deviation

61-70

27

4.16 mm

1.09 mm

71-80

25

4.3 mm

1.1 mm

81-90

18

5.61 mm

2.06 mm

Mean CBD diameter in group 1 was 4.16±1.09mm (95% CI: 3.70-4.62). Mean CBD diameter in group 2 was 4.3±1.11mm (95% CI: 3.84-4.75) and mean CBD diameter in group 3 was 5.61± 2.06mm (95% CI: 4.58-6.63) One-way analysis of variance test (ANOVA), showed a statistically significant difference in the CBD diameter (p=0.003) between three age groups. Spearman’s rho test shows a positive correlation between age and CBD diameter (R=0.301; p=0.013) Conclusion: An upward trend is seen in the CBD diameter across the three age groups which is statistically significant. Significantly positive correlation is present between age and CBD size. Normal range for CBD diameter in all three age groups was also calculated.

99 Expression of Estrogen Receptor Beta 1, 2, and 5 in Pancreatic Adenocarcinoma Presidential Poster

97 Predicting the Severity of Gallstone Pancreatitis Using BISAP Score Gaurav Singhvi, MD1, Raghav Bansal2, Ishita Rajnish2, Melik Tiba2, Loveleen Sidhu2, Umer M. Syed, MD2, Aaron Walfish3, Vishal Ghevariya4, Ilnaz Salehi, MD3. 1. UCLA, Sylmar, CA; 2. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), Elmhurst, NY; 3. Icahn School of Medicine at Mount Sinai, Elmhurst, NY; 4. Bay Area Endoscopy Center, Elmhurst, NY. Introduction: It is generally recommended that patients who suffer a mild attack of gallstone pancreatitis have their gallbladder removed during the index hospitalization in order to prevent recurrent attacks. One difficulty has been differentiating mild attacks from more severe attacks. The Bedside Index of Severity in Acute Pancreatitis (BISAP) Score is a simple, validated test with which to determine this. Accordingly the goal of this study was to determine the percentage of patients at our institutions who had their gallbladder removed during the initial hospitalization. Secondarily we used the BISAP score to determine the severity of the pancreatitis. Methods: A retrospective chart review of patients presenting with gallstone pancreatitis since 2010 was conducted at two county hospitals, one in New York City and the other in Los Angeles. Pancreatitis was diagnosed by a lipase > 3x the ULN in the setting of gallstones. The number of patients who had surgery, the BISAP score, and the length of stay were documented. We also determined what percentage of patients had recurrence. BISAP scores of 0 and 1 were considered mild, 2 moderate, while 3 and 4 considered severe. Results: There were a total of 174 patients who were evaluated. The mean length of stay was 7.2 days while the mean BISAP score was 0.71. The number of patients who had surgery was 136. (78%) Notably 25 patients (14%) had a recurrent episode. The vast majority of the patients who did not get surgery (29/38) had mild pancreatitis (BISAP score of 0 or 1) and 71% (27/38) were hospitalized for 4 or more days. Conclusion: Our data indicate that most patients with gallstone pancreatitis have mild disease as judged by low BISAP scores. The cholecystectomy rate at our hospitals was quite good, at 78%, but the data suggest that this rate could perhaps be even higher since 74% of patients who did not get surgery had mild pancreatitis. With the average length of stay being greater than a week, plenty of time was available to get the operation done prior to discharge. Timely intervention in these patients could have prevented recurrence of gallstone pancreatitis, led to better hospital resource utilization, and perhaps decreased health care costs. Based on our study the BISAP score should be evaluated further to risk stratify patients presenting with gallstone pancreatitis.

Mamoun Younes, MD1, Charlie Ly, BS2, Jennifer Bailey, PhD3, Sushovan Guha, MD, PhD1, Atilla Ertan, MD4. 1. University of Texas Health Science Center, Houston, TX; 2. University of Texas Medical School, Houston, TX; 3. Department of Internal Medicine Division of Gastroenterology, Hepatology and Nutrition University of Texas Medical School, Houston, TX; 4. UT Medical School at Houston, Houston, TX. Introduction: There had been several limited trials in which tamoxifen efficacy was tested in patients with pancreatic adenocarcinoma (PAC). Most of these studies were small series of patients with unresectable PAC with mixed results: some showing improved survival with tamoxifen while others did not. Patients were not stratified for estrogen receptor expression in these studies because at the time estrogen receptor beta (ER-b) had not yet been identified, and PAC did not express the traditional ER-alpha. More recent studies showed that the effects of estrogens, phytoestrogens and tamoxifen on PAC cell lines depended on ER-b expression. The aim of this study was to identify the expression pattern of ER-b isoforms in PAC. Methods: Sections of 19 formalin fixed and paraffin embedded PAC tissues were stained by immunohistochemistry using specific antibodies to ER-b isoforms 1, 2, and 5 (ER-b1, ER-b2, and ER-b5, respectively). The staining results were evaluated using the Allred method, which combines the staining intensity score with the proportion of positive cells score for a total score (TS) that ranges from 0 to 8. For the purpose of this study, TS of 1-4 was regarded as low expression, 5-6 intermediate, and 7-8 high. Results: For ER-b1, one case (5%) was completely negative, 6 (31%) had low, 10 (53%) had intermediate, and 2 (11%) had high expression. For ER-b2, two (11%) were negative, one had low (5%), 5 (26%) had intermediate, and 11 (58%) had high expression. For ER-b5, three (16%) had low, 10 (53%) intermediate, and 6 (32%) had high expression. Conclusion: A significant percentage of PAC in this series expresses intermediate to high levels of ER-b1, ER-b2, and ER-b5. These findings raise the possibility that the growth of PAC may be influenced by sex steroids and dietary intake of phytoestrogens, and that these tumors may respond to selective estrogen receptor modulators (SERMs) including tamoxifen.

Am J Gastroenterol 2015; 110:S40–S550; doi:10.1038/ajg.2015.270

CLINICAL VIGNETTES/CASE REPORTS - BILIARY/PANCREAS

98 CT-Based Assessment of Bile Duct Size: Assessing if There Is Any Correlation of the Bile Duct Size With the Advancing Age Malav Parikh1, Niyati Gupta, MBBS2, Jay Vasani, MD3, Venu Gopalakrishnan, MD3, Venu Ganipisetti3. 1. St. Francis Hospital, Evanston, IL; 2. Grant Medical College, Mumbai, Evanston, IL; 3. Presence Saint Francis Hospital, Evanston, IL. Introduction: Dilatation of the biliary system is seen with a variety of intrahepatic and extra hepatic conditions. While assessing the pathological significance of a dilated common bile duct (CBD), it is important to compare the bile duct size with age controlled normal values. Prior studies have evaluated the bile duct diameter in autopsy series or by ultrasonography; however there is limited data on computerized tomography (CT) based measurement of bile duct size. This study was designed to determine the normal CBD diameter from CT imaging and assess if there is a statistically significant change in the CBD diameter with age. Methods: Retrospective review of the CT scans of the abdomen was performed for patients between the age of 61 and 90. The study was carried out at a single center by a single radiologist. Patients with any liver, gall bladder, biliary, pancreatic or duodenal pathologies were excluded from study. A total of 70 patients were included in the study after fulfillment of the above criteria. Diameter of the CBD was measured at the distal end near the ampulla of vater. Patients were divided in three age groups [(Group 1: age 61-70 years), (Group 2: age 71-80 years) and (Group 3: age 81-90 years). Results: Mean CBD diameter in the above population was calculated to be 4.59±1.52 mm.

The American Journal of GASTROENTEROLOGY

100 Getting into the Groove: Case Report of a Rare Form of Chronic Pancreatitis Sarah Fishman, MD, PhD, Dmitry Kozekhnikov, DO. Lenox Hill Hospital, New York, NY. Groove pancreatitis is a rare type of segmental pancreatitis that can mimic the effects of a mass leading to gastric outlet obstruction. The clinical manifestations as well as the radiographic appearance make this entity a diagnostic challenge. A 61 year old male with a history of heavy alcohol use and multiple admissions for chronic pancreatitis presented with a four day history of nausea and vomiting. Nine months earlier he had been evaluated by his primary care doctor for a one month history of progressive jaundice. Initial workup was notable for a cholestatic elevation in liver enzymes and a direct bilirubinemia. MRCP suggested distal common bile duct stricture. ERCP confirmed this finding and suggested possible cholangiocarcinoma or pancreatic adenocarcinoma. Tumor markers including CA 19-9 and CEA were normal. A biliary stent was placed and jaundice resolved. Subsequent ERCP to exchange the stent revealed chronic calcified pancreatitis and adenopathy in the peripancreatic and porta-hepatis areas with persistent distal common bile duct stricture. Biopsies were taken from the pancreatic head which were suggestive of chronic pancreatitis but were negative for malignant cells. On admission, lab values were consistent with a severe metabolic alkalosis and a cholestatic pattern of hepatic enzyme elevations. Abdominal CT with oral contrast revealed partial gastric outlet obstruction. A nasogastric tube was placed to decompress the stomach. Repeat MRCP was notable for gastric outlet obstruction and a pancreatic head mass involving

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Abstracts discharged. He was readmitted five days later with biliary sepsis, and severe gastric outlet obstruction. He was medically managed with antibiotics and hydration and subsequently transferred to the surgical service where he underwent gastrojejunostomy. At three month follow up he reported feeling well, resolved nasuea, and weight gain. A rare condition in the US, groove pancreatitis is associated with male gender and alcohol abuse. Pathogenesis likely involves increased viscocity of pancreatic secretions from alcohol use in susceptible patients, leading to stasis. inflammation, and obstruction of the minor papilla. Case series describing this condition suggest that definitive treatment is pancreatoduodenectomy, however this case demonstrates that pancreatic sparing surgical approaches may be feasible.

101 Sump Syndrome as a Complication of Endoscopic Sphincterotomy Omar N. Metwally, MD1, Gregory Fung, MD2, Kevin Man, MD2. 1. St. Mary’s Medical Center in San Francisco, San Francisco, CA; 2. San Francisco Digestive Medicine, San Francisco, CA.

[100A] Figure 1.

Sump Syndrome is an uncommon complication of choledochoduodonostomy in which bile refluxes and stagnates in a blind segment of the common bile duct (CBD) between the anastomosis and the distal end of the CBD. This anatomy predisposes to recurrent episodes of cholangitis resulting from infection of stagnant debris. Sump Syndrome is typically managed by endoscopic sphincterotomy and bile duct clearance but can recur. An unusual case of spontaneous Sump Syndrome due to choledochoduodenal fistula has been reported. We report here a case of Sump physiology in a patient who underwent prior endoscopic sphincterotomy and was found to have a periampullary duodenal diverticulum, which predisposes to bile reflux and obstructive jaundice. The patient developed cholangitis, which resolved after repeat endoscopic sphincterotomy and CBD sweep. This case demonstrates that Sump Syndrome physiology can also occur in patients without a history of biliary surgery but who have predisposing anatomy.

102 Chronic Cholecystitis: A Lost Clinical Differential and Diagnosis Rukevwe Ehwarieme, MD1, Neha Jain, MD1, Ujwala Koduru, MD2, Gurunanthan Palani1. 1. McLaren Flint, Flint, MI; 2. McLaren Flint, Holly, MI.

[100B] Figure 2.

Chronic cholecystitis is a clinical entity which is yet to be clearly defined.Its diagnosis is established by the co-operation of a clinician and pathologist, but over years it has become more of a pathologic finding on cholecystectomy and less of a clinical differential diagnosis.Although the diagnosis is fairly common, literature search did not reveal any case reports. 36 y/o Caucasian female presented with epigastric pain radiating to the right upper quadrant. She had suffered intermittent epigastric pain for 4 months. Pain was associated with nausea and diaphoresis. She denied fever, chills, bowel or bladder symptoms. On physical examination, she was hemodynamically stable with mild abdominal tenderness on deep palpation of the right hypochondrium; her physical examination was otherwise unremarkable. Her laboratory findings showed elevated AST 385 and ALT 260. Her Alk-p, total bilirubin, lipase, CBC and BMP were normal. An abdominal ultrasound was negative for cholelithiasis, CBD dilatation, or findings of acute cholecystitis. CT abdomen with contrast showed thickening of the gall bladder wall. MRCP showed a 3 mm non-obstructive calculus in the distal CBD, a distended gallbladder with wall thickening and minimal pericholecystic edema. On ERCP, a normal intra- and extra-hepatic biliary duct; there was CBD sludge but no CBD stones. She underwent laparoscopic cholecystectomy, her elevated AST, ALT and symptoms resolved. On gallbladder pathology, chronic cholecystitis with cholesterolosis. Although chronic cholecystitis does not correlate with any specific physical exam findings, it remains a clinical entity and should be considered in the differential diagnosis of patients with such clinical presentation. Though a diagnosis of exclusion, clinicians should recognize that early consideration can lead to early interventions and symptomatic relief. Treatment of all types of cholecystitis is cholecystectomy as 90% of patients become asymptomatic.

103 Hemorrhagic Pancreatitis and Ketoacidosis Associated With Severe Hypertriglyceridemia Following Conjugated Linoleic Acid Use James D. Haddad, MD, Alfred F. Shwayhat, DO, MPH, Ryan C. Maves, MD. Naval Medical Center San Diego, San Diego, CA.

[100C] Figure 2.

the second portion of the duodenum. Repeat ERCP showed partial obstruction in the duodenal cap with edematous folds. Biopsies were again taken from the pancreatic head, which were negative for malignancy. The patient underwent PEJ placement for nutrition and placement of a venting PEG tube for oral liquid intake. The patient was started on prednisone 40mg daily to reduce pancreatic inflammation and

© 2015 by the American College of Gastroenterology

Hypertriglyceridemia-induced acute pancreatitis accounts for less than 5% of all cases of acute pancreatitis and is typically associated with serum triglyceride levels greater than 1000 mg/dL. Conjugated linoleic acids (CLAs) are a diverse group of isomeric derivatives of linoleic acid, naturally present in foods originating from ruminant species. We present a case of hypertriglyceridemiainduced pancreatitis and concomitant diabetic ketoacidosis (DKA) temporally related to consumption of CLAs. A previously healthy, 27-year-old African American man presented to a community hospital with nausea, vomiting, and abdominal pain. Initial studies revealed grossly lipemic blood, uninterpretable serum potassium levels, hyperglycemia, an anion gap metabolic acidosis, and an elevated amylase of 515 U/L (25-115 U/L). Contrast-enhanced computed tomography demonstrated an edematous pancreas with a small amount of peripancreatic fluid, without evidence of necrosis. A presumptive diagnosis of DKA complicating acute pancreatitis was made, and the patient was transferred to our critical care unit. Serum triglycerides were measured at 4371 mg/dL (50-199 mg/dL). The patient underwent apheresis with a reduction in his triglycerides to 649 mg/dL. His course was further complicated by acute kidney injury requiring hemodialysis and hemorrhagic pancreatitis requiring erythrocyte transfusion. Routine lipid analysis several months prior to presentation revealed a fasting triglyceride level of 346 mg/ dL. Further history revealed the patient had been using a synthetic CLA supplement for the 10-14 days prior to his presentation. He had not been a known diabetic, and autoimmune markers were negative.


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status. Labs [Table 1] demonstrated elevated proinsulin and C-peptide levels with negative urine toxicology screen and sulfonylurea assay. CT scan of the head and abdomen were unremarkable. Gastroenterology (GI) was consulted for an evaluation with endoscopic ultrasound (EUS) to rule out insulinoma. Although insulinoma was the working diagnosis in-addition to other differential diagnoses as listed [Table 2], a negative monitored 72-hour fasting test [Fig.1] without any symptomatic hypoglycemic episodes essentially ruled out insulinoma. Recurrent post-prandial hypoglycemia with neuroglycopenic symptoms in the setting of RYGB and endogenous hyperinsulinism with negative 72-hour fasting test suggested nesidioblastosis as the likely diagnosis. Our patient was managed with Diazoxide (3-8mg/kg/ day divided into 3 doses) and, complex carbohydrates were added to his diet. His hypoglycemic symptoms improved at subsequent follow-ups. Nesidioblastosis is rare in adults and, seen in patients who had undergone gastric bypass surgery with etiology linked to persistent hyper-secretion of glucagon-likepeptide-1 causing beta cells hypertrophy. Post-prandial neuroglycopenia is a classic manifestation but can be challenging to diagnose due to its rarity and the difficulty to localize on imaging. Selective arterial calcium stimulation and venous sampling can confirm the diagnosis, invasively [1-3]. Often patients are referred to GI for evaluation with EUS, but with RYGB, EUS is technically not feasible to evaluate pancreas due to the altered anatomy. However, a certain diagnosis can be made based on the history, labs [Table1] and a negative 72-hour fasting test without the need for invasive tests. With increasing prevalence of obesity and gastric bypass surgeries, we as gastroenterologists shall expect to see more of this rare, but interesting metabolic complication of gastric bypass surgery. Reference: [1] Service, G.J., et al. N Engl J Med, 2005. 353(3): p. 249-54. [2]. Kellogg, T.A., et al. Surg Obes Relat Dis, 2008. 4(4): p. 492-9. [3] Ritz, P. and H. Hanaire. Diabetes Metab, 2011. 37(4): p. 274-81.

[103A] Figure 1.

[104A] Figure 1.

[104B] Figure 2. [103B] Figure 2.

Hemoglobin A1c level drawn prior to transfusion was 9.3%. His demographics and dramatic presentation suggested an antecedent diagnosis of ketosis-prone type II diabetes mellitus. CLAs have been widely marketed as dietary supplements and are generally regarded as safe for human consumption. Commercially available CLAs contain mostly the cis-9, trans-11 and trans-10, cis-12 isomers which have been shown to be active in adiposity and insulin sensitivity regulation via multiple mechanisms. The patient’s predisposition for hypertriglyceridemia was potentiated by ingestion of CLAs, resulting in severe hypertriglyceridemia and resultant pancreatitis that precipitated his DKA. Our case adds to the growing body of literature documenting the risks associated with consumption of CLAs.

104 Nesidioblastosis: A Rare Case of Post Prandial Hypoglycemia in a Patient With Gastric Bypass Surgery Pradeep R. Atla, MD, MPH1, Jagrati Mathur, MD1, Devang N. Prajapati, MD2. 1. University of California San Francisco, Fresno, CA; 2. VA Central California Health Care System, University of California San Francisco, Fresno, CA. A 46-year-old man with recurrent episodes of hypoglycemia for two-years admitted with recent worsening of symptoms that ranged from dizziness, diaphoresis and disorientation to seizures and loss of consciousness. His symptoms were mostly postprandial with low random home sugars (50-80 mg/dL) despite consuming sugary drinks and candies. History remarkable for Roux-en-Y gastric bypass (RYGB) surgery 5 years ago for obesity, anxiety disorder and daily alcohol use (40 g/day). Denied diabetes, use of diabetic medications or weight loss supplements. Unremarkable physical exam with normal mental


[104C] Figure 3.


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Abstracts 105 Pancreatitis by Compression Hirsh D. Trivedi, MD, Manish Tandon, MD, Blanca Lizaola, MD, David Lee, MD. St. Elizabeth’s Medical Center, Brighton, MA. Diverticula are a rare cause of pancreatitis. We present a case of acute pancreatitis secondary to compression from a periampullary duodenal diverticulum (PAD). A 38-year-old male presented with acute epigastric abdominal pain. He denied other symptoms and had no history of alcohol intake, trauma, or taking any medications. He was afebrile and hemodynamically stable. On exam, his abdomen was tender to palpation in the epigastrium. His labs were notable for a WBC 11.5 k/mm3, lipase 5,410 IU/L, AST 87 IU/L, ALT 72 IU/L, ALP 126 IU/L, total bilirubin 0.5mg/dL, normal triglycerides and calcium levels. He was admitted with suspected biliary pancreatitis and medical management was initiated with intravenous fluids, bowel rest, and pain control. His liver enzymes subsequently increased to an AST 469 IU/L, ALT 503 IU/L and total bilirubin 1.4 mg/dL. An abdominal ultrasound done prior to admission for similar symptoms was negative for gallbladder stones or sludge. Computed Tomography Scan showed mild common bile duct and pancreatic duct dilatation with an edematous pancreatic head consistent with pancreatitis. An Endoscopic Retrograde Cholangiopancreatography showed a large diverticulum with food impaction obscuring the major duodenal papilla. Some food particles were removed from the diverticulum using a grasping snare and a Roth net. Due to remnant food debris, the ampulla could not be located to allow for cannulation within the large diverticulum. Magnetic Resonance Cholangiopancreatography revealed an enlarged pancreatic head with a large 3cm duodenal diverticulum compressing its inferior portion at the ampulla of Vater with no evidence of biliary stones. The patient’s symptoms and laboratory abnormalities improved after ERCP, and he was discharged with surgical follow-up for possible intervention in event of recurrent pancreatitis attacks. Duodenal diverticula rarely cause pancreatitis, but should be kept in mind as a potential etiology. About 70-75% of duodenal diverticula occur in the periampullary region. Factors that contribute to the development of these diverticula include age, weakening of intestinal smooth muscles, and increased

[105C] Figure 3.

intraduodenal pressure. Mechanical pressure from the diverticulum and diverticular inflammation from narrowing at the duodenal papilla leads to complications of PAD. Surgical intervention is not indicated for asymptomatic patients. Patients who are symptomatic may necessitate surgical or endoscopic intervention, such as sphincterotomy. We present a rare case of acute pancreatitis caused by compression from a periampullary duodenal diverticulum.

106 Splenic Abscess: A Rare Complication of a Common Disease Julia Shor, MD1, Darren Vo, MD2, Matthew Czaja, MD2. 1. Rutgers Robert Wood Johnson University Hospital, Highland Park, NJ; 2. Rutgers Robert Wood Johnson University Hospital, New Brunswick, NJ.

[105A] Figure 1.

Introduction: Chronic pancreatitis is a common disease that is usually caused by alcoholism or gallstones. The complications of chronic pancreatitis are myriad, including splenic vein thrombosis due to chronic inflammation surrounding the splenic vein. In 1-5% of cases, chronic pancreatitis involves the spleen in the form of infarction, intrasplenic pseudocyst, and hemorrhage. We present a case of chronic pancreatitis causing splenic vein thrombosis related infarct and splenic abscess. Case: A 52-year-old male with DM, HTN, and chronic pancreatitis due to alcohol abuse was admitted for left upper quadrant abdominal pain. Initial CT scan showed splenic vein thrombosis, splenic infarct, and a small pancreatic pseudocyst. He was initially treated with pain control, IV fluids, and bowel rest. However, his abdominal pain increased, he became febrile, and the WBC count increased from 16,000 to 24,000 cells/microliter. Empiric piperacillin-tazobactam was started. A repeat CT scan of the abdomen revealed the presence of a subcapsular splenic fluid collection, concerning for abscess vs. hematoma. CT guided aspirate was performed which yielded 60cc of purulent fluid, and a JP drain was left in place. Abscess cultures were positive for Escherichia coli. Blood cultures drawn prior to the initiation of antibiotics were negative. The patient markedly improved after abscess drainage and was discharged home with the drain in place to complete a course of levofloxacin and metronidazole. Discussion: The most common locations for the development of an abscess in chronic pancreatitis are pancreatic and hepatic. The above case highlights the rare occurrence of splenic abscess in the setting of chronic pancreatitis. Splenic abscesses usually occur due to hematogenous spread from infectious sources such as endocarditis, but they can occur as complications of splenic pseudocysts, which can extend from pancreatic pseudocysts in chronic pancreatitis. Additionally, while splenic infarcts do occur in chronic pancreatitis due to inflammatory encasement of the artery, splenic vein thromboses are usually self-limited. We hypothesize that our patient had chronic pancreatitis complicated by pancreatic tail pseudocyst. The splenic vein, with close proximity to the pancreas, became occluded by thrombus and caused a splenic infarct secondary to venous congestion. In a separate process, a splenic abscess formed by contiguous spread of bacteria from the pancreatic pseudocyst. To our knowledge, there have been only two case reports of chronic pancreatitis causing splenic abscess, in 1998 and 1999. Our case is the third reported case and the first to also showcase splenic vein thrombosis leading to infarct.

107 Biliary Intraductal Papillary Mucinous Neoplasm (B-IPMN) Presenting as Obstructive Jaundice Mehran Moradi, DO, Thomas Dorsey, MD, FACG. Ohio Valley Medical Center, Wheeling, WV.

[105B] Figure 2.


Purpose: B-IPMN is a rare disorder of the biliary tract characterized by projections into the biliary lumen. We describe a case of Intraductal Papillary Mucinous Neoplasm Presenting as Obstructive Jaundice.


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108 An Unusual Bug in the Biliary Tree and Beyond Moira Hilscher, MD1, James H. Tabibian, MD, PhD2, Stephanie Hansel, MD, MS3. 1. Mayo Clinic, Rochester, MN; 2. Division of Gastroenterology& Hepatology, Mayo Clinic, Rochester, MN; 3. Division of Gastroenterology, Mayo Clinic, Rochester, MN.

[107A] Figure 1.

Introduction: Achromobacter xylosoxidans is a gram-negative bacillus which inhabits hospital environments and rarely causes infection. Despite its low virulence, it has a high degree of intrinsic antibiotic resistance and is emerging as an opportunistic pathogen in immunocompromised patients. A. xylosoxidans infection generally manifests as bacteremia, endocarditis, or pneumonia and has a high mortality rate. This organism has rarely been isolated from the human hepatobiliary system and the few reported outcomes have been poor. We report a challenging case of biliary infection presenting with protean manifestations which were ultimately due to bacteremia and discitis originating from biliary infection with a rare organism. Case report: A 62 year old man presented with severe back pain. His medical history was significant for diabetes mellitus and remote necrotizing pancreatitis requiring multiple necrosectomies, Roux en Y choledochojejunostomy, cholecystectomy, splenectomy, and placement of a self-expanding metal stent in the biliary tree which had become embedded in the common bile duct (CBD). Serum laboratory evaluation was remarkable for leukocytosis (21.8 x 109) and elevated alkaline phosphatase (ALP) (543 U/L; upper limit of normal 130 U/L). Review of prior serologic tests suggested that the presenting ALP value was the patient’s new baseline as the value had doubled during two prior episodes of clinical acute cholangitis. Liver enzymes were otherwise normal. Blood cultures grew A. xylosoxidans at 24 hours in two out of three bottles. Further evaluation was pursued to identify the source of infection. Abdominal ultrasound revealed dilation of the CBD to 20 mm without cholelithiasis or sludge. Computerized tomography of the chest/abdomen/pelvis revealed stable pneumobilia and multiple thoracic vertebral body fractures. Positron emission tomography scan demonstrated increased fluorodeoxyglucose (FDG) activity near the vertebral compression deformities and increased FDG uptake just inferior to the diaphragm and extending to the dome of the liver. Transesophageal echocardiogram was negative for endocarditis. Due to concern for a biliary nidus of infection despite stable serum liver tests, endoscopic retrograde cholangiography (ERC) was performed. This revealed grade II duodenal varices without esophageal or gastric varices. Balloon sweeping of the CBD resulted in extraction of stones, sludge, and frank pus consistent with pyogenic cholangitis and a source of bloodstream and skeletal infection. The patient was treated with two weeks of ertapenem and daptomycin with continuation of indefinite suppressive antimicrobials.

109 A Rare Case of Oriental Cholangiohepatitis Naga Saranya Addepally, Jagpal Singh Klair, MD, Aneet Kaur, Abhishek Agarwal, Farshad Aduli. University of Arkansas for Medical Sciences, Little Rock, AR.

[107B] Figure 2.

Case Report: Patient is an 81-year-old male who presented with chest pain and right upper quadrant abdominal pain. Pain radiated to the back and associated with nausea without vomiting. He had guarding on the physical exam. Bilirubin was 6.4 MG/DL and Alkaline Phosphatase was 370 U/L on admission. Hida Scan failed to show excreting of nucleotide from the liver parenchyma after four hours. CT of the abdomen with IV contrast showed dilated gallbladder with surrounding inflammatory changes including biliary dilatation. Ultrasound showed mild dilatation of the common bile duct measuring 8mm. Patient underwent laparoscopic cholecystectomy and intra operative cholangiogram which was interpreted as distal common bile duct stones with incomplete obstruction (Fig 1). Postoperative ERCP showed multiple tiny filling defects throughout common bile duct (Fig 2). Several sweeps were made with balloon and basket yielding mucus but no stony material. The filling defects were fixed 2-3 mm in size polypoid lesions. Spy Glass procedure targeted biopsy performed and histopathology was consistent with B- IPMN. Covered Self-Expanding Metal Stent was placed. Patient did well post procedure. Bilirubin and Alkaline Phosphatase have returned to normal. B-IPMN is characterized by multiple papillary tumors within the intrahepatic biliary tree that can cause biliary obstruction. 41%-83% of these lesions undergo malignant transformation. B-IPMN presents with recurrent episodes of abdominal colic, jaundice, acute cholangitis, weight loss, and the presence of biliary stones. Medical imaging can sometimes help in the diagnosis with ERCP showing multiple filling defects and irregularity of the bile duct wall. The diagnosis can be confirmed by intra ductal biopsies or by studying the cytology of any secretions. B-IPMN that does not undergo malignant transformation eventually leads to chronic cholestasis due to mechanical obstruction resulting in septic cholangitis and hepatic failure. Treatment is based on the location of the neoplasm. In diffuse papillomatosis, liver transplantation has been performed with promising results. If the lesion is located in the lower third of the common bile duct or in the pancreatic duct, pancreaticoduodenectomy is an indication. This case is a rare presentation of obstructive jaundice similar to choledocholithiasis, but with no stone in the common bile duct. B-IPMN requires prompt diagnosis, since it has a high malignant transformation potential.


Introduction: Oriental cholangiohepatitis is commonly seen in Asian with prevalence of < 1% in Western countries. It is thought to be secondary to parasitic infection of bile system with concomitant biliary infection that leads to production of beta-glucuronidase that play key roles in bilirubin precipitation, stone and stricture formation. Case: A 73 year-old caucasian female with history of diabetes mellitus presented with nausea, vomiting, epigastric abdominal pain, diarrhea for 1 week. Reported 70-lb weight loss over past year. CT scan was concerning for possible pancreatic mass, omental metastasis, numerous tumor nodules in mesentery and possible thrombus in portal vein. Labwork showed ALP 230, albumin 1.6, CA 19/9 45.2. US Liver showed moderate intrahepatic biliary dilation, dilated proximal common duct measuring 1.4cm. MRCP showed moderate intra and extrahepatic biliary ductal dilatation with multiple large filling defects within both intrahepatic and extrahepatic bile ducts, consistent with stones (Fig1). EUS was done which showed normal visual exam, diffuse pancreas with mixed echogenicity. FNA of pancreatic head/body negative for malignancy. ERCP showed CBD of 1.8 cm with atleast 4 (~1cm stones) with largest being ~1.2cm (Fig2). Biliary sphincterotomy was performed followed by mechanical lithotripsy, balloon extraction. A 10 Fr 9cm plastic biliary stent was placed in CBD proximal to retained stones. Repeat ERCP was done in OR with laser lithotripsy and residual stone removal in 2-3 weeks. Discussion: It is a serious condition owing to its intractability, frequent recurrence and predisposition of cholangiocarcinoma. Presenting symptoms include abdominal pain, jaundice, cholangitis and can lead to production of strictures and liver abscesses. US liver is first diagnostic modality as it can clearly show intrahepatic stones and biliary dilation. MRCP is the best non-invasive imaging that shows intrahepatic stones, biliary strictures and hepatic abscess. Direct cholangiography remains the gold standard with sensitivity of almost 100% in the detection of obstruction. The goals of treatment include treating cholangitis (fluids/antibiotics), preventing recurrence, clearance of stones, correction of strictures, restoration of biliary drainage and to stop the progression of the disease. There is no definitive treatment owing to the complicated nature of the disease. Urgent endoscopic biliary decompression prevents patient from going into shock. Hepatic resection has shown to reduce the risk of recurrence of stones, since it removes not only intrahepatic stones but also the associated pathological bile ducts damaged by strictures. Liver transplantation is usually the only treatment option in cases of diffuse liver parenchyma involvement and development of cirrhosis.

[109]

Table 1. Grading the severity of hepatolithiasis

Grade 1

Asymptomatic

Grade 2

Having abdominal pain

Grade 3

Presence of either transient jaundice or cholangitis

Grade 4

Having continuous jaundice, sepsis, or cholangiocarcinoma.


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[109A] Figure 1.

[110B] Figure 2.

[109B] Figure 2.

110 An Atypical Cause of Intermittent Biliary Obstruction Blanca Lizaola, MD, Hirsh Trivedi, MD, David Lee, MD, Manish Tandon, MD. St. Elizabeth’s Medical Center, Brighton, MA. Periampullary diverticula (PAD) can rarely cause biliary obstruction resulting in obstructive jaundice or transaminitis. PAD therefore should be on the differential for patients presenting with suspected biliary obstruction. We present a case of biliary ductal dilation with intermittent transaminitis due to PAD causing obstruction. A 76-year-old Asian female with history of paranoid schizophrenia, hypertension and remote open cholecystectomy presented with altered mental status. She denied nausea, vomiting, abdominal pain, weight loss, dark urine or pale stools. Physical exam was benign. Laboratory tests revealed AST 82 IU/L, ALT 75 IU/L, ALP 122 IU/L and total bilirubin of 0.2 mg/dl. The liver enzymes had been within normal range prior to her presentation. An abdominal ultrasound showed normal biliary ducts and suggested mild hepatic steatosis. A subsequent abdominal Computed Tomography (CT) scan demonstrated dilation of the common bile duct (CBD) with associated pancreatic ductal enlargement, which raised concern for an ampullary lesion. Magnetic Resonance Cholangiopancreatography confirmed CBD dilation to 17 mm along with intrahepatic ductal dilation, and a pancreatic duct measuring 6 mm. An Endoscopic Retro-

[110C] Figure 3. grade Cholangiopancreatography showed that the major papilla was located within a diverticulum containing particulate debris. The biliary tree was diffusely dilated with the largest CBD diameter measuring 17 mm in the mid portion with gradual smooth tapering towards the ampulla. Sphincterotomy and balloon sweeps were done and no stones were noted. Biopsies of the ampulla were negative for adenoma and confirmed the presence of chronic inflammation. The patient’s symptoms and transaminitis normalized after ERCP and the patient was discharged. Upper gastrointestinal studies have reported a duodenal diverticula incidence of 1-6% and a prevalence of 22% in cadavers. 75% of the duodenal diverticula are periampulary in location and can cause obstruction which presents as jaundice or as in our case, intermittent transaminitis. Lemmel’s Syndrome is the obstruction of the hepatopancreatobiliary drainage secondary to inflammation and chronic fibrosis of the Papilla, dysfunction of the sphincter of Oddi and/or direct compression of the distal CBD or Ampulla by the diverticula. Its diagnosis may be challenging and should be considered in the absence of choledocholithiasis and other pancreatobiliary tumors. Diagnosis is made through endoscopy and the most appropriate treatment is endoscopic sphincterotomy.

111 Shoulder Pain as the First Sign of Pancreatic Cancer Syed Amer, MBBS1, Huma S. Manzar, MBBS2, Jennifer L. Horsley-Silva, MD1. 1. Mayo Clinic, Phoenix, AZ; 2. Shadan Institute of Medical Sciences, Hyderabad, India.

[110A] Figure 1. © 2015 by the American College of Gastroenterology

A fifty-four year-old Caucasian male presented to the emergency department with a chief complaint of progressively worsening left shoulder pain that had been ongoing for the past three weeks. He described the pain as initiating in his left shoulder radiating down his arm, worsening with movement and improving with rest. He had been evaluated by his primary care provider a week before


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presentation, was thought to have a muscle spasm, and was prescribed a muscle relaxant. The pain progressed despite muscle relaxant administration and he noticed weakness developing in his left extremity. He denied any trauma to his shoulder, any numbness or tingling, or any similar symptoms in the past. On physical exam, he was unable to abduct his left shoulder, and had diminished strength and absent deep tendon reflexes on the left upper extremity. The rest of his physical examination was normal. Magnetic resonance imaging (MRI) of the cervical spine was performed, revealing a left C5 vertebral body lesion (Image 1) with an extraosseous extension likely compressing the exiting C5 nerve root, with neoplasm being the primary consideration. He subsequently had a computed tomography (CT) of the chest and abdomen. CT revealed an hypoenhancing mass in the pancreatic tail, concerning for malignancy (Image 2). His CA 19-9 was elevated at 323 U/ml. MRI of the abdomen confirmed the pancreatic tail lesion and also revealed multiple hepatic lesions concerning for metastatic lesions. A subsequent bone biopsy of the C5 vertebrae revealed moderately differentiated metastatic adenocarcinoma (Image 3). Oncology service was consulted. They felt that he would not benefit from chemotherapy, given the grave diagnosis of metastatic pancreatic cancer. He subsequently underwent palliative radiation to the C5 lesion. Unfortunately, he passed away three months after his diagnosis. The usual sites of metastases in pancreatic cancer include the liver and peritoneum. Other less common sites are the lung, brain, kidney, and bone. Skeletal metastases are less prevalent but contribute to significant morbidity associated with pancreatic cancer. The exact prevalence of osseous metastases is not known, but has been estimated to be between 5% and 20%. The most common osseous lesions are osteolytic in nature, but rarely the osteoblastic ones can be seen. The spine, in the form of vertebral metastases is the most common site of skeletal metastasis of pancreatic cancer. Bone pain, pathological fractures, and hypercalcemia are possible symptoms of skeletal metastases. Early diagnosis and treatment for bone metastases is important to maintain quality of life.

[111A] Figure 1.

112 Acute Pancreatitis in the Setting of Normal Serum Pancreatitic Enzyme Levels Carmine Catalano, MD1, Hassan Alkhawam2, Mariya Fabisevich2, Neil Vyas2. 1. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), East Rockaway, NY; 2. Elmhurst Hospital Center, Elmhurst, NY.

[111B] Figure 2.

There have been many reports of acute pancreatitis with normal serum amylase levels but acute pancreatitis with normal serum lipase levels is exceedingly rare. This is not uncommon given that amylase has a relatively short half-life of about ten hours with normalization in about three to five days while lipase may remain elevated for up to two weeks. A 44 year-old male with a past medical history of hypertension and diabetes mellitus presented to the Emergency Department complaining of nausea with non-bloody and non-bilious emesis, non-bloody diarrhea, epigastric pain, anorexia and chills for the past several days. The epigastric pain is sharp and radiates to the back. It is aggravated with food intake and lying supine. The patient admits to using alcohol every weekend and consumes several beers each session. His last alcohol intake was about one week prior. He denies tobacco or illicit drug use.His vitals on admission were notable for a fever of 101.5 degrees Fahrenheit and sinus tachycardia.The physical exam was notable for dry mucous membranes and severe epigastric tenderness with guarding.The remainder of the exam was unremarkable. His complete blood count and basic metabolic panel were within normal limits. Liver function tests were only notable for an elevated gammaglutamyl transpedtidase and an elevated lactate dehydrogenase. Serum amylase and lipase levels were found to be within normal limits. A lipid panel including triglycerides was also found to be within normal limits. A chest x-ray showed a small left-sided pleural effusion. The patient was admitted to the medicine service for the inability to tolerate oral intake and treatment for acute gastroenteritis.On day three of hospitalization, the patient was still not able to tolerate oral intake, developed worsening abdominal pain and a low grade fever. Repeat blood work revealed a white blood cell count of 15,300 cells per microliter. A Computed Tomography (CT) scan of the abdomen and pelvis with intravenous and oral contrast was pursued and showed extensive pancreatic edema and peripancreatic stranding consistent with acute pancreatitis. No pseudocysts or calcifications were seen. A repeat serum amylase and lipase were within normal limits. Based on clinical presentation and radiological findings, the diagnosis of acute pancreatitis was made. The patient was started on aggressive intravenous fluid hydration, pain management and bowel rest, with improvement in symptoms. On day five of hospitalization the patient was able to tolerate a regular diet with almost complete resolution of his epigastric pain. Clinical symptoms and radiological findings are all that is needed to make the diagnosis of acute pancreatitis and medical care providers should not exclude this diagnosis based on normal serum levels of amylase and lipase enzymes as they can normalize early on in the course of this disease.

113 Transjugular Liver Biopsy and the Bloody Mess That Follows: A Rare Case of Hemobilia and Hemocholecystitis Kristen A. Suchniak-Mussari, MD1, Beth A. Foreman, DO1, Amol Sharma, MD2, Charles E. Dye, MD1. 1. Penn State Milton S. Hershey Medical Center, Hershey, PA; 2. Penn State Hershey Medical Center, Hershey, PA. A 59-year-old woman with hepatitis C presented with right upper quadrant abdominal pain. One day prior, she underwent transjugular liver biopsy to evaluate for cirrhosis. Physical exam revealed stable vital signs, jaundice, scleral icterus, and guarding to right upper quadrant palpation. Liver function tests were consistent with total bilirubin 11.2 mg/dL, AST 354 unit/L, and ALT 209 unit/L. Hemoglobin was 8.9 g/ dL, decreased from a baseline of 15 g/dL. Abdominal CT showed a large soft tissue density extending the entire length of the common bile duct (CBD). ERCP was performed, finding a dilated CBD greater than 2.5 cm with multiple large, amorphous filling defects. Repeated balloon sweeps revealed blood clots, and a nasobiliary tube was left in place for flushing. Despite this, the patient developed hemorrhagic shock. She underwent angiography revealing distal hepatic artery laceration, and subsequent coil embolization achieved hemostasis. Post-procedure, hemoglobin and vital signs stabilized. However, on hospital day 12, she again developed severe right upper quadrant pain. Abdominal ultrasound revealed an enlarged gallbladder with a thickened wall and a positive Murphy’s sign. HIDA scan showed non-visu-

[111C] Figure 3. The American Journal of GASTROENTEROLOGY


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Abstracts nine 1.49mg/dl, total bilirubin 2.3mg/dl (which peaked at 3.5mg/dl), direct bilirubin 1.4mg/dl (peaking at 2.2mg/dl), alkaline phosphatase 357U/L (peaking at 379U/L), AST 24U/L, ALT 44U/L, GGT 722U/L. ASMA, AMA and anti-LKM1 antibody were negative as was a viral hepatitis panel. Liver ultrasound showed no evidence of biliary obstruction, and HIDA scan did not demonstrate cholecystitis or biliary obstruction. MRCP was unremarkable. Her current medications were reviewed for their side effects, and drug-induced liver disease was deemed unlikely. Her decompensated heart failure was managed, and the alkaline phosphatase trended down, but pruritus remained. Ursodeoxycolic acid was administered, and within 12-18 hours there was marked improvement of pruritus. The patient was continued on ursodeoxycolic acid, and the pruritus was completely resolved in about 72 hours.

115 A Case of Concomitant Diagnosis of PSC and Cholangiocarcinoma (CCA) in a Patient With History of Surgically Treated UC for 25 Years Mahreema Jawairia, MD, Ghulamullah Shahzad, MD, Paul Mustacchia, MD. Nassau University Medical Center, East Meadow, NY.

[113A] Figure 1.

A 72 year old Indian male with history of UC for 25 years and colon cancer s/p proctocolectomy presented with epigastric pain, fevers and chills for 10 days for last 3 days. Pain was 8/10 in intensity, nonradiating, sharp, and was associated with decreased appetite. He denied any nausea, vomiting, diarrhea or constipation or weight loss. His LRTs showed cholestatic picture, of note for past five years they were within normal range. A CT scan of abdomen showed intrahepatic biliary ductal dilatation the transition to normal-caliber at the porta hepatis and a questionable filling defect at the point of transition within the CBD. A stone or mass could not be excluded. Surgey said no intervention needed at this time. MRCP showed marked bilobar intrahepatic biliary ductal dilatation with normal caliber distal CBD concerning for obstructing stricture or neoplasm. ERCP showed small filling defects in the CBD, likely due to choledocholithiasis. A stricture was noted in the distal right hepatic duct proximal to the hilum. Left hepatic duct appeared irregular and dilated likely secondary to PSC and gallbladder was normal. CA-199 was abnormal with a level of 8589 and brush cytology was negative for malignancy. Patient was informed of high suspicion of biliary ductal tumor and was given the option to seek treatment at a specialized biliary center. He opted to continue treatment in India. There, he underwent percutaneous biopsy and PET scan showed CCA with metastasis. PSC is a cholestatic liver disease characterized by multiple fibrotic strictures of the intra- and extrahepatic biliary tree. Although PSC is generally slow progressive, it is refractory to therapy, and frequently results in advanced liver cirrhosis. CCA is the most feared complication of PSC and the occurrence of CCA leads to a poor prognosis for PSC patients. The prevalence of CCA in patients with PSC is reported to be approximately 7–15% in USA. The average follow-up period between PSC and CCA diagnosis is relatively short (2.6 to 3.5 years). Also, PSC patients with IBD are less likely to develop CCA. Although most PSC patients die from liver failure or cholangitis-associated sepsis, some die from CCA, which occasionally accompanies the natural course of PSC. In the US and Europe, PSC is the major risk factor associated with the development of CCA and rapidly complicates PSC, usually leading to death within a few months of diagnosis. Patients with PSC have a 10-15% lifetime risk of developing CCA. The highest risk is in newly diagnosed patients within the first year, and thereafter, the incidence of CCA is about 1% per year. Unlike CCA without PSC, it is difficult to diagnose CCA in patients with PSC because PSC itself shows similar diffuse radiographic findings of bile duct derangement, and brush cytology and biopsy often fail to detect cancer cells because of the desmoplastic nature of CCA.

116 A Case of Pancreatic Pseudocyst Extending Into the Mediastinum Nabeel Chaudhary, MD1, Wahid Wassef, MD, MPH, FACG2. 1. UMass Memorial Medical Center, Boston, MA; 2. UMass Memorial Medical Center, Worcester, MA.

[113B] Figure 2.

alization of the gallbladder, consistent with acute cholecystitis. She underwent laparoscopic cholecystectomy, confirming hemocholecystitis. Hemobilia is a rare complication of liver biopsy with an incidence less than 1%, occurring immediately or within one week after biopsy. Classic clinical presentation with Quincke’s triad (right upper quadrant pain, jaundice, and gastrointestinal hemorrhage) occurs in only 20% of patients with hemobilia. Resultant biliary obstruction requires ERCP with sphincterotomy and clot extraction. While half of cases reach hemostasis spontaneously, the remaining cases require embolization. Hemocholecystitis following liver biopsy is even more uncommon with only a few cases reported in the literature. When right upper quadrant pain worsens despite proper treatment of hemobilia, hemocholecystitis should be suspected and can be confirmed with a HIDA scan. Without prompt diagnosis, gallbladder perforation can occur in 2-15% of hemocholecystitis cases as a result of gangrenous cholecystitis. Treatment involves early cholecystectomy.

114 Devastating Pruritus in Congestive Heart Failure Exacerbation

Introduction: Pancreatic pseudocyst are walled-off fluid collections usually occurring in cases of acute pancreatitis but can also occur in chronic pancreatitis, blunt, and penetrating pancreatic trauma. They can range in size from very small to very large and can extend outside the abdomen into the mediastinum or even into the pelvis. Here we report a case of a pancreatic pseudocyst extending into the mediastinum which was treated successfully by endoscopic cystgastrostomy. Case Report: Patient is a 50 year old female who has a history of chronic pancreatitis secondary to alcohol abuse. She had multiple admissions to the hospital 6 months prior to this hospitalization for acute on chronic pancreatitis and chest pain. She was found to have a small developing pseudocyst on initial CT scan. Upon this admission for chest and abdominal pain, an abdominal CT scan showed increase in size of pancreatic pseudocyst extending into the mediastinum, persistent pancreatic stranding, and new pseudocysts. Amylase was 348 and lipase was 212. An EUS with fluid aspiration confirmed that this was a pseudocyst. Fluid cultures grew streptococci viridians, candida albicans, and lactobacillus species. A step-up approach cystgastrostomy with stent placement followed by necrosectomy was successfully performed. Subsequently, patient did well, pseudocyst resolved and stents were removed uneventfully. It has now been six months since stent removal and she is doing well without any recurrent hospital or ER visits. Conclusion: Pancreatic pseudocysts occur in about 10 percent of acute pancreatitis cases but can also be seen in chronic pancreatitis, blunt, or penetrating pancreatic trauma. These pseudocyst if asymptomatic require no intervention. If symptomatic, they need to be drained. This can be successfully performed wherever the pseudocysts extend, even into the mediastinum as in this case as long as the same principles of step-up-approach for cystgastrostomy are followed.

Rukevwe Ehwarieme, MD1, Suhag Patel 2, Murray Ehrinpreis, MD3. 1. McLaren Flint, Flint, MI; 2. Harper Hospital, Detroit, MI; 3. Department of Gastroenterology, Wayne State University School of Medicine, Detroit, MI. Congestive hepatopathy can have elevations in liver specific alkaline phosphatase in decompensated heart failure. In contrast to other end organ damages associated with congestive heart failure such as cardio-renal syndrome, less is known about impaired liver function in patients with heart failure. Although there are a number of case reports regarding describing elevated alkaline phosphatase in congestive hepatopathy, there are no known reported cases of pruritus associated with this condition. A 68 year old female with a known history of end stage congestive heart failure presented with decompensated heart failure, severe pruritus and persistently elevated alkaline phosphatase. The pruritus was resistant to diphenhydramine, hydroxyzine, and prednisone. Laboratory work-up: BUN 26mg/dl, creati-


117 Spontaneous Rupture of an Intrahepatic Biliary Duct Causing a Right Pleural and Retroperitoneal Biloma Eduardo A. Rodriguez, MD1, Kartik Valluri, MD2, Diana Otero, MD3, Frederick Williams, MD2. 1. University of Miami Palm Beach Campus, West Palm Beach, FL; 2. University of Miami Palm Beach Campus, Atlantis, FL; 3. Mount Sinai Bronx Program, Bronx, NY. Bilomas are encapsulated collections of bile outside of the biliary tree and are mainly caused by iatrogenic injury or abdominal trauma. Spontaneous rupture of the biliary tree is not common. We report a case


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of a patient with spontaneous rupture biloma treated with percutaneous and internal-external biliary drainage. A 68-year-old man with significant history of amyloidosis and monoclonal paraproteinemia was admitted for progressively worsening right upper quadrant abdominal pain and nausea for the last week. Vital signs were unremarkable and physical exam revealed mild jaundice and a positive Murphy sign. No rebound or guarding. Laboratory results revealed total bilirubin of 1.7 mg/dL, direct bilirubin of 0.8 mg/dL, alkaline phosphatase of 328 IU/L, AST of 190 IU/L, ALT 154 IU/L. Pancreatic enzymes and Ca 19-9 were within normal limits. Right upper quadrant ultrasound showed a distended gallbladder with biliary sludge and a dilated common bile duct (CBD) measuring 11mm. MRCP suggested a pancreatic head mass. Subsequent ERCP showed narrowing at the CBD making it difficult for cannulation. However fine needle aspiration samples were obtained and came back positive for malignancy. Over the next few days, the patient became febrile, continued having the abdominal pain and developed worsening liver function tests. CT of the abdomen revealed a large retroperitoneal fluid collection, intra and extrahepatic biliary duct dilation and a right pleural effusion. Patient underwent right chest tube placement, which drained 2 L of bilious pleural fluid. She also underwent percutaneous transhepatic cholangiogram, which showed bilious leakage from third order branch of the right hepatic duct at the level of the superior aspect of the right lobe of the liver, which was causing complete obstruction of the distal CBD. Subsequent internal-external biliary drain was placed without complications, followed by resolution of the patient’s jaundice over the next days. Follow up CT of the abdomen confirmed resolution of the retroperitoneal and right pleural bilomas. After discharge, patient underwent Whipple procedure for resection of what was found to be a well differentiated cholangiocarcinoma of the CBD. He has been following with general surgery and hematology/oncology since then. Spontaneous biloma is a rare occurrence which needs to be promptly assessed and treated. Percutaneous biliary drainage with placement of an internal-external drain is an effective procedure which can be used, especially if endoscopic sphincterotomy is not feasible.

118 Pancreatic VIPoma: A Rare Clinical Entity Captured at the Dawn of Its Manifestation Mohsen Pourmorteza, MD1, Mehdi Pourmorteza, DO1, John Litchfield, DO2, Thomas Borthwick 3. 1. Department of Internal Medicine, East Tennessee State University, Johnson City, TN; 2. East Tennessee State University, Department of Internal Medicine, Division of Gastroenterology, Johnson City, TN; 3. East Tennessee State University, Johnson City, TN.

consistent with VIPoma and margins negative for neoplasm. Discussion: Fewer than 300 cases of VIP-secreting islet cell tumors have been reported in the medical literature. Perfuse secretory diarrhea is the hallmark of the disease process with 1 L to more than 3 L of stool output daily. Associated symptoms include hypokalemia-89%, achlorhydria-43%, and weight loss36%. The majorities of tumors are malignant and present with metastatic disease and local lymph node involvement (78%) ranging from 2-6 cm in size. Our patient’s presentation was inconsistent with the WDHA syndrome. To our knowledge this is the smallest (13mm) reported solitary tumor of its kind. Considering the natural slow progression of the tumor in terms of size and clinical constellation in a setting of acute worsening diarrhea with newly identified small size pancreatic lesion has raised our suspicion of an early clinical manifestation of VIPoma. The lack of evidence of electrolyte abnormality and metastasis with normal radiologic finding one year prior to the diagnosis has furthermore strengthened our notion of such early presentation.

119 Neuroma of the Bile Duct Mimicking Cholangiocarcinoma Natasha Shah, MD1, Imad Elkhatib, MD2, Thomas Savides, MD3. 1. University of Illinois at Chicago/ Advocate Christ Medical Center, Oak Lawn, IL; 2. Advocate Christ Medical Center, Oak Lawn, IL; 3. Division of Gastroenterology/University of California San Diego, La Jolla, CA. A 75 year old female presented with intermittent right upper quadrant and epigastric pain for several months. Her past medical history was notable for an open cholecystectomy for gallstones 50 years prior and endoscopic retrograde cholangiography (ERCP) with sphincterotomy 20 years earlier for choledocholithiasis. Blood tests were normal. Ultrasound found dilated intra and extra-hepatic bile ducts. Magnetic resonance cholangiopancreatogram revealed a 14mm common bile duct with a 5mm filling defect within the distal duct (Figure 1). An ERCP was unable to remove the filling defect. Brush cytology was benign.Endoscopic ultrasound revealed a hypoechoic well defined nodule in the distal common bile duct, consistent with a soft-tissue lesion(Figure 2). The bile duct was 14 mm upstream of the lesion. ERCP revealed a filling defect within the bile duct and a10-11-12 mm balloon sphincteroplasty was performed to allow passage of a diagnostic upper endoscope (outer diameter 9.8mm). Cholangioscopy revealed a 7mm nodule in the distal duct. When biopsy forceps were used for sampling, the lesion was firm and adherent to the bile duct wall.(Figure 3). The nodule biopsy

Introduction: VIPomas are rare pancreatic endocrine tumors that usually presents with symptoms of chronic refractory diarrhea, hypokalemia, and achlorhydria (WDHA).The diagnosis is confirmed by identifying hypersecretion of VIP in a setting of the localized pancreatic tumor.We demonstrate a rare glimpse at an unusual small size of VIPoma at its earliest clinical presentation. Case Report:A 71 Year old male with a past medical history of diabetes mellitus was referred to GI clinic for three month history of worsening diarrhea.Stool output ranged from 5-6 bowel movements daily.1 month following the onset of diarrhea he presented to the ED with upper quadrant abdominal pain as a new 0.4cm calcified lesion was identified on abdominal CT which was not evident on a previous CT one year ago.On examination he was dehydrated with elevated creatinine/BUN (2.1/28mg/dL) from baseline (1.4/21mg/dL) while denying fever, blood in stool, nausea/vomiting.Blood investigations demonstrated Potassium 4.7mmol/L, Sodium 142mmol/L and Chloride 102mmol/L.Blood count and liver enzymes were all within normal limits.MRI exhibited a well circumscribed 13mm solitary lesion within the ventral pancreatic body consistent with pancreatic neuroendocrine tumor.The serum VIP was in excess of 261pg/ml with a repeat of 245.7pg/ml. Total body Octreotide Scan failed to demonstrate any evidence of metastasis.Pathology results described a well differentiated pancreatic neuroendocrine neoplasm 1.4cm

[119A] Figure 1.

[118A] Figure 1.

[118A] Figure 1.


[119B] Figure 2.


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[119C] Figure 3. revealed atypical cells suspicious for adenocarcinoma: patient was referred for a Whipple procedure. Pathology revealed a benign neuroma of the distal common bile duct with no evidence of malignancy. Bile duct neuromas have been reported in fewer than 100 cases since 1928 (1). Biliary neuromas are not considered malignant, but a benign reactive proliferation of pericholangial nerve tissue in response to trauma (2). They have been described in patients who have had previous cholecystectomy hepatico- or choledochojejunostomies, or previous ERCP (3), as well as post-liver transplant(4). Neuromas may occur within a few months to decades after the injury (3).The presence of clinically silent biliary neuromas in post-cholecystectomy patients may be common, with one autopsy study demonstrating neuromas in 10% of post-cholecystectomy patients (2). On histology, specimens appear as disorganized proliferation of axons, Schwann cells and peri-neural cells encased in collagenous and fibrous stroma.The majority of neuromas of the bile duct are asymptomatic, and the leading diagnosis tends to be cholangiocarcinoma. Given that pre-operative diagnosis is often not known,and malignancy is a consideration, most surgeons advocate for extrahepatic bile duct resection with negative margins, periportal lymphadenectomy and Roux-en-y hepaticojejunostomy (5). This case demonstrates the first available cholangioscopic image of a bile duct neuroma. With such a pre-operative diagnosis, a simple excision and hepaticojejunostomy would suffice.The possibility of a bile duct neuroma should be on the differential for soft tissue lesions of the bile duct in patients who have had biliary surgery.

U/L. The patient was admitted and treated for acute on chronic pancreatitis. His hospital course became complicated when he developed melena and a decrease of hemoglobin from 7.8 to 3.9, for which he was transfused packed red blood cells. An upper esophagogastroduodenoscopy demonstrated retained blood within the duodenum, with no source of active bleeding. Interventional Radiology was consulted and angiography of the superior mesenteric artery was performed, which demonstrated an arteriovenous fistula (AVF) located in pancreatic bed (see figure 1). A subsequent embolization was attempted. There was no extravasation of contrast observed, indicating that the bleeding had spontaneously resolved and, therefore, embolization was canceled. The patient’s hemoglobin stabilized and he remained hemodynamically stable upon discharge. Upon follow up at an outpatient gastrointestinal clinic one month later, patient’s hemoglobin remained stable. Discussion: Hemosuccus pancreaticus is defined as bleeding expelled from the pancreatic duct into the duodenum at the site of the ampulla of Vater. It is a rare cause of upper gastrointestinal bleeding (1/1500). The biggest risk factor for hemosuccus pancreaticus is chronic pancreatitis, in which the inflammation results in the formation of aneurysms or pseudoaneurysms, which can rupture. Other risk factors include trauma, pancreatic tumor, and vascular malformation. HP is a diagnostic challenge because it presents as an obscure upper gastrointestinal bleed. Endoscopy is necessary to rule out other etiologies of bleeding, but does not always help determine an etiology. Ultimately, angiography is the gold standard for diagnosis. Surgery and angiographic embolization are the recommended treatment options. Left untreated, mortality can be as high as 90%. Transcatheter embolization of the bleeding artery is attempted first, with success rates of 80-100%. If bleeding cannot be stopped, then distal pancreatectomy is performed. Conclusion: Our case demonstrates that hemosuccus pancreaticus should be on the differential for the etiology of a upper gastrointestinal bleed in a patient with a history of pancreatic disease.

121 Ascending Cholangitis With Normal Bilirubin in Patients With Prior Biliary Instrumentation: A Case Series Keyur Parikh, MD1, Eileen Zhuang2, Emily Pontzer, PhD3, Meer A. Ali, MD4, Hazel Veloso, MD5, John Dumot, DO6, Amitabh Chak, MD3. 1. University Hospitals Case Medical Center, Cleveland, OH; 2. Case Western Reserve University School of Medicine, Pittsburgh, PA; 3. Case Western Reserve University, Cleveland, OH; 4. Case Western Reserve University, Cleveland Heights, OH; 5. University Hospitals Case Medical Center, Cleveland , OH; 6. Case Western Reserve University, Beachwood, OH. Introduction: Patients with prior instrumentation or biliary surgery may not present with classic laboratory changes associated with ascending cholangitis. Here we describe two cases of acute cholangitis in patients with normal bilirubin levels.

[121]

Table 1. Laboratory Values at Presenation Case 1

Case 2

Normal Values

WBC (109/l)

20.5

32.2

4.4–11.3

120

ALP (units/l)

175

115

45–117

Hemosuccus Pancreaticus: A Rare Upper Gastrointestinal Bleed

AST (units/l)

36

13

10–37

Steven Shamah, MD1, Angelica Nocerino, MD2, Valerie Gustave, MD3. 1. North Shore-LIJ Lenox Hill Hospital, New York , NY; 2. North Shore-LIJ Lenox Hill Hospital, Bronx, NY; 3. North Shore-LIJ Lenox Hill Hospital, New York, NY.

ALT (units/l)

45

10

7–54

TB (mg/dl)

0.9

0.7

100,000 RBCs, 535 WBC (33% PMN) suggestive of hemoperitoneum with no bacterial peritonitis. Repeat fluid analysis revealed amylase >99,000 suggestive of pancreatic ascites, which raised concern for possible pancreatic duct disruption. ERCP was subsequently performed, and pancreatogram revealed an ansa deformity of the ventral pancreatic duct with a very narrow ductal connection between the ventral and dorsal duct, consistent with incomplete pancreatic divisum. Only the proximal dorsal duct could be visualized revealing a filling defect, however, upstream duct could not be filled likely due to partial divisum and ductal obstruction. At that point, we elected for EUS guided access to better evaluate the dorsal pancreatic duct for leak. EUS revealed a fluid collection


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[161A] Figure 1.

[162A] Figure 1.

[162B] Figure 2.

[161B] Figure 2.

adjacent to the pancreatic head representing residual GDA pseudoaneursym with pancreatic duct dilation to 4mm starting at the neck. A 25 gauge needle was used to access the dorsal duct, and 20 cc of maroon colored fluid consistent with old blood was aspirated until clear fluid was noted. Pancreatogram of the dorsal duct revealed beaded appearance of the dorsal pancreatic duct with dilated side branches, likely due to partial pancreatic duct obstruction by clot from partial communication with GDA pseudoaneurysm. Stent placement to facilitate pancreatic drainage and prevent further obstruction from hemosuccus pancreaticus was not technically possible in setting of incomplete divisum. During the course of admission, patient was also diagnosed with a DVT, and an IVC filter was placed. Anticoagulation was deferred given concern for recurrent hemoperitoneum and pancreatic duct obstruction.This is the first reported case of a GDA aneurysm with pancreatic ductal communication resulting in hemosuccus pancreaticus, and this should be considered in the differential for gastrointestinal bleeding in these patients.

162 Failure of Biliary Stent Requiring Second ERCP With Stone Extraction in Acute Cholangitis

[162C] Figure 3.

Colin Wolslegel, DO, Charles Ruskowski, MD, Henrique Fernandez, MD. Parkview Medical Center, Pueblo, CO. Case Report: An 87 year old male was admitted with epigastric pain and taken emergently for coronary catheterization, resulting in placement of a drug eluding stent in his RCA, although this did not resolve his symptoms. He continued to decompensate leading to vasopressor support with norepinephrine, phenylephrine and vasopressin. His lactic acid was found to be 11.8 mmol/L and he had a rigid abdo-


men therefore he was taken for emergent exploratory laparotomy which was unrevealing. Blood cultures grew Klebsiella pneumonia and his total bilirubin was found to be 11mg/dL so a gastroenterology consult was placed. He was taken to the OR for an emergent endoscopic retrograde cholangiopancreatography.


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Abstracts Cholangiogram showed multiple common bile duct stones and a sphincterotomy was performed resulting in flow of pus, sludge and a small stone. We decided against a balloon sweep secondary to his decompensated state and current literature that recommends biliary decompression as the initial therapy and stone extraction being done at a later date when the patient is more stable. A 10Fr x 10 cm straight plastic biliary stent was placed with good bile flow. The following day he was weaned to norepinephrine alone and his bilirubin decreased to 7mg/dL. Over the following 2 days his bilirubin continued to decrease to 5.9mg/dL and then 4.4mg/dL; however his dependence on vasopressors continued and day 3 post ERCP vasopressin was restarted. We were asked to perform a 2nd ERCP, which revealed an appropriately positioned common bile duct stent with good bile flow. Following removal of the stent, balloon extraction of all the gallstones, the largest being 12mm, was performed. We then placed an 11.5Fr x 7cm plastic stent in the CBD and returned the patient to the ICU. Over the next 2 days he was weaned off of vasopressors and his sepsis resolved. Discussion: Current accepted practices and recommendations for the treatment of acute cholangitis include antibiotics and biliary decompression with either sphincterotomy and/or biliary stenting, if ERCP is able to be performed. It is accepted that the complications arise from the increased pressure in the biliary tree and by relieving these patients should improve. We have presented a case where biliary decompression alone was not successful and removing the nidus of infection was required to treat the acute cholangitis.

163 A Rare Case of Hypoplastic Pancreas Presenting as Normal Lipase Pancreatitis Joana Vicente Vargas, MD1, James Mellone, MD1, Leslie Soto, MD1, Lillian Gonzales, MD2, Shams Tabrez, MD3. 1. University of Central Florida , Orlando, FL; 2. University of Central Florida Internal Medicine Residency Program, Way Orlando, FL; 3. Saxon Medical Group, PA, Kissimmee, FL. Partial agenesis of the dorsal pancreas is a rare condition resulting in varying degrees of pancreatic body and tail hypoplasia. This embryologic underdevelopment is usually associated with reduced endocrine function and diabetes mellitus; in this case, however, we examine how this anomaly impacts pancreatic exocrine function, known to be concentrated in the affected area. We discuss the case of a 47 year old woman with history of diabetes who was seen in the ED complaining of two days of epigastric pain radiating to her left back, nausea, and vomiting. She denied history of NSAID use, alcohol ingestion, or gallstones. Initial vitals were normal, and examination was remarkable for left upper quadrant tenderness without rebound. The patient’s presentation was suspicious for acute pancreatitis (AP), yet amylase and lipase levels were normal at 40 U/L (25-150 U/L) and 251 U/L (73-393 U/L), respectively. Serum calcium was also normal, however triglycerides (TG) were elevated at 537 mg / dL. Clinical suspicion for AP remained, and while abdominopelvic computed tomography (CT) did confirm marked inflammatory changes in the peripancreatic mesentery consistent with the diagnosis, it was also noteworthy for congenital absence of the pancreatic tail. Gallbladder ultrasound demonstrated no evidence of cholelithiasis, and cholescintigraphy confirmed patency of the common bile duct and hepatopancreatic ampulla. The patient was managed in the usual fashion without issue, and lipase remained normal throughout her one-week admission. Repeat CT scan two months later revealed a pancreatic pseudocyst and resolution of the previously noted inflammation. This is a rare case of clinical and radiographic normal-lipase pancreatitis (NLP). The estimated negative predictive value of this enzyme in diagnosing AP is 94-100%; in fact, less than ten cases of NLP are described in the English literature, none of which occur in the setting of partial agenesis of the dorsal pancreas. We propose that reduction in exocrine pancreatic mass due to this defect decreases measurable serum lipase. In fact, this abnormality may even predispose the patient to hypertriglyceride-associated pancreatitis (HTGP); while HTGP is generally involves TG levels over 1000 mg / dL, we theorize that TG levels in this case were sufficient to induce AP because of decreased available enzymatic activity. Thus, we believe this case establishes a link between total exocrine mass and the somewhat uncertain mechanism of HTGP.

164 Intrapancreatic Accessory Spleen Presenting Diagnosed by Endoscopic Ultrasound-Guided Fine Needle Aspiration Nathan Jaqua, MD1, Scott E. Cunningham, MD2, Jeffrey Laczek, MD3. 1. Walter Reed National Military Medical Center, Colesville, MD; 2. Walter Reed National Military Medical Center, Southern Pines, NC; 3. Walter Reed National Military Medical Center, Bethesda, MD. Intrapancreatic accessory spleen (IPAS) is a rare congenital anomaly that may mimic pancreatic malignancy. We present a case of IPAS that was diagnosed by endoscopic ultrasound-guided fine needle aspiration. A 59 year old female presented to the emergency department with two days of mid-epigastric abdominal pain. Abdominal computed tomography (CT) with intravenous and oral contrast demonstrated a 2.8 x 2.4 cm enhancing mass in the body of the pancreas. Subsequent magnetic resonance imaging (MRI) showed a 2.9 x 1.9 x 1.7 cm mass in the distal body of the pancreas. The mass enhanced on arterial phase, portal venous phase, and delayed images. No pancreatic ductal dilation or pancreatic atrophy was noted. Chromogranin A was normal. She underwent an endoscopic ultrasound (EUS) of her pancreas which revealed a 3.5 x 2.0 cm hyperechoic mass in the body of the pancreas with a 1.7 x 1.1 cm hypoechoic focus. Fine needle aspiration (FNA) with cytology of the pancreatic mass demonstrated benign pancreatic acini with hematopoietic elements. Technetium-99 scinitgraphy was negative. A follow-up CT 9 months later demonstrated stability of the size and character of the mass. IPAS is a rare congenital anomaly with increasing frequency of diagnosis likely secondary to frequent use of CT for unrelated symptoms. Based on autopsy studies accessory spleens are found in 10 to 17% of people, with sites including the splenic hilum, pancreas and, less frequently, the jejunum. Based on two autopsy studies, 17% of accessory spleens were found in the pancreas, all of which were in the tail. An IPAS is usually 1-2 cm in diameter and appears similar to hypervascular pancreatic tumors (e.g. neuroendocrine tumors) on radiologic imaging. Non-invasive diagnosis is difficult, and technetium-99 scinitgraphy is helpful; however, scinitgraphy is limited by low resolution and the small size of most IPAS. EUS-guided FNA can confirm the diagnosis. IPAS presents a diagnostic challenge and differentiation from pancreatic neoplasms is imperative to avoid unnecessary surgical resection. Collaboration between radiology, gastroenterology, and pathology is necessary for the diagnosis of IPAS.

[164A] Figure 1.

165 Low CEA Cystic Pancreatic Tumors: A Tail of Two Cysts Patrick Hickey, DO1, Hiral Shah, MD2, Shashin Shah, MD3. 1. Lehigh Valley Health Network, Breinigsville, PA; 2. Lehigh Valley Health Network; EPGI, Center Valley, PA; 3. Lehigh Vally Health Network; EPGI, Allentown, PA.

[163A] Figure 1.


Background: Cystic pancreatic tumors (CPT) have variable malignant potential and are increasingly recognized. Generally, cross-sectional imaging cannot definitely differentiate mucinous from non-mucinous cysts. Endoscopic ultrasound (EUS) with fine needle aspiration (EUS-FNA) is used to evaluate morphologic appearance and fluid. Fluid analysis can help differentiate CPT. In this case series we will review two cases of low carcinoembryonic antigen (CEA) pancreatic tail CPTs with similar preoperative diagnostic evaluation, but differing final diagnoses. Cases: 1) A 71 year old asymptomatic male was found to have an incidental pancreatic tail cyst on imaging. EUS showed an anechoic, lobulated pancreatic tail cyst (4.2 x 2.8 cm) communicating with a small side branch without septation or nodules. FNA yielded viscous clear fluid with cytology negative for malignancy, amylase 5420 IU/L and CEA 99 ng/mL. Surveillance EUS-FNA fluid was inadequate for cytology, however DNA showed KRAS mutation. Robotic distal pancreatectomy showed a pancreatic tail side-branch IPMN (4.3 x 3.0 x 2.4 cm) with low grade intraepithelial dysplasia. 2) A 51 year old female presented with abdominal pain and hematuria. CT scan to rule out nephrolithiasis incidentally showed a cystic lesion of the distal pancreas confirmed with MRI. EUS revealed a pancreatic tail cyst (2.1 x 1.9 cm) with numerous 1mm septations and large pockets within the cyst. FNA


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yielded thin fluid with cytology negative for malignancy, amylase 44 IU/L and CEA 4.4 ng/mL. Robotic distal pancreatectomy showed a 1.5 x 1.4 x 1.2 cm well differentiated cystic pancreatic neuroendocrine tumor (cPanNET). Discussion: CPT may be malignant and require evaluation prior to resection. EUS appearance can be diagnostic, and cytology has low sensitivity for diagnosing malignancy. A CEA concentration cut-off of 192 ng/mL helps differentiate mucinous from nonmucinous (sensitivity 73%, specificity 84%). Fluid KRAS mutations are associated with mucinous cysts and the development of malignancy. Our IPMN patient had uncharacteristic low CEA, but expected DNA KRAS mutation and high amylase. cPanNETs have fluid findings similar to serous cystadenocarcinomas and presents a diagnostic challenge. Our patient’s surgery was necessitated by young age, septations, and the need for long-term follow-up. In this case series we reviewed the diagnostic course of pancreatic tail cysts with low CEA found to be an IPMN and a cPanNET.

166 Incomplete MEN in a Female Sridivya Parvataneni1, Zia Ur Rahman2, Dhara Chaudhari1, Puneet Goenka2, Mark Young2. 1. East Tennessee State University, Johnson City, TN; 2. East Tennessee State University, Johnson City , TN.

[167A] Figure 1.

Introduction: Symptomatic hypoglycemia without diabetes is unusual and prompts further evaluation including use of exogenous insulin or oral hypoglycemic agents and insulinoma. Insulinoma could present sporadically or as a part of syndrome; most commonly MEN (multiple endocrine neoplasia) 1or Wermer Syndrome. It is usually diagnosed at younger age but reported in elderly population on rare occasions. We present an old female presenting with hypoglycemia and found to have incomplete MEN 1 syndrome. Case: A 72 year old female was brought to hospital by EMS after being found unconscious at home. Her initial blood glucose was 22 when checked by EMS with transient improvement after giving dextrose 50%. In the emergency room, again she was noted to have blood glucose 33 and started on D5-normal saline infusion. Her past medical history included chronic kidney disease, hypertension, and stroke with residual right hemiplegia. Initial physical exam was significant for elevated BP: 220/118, slurred speech, altered mental sensorium, residual right arm and leg weakness. Laboratory values: Ca 11 mg/ dl (corrected calcium 11.32), creatinine 2.07 mg/dl (baseline), Albumin 3.6 g/dl, Vitamin D 70 ng/ ml, unremarkable CBC. Computed tomography (CT) of head was negative for intracranial abnormality. Patient met the criteria of Whipple’s traid and further workup for hypoglycemia revealed elevated serum Insulin 33.4 U/IU/ml, Pro insulin 65.2 pmol/l, C Peptide 27.1 ng/ml, parathyroid hormone 147 pg/ml. The sulfonylurea screen was negative. MRI abdomen, endoscopic ultrasound and octreotide scan failed to show any obvious pancreatic lesion. Parathyroid scan revealed parathyroid adenoma in left lower neck. Due to patient’s age and medical co-morbidities, decision was made for medical management with diazoxide and bisphosphonate with parathyroidectomy later on and genetic testing for family members. Discussion: Insulinoma, rare fascinating tumor is associated with MEN1 in less than 10% of cases. MEN 1 is autosomal dominant inheritance with 95% penetrance of gene by 50 years, but sporadic mutations occur and usually presents with hyperparathyroidism. Pancreatic islet cell tumors are the second most common presentation and can occur in 30-80% of MEN1 patients. Patients with MEN1 have decreased life expectancy and 70% of these patients die of causes directly related to MEN1 as reported by a multicenter trail. Our patient had incomplete expression of MEN 1 with only parathyroid adenoma and Insulinoma. It should be noted that these tumors could present in the elderly patients and one needs to look for these when dealing with elderly patients with hypoglycemia and other typical presentation of MEN1.

[167B] Figure 2.

167 Endoscopic Resection of Ampullary Carcinoid in a Patient With Advanced Cirrhosis: Case Report and Review Mohammad K. Choudhry, MD1, Kevin Tin, MD, MBA2, Kadirawelpillai Iswara, MD, FACG2, Ira E. Mayer, MD, FACG2, Rabin Rahmani, MD, FACG2. 1. Maimonides Medical Center/Coney Island Hospital, Brooklyn, NY; 2. Maimonides Medical Center, Brooklyn, NY. Carcinoid tumors are low-grade tumors that originate from endoderm and mostly arise in gastrointestinal tract. The large majority of these tumors involve appendix, ileum, rectum, stomach, and, very rarely at the ampulla of Vater. We present a case of a carcinoid tumor of the ampulla of Vater that was incidentally found on abdominal sonogram in a patient with advanced cirrhosis treated with endoscopic ampullectomy. A 52 year old female with past medical history of diabetes mellitus, hypertension, and Hepatitis C cirrhosis was being treated for genotype 3A HCV with Sovaldi and Ribavirin. The patient had been complaining of gastroesophageal reflux symptoms that did not respond to dietary changes and proton pump inhibitors. She underwent an EGD for further evaluation which revealed a 1.5 cm bulging ampulla. Biopsy was performed and revealed a well-differentiated neuroendocrine tumor. Laboratory studies and physical examination were consistent with Child-Pugh-B(score=9) cirrhosis. MRI of the abdomen revealed a cirrhotic liver, normal biliary tree without any filling defects, and a 1.1 x 0.8 cm nodular lesion at the level of the papilla projecting into the second portion of the duodenum. Endoscopic ultrasound identified a single hypoechoic sessile mass in the ampulla which measured 1.7 cm by 0.8 mm in maximal cross-sectional diameter. The lesion appeared confined to the mucosa, without extension into the deeper wall layer consistent with a T1a lesion. After discussion with the patient, a decision was made to remove the lesion endoscopically. ERCP and ampullectomy was performed using hot snare with pancreatic duct and common bile duct stents placement. The residual tissue was coagulated partially with a coagrasper. Argon plasma coagulation was then used to coagulate the residual tissue. Histopathology was consistent with a neuroendocrine tumor with no margin or lymphovascular invasion. Patient did not have any procedure related complications, and was asymptomatic at 3 months follow up. Ampullary carcinoid is a rare entity as only approxiamtely 100 cases have thus far been reported. Management must ensure complete removal with negative margins as ampullary carcinoids tend to have a


[167C] Figure 3.

high metastatic potential. Resection options typically involve a Whipple procedure though endoscopic managment can be considered for smaller lesions or non-operative candidates. In general, for lesions > 2 cm, Whipple procedure or pylorus-preserving pancreaticoduodenectomy are considered to be the


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Abstracts treatment of choice. For lesions that are < 2 cm, local excision has been deemed a good option, although operative morbidity and recurrence could be high. In patients with advanced cirrhosis and multiple medical comorbidities, endoscopic ampullectomy for carcinoid tumors can be performed as a safe and effective therapy.

168 A Rare Case of Isolated Pancreatic Tuberculosis Daniel J. Waintraub, MD1, Lionel S. D’Souza, MD1, Gil I. Ascunce, MD2. 1. Mount Sinai Beth Israel Medical Center, New York, NY; 2. Icahn School of Medicine at Mount Sinai, New York, NY. Tuberculosis (TB) is a systemic disease that can affect any organ. While abdominal TB is common in endemic countries, pancreatic tuberculosis is rare. Its clinical and radiologic features may mimic pancreatic malignancy, making it difficult to diagnose clinically. A 31 year-old previously healthy man presented with fevers, epigastric pain, poor appetite, night sweats and a 12 kilogram weight loss over 1 year. The patient denied a history of tuberculosis. Abdominal MRI revealed a 3cm x 4cm mass indenting the pancreatic head and uncinate process and compressing the mid-common bile duct. Lab work showed a white blood cell count of 12,200 cells/ul, amylase of 152 mg/dL, and lipase of 623 U/L. Malignancy workup including CA 19-9, CA 125, and alpha fetoprotein was negative. Quantiferon gold was positive. The chest x-ray was unremarkable. Endoscopic ultrasoundguided fine needle aspiration (EUS-FNA) of the pancreatic head mass was performed (Figure 1). Pathology revealed caseating granulomas and a positive acid-fast bacilli stain. The patient was treated with rifampin, isoniazid, pyridoxine and ethambutol for 14 months. Follow up MRI one year after starting treatment showed resolution of the pancreatic head mass. While TB is a health concern worldwide, isolated pancreatic TB is uncommon even in endemic areas. The prevalence of pancreatic TB is similar in males and females with a mean age of 40 years. A large case series evaluating abdominal TB reported no cases of pancreatic TB. Patients may present with obstructive jaundice and a pancreatic mass clinically indistinguishable from a pancreatic neoplasm. Consequently, most previously reported cases were diagnosed after exploratory laparotomy for pancreatic malignancy. Pancreatic TB most commonly affects the head or body of the pancreas. There are no radiologic features pathognomonic for pancreatic TB. Typically, pancreatic lesions from TB are heterogeneous and multicystic. The diagnosis of pancreatic TB requires histologic, cytologic and bacteriologic confirmation. EUS-FNA is the diagnostic modality of choice. Treatment with 6-12 months of anti-tuberculosis therapy is effective. Isolated pancreatic TB is a rare disease that must be considered in the differential diagnosis of a pancreatic mass, especially in endemic regions. A high index of suspicion and an accurate diagnostic approach with EUS- or CT-guided FNA are necessary.

[169A] Figure 1.

[169B] Figure 2.

[168A] Figure 1.

169 Hepatic Angiomyolipoma Jennifer Behzadi, MD1, Ilona Chepak, MD1, Carl Schmidt2, Peter Stanich, MD3. 1. The Ohio State University Wexner Medical Center, Columbus, OH; 2. The Ohio State University, Columbus, OH; 3. Section of Intestinal Neoplasia and Hereditary Polyposis, Division of Gastroenterology, Hepatology & Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH. Introduction: Comprehensive analysis is essential in determining the appropriate etiology of clinical manifestations. Pathological analysis and immunohistochemistry can differentiate hepatic angiomyolipoma (AML), a rare yet benign tumor, from other more common liver lesions. Case Description: A 62-year-old male with human immunodeficiency virus and Hepatitis B presented with epigastric pain, nausea, and a 30 pound weight loss over 6 months. Physical examination was significant for mild epigastric and right upper quadrant tenderness. Computed tomography (CT) of the abdomen and pelvis revealed a large, well defined heterogeneous mass of the right hepatic lobe measuring 9.6cm in maximal diameter, with vascular soft tissue intermixed with macroscopic fat. Radiologic differentials included a primary hepatic neoplasm such as hepatocellular carcinoma or hepatic AML. Magnetic resonance imaging (MRI) of the liver with triple phase contrast was performed and the lesion remained suspicious for hepatocellular carcinoma. AFP was 3.7 (normal ‹8.5 ng/mL). A percutane-


[169C] Figure 3.

ous CT-guided biopsy of the mass was performed. Histology showed large cells with eosinophilic and fibrillar cytoplasm, admixed with adipocytes, inflammatory cells and extramedullary hematopoiesis consistent with a hepatic AML. This was confirmed with positive staining for smooth muscle actin, Melan-A and HMB-45. Given the size of the AML and the symptoms, the patient underwent open excision of the mass with partial right hepatic lobectomy. Intraoperatively, the lesion was found to be encapsulated. The resected mass was 9.3 x 7.4 x 4.3cm in size and histology confirmed the initial biopsy findings. There were no postoperative complications and he remained symptom free at his follow-up appointment.


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Discussion: Hepatic AML is a benign mesenchymal tumor composed of variable proportions of smooth muscle cells, adipocytes, and blood vessels. It is most often a solitary tumor found incidentally, although a minority present with upper abdominal discomfort related to mass effect. MRI is considered to be the imaging study of choice but has been reported to misdiagnose between 48-90% of cases given variability in tumor composition. They can be mistaken for hepatocellular carcinoma, hemangioma or hepatic adenoma. Definitive diagnosis is dependent on tissue histopathology and immunostaining for muscle-specific markers such as smooth muscle actin as well as melanoma markers HMB-45 and melan-A.

170 Biliary Colic and Jaundice Presenting as Ampullary Neuroendocrine Tumor Jennifer Behzadi, MD1, Reshi Kanuru, MD2, Jeffery R. Groce, MD1. 1. The Ohio State University Wexner Medical Center, Columbus, OH; 2. The Ohio State University Wexner Medical Center, Dublin, OH. Introduction: Carcinoids are relatively rare neuroendocrine tumors of the gut. Ampullary neuroendocrine tumor (ANET), a subset of this group, is less recognized as its clinical manifestation can present similarly to more common diseases. We present an unusual case of ANET in a patient with biliary colic and jaundice. Case Report: A 39 year old male with a past medical history of renal cell carcinoma with right partial nephrectomy presented with jaundice and pruritus for 4 months. He also had crampy periumbillical pain worsened by eating for the past year that had become more constant over the past few months. He denied alcohol intake but had a 50 pack-years of smoking. CT abdomen/pelvis with contrast showed hepatomegaly with mild to moderate intrahepatic ductal dilation. His gallbladder was partially distended with multiple stones. The common bile duct (CBD) was dilated up to the ampulla which was notably protruding into the duodenum and was 2.2 cm in maximum caliber. There were no identified stones in the CBD. The pancreas was normal with mild prominence of the main pancreatic duct in the head and body. His AFP, CEA, and CA 19-9 were normal. Endoscopic ultrasound (EUS) showed a bulging ampulla with a well-defi ned round lesion in the deep mucosa/ submucosa of the ampulla obstructing the pancreatic and main bile ducts. An ERCP was completed with biliary sphincterotomy, sweeping of the bile ducts and biopsy of the ampullary mass. Pathology showed a grade 1 neuroendocrine tumor. Octreotide scan revealed no abnormal uptake to suggest somatostatin receptor positive tumor. His neurotensin level was 190 pg/mL (nl < 100 pg/mL) and pancreatic polypeptide was 960 pg/mL (nl < 500pg/mL). He underwent a pylorus saving pancreaticoduodenectomy. Pathology showed a well differentiated grade 1 neuroendocrine tumor with 2 of 17 lymph nodes positive and negative margins. Postoperatively his neurotensin level decreased to 178 and his pancreatic polypeptide normalized to < 40. Almost one year later he is doing well with no evidence of metastatic disease. Discussion: ANET accounts for less than 1% of all gastrointestinal cancers and less than 2% of all tumors at the ampulla. Clinically, its presentation can mimic other more common gastrointestinal disorders. Different imaging modalities such as EUS and ERCP may be needed to assist with the diagnosis. Immunohistochemisty has been suggested as a complimentary aid however hormone markers have not yet been widely identified in all ANETs.

[170B] Figure 2.

[170C] Figure 3.

171 Severe Chronic Diarrhea Secondary to Primary Lymph Node Gastrinoma

[170A] Figure 1.

Mouhanna Abu Ghanimeh, MD1, Khalil M. Abuamr2, Esmat Sadeddin, MD3, Osama Yousef, MD4. 1. University of Missouri, Kansas City, Mission, KS; 2. University of Missouri, Kansas City, Overland Park, KS; 3. University of Missouri/Truman Medical Center, Kansas City, MO; 4. University of Missouri/Truman Medical Center, Kasas City, MO. Introduction: Gastrinoma is the most common type of pancreatic neuroendocrine tumors (PETs). It exists in multiple forms including sporadic and as part of Multiple endocrine neoplasia (MEN-I) syndrome, and can be malignant and metastatic. The majority of sporadic gastrinomas (90%) occur in the gastrinoma triangle with the wall of the duodenum and the pancreas being the most common sites, however ectopic sites have been reported as well. The existence of primary lymph node (LN) Gastrinomas is controversial, even-though it is described by many case reports, and supported by prospective studies. The main challenge is to determine whether it represents a primary tumor or metastasis from an occult primary site. There are some criteria used to diagnose patients with primary LN Gastrinoma, however it remains a diagnosis of exclusion and a carful follow up is always warranted.



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Abstracts Case report:48 year-old female presented with chronic abdominal pain, and severe watery diarrhea causing significant renal insufficiency. She had an extensive blood, stool, radiological and endoscopic workup without explanation of her chronic symptoms. Suspicion of an endocrine cause of her secretory diarrhea warranted testing serum gastrin and Chromogranin, which were elevated and suspicious for Gastrinoma. The diagnosis was confirmed radiologically by Octroetide scan, and Endoscopic Ultrasound (EUS), which showed a lesion in the posterior aspect of the head of the pancreas. Secretin stimulation test confirmed the diagnosis. Screening for MEN-I syndrome was negative. She underwent a surgical intervention for tumor enucleation near the head of pancreas. Samples were sent for histological evaluation and they showed LN with neuroendocrine tumor. No additional lesions were found in the Gastrinoma triangle after carful surgical exploration. The patient improved clinically post-operative, her serum gastrin decreased to normal range and repeated Octroetide scan was negative. Conclusion: The existence of primary LN Gastrinomas is controversial. It remains a diagnosis of exclusion and a carful follow up is warranted, and it should be in the differential diagnosis of severe chronic diarrhea.

[171]

Table 1. Patient's serum gastric level Result (pg/ml)

Note

Result 1

3530

Patient was on proton pump inhibitor

Result 2

583

After one week off proton pump inhibitor

Result 3

2882

Secretin stimulation test baseline value

Result 4

6677

Secretin stimultion test maximum value, this provided biochemical confirmation for Gastrinoma

Result 5

70

Post-operative gastrin level

172 Colopancreatic Fistula: Uncommon Complication of Recurrent Acute Pancreatitis Mouhanna Abu Ghanimeh, MD1, Khalil M. Abuamr2, Esmat Sadeddin, MD3, Osama Yousef, MD4. 1. University of Missouri, Kansas City, Mission, KS; 2. University of Missouri, Kansas City, Overland Park, KS; 3. University of Missouri/Truman Medical Center, Kansas City, MO; 4. University of Missouri/Truman Medical Center, Kasas City, MO. Introduction: Acute pancreatitis is not uncommon, and it can affect nearby organs including the colon. Colonic complications are uncommon but are reported and serious. Colopancreatic fistula (CPF) is one of these colonic complications and can be associated with chronic pancreatitis as well. Usually it presents with either colonic symptoms or with similar presentation to acute pancreatitis. Since CPFs in general are less likely to close spontaneously, and it’s associated with a higher risk of complications; more definitive treatment is required which include surgery and endoscopic treatment. Case report: A 62 year-old male patient with history of heavy alcohol intake and recurrent episodes of acute pancreatitis presented with 6 month history of diarrhea and abdominal pain. His previous blood, stool, radiological and endoscopic workups were without explanation of his chronic symptoms. Repeated Abdominal imaging showed circumferential colonic wall thickening and cystic foci in the pancreatic tail. The pancreatic tail was inseparable from the colon with possible connection between colon and pancreas. Colonoscopy was done afterward and was significant for a localized edematous area with bluish discoloration that correlate with the area described in imaging. He had subsequently more workup including Endoscopic ultrasound (EUS) with Fine Needle Aspiration (FNA) which showed hypo echogenic cystic structure in pancreatic tail with Gram negative rods in FNA increasing the suspicion of colonic connection. Endoscopic retrograde chloangiopancreatogram (ERCP) was performed and didn’t show significant extravasation of contrast. The suspicion of CPF was still high, so subsequently the patient was referred to surgery and underwent exploration and the diagnosis of CPF was confirmed. Distal Pancreatectomy, splenectomy and partial left colectomy were done and he showed improvement afterward. Conclusion: CPFs in general are less likely to close spontaneously, and it’s associated with a higher risk of complications; so more definitive treatment with surgery is recommended. Endoscopic treatment has been described in many cases, however there’s no clear guidelines for the use of these techniques as standard treatment option until now.

[171A] Figure 2. [172A] Figure 1.




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[173B] Figure 2. [172C] Figure 3.

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174

Biloma: A Rare, Late Complication of Incomplete Laparoscopic Cholecystectomy

Lamivudine-Induced Acute Pacreatitis: A Unique Case

Lediya Cheru, MD. Albany Medical College/Albany Medical Center, Albany , NY.

Jalaluddin Umar, MBBS, Rushikesh Shah, MBBS, Divey Manocha, MBBS, Sekou Rawlins, MD. SUNY Upstate Medical University, Syracuse, NY.

Case: A 53 year-old woman with history of biliary dyskinesia status post laparoscopic cholecystectomy 3 years ago. A year following the procedure patient began to experience abdominal pain and nausea. She had multiple outpatient evaluation at an outside facility without definitive diagnosis. She eventually was evaluated at our facility and underwent ultrasound that was concerning for possible bile leak. MRCP and HIDA scan that confirmed the suspected bile leak within gallbladder bed. ERCP revealed possible retained gallbladder versus bile leak and stent was placed. After multiple failed attempts with biliary stents, she underwent pigtail drain. On day two, she developed fever and back pain. Physical exam was notable for right upper quadrant and epigastric pain without murphy sign and spinal tenderness over L2-L5 without neurological deficits. Significant laboratory findings showed WBC 10,800/uL, alkaline phosphates of 583 U/L, AST of 38 U/L, and ALT of 76 U/L. Blood and pigtail drain cultures grew MSSA. MRI showed L4-L5 epidural abscess. With regards to her biliary leak, she underwent another ERCP that was suspicious for retained gallbladder and had stent exchange. Due to active bacteremia, it was decided to continue pigtail drainage and monitor as outpatient. Once bacteremia resolved, patient was admitted for ex-laparotomy. Intraoperatively, 80% of the gallbladder was retained. She underwent cholecystectomy with resolution of symptoms. Discussion: Biloma is a rare finding of intrahepatic or extrahepatic bile collection. Biloma is most commonly due to iatrogenic complication from laparoscopic cholecystectomy, partial hepectomy, and bile duct catheter drain (1). Biloma is recognized intraoperatively. Laparoscopic procedure can be converted into exploratory laparotomy if bile leak is uncontrolled. In rare cases, biloma can present on postoperative day 5-15 and infrequently, past 1 year (1). Most patients typically present with right upper quadrant pain, nausea, and fever (1, 2). Initial evaluation in patients suspected of biliary leak should undergo abdominal ultrasound to identify the type of leak. CT is a sensitive method of evaluating extends of the leak in the abdominal or pelvic cavity. To confirm the biloma, hepatobiliary imino-diacetic scan (HIDA) can be applied (3). Once Biloma is diagnosed, ERCP can be used to further confirm diagnosis and stent placement proximal to the leak to reduce the pressure in the biliary system (4). If biloma is not controlled with stent, placement of percutaneous drainage is considered for decompression in patients who continue to have symptoms. Exploratory laparotomy should be performed for patient with unresolved biloma despite nonsurgical interventions.

Lamivudine is a potent nucleoside analog reverse transcriptase inhibitor (NRTI). It is used in treating HIV and Hepatitis B patients. Lamivudine has been reported to cause a wide array of side effects but literature offers only a handful of cases of Lamivudine induced acute pancreatitis. We present a first of its kind case of recurrence of acute pancreatitis in a patient who was (non-deliberately) re-challenged with Lamivudine haivng ruled out all other causes of pancreatitis. Case: A 45-year-old male with HIV was admitted with a two-day history of sharp epigastric pain arising after meals and associated with nausea and vomiting. Past medical and surgical history other than diagnosis of HIV was unremarkable. He denied smoking, alcohol intake or use of illicit drugs. On presentation, vitals included HR of 130, BP of 92/58, RR 27 and saturation of 92% on RA with temperature of 37.2 C. Laboratory studies showed leukocytosis of 17,000 with left shift, blood glucose of 566 with anion gap of 23, BUN of 19, creatinine of 1.5, lactic acid of 4 and elevated lipase at 1129. His blood alcohol level was negative, triglycerides were 289, abdominal sonogram and IgG4 were within normal limits. CT abdomen confirmed acute pancreatitis. He was discharged only a week ago after treatment of acute pancreatitis which was deemed to be drug induced secondary to HAART therapy drug Triumeq (Lamivudine, Dolutegravir and Abacavir). The medication was held on discharge with outpatient referral to HIV clinic. However, the patient continued to take his medication unknowingly. He was admitted to MICU and after negative work up for other etiologies his pancreatitis was again believed to be secondary to Lamivudine component of his HAART therapy (no evidence of either Dolutegravir or Abacavir causing acute pancreatitis independently). He was instructed strictly to destroy the medication Lamivudine at home and his prescription was held at pharmacy. Subsequently, patient’s HAART therapy was switched to atripla (Efavirenz/Emtricitabine/Tenofovir ) and he has been doing well till date. We present a unique case which reports re-occurrence of acute pancreatitis with re-challenge of Lamivudine after ruling out other causes of pancreatitis- an evidence strongest to date. Naranjo probability score is 9 indicating a definite adverse drug reaction. Although exact mechanism is not clear, NRTI-induced mitochondrial injury seems to be plausible hypothesis behind Lamivudine induced pancreatitis.

175 Balint’s Syndrome With Metastatic Pancreatic Cancer: A Case Report Abhik Bhattacharya, MD, Bhavana Bhagya Rao, MD, Kenneth E. Fasanella, MD. University of Pittsburgh Medical Center, Pittsburgh, PA.

[173A] Figure 1.


Introduction: Pancreatic cancer has been linked to hypercoagulability associated thromboembolic phenomena. Bálint’s syndrome, a triad of neurologic deficits including inability to perceive visual field as a whole (simultanagnosia), difficulty in fixating the eyes (oculomotor apraxia), and inability to move the hand to a specific object by using vision (optic ataxia) is a rare stroke type. We present a case of Bálint’s syndrome leading to the diagnosis of pancreatic cancer. Case Report: A 64 year old hypertensive male presented with 4 days of blurred vision and right hand heaviness. At presentation he was hemodynamically stable with physical examination notable for simultanagnosia, optic ataxia, ocular apraxia and right arm paresis. Initial laboratory tests including blood counts, complete metabolic and coagulation profiles were only notable for an elevated troponin of 7.21. Magnetic resonance (MR) imaging of the brain (Figure 1) showed multiple acute/ subacute infarcts in the right parietal, left occipital and left cerebellar lobes. Transthoracic echocardiogram showed anterior wall hypokinesis with decreased ejection fraction (40%), with no intra-cardiac thrombus or patent foramen ovale. Carotid ultrasound and MR angiography of the neck were unrevealing. Heparin drip was initiated for anticoagulation.Two days later he developed


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Abstracts dural pancreatitis, retroperitoneal hematoma and sepsis needing vasopressor support. In view of the advanced cancer with poor prognosis, the patient opted against further aggressive management and died 2 days later. Discussion: Cerebral ischemia as the initial manifestation of pancreatic cancer has been reported only once before. In the absence of conventional etiologies of stroke, underlying malignancy should be considered as a possible alternative.

176 Your Bile Ducts Are What You Eat: A Rare Etiology of Cholangitis Presidential Poster Soohwan Chun, MD, Adam C. Lessne, MD, Sammy Ho, MD. Montefiore Medical Center, Bronx, NY.

[175A] Figure 1.

Introduction: Acute bacterial cholangitis is a dreaded complication of obstructed bile ducts, most commonly by gall stones (1). We report a rare cause of cholangitis, with an obstructed bile duct by food chyme from a choledocho-gastric fistula. Case Report: A 61 year old woman with cholecystectomy for chronic cholecystitis one month ago presented with right upper quadrant abdominal pain, darkened urine, and acutely elevated cholestatic liver tests with direct bilirubin level of 5.4 mg/dL. MRCP showed new intrahepatic and extrahepatic bile duct dilation with multiple intraductal hypointense structures and pneumobilia. During admission, patient developed worsening abdominal pain with sepsis. An urgent ERCP was performed for biliary decompression for presumed ascending cholangitis. Endoscopy revealed a pre-pyloric choledocho-gastric fistula. Cholangiogram via the fistula showed dilated common bile duct (1.5cm) with multiple filling defects. A biliary sphincterotomy was performed with drainage of pus, followed by balloon-sweep extraction of food chyme and placement of a 10mm x 6cm biliary metal stent. Patient had significant clinical improvement with resolution of her sepsis, abdominal pain, and elevated liver tests. 2 weeks later, patient had repeat ERCP for stent removal and biliary clearance. The persistent choledocho-gastric fistula was closed with an over-the-scope clip system (Bear-Claw). Discussion: Bilio-enteral fistulae are rare complications of cholecystitis with reported intra-op incidence of 0.15%-4.8% (2). The most common types of fistulae are cholecysto-duodenal, cholecysto-colonic, and choledocho-duodenal fistula (3). Choledocho-gastric fistula is a rare type of bilio-enteral fistulae, described only anecdotally. Definitive diagnosis often requires ERCP (4). For treatment, laparoscopic fistula closure using an endo-stapling device had been described during concurrent cholecystectomy (5). However, most often, endoscopic approach is taken that involves placement of a biliary stent to lower intra-ductal pressure and reduce flow through the fistula (6). The fistula typically resolves spontaneously within a few weeks, however sometimes requires endoscopic closure. Newer endoscopic techniques, utilizing overstitch endoscopic suturing system or over-the-scope clip system (our case), have been reported successful in closing the persistent fistula (7).

177 [175B] Figure 2.

Two Cases of a Unique Variant of Duplicated Extrahepatic Bile Ducts With Coexistence of Distal Klatskin Tumor Surgically Treated by Whipple Procedure and Hepaticojejunostomy Tariq Hammad, MD1, Yaseen Alastal, MD1, Muhammad Ali Khan, MD2, Osama Alaradi, MD3, Ankesh Nigam, MD4, Thomas Sodman , MD1, Ali Nawras, MD, FACG1. 1. University of Toledo Medical Center, Toledo, OH; 2. University of Tennessee Health Science Center, Memphis, TN; 3. University of Toledo, Canton, MI; 4. Albany Medical College, Albany, NY.

gross hematuria. Computed tomography scan of the abdomen (Figure 2a and 2b) was obtained that revealed a 3.9X4.1 cm mass in the neck/body of the pancreas, hypodense lesions in the liver and 9th & 12th thoracic vertebral bodies, retroperitoneal lymphadenopathy and small splenic infarcts. Cytologic analysis of the pancreatic mass after endoscopic ultrasound guided fine needle aspiration showed adenocarcinoma. Subsequently patient developed features of obstructive jaundice. Endoscopic retrograde cholangiopancreatography guided biliary stenting was unsuccessful, hence percutaneous trans-hepatic catheter was placed. Further course was complicated by post-proce-

Duplication of the extrahepatic bile duct (DEHBD) is a rare anomalous of the biliary system. Here we report two unique cases of DEHBD coexistent with hilar cholangiocarcinoma (Klatskin tumor). The two cases were diagnosed preoperatively and treated with a modified surgical technique. Case 1: A 77-year-old female presented with obstructive jaundice. Abdominal computed tomography (CT) scan revealed diffuse bile duct dilatation (BDD). Magnetic resonance cholangiopancreatography (MRCP) showed diffuse BDD, stone in the extrahepatic duct with distal common bile duct (CBD) stric-

[176A] Figure 1.



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ture. Endoscopic retrograde cholangiopancreatography (ERCP) was attempted at other hospital and reported diffuse BDD. The procedure was aborted due to suspected contrast extravasation and the patient was transferred to our facility for further evaluation. Repeated ERCP revealed EHBDD with single biliary drainage to the duodenum (Fig.1A). Findings were consistent with type Va EHBDD (Fig.2). Brushing cytology was done. Rapid on-site evaluation (ROSE) by cytopathologist was suggestive of cholangiocarcinoma. Case 2: A 78-year-old female presented with obstructive jaundice for one month. Abdominal CT showed diffuse BDD. MRCP showed diffuse BDD to the level below CD take off. The patient had ERCP at other facility that showed distal CBD stricture. The stricture was dilated and stented with a 10 French x 5 cm PS. Brush cytology was negative. Patient’s jaundice persisted; so she was referred to our institution for further evaluation. Endoscopic ultrasound showed hypoechoic and well-demarcated mass of 21.3x17.2 mm at the neck of pancreas. Fine needle aspiration was done and ROSE by cytopathologist was suggetive of cholangiocarcinoma. Old stent was removed. ERCP was repeated and showed type Va EHBDD(Fig.1C). The biliary hilum was obstructed by the mass mimicking Klatskin tumor (Fig.1C). In both cases, biliary strictures were dilated and stented with 2 plastic stents placed up to the right and left main extrahepatic bile ducts (Fig.1B&D). Both patients were referred for pylorus-preserving Whipple surgery with hepaticojejunostomy. Intra-operative evaluation and surgical pathology confirmed

[177C] Figure 3.

the diagnosis of type Va EHBDD with cholangiocarcinoma involving a distally located biliary hilum (Klatskin tumor) (Fig.3A&B). Preoperative diagnosis of type V EHBDD coexistent with distal hilar cholangiocarcinoma (Klatskin tumor) is challenging and necessitates surgical approach modification. Instead of major hepatic resection or traditional Whipple procedure; Whipple procedure with hepaticojejunostomy was used to manage those potentially resectable Klatskin tumors in the setting of this anomaly.

178 Masquerading Malignancy: Intrahepatic Cholangiocarcinoma Presenting With Perianal Mass Ali Fakhreddine, MD1, Theresa Yang, MD2, Kathy Pan, MD2, Guanghong Liao, MD2, Bahman Chavoshan, MD, MAvMed3. 1. Harbor-UCLA Medical Center, Long Beach, CA; 2. Harbor-UCLA Medical Center, Torrance, CA; 3. David Geffen School of Medicine at UCLA, Torrance, CA.

[177A] Figure 1.


Introduction: Intrahepatic cholangiocarcinomas (ICC) are notorious for surreptitious presentation and poor outcome. We present an unusual case of intrahepatic cholangiocarcinoma in a young African American male presenting with perianal mass and bone marrow failure. The diagnosis of ICC was only made on autopsy examination. Case: A 40 year-old male presented to the emergency department (ED) with difficulty walking due to severe gluteal swelling and pain. The patient had an 18 month history of biopsy-proven hidradenitis suppurativa previously managed with antibiotics and multiple incision and drainage procedures. Examination under anesthesia disclosed a 9 cm left perianal mass and a 5 cm right peri-scrotal mass; both masses were excised and sent for histological evaluation. CT scan of the abdomen and pelvis was remarkable for left perianal induration and multiple new low-density lesions in the liver (Image 1). Biopsy of presumed hepatic metastases was unsuccessful and the patient was discharged with outpatient follow-up. Histologic evaluation of the excised perineal masses revealed adenocarcinoma with signet ring cell differentiation (Image 2). Immunohistochemical stains suggested a bladder or pancreas primary. The patient re-presented to the ED soon after discharge with complaint of difficulty urinating. Admission CT pelvis demonstrated new density invasion into the left corpus cavernosum. Additionally, bone marrow biopsy to evaluate new pancytopenia demonstrated near-total replacement with metastatic adenocarcinoma with signet ring cell morphology. A diagnosis of metastatic primary perianal adenocarcinoma with signet cell morphology arising in the setting of hidradenitis suppurativa was made. Initiation of palliative capecitabine was planned; however, the patient decompensated and expired one month from the time of his diagnosis.


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Abstracts many presentations of widely metastatic ICC are classified as adenocarcinoma of unknown primary, especially given that 90% of ICC are histologically adenocarcinoma. The importance of considering ICC in the differential of any case of metastatic adenocarcinoma of unknown origin with liver lesions is therefore crucial. This case not only highlights the epidemiologic concerns of ICC under-diagnosis but also emphasizes the importance of autopsy-proven diagnoses.

179 Liver Biopsy-Induced Hemobilia Complicated by Cholangitis and Cholecystitis Padma Chamarthy, MD1, Beatrice Wong, MD2, Schweta Arakali, MD1, Lauren Hogshire, MD1. 1. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ; 2. Rutgers Robert Wood Johnson Medical School, Staten Island, NY.

[178A] Figure 1.

Hemobilia is a rare consequence of liver biopsy occurring less than 1% of the time with 96% of complications found within 24 hours of the procedure. Prior to the introduction of percutaneous liver penetration for biopsy, cholangiography, and biliary drainage, hemobilia was most commonly caused by blunt abdominal trauma. A 72 year old woman with Hepatitis C and multiple abdominal surgeries initially presented with severe epigastric abdominal pain after elective ultrasound guided percutaneous liver biopsy for hepatitis C staging. CT abdomen/pelvis demonstrated a mild hemoperitoneum adjacent to the liver and in the right paracolic gutter. Three days after discharge, patient returned with nausea, vomiting and intense right upper quadrant (RUQ) pain radiating to the right shoulder. Significant labs included a total bilirubin 2.2 mg/dL, alkaline phosphatase 120 IU/L, aspartate aminotransferase 214 IU/L, alanine aminotransferase 109 IU/L, and a WBC count of 9.2 k/uL. RUQ ultrasound showed cholelithiasis and a 10mm dilated common bile duct (CBD). ERCP visualized blood in the CBD and a subsequent sphincterotomy was performed with placement of a CBD stent. Two days post procedure, patient developed fever, leukocytosis, a four-fold increase in total bilirubin with worsening jaundice, mental status changes, tachycardia, and hypoxia. Clinical presentation was consistent with ascending cholangitis. New gallbladder wall thickening was noted on RUQ ultrasound. Vancomycin and piperacillin-tazobactam were started as empiric antibiotic therapy. Blood cultures eventually speciated bacteroides fragilis. IR guided percutaneous cholecystostomy drain was placed urgently. Patient condition stabilized and she was discharged on cefpodoxime and metronidazole. Hemobilia is characterized by blood clots in the biliary tree and can lead to cholangitis, cholecystitis, or pancreatitis. Treatment of hemobilia is focused on restoring blood flow through the bile ducts and achieving hemostasis. Angiographic occlusion is recommended as initial treatment to control hemobilia and is found to be the most efficacious method for controlling intrahepatic bleeding. In our case, hemobilia was a late complication of liver biopsy, occurring 3 days after initial intervention. It was further complicated by both acute cholecystitis and ascending cholangitis. Treatment with percutaneous drainage and empiric antibiotics are reasonable therapeutic options in this situation.

180 Groove Pancreatitis Complicated by Pancreatic Hematoma

[178B] Figure 2.

[178C] Figure 3.

Autopsy revealed a 3440 gram liver with histology and staining (CK7, CK20, Hep-Par, CA19-9) consistent with intrahepatic cholangiocarcinoma with signet-ring cell features. (Image 3) Discussion: Diagnosis, reporting, and staging of intrahepatic cholangiocarcinoma (ICC) has been epidemiologically elusive until more recent efforts by investigators such as Welzel and Nathan, et al, provided more concrete topographic and histologic standards of classification. It remains unclear however how


Khushbir Bath1, Israr Sheikh2, Frances Briones Horenstein, MD1, Sanjiv Gray, MD3, Leaque Ahmed, MD1, Joan Culpepper-Morgan1, Joan Culpepper-Morgan, MD, FACG4. 1. Harlem Hospital Center, New York, NY; 2. Columbia University/Harlem Hospital Center, New York, NY; 3. Harlem Hospital Center, Palmetto, FL; 4. Harlem Hospital/ Columbia University, New York, NY. Groove pancreatitis is a rare benign disorder which is frequently confused with more ominous conditions due to its presentation, location and radiological findings. A multidisciplinary approach is recommended with emphasis on quality radiological assessment and involvement of the gastroenterologist and pancreatic surgeon. Prompt diagnosis of this disease leads to early initiation of effective treatment and may prevent the patient from being subjected to pancreaticoduodenectomy. A 47 y/o male with PMH of cigarette smoking and alcohol abuse, admitted with TIA developed epigastric pain with nausea and vomiting. On examination he was noted to have soft abdomen with epigastric and periumblical tenderness; Labs were significant for elevation of WBC, Lipase and Amylase. Abdominal CT showed a heterogeneous hyper dense, non-enhancing round lesion approximately 5 cm in diameter, which appeared to arise in the head or uncinate process of the pancreas. Patient underwent MRCP which showed Groove pancreatitis complicated by pancreatic hematoma. He was managed with IV fluids and analgesics and was discharged home in stable condition. An abdominal CT 1 month following discharge showed decrease in size of the hematoma to approximately 1.7 cm in size and at 6 months, MRI showed complete resolution. Patient was followed up in clinic for chronic pancreatitis with enzyme insufficiency, malnutrition and pain management. This case describes a distinct form of chronic segmental pancreatitis. In patients undergoing pancreaticoduodenectomy, the incidence varies from 2.7% - 24.5%, and is frequently associated with anatomical or functional obstruction of the minor papilla, absent or narrow Santorini duct. The clinical presentation is similar but more severe than chronic pancreatitis. Laboratory tests show moderate elevation of serum pancreatic enzymes and if common bile duct is involved serum hepatic enzymes. Imaging plays and important role in differentiating from other conditions with similar presentations. US, endoscopic US can help accurate location and demonstration of the extent of the disease & CT can help in differentiating the two forms. MRCP can help to differentiate in between groove pancreatitis and pancreatic neoplasm, a gradual tapering of common bile duct is observed in groove pancreatitis as compared to abrupt stenosis in malignancy. For patients with high index of suspicion for pancreatic head adenocarcinoma, endoscopy with FNA is recommended. Medical treatment with analgesics, smoking cessation, and alcohol abstinence may help in providing symptomatic relief, albeit they are only temporary with Surgery, Pancreaticoduodenectomy and pylorus-


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preserving pancreaticoduodenectomy, remains the treatment of choice for complete symptomatic relief and provides a definite diagnosis that rules out pancreatic neoplasm.

181 Periampullary Psammomatous Somatostatinoma in a Patient With Neurofibromatosis Type 1 Jacob Sadik, MD1, Caroline Soyka, DO2, Ashley Faulx, MD3, Meer A. Ali, MD4. 1. University Hospitals Case Medical Center, Lakewood, OH; 2. University Hospitals, Case Western Reserve University, Cleveland, OH; 3. University Hospitals Case Medical Center, Division of Gastroenterology, Cleveland, OH; 4. Case Western Reserve University, Cleveland Heights, OH. A 33 year-old male with a history of neurofibromatosis type 1 (NF1) was admitted with new periumbilical abdominal pain. Labs only revealed a mild cholestatic picture with elevated alkaline phosphatase and total bilirubin. CT abdomen showed biliary ductal dilatation to the ampulla with demonstration of a 3 x 2.5 cm ill-defined pancreatic head hypodensity. CA 19-9 was elevated at 2600. An endoscopic retrograde cholangiopancreatography (ERCP) was performed with biopsy of the ampullary mass. Ki-67 antigen was seen with low reactivity in the tumor cells, which stained positive for chromogranin, somatostatin and S-100 protein (nuclear). These findings were consistent with psammomatous somatostatinoma. PET/CT showed low metabolic activity near the pancreatic head and ampulla, but no metastatic disease, which was further supported by a 3-day octreotide scan. The patient underwent a classic pancreaticoduodenectomy (Whipple procedure), cholecystectomy, appendectomy as well as a portal and hepatic lymphadenectomy given his localized disease. Final pathology was consistent with somatostatinoma with 5/18 lymph nodes involved. NF1 patients have a 2.5-4 fold increased risk of developing malignancy compared to the general population and 10-25% have gastrointestinal (GI) tumor involvement, with only 5% presenting symptomatically. When symptoms are present, weight loss, abdominal pain, GI bleeding, obstructive jaundice and anemia are common. GI manifestations of NF1 usually arise during midlife or later. The true frequency of somatostatinoma is extremely rare, with an incidence of one in forty million. As of 2010, only 76 cases of periampullary and duodenal neoplasms in NF1 patients have been reported in the literature. According to a literature review by Kim et al. in 2011, following the first case reports of somatostatin-secreting tumors in 1977, less than 200 cases in total have been reported, a fraction of which are associated with NF1. As a consequence of non-familiarity with their frequency and wide clinicopathological spectrum, GI manifestations of NF1 are seldom thought of in routine clinical practice and might thus be significantly under-recognized. This case illustrates the benefit of early recognition of periampullary tumors in NF1 patients. Although rare, periampullary tumors have variable malignant potential. One can postulate that having a low threshold to evaluate the hepatobiliary and GI tract in a NF1 patient may have significant impact in clinical management.

[182B] Figure 2.

182 A Case of Pancreaticobiliary Adenocarcinoma Secondary to Malignant Transformation of Remnant Tissue From a Type I Choledochal Cyst Hao Chi Zhang, MD, Rohini Vanga, MD, Shilpa Jain, MD, Sahil Mittal, MD. Baylor College of Medicine, Houston, TX. Introduction: Surgical resection of the choledochal cyst reduces but does not eliminate the risk of malignant transformation, suggesting the important role of continued surveillance. Case presentation: A 38-year-old man with a history of cadaveric liver allograft and a peripancreatic cystic mass presented with right upper quadrant abdominal pain, nausea, and involuntary weight loss. Eight years prior, the patient suffered from acute cholangitis and hepatic failure. He was diagnosed with a type I choledochal cyst. He underwent liver transplantation with cyst resection. Hepatic fibrosis and cholangitis were identified. A surveillance abdominal CT later revealed a 12-mm

[182C] Figure 3.

hypodense cystic lesion at the head of the pancreas. Differential diagnoses considered were intraductal papillary mucinous neoplasm (IPMN) and pancreatic pseudocyst. Abdominal MRCP later demonstrated a larger cystic mass with a tubular connection to the main pancreatic duct, suspicious for branch duct IPMN. Fine needle aspiration (FNA) of the cyst was not diagnostic. The physical exam revealed a tender abdomen at the right upper quadrant, without a palpable mass or jaundice. Laboratory studies revealed an elevated serum alkaline phosphate level and otherwise normal liver function tests. Serum CEA and CA-19-9 levels were elevated. The abdominal CT demonstrated a heterogeneous hypodense solid mass at the pancreatic head with surrounding desmoplastic reaction, portal vein invasion, regional adenopathy, and multiple liver lesions. Deep FNA was performed on one liver lesion: Metastatic pancreaticobiliary adenocarcinoma was diagnosed. The patient was initiated on chemotherapy, but the disease continued to progress. Discussion: We report a case of adenocarcinoma of pancreaticobiliary origin, secondary to malignant transformation of presumed remnant tissue from a type I choledochal cyst, despite efforts in surveillance. The choledochal cyst, a congenital abnormality from embryological development, is usually a pediatric diagnosis. The Todani classification delineates different anatomical features of a choledochal cyst. Complications include acute cholangitis and hepatic injury with fi brosis. While the management is generally early surgical resection due to the risk of malignant transformation to cholangiocarcinoma, removal does not eliminate the risk entirely, as remnant tissue could transform. Therefore, close surveillance remains a priority after resection of a choledochal cyst.

183 A Rare Case of Intraductal Papillary Mucinous Neoplasm of Biliary Duct in a Patient With Prostate Adenocarcinoma Ravish Parekh, MD1, Gregory Krol, MD2, Cyrus Piraka, MD1, Atsushi Yoshida, MD3, Surinder K. Batra, MD1. 1. Henry Ford Hospital, Gastroenterology, Detroit, MI; 2. Henry Ford Hospital, Internal Medicine, Sterling Heights, MI; 3. Henry Ford Hospital, Transplant and Hepatobiliary Surgery, Detroit, MI.

[182A] Figure 1. The American Journal of GASTROENTEROLOGY

A 80-year-old male was evaluated for elevated prostate specific antigen (PSA) level and biopsy of prostate gland revealed Adenocarcinoma. Patient underwent cross sectional tomography (CT) imaging of abdo-


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Abstracts men which showed 2.3 x 2.7 cm soft tissue mass centered at porta hepatis with diffuse dilatation of left intrahepatic biliary ductal system and mild prominence of right intrahepatic ductal system. On physical examination, head, eyes, ears, nose and throat were normal. There was no jaundice. Abdomen was soft, non-tender, non-distended, no masses or free fluid and normal bowel sounds. Laboratory evaluation showed normal liver enzymes, lipase and amylase. Carbohydrate Antigen (CA 19-9) was 35.2 units/ml. The patient underwent endoscopic ultrasound (EUS) and endoscopic retrograde cholangiopancreaticography (ERCP). EUS showed 2 adjacent hilar masses involving common hepatic duct and left hepatic duct with protrusion of the tissue into the lumen of the duct and upstream ductal dilatation with parenchymal atrophy. ERCP revealed a large filling defect in the common hepatic duct extending into the left hepatic duct. A large amount of clot and soft tissue with a fish-egg appearance was retrieved. Two pigtail biliary stents were placed into the left hepatic duct upstream from soft tissue mass. The biopsy of the soft tissue revealed intraductal papillary neoplasm of the bile duct with diffuse high-grade dysplasia and intramucosal carcinoma. The patient underwent radical resection of common hepatic duct, left hepatic lobectomy with Roux-en Y hepaticojejunostomy to the right hepatic duct. Histopathological examination of the resected specimen revealed intraductal papillary neoplasm with diffuse high-grade dysplasia. The surgical margins and lymph nodes were negative for carcinoma. Post-operative course was complicated by intra-abdominal abscesses and pneumonia requiring intravenous antibiotics and CT guided drainage. Follow up CT scan, 2 months after the surgery was negative for any masses. Patient feels well and is asymptomatic 12 months since surgery. Intraductal Papillary Mucinous Neoplasms (IPMNs) are intraductal mucin-producing tumors arising from epithelial cells and have malignant potential. It usually arises from the pancreatic duct. It can lead to cyst formation or papillary proliferation and may have varying degrees of cellular atypia. The malignant potential rises with increasing size (> 3cm). Multiple genetic mutations have been described. IPMN of the biliary tract are rarely reported in literature. It is more often associated with higher levels of CA 19-9 and Carcinoembryonic antigen (CEA). Most IPMNs are benign and non invasive, however due to increasing size and malignant potential, surgical resection is the treatment of choice. Our patient’s IPMN was 2.7 cm with high-grade dysplasia that was treated with surgical resection.

surgical procedures are available. Our case is unusual because of the profound degree of anemia on presentation attributable to a combination of acute bleeding and chronic liver disease. In conclusion, hemosuccus pancreaticus is a rare cause of upper gastrointestinal bleeding which should be considered in patients with melena or hematemesis and a negative upper endoscopy.

186 Self-Induced Pressure Necrosis as a Mechanism to Free an Embedded Metal Stent From the Bile Duct Jaycen Brown, BS1, Keng-Yu Chuang, MD2, Fakhri Kalolwala , MD3, Adbul Nadir, MD4. 1. University of Arizona College of Medicine, Mesa, AZ; 2. Maricopa Medical Center, Phoenix, AZ; 3. Maricopa Medical Center, Chandler, AZ; 4. Maricopa Medical Center, Gilbert, AZ. A 68-year-old Hispanic male received a covered metal stent (Wallflex RX, Boston Scientific) through ERCP for benign biliary stricture. Sixteen weeks later, another ERCP was performed to remove the stent but it was noted that the entire stent has migrated proximally into the bile duct. As significant amount of epithelialization has occured to the uncovered portions of the stent, only a small uncovered portion of the embedded stent could be brought out of the bile duct using a 12-15 mm

184 Prolonged Survival in a Case of Metastatic Cholangiocarcinoma Raj Shah1, Hirak Shah2, Neal Akhave2, Aditya Gutta, MD1, Reem Mustafa1, Fadi Bdair3. 1. University of Missouri, Kansas City, MO; 2. Washington University in Saint Louis, St. Louis, MO; 3. Mosaic Life Care, St Joseph, MO. Introduction: Each year about 2000 to 3000 people develop cholangiocarcinoma. Multiple studies have shown the median survival to be less than 6 months in unresectable cholangiocarcinoma. Here we present a case of an unusually prolonged survival in a case of metastatic cholangiocarcinoma. Case Description: A male over the age of 70 with a past medical history of insulin dependent diabetes mellitus presented with complaints of generalized itching, jaundice, and 15 pound weight loss over 3 months. An ERCP showed diffuse stricture of the common bile duct. Brushings were obtained for cytology and a biliary stent was placed. Cytology was negative for malignancy. He was lost to follow up but presented again eight months later and underwent repeat ERCP. Brushings were repeated and came back positive for malignancy. A diagnostic laparoscopy with the intent of performing palliative resection and hepaticojejunostomy was terminated due to a suspicious peritoneal nodule. Biopsy of the nodule revealed adenocarcinoma with CK 7 (+) and CK 20 (-) consistent with metastatic aberrant cholangiocarcinoma. The patient refused palliative chemotherapy and he remains stable clinically and is still alive at 24 months after his symptoms started and 16 months since primary diagnosis. Discussion: This patient’s good functional status prior to diagnosis is an integral part of his lengthy survival. Further investigation in survival for aberrant versus classic metastatic cholangiocarcinoma is warranted. Better understanding of different prognostic factors that lead to prolonged survival and overall further research needs to be undertaken for this deadly disease.

[186A] Figure 1.

185 Hemosuccus Pancreaticus Causing Profound Anemia in a Jehovah’s Witness With Cirrhosis Vadim Bul, MD1, Brian Boulay, MD2. 1. University of Illinois College of Medicine at Chicago, Department of Internal Medicine, Chicago, IL; 2. University of Illinois College of Medicine at Chicago, Department of Gastroenterology and Hepatology, Chicago, IL. Case Description: A 52 year old Jehovah’s Witness female with a past medical history of alcohol abuse, anemia and a solitary episode of acute pancreatitis presented to an outside hospital complaining of multiple episodes of hematemesis and intermittent abdominal pain for several days. On presentation, Hemoglobin was 3.1 g/dl and INR was 1.5 but the patient was normotensive. She eventually consented to resuscitation with blood products with appropriate response. An initial esophagogastroduodenoscopy showed no active bleeding. Computed tomography of the abdomen showed enlargement of the pancreas with infiltration of the peripancreatic fat and a fluid collection concerning for a pseudocyst or pseudoaneurysm. The patient had continued melena requiring additional blood transfusions while hospitalized. A tagged technetium 99-m red blood cell scan showed bleeding from the location of the ampulla within the duodenum and an abdominal ultrasound with Doppler showed flow within the pancreatic fluid collection, consistent with vascular etiology. The patient underwent celiac mesenteric angiography with embolization of a 6.4 cm x 2.8 cm pseudoaneurysm of the pancreatic magna artery. The patient had no further episodes of abdominal pain and her hemoglobin stabilized following angiography. Discussion: Hemosuccus Pancreaticus is defined as bleeding from the pancreatic duct via the ampulla of Vater. It is a very rare cause of upper gastrointestinal bleeding with fewer than 100 cases previously reported. The condition usually occurs in patients with acute on chronic or chronic pancreatitis and the classic triad for the disease is episodic abdominal pain followed by melena and hyperamylasemia. Due to the intermittent nature of bleeding, patients’ hemoglobin levels will rarely fall to critical levels. Hemodynamically stable patients should undergo angiographic embolization of the culprit vessel. For patients who are hemodynamically unstable or who have bleeding refractory to angiographic intervention several


[186B] Figure 2.


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188 Novel Endovascular Technique in the Management of Splenic Artery Pseudoaneurysm Jagrati Mathur, MD, Jeffrey Saavedra, MD, Rabindra Kundu, MD. University of California San Francisco, Fresno, CA.

[186C] Figure 3.

A 42 yr female with history of chronic alcoholic abuse and early cirrhosis presented to the clinic with severe acute upper abdominal pain, bloating, significant weight loss 20 lb, non-bloody diarrhea, early satiety and loss of appetite. She stopped drinking alcohol 6 months prior to presentation and joined AAA. Medications- diuretics & protonix. Vitals stable. Exam revealed a cachetic woman, normal abdominal, cardiac and respiratory exam, pitting pedal edema 2+. EGD showed gastritis & LA grade B esophagitis. US abdomen showed hepatic steatosis, hepatomegaly, small hepatic cyst 6x5x6mm, patent portal vein and small ascites. CT abdomen showed prominent cystic changes replacing the entire pancreas, sparing the head and uncinate and a markedly dilated pancreatic duct. MRI abdomen showed extensive serpiginous cystic pancreatic parenchyma in body and tail, ascites and hepatic steatosis. Endoscopic US showed a heterogenous pancreas in the body and tail, a cystic lesion 2.3 x 2.4 cm in the pancreatic body and arterial flow in anechoic structure 3 x 3 cm likely a splenic artery pseudoaneurysm. She was referred to IR for a SMA angiogram and a 5 x 5 cm viabahn stent was placed across the splenic pseudoaneurysm. After stenting, retrograde filling to the aneurysm was noted suggesting a leak and transcatheter embolization with coiling of the splenic artery was achieved. Immediate post procedure complication included a small splenic infarct, which was managed conservatively. EUS a month later, showed no blood flow in the area of the pseudoaneurysm, suggesting resolution. The anechoic 30 x 35 mm cystic lesion seen prior in the pancreatic body was aspirated. The fluid analysis showed a CEA of 347 ng/ml & Amylase of 19,269 U/L consistent with either a MCN or IPMN. Patient was started on TPN for malnutrition and referred to hepatobiliary surgery for further management of the pancreatic cyst. Splenic artery aneurysms (SAA) are rare, with an incidence of about 0.1% in the general population, 10% in age 60 years and older and up to 50% in those with portal hypertension. Risk factors of SAA include portal HTN, systemic HTN, cirrhosis, post liver transplantation, post pancreatitis, atherosclerosis, arte-

extraction balloon, rat tooth forceps, and a 10 mm wire-guided CRE balloon. While attempting to pull the rest of the stent out using a snare, the exposed portion of the stent was seen rolling onto itself. The stent remained stuck in the bile duct and the endoscopist decided to abort the procedure (image1). An ERCP was performed four weeks later and showed that the stent has freed itself from the bile duct wall and was easily removed using a snare this time (images 2 and 3). It has been reported that when a covered metal stent becomes embedded to the bile duct, it can be removed by placing another metal stent inside of it to induce pressure necrosis of the bile duct tissue epitheliazing the stent. Our case report supports this observation but it is unique as our embedded stent freed it self from the bile duct not due to the placement of another stent but from the eversion of the exposed portion of stent which occured incidentally during our first attempt to remove it. In lieu of an actual second stent placement, this everted portion of the stent acted as a second stent to cause pressure necrosis in the bile duct.

187 The Paan Pancreatitis Problem Niket Sonpal, MD1, Samit Datta, MD2, Sonja Olsen, MD3. 1. Lenox Hill Hospital, Happauge, NY; 2. North Shore-LIJ Lenox Hill Hospital, New York, NY; 3. Lenox Hill Hospital, New York, NY. Paan is a commonly abused substance in Southeast Asian countries and India, which is mainly composed of the betel leaf and areca nut. Nicotine, caffeine, and alcohol are three common addictive substances that are more commonly used that paan, however like cigarettes the total number of additives is unknown. One mouse-model study showed the betel causing increased pancreatic lipase stimulation, and decreased trypsin and chymotrypsin secretion. In this case study, we present a case where Paan is believed to have caused pancreatitis in an 18 year-old female. An 18-year-old Bangladeshi female was recently discharged from an outside hospital with a diagnosis of pancreatitis for similar symptoms. Following discharge, patient noted the pain never fully resolved and began to worsen 3 days prior to presentation. Patient reported no alcohol or cigarette usage, no trauma, and no recent travel. She denies any medication use, and was not any antibiotics prior. She did however endorse paan usage for approximately 4-5 years, and has noted issues with anorexia with a 12 pound weight loss and nausea for approximately 1 year. Physical exam was notable was significant tenderness in the epigastrum. Notable labwork showed Lipase of 20251 U/L, and a normal triglyceride level. An ultrasound showed no evidence of gallstones, and a CT of the abdomen and pelvis which showed mild stranding and fluid surrounding the pancreas, and MRCP which showed acute pancreatitis, with no evidence of cholelithiasis, choledocholithiasis, or evidence of pancreas divisum. Patient was also found to be negative for HIV, VZV, CMV, and mumps. Pancreatitis is a very severe disease that has been well described in the literature with clear evidence for risk factors. Our patient was negative for alcohol use, gallstones, hypertriglyceridemia, trauma, and medication use. While there has been one study linking the use of smokeless tobacco to pancreatic cancer in the Swedish population, there is very little research for the effects of paan use on the human body. This case report demonstrates a need for prospective studies to detail and evaluate the exposure to paan in the budding immigrant Indian and Southeast Asian population and the deleterious health effects, namely pancreatic stimulation and pancreatitis.

[188A] Figure 1.

[188B] Figure 2.



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[188C] Figure 3.

rial fibrodysplasia, chronic inflammatory process and pregnancy. Due to the high risk of rupture and high mortality rate, early intervention is critical. Traditional treatment of choice is splenectomy with or without partial pancreatectomy and carries a high risk of mortality 5-40% and morbidity 10-25%. Endovascular techniques are rapidly gaining interest as they are less invasive, have less morbidity and require shorter hospital stays than surgical approach. The success rate of percutaneous coil embolization has been reported as high as 90%. In this case, transcatheter stent placement and coil embolization was effective in treating the SAA and preventing surgery.

[189B] Figure 2.

189 A Vary Rare Congenital Anomaly of the Adult Biliary System- Type Vb Double Common Bile Duct Sandar Linn, Hernan Lopez-Morra, MD, Amandeep Kaur, Mahmoud Dakhel, MD, Moshe Fuksbrumer, MD, Mahesh Krishnaiah , Sury Anand, MD. The Brooklyn Hospital Center, Brooklyn, NY. Introduction: Duplication of the common bile duct (DCBD) is a rare anomaly especially in the western world; more cases have been reported in Asia. Based on the modified classification proposed by Choi et al. there are five subtypes of this anomaly. Type V is the least common with only five cases reported and one reported as type Vb). Case Report: We present a 57-year-old Hispanic male seen for evaluation of choledocholithiasis. He had a history of cholecystectomy for cholelithiasis and cholecystitis. His only complaint was an occasional feeling of being distended and gassy. No family history of biliary problems was reported.

Physical examination was not remarkable. Routine biochemistry revealed no abnormalities of hepatic or renal function with normal bilirubin, alkaline phosphate and c-reactive protein. Magnetic resonance cholangiopancreatography (MRCP) revealed duplicated extrahepatic bile ducts running parallel with proximal communication and a common channel distally as it enters the duodenum. The finding is consistent with type Vb double common bile duct according to the Choi classification. The extrahepatic biliary ducts measured 7.5 and 4.5mm. Two filling defects were seen in the 7.5 mm extrahepatic biliary duct suspicious for choledocholithiasis. On Endoscopic retrograde cholangiopancreatography (ERCP), the finding of MRCP was confirmed, and two stones were extracted from the dominant common bile duct. No complications occurred after the procedure and patient was doing well three months later. Conclusion: This is the second case of type Vb DCBD in a Hispanic male complicated by choledocholithiasis. The awareness of this anomaly is essential due to its association with congenital conditions like choledochal cysts, biliary atresia or complications like choledocholithiasis and malignancy. Moreover, it is important to identify this anomaly to prevent intraoperative injury to the other extrahepatic ducts.

190 A Curious Case of Coil Cholangitis Alexander Perelman, DO, MS1, Neil Gupta, MD1, Jason Puckett, MD2, David J. Hass, MD2, Ramon Generoso, MD3. 1. Yale University School of Medicine, New Haven, CT; 2. Yale University School of Medicine, Hamden, CT; 3. Gastroenterology Center of Connecticut, Hamden, CT.

[189A] Figure 1.


Case Summary: A 59-year-old female with a surgical history of a laparoscopic cholecystectomy, complicated by a biliary leak repaired using an Azur endovascular coil, three years prior to presentation was admitted with eight days of abdominal pain, jaundice, and fevers. Review of systems was significant for anorexia, fatigue, shortness of breath and nausea. On exam she was hypotensive to 80/50 and febrile to 100.4 with jaundice, scleral icterus, and tenderness in the right upper quadrant and epigastrium. Labs were significant for a white blood cell count 44.6 x1000/uL, hemoglobin of 10.9 g/dL, and sodium to 118. Her liver enzymes were significant for total bilirubin of 20.88 mg/dL, an alkaline phosphatase of 659 U/L, Alanine Aminotransferase and Aspartate Aminotransferase of 93U/L and 117 U/L respectively. An ultrasound of the liver demonstrated a common bile duct (CBD) dilatation to 1.5 cm thought to be from a 1.3 cm hyperechoic density. A percutaneous biliary drainage catheter (PTC) was placed for decompression of the biliary tree; broad-spectrum antibiotics, aggressive crystalloid resuscitation and eventually pharmacologic blood pressor support was started. Her blood cultures grew E. coli and Bacteroides fragilis. After initial improvement, her status declined and it was discovered that her PTC had become dislodged, requiring a repeat cholangiogram. During the study it was discovered the 1.3 cm hyperechoic density seen on ultrasound was the Azur coil, which had migrated to the distal CBD. With the PTC drain repositioned the patient completed a course of antibiotics and symptoms resolved. Discussion: Acute cholangitis is thought to develop secondary to biliary stasis and infection in the biliary tract. We describe a unique case of acute cholangitis secondary to obstruction of the CBD by a migrating Azur coil which was placed previously to treat a biliary leak. Bile leaks are a known complication of cholecystectomy, usually treated by decompression of the biliary system. There are few case reports describing embolization of biliary leaks by endovascular coils (Oliva, Hunt.) To our knowledge, there has never been another case report of a patient developing acute cholangitis with septic shock secondary to coil migration requiring an ICU admission and pressor support. As the use of endovascular


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[191B] Figure 2.

192 Signet Ring Cell Adenocarcinoma of Ampulla of Vater: A Rare Case With Concurrent Non-gastrointestinal Malignancies Sandar Linn1, Nami Safai Haeri1, Hernan Lopez-Morra, MD1, Juan Tejada, MD1, Sofia Nigar, MD2, Shah Giashuddin, MD1, Jonathan Chow1, Mahesh Krishnaiah 1, Sury Anand, MD1. 1. The Brooklyn Hospital Center, Brooklyn, NY; 2. The Brooklyn Hospital Center, Yonkers , NY.

[190B] Figure 2.

Background: Signet-ring cell adenocarcinoma (SRCC), a histological variant of ampullary carcinoma, is an extremely uncommon malignancy. There is an established correlation between ampullary carci-

coils becomes more widespread, it is important to recognize cholangitis as a significant complication and explore other ways to prevent migration.

191 Year of the Dragon: A Remarkable CT Scan From a Chronically Obstructed Bile Duct Sandar Linn, Nami Safai Haeri, Hernan Lopez-Morra, MD, Mahmoud Dakhel, MD, Sury Anand, MD. The Brooklyn Hospital Center, Brooklyn, NY. We present a remarkable case of chronic common bile duct (CBD) obstruction resulting in massive dilatation with a dragon like appearance (picture 1). This was a 78 year-old female with a history of cholecystectomy and sphincterotomy over 20 years ago. She had been asymptomatic until recently and presented with jaundice. CT scan findings are shown in pictures 1 and 3. ERCP was performed confirming the CT findings of a large CBD stone with this remarkable upstream dilatation. Due to comorbidities, the stone was bypassed with a stent with resolution of jaundice (picture 2 and 4). Abbreviation, CBD: Common Bile Duct, S: CBD stone, IHD: Intrahepatic ducts.

[192A] Figure 1.



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noma and an attenuated form of Familial Adenomatous Polyposis syndrome. However, SRCC has not been reported with other gastrointestinal or non-gastrointestinal malignancies. To our knowledge, this report is the first case of SRCC with concurrent non-gastrointestinal malignancies. Case Report: A 66 year old male with history of prostate cancer and anglioblastoma multiforme presented with obstructive jaundice and abdominal pain for one week duration. Endoscopic retrograde cholangiopancreatography (ERCP) and Endoscopic Ultrasound (EUS) suggested a duodenal tumor at the Ampulla of Vater invading the duodenal wall and pancreatic parenchyma without local lymphadenopathy. Immunohistological examination confirmed poorly-differentiated SRCC of the Ampulla of Vater. The tumor was staged as T3N0M0 (stage 2A). Because of his poor prognosis of coexisting malignancy, surgical intervention was not considered. Conclusion: We highlight a rare case of SRCC of the Ampulla of Vater with local invasion of the duodenal wall and pancreatic parenchyma without lymph node infiltration or distant metastasis in a patient with concurrent non-gastrointestinal malignancies.

193 Acute Cholangitis Complicating Bear Claw Placement for Closure of Duodenocutaneous Fistula from a Billroth II Afferent Limb Yaseen Alastal, MD1, Tariq Hammad, MD1, Mohammad Nawras2, Basmah Khalil, MD2, Osama Alaradi, MD3, Ali Nawras, MD, FACG1. 1. University of Toledo Medical Center, Toledo, OH; 2. University of Toledo, Toledo, OH; 3. University of Toledo, Canton, MI. Introduction: Bear Claw endoclip is a novel endoscopic modality used for closure of gastrointestinal defect with high efficacy and safety. Few complications have been reported. Herein we present a patient who developed acute cholangitis one day after placement of bear claw clip for closure of duodenocutaneous fistula from the afferent enteric limb of Billroth II. This complication is unreported in the literature. Case presentation: 28-year-old female patient with history of eosinophilic gastroenteritis and multiple abdominal surgeries including Billroth II gastrectomy referred to our hospital for treatment of duodenocutaneous fistula. She had large chronic duodenocutaneous fistula extending from Billroth II afferent limb. She was scheduled for cutaneous and enteric closure of the fistula with Fibrin glue and Bear Claw endoclip placement, respectively. During the procedure, pediatric colonoscope was introduced to the afferent limb of Billroth II. India ink was injected through the cutaneous orifice to localize the internal orifice of the fistula (Fig 1A). A guide wire was introduced through the cutaneous orifice and grasped by forceps and pulled out through the scope for scope reinsertion purpose. An 11/6 t Bear Claw endoclip was secured on the tip of the gastroscope, and the gastroscope was reintroduced into the afferent duodenal limb. The enteric orifice of the fistula was suctioned inside the cap of the Bear Claw with the wire still inside the fistula and scope channel. The guide wire was then removed and the

[193C] Figure 3.

clip was deployed successfully (Fig 1B). The patient tolerated the procedure well without immediate complications. On the next day, the patient developed fever, jaundice, changes in mental status and abdominal pain. Abdominal ultrasound revealed dilation of the common bile duct (1.2 cm). Abdominal CT scan showed mild edema surrounding the endoclip in the afferent loop of the Billroth II (Fig 2). Patient was diagnosed with acute cholangitis secondary to biliary obstruction due to Bear Claw placement close to the major papilla and was managed with empirical antibiotics and supportive care. PTC showed diffuse dilation of the biliary tree down to the papilla then a guide wire was advanced into the duodenum through the major papilla adjacent to the Bear Claw clip which was causing partial obstruction (Fig 3). An 8 French pigtail catheter was placed down to the duodenum. As a result, the patient had clinical and laboratory improvement. Conclusion: Acute cholangitis due to papillary obstruction is a potential complication of bare claw placement at the dome of the afferent limb in patient with Billroth II surgery due to its close proximity to the major papilla.

[193A] Figure 1.



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194 A Slipped Clip: Surgical Clip-induced Choledocholithiasis Following Cholecystectomy David C. Olson, MD, Andrew M. Dries, MD. Carolinas Medical Center, Charlotte, NC. Laparoscopic cholecystectomy has become the gold standard for management of symptomatic cholelithiasis since it was first reported in 1988.1 While immediate post-surgical complications of the biliary tract are most common, long term complications due to clip migration been reported.2 We report a case of a biliary obstruction as a complication of cholecystectomy four years prior. A 54-year-old female with a history of laparoscopic cholecystectomy for symptomatic cholelithiasis four years prior presented to our emergency department with right upper quadrant pain associated with nau-

consistent with stone adherent to a radiopaque clip was noted. A biliary sphincterotomy was performed and the biliary tree was swept with a 12 mm balloon. One stone was successfully removed and subsequent cholangiogram revealed no stones remaining in the bile duct. Upon closer inspection of the removed stone, a surgical clip was noted to be embedded in the center of the stone. The patient’s symptoms and transaminases subsequently improved and she was discharged home. “Clip-choledocholithiasis” from a migrated surgical cystic-duct clip was first reported in 1979.3 In such cases, the migrated surgical clip serves as a nidus for the formation of common bile duct stones.4 The precise pathophysiological mechanism leading to surgical clip migration is unclear. Despite the increasing frequency of laparoscopic cholecystectomies, surgical clip-induced choledocholithiasis remains a rare complication. However, this case highlights the importance of considering post-cholecystectomy clip migration leading to biliary complications in the differential diagnosis of patients presenting with typical biliary colic symptoms and a remote history of cholecystectomy. References: [1]. Laser Med Surg News 1989; 7: 38-40. [2]. J Gastrointest Surg 2010; 14: 688–696 [3]. Cholangitis with a silver lining. Arch Surg 1979; 114: 214–215. [4]. Gastrointest Endosc 1982; 28: 222–3.

195 Groove Pancreatitis: A Rare Form of Chronic Pancreatitis Bhairvi S. Jani, MBBCH, Fadi Rzouq, MD, Shreyas Saligram, Carly Ernst, Atta Nawabi, Katie Dennis, MD, Nicola Marian, Ali Abbaszadeh, John Bonino, Mojtaba Olyaee. University of Kansas Medical Center, Kansas City, KS.

[194A] Figure 1.

Introduction: Groove Pancreatitis is an uncommon form of chronic pancreatitis. Its presentation is very similar to pancreatic head adenocarcinoma and its diagnosis is extremely challenging. EUS FNA is generally inconclusive therefore most patients eventually require surgery. Case Presentation: A 57 year old male with a history of HIV, Hepatitis B and Fournier gangrene presented with four days of epigastric pain. He was mildly tachycardic and had dry mucous membranes. Abdominal exam revealed absent bowel sounds and epigastric tenderness. Laboratory evaluation revealed a creatinine of 1.72 mg/dL, potassium of 2.9mmol/L and a normal lipase level of 86 U/L. Liver enzymes and total bilirubin were normal. CT imaging of his abdomen and pelvis showed high grade obstruction of the second portion of the duodenum without any obvious mass. EGD showed a mass at the duodenal bulb causing luminal narrowing. Biopsies of were negative for malignancy. MRI of the abdomen revealed a mass in the region of the pancreatic head and descending duodenum. PET scan demonstrated hypermetabolic activity of the mass without lymph node involvement. CEA and CA 19-9 were normal. EUS revealed a 3 cm mass in the region of pancreatic head with irregular borders and no vascular invasion. FNA was non-diagnostic. Pt then underwent a Whipple’s procedure. Pathology of these specimens was negative for malignancy but were consistent with paraduodenal or “groove” pancreatitis. The duodenal submucosa had Brunner’s gland hyperplasia with fibrosis and into the pancreas. The patient was discharged after pain was controlled and he was tolerating an oral diet. We suspect the Brunner’s gland hyperplasia as confirmed by pathology to be the cause of Groove pancreatitis in our patient. Discussion: The low incidence of groove pancreatitis is partly due to lack of familiarity. The exact cause is unknown, although there are strong associations with long-term alcohol abuse, functional obstruction of the duct of Santorini and Brunner gland hyperplasia. Groove Pancreatitis should always be considered in the differential for patients presenting with pancreatic head lesions with no cholestatic jaundice especially when duodenal obstruction is present and neither duodenal biopsies nor pancreatic head FNA confirm adenocarcinoma.

[194B] Figure 2.

sea and vomiting that had been occurring intermittently for one week. She felt that this pain was similar to her previous biliary colic pain before cholecystectomy, but more severe in intensity. On physical examination, she was noted to have mild scleral icterus and right upper quadrant abdominal tenderness. A CT scan of the abdomen and pelvis was performed which revealed a surgically absent gallbladder and a surgical clip which appeared to be located within the lumen of the common bile duct. The common bile duct was mildly dilated at 9 mm. Her transaminases were elevated with AST 118, ALT 183, alkaline phosphatase 337, and total bilirubin 6.7. She subsequently underwent endoscopic retrograde cholangiopancreatography (ERCP) which revealed a 6 mm common bile duct stone. A mobile filling defect


[195A] Figure 1.


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[196A] Figure 1.

[195B] Figure 2.


196 Anuria as Presenting Symptom of Pancreatic Adenocarcinoma Yaseen Alastal, MD1, Tariq Hammad, MD1, Basmah Khalil, MD2, Turki Alkully, MD1, Abdallah Kobeissy1, Ali Nawras, MD, FACG1. 1. University of Toledo Medical Center, Toledo, OH; 2. University of Toledo, Toledo, OH. Pancreatic adenocarcinoma has different common presentations, but anuria is a rare presentation that was only reported in very few case reports. Here we present a case of pancreatic adenocarcinoma presented to hospital with a chief complain of anuria. 72-year-old female patient with no significant past medical history referred from outside facility for further evaluation of anuria for 2 days. On further questioning, the patient stated that she had jaundice for 2 weeks and she lost over 20 pounds of her weight in 2 months. No significant history of abdominal pain, nausea or vomiting. Patient used to smoke one pack daily for 50 years but stopped 5 years ago. Abdominal exam showed soft, nontender abdomen. Laboratory work up showed: creatinine 7.57 mg/dL, BUN: 81 mg/dL, total bilirubin: 6.4 mg/dL, direct bilirubin 4.7mg/dL, alkaline phosphatase: 328 IU/L, ALT: 111 IU/L, AST: 50 IU/L, CA 19-9: 113 U/mL (normal rage : 0-37 Units/mL), CEA : 25.4 ng/mL (normal rage: 0-3 ng/mL), CA 125 : 58 Units/mL (normal rage : 0-35 U/mL). Non contrast abdominal CT scan revealed bilateral hydroureteronephrosis secondary to extrinsic compression from severe retroperitoneal lymphadenopathy along with 4 cm abdominal mass in portal area (Fig 1). Bilateral emergent percutaneous nephrostomy tubes were inserted for short term drainage of the urinary tract. Endoscopic ultrasound revealed large paraduodenal pancreatic mass measured 58.5 mm x 55.5 mm, obstructing the bile duct and causing external compression on the duodenum. Fine needle aspiration was performed. ERCP showed high grade distal common bile duct stricture, which was dilated and stented with a 10 mm × 60 mm partially covered metallic biliary stent (Fig 2). A duodenal 22 mm × 120 mm uncovered metallic stent was also used to relieve the duodenal obstruction. Under CT guidance, the patient also underwent


[196C] Figure 3.


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bilateral ureteric stent insertion through nephrostomy tubes to overcome the ureteric obstruction. FNA cytology results showed moderately differentiated pancreatic adenocarcinoma. The patient was referred to oncologist for further evaluation and management. Anuria can be the presenting symptom of pancreatic adenocarcinoma. It can result from bilateral ureteric obstruction secondary to severe retroperitoneal lymphadenopathy.

197 Bile Duct Papillary Adenoma Degenerating Into Cholangiocarcinoma Brent T. Cengia, MD1, Jason D. Jones, MD1, Lucy Lan, BA2, Ling Guo, MD3, Barry DeYoung, MD3, Rishi Pawa, MBBS4. 1. Wake Forest School of Medicine, Department of Internal Medicine, Winston-Salem, NC; 2. Wake Forest School of Medicine, Winston-Salem, NC; 3. Wake Forest School of Medicine, Department of Pathology, Winston-Salem, NC; 4. Wake Forest School of Medicine, Department of Gastroenterology, Winston-Salem, NC. A 79 year old Caucasian female was incidentally discovered to have transaminitis on routine labs and underwent right upper quadrant ultrasound revealing a dilated bile duct. MR Abdomen revealed a solid mass in the proximal common hepatic duct. She was asymptomatic without jaundice, weight loss, pruritus or abdominal pain. Additional and repeat labs showed a mildly elevated carbohydrate antigen 19-9 (CA-19-9) at 41.49 and normal carcinoembryonic antigen (CEA). Endoscopic Ultrasound (EUS) revealed a 1.5 x 2 cm mass in the common hepatic duct and fine needle aspiration showed atypical glandular papillary cells with no evidence of neoplasm. Endoscopic Retrograde Cholangiopancreatography

[197C] Figure 3.

(ERCP) with cholangioscopy demonstrated a frond-like mass in the common hepatic duct with pathology indicative of dysplastic epithelium consistent with low-grade dysplasia without frank malignancy. Repeat CA-19-9 level normalized at 30.11. She underwent pre-operative evaluation and was found to have severe aortic stenosis necessitating valve replacement and thus biliary surgery was delayed. Repeat labs four months later showed highly elevated CA-19-9 at 1382.10 concerning for degeneration of adenoma to malignancy. She underwent diagnostic laparoscopy with resection of the extrahepatic biliary tree including bifurcation, Roux-en-Y hepaticojejunostomy, hilar lymphadenectomy and cholecystectomy. Hepatic duct mass pathology showed a 3 x 1.4 cm exophytic papillary adenoma with high grade dysplasia, within which was a 0.3 cm moderately differentiated adenocarcinoma involving the left proximal hepatic duct invading into but not through the hepatic duct wall with negative margins. Final diagnosis was Stage I cholangiocarcinoma (T1N0M0) within a papillary bile duct adenoma. Bile duct adenomas (BDA) are rare bile duct tumors accounting for roughly 6% of extrahepatic tumors. Adenomas of the extrahepatic bile ducts may present with obstructive symptoms or may be asymptomatic, found incidentally on physical exam or imaging. Though defined as a benign tumor, BDAs have carcinogenic potential. The incidence and timing of malignant transformation is not well defined and thus prompt surgical resection is indicated for treatment. In our case, after a necessary delay in therapy, CA-19-9 levels dramatically increased and her tumor that was initially felt to be BDA degenerated to cholangiocarcinoma.

198 [197A] Figure 1.

“An Invisible Insulinoma -- Or Is It?”: The Role of EUS Elastography in Detection of Sub Centimeter Pancreatic Neuroendocrine Tumor Siddharth B. Javia, MD, Dishita Pandya, MBBS, Asha Kuruvilla, MD, Erik Rahimi, Jennifer Lamberth, MD, Nirav Thosani, MD. University of Texas, Houston, TX.

[197B] Figure 2.


Introduction: Endoscopic ultrasound (EUS) role is well established for detection of solid pancreatic lesions. We report utility of EUS with elastography for improved localization of insulinoma in a patient with a subcentimeter insulinoma not seen on CT, MRI and Somatostatin receptor scintigraphy (SRS). Case: A 34-year-old female presented with several episodes of altered sensorium. These episodes were associated with symptoms of shakiness and sweating. She was found to have hypoglycemia during these episodes. Her symptoms improved with eating. She gained 10 pounds over few months period. Diagnostic evaluation: On supervised 72-hour fast test, patient developed symptomatic hypoglycemia (glucose=40 mg/dl) 7 hours after last calorie intake. Her symptoms and blood glucose values improved with glucagon and meal ingestion. Her proinsulin level was 26.4 pMol/L (normal < 18.8pMol/L) and C peptide levels were 1.59 ng/ml (normal 0.48-5.55 nm/ml). Her plasma sulfonylurea testing was negative. Biochemical diagnosis of insulinoma was made. Imaging (Localization of insulinoma): Pancreas protocol CT Scan, MRI with contrast, SRS (Indium labeled Octreotide scan) failed to localize insulinoma. EUS with elastography showed a 6 x 9 mm isoechoic, homogenous mass with fine capillary flow in the neck of the pancreas near the level of portal confluence. On elastography, the mass demonstrated diffuse solid blue patter with scattered green color with EUS elastography color score of 4. Quantitative real time elastography suggested strain ratio of 8. Immunohistochemical analysis of fine needle aspiration(FNA) supported diagnosis of a benign insulinproducing pancreatic endocrine lesion-islet B cell hyperplasia vs. insulinoma. Patient was referred for laparoscopic enucleation. Learning points: In patients with suspected pancreatic neuro-endocrine tumors (NET) undergoing EUS and CT, the sensitivity of EUS is greater than MSCT (92% vs 63%, respectively), particularly for insulinomas (84% vs 32%, respectively) and for lesions smaller than 2 cm, EUS may detect up to 91% of insulinomas missed by MSCT. The sensitivity of EUS for insulinomas depends on the location and size of the tumor; sensitivity is greatest for tumors in the head of the pancreas and lowest for those in the tail of the pancreas. EUS elastography can be a useful additional tool to locate and further characterize small insulinomas and may improve yield of diagnostic FNA.


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Abstracts tion. IVC filter placement has been reported to have an overall complication rate 0.3%. IVC filter migration and extrusion into extravascular space is uncommonly reported in the literature. A 31 year-old woman with history of a right common iliac deep vein thrombosis status post IVC filter placement 7 years ago presents to the hospital with acute onset non-radiating epigastric pain for 2 days associated with nausea and bilious emesis. Upon presentation, she was febrile to 100.1ºF and tachycardic to 140 bpm. On physical exam, the patient was in mild distress from pain and anicteric. She had moderate epigastric tenderness with voluntary guarding but no rebound tenderness. Her laboratory results were notable for leukocytosis (17.18 k/uL), lactic acidosis (4.7 mmol/L), and elevated amylase (283 U/L) and lipase (1595 U/L). She had normal liver tests. Pan-cultures and chest radiograph were negative for infection. Computed tomography of the abdomen and pelvis revealed peri-pancreatic stranding and fluid consistent with acute pancreatitis with possible signs of necrosis. The common bile duct measured 11mm in diameter. A strut of the IVC filter was observed extending anteriorly into the small bowel. An endoscopic retrograde-cholangio-pancreatography demonstrated a foreign body metal wire projecting out of the ampullary orifice that upon fluoroscopic evaluation appeared to be one of the struts of the IVC filter eroding into the duodenal wall. Vascular surgery was consulted and attempts at removing the IVF filter were unsuccessful. The patient clinically improved with supportive care. IVC filter migration can occur in the immediate post-procedure setting or long after placement. Approximately one third of complications from IVC filter placement are caused by migration, though the vast majority of these migrated filters remain in the intravascular space. Only a handful of cases have been reported to have IVC filter extrusion into the gastrointestinal tract. This case is one of two cases reported in the literature of a migrated IVC filter causing pancreatitis.

[198A] Figure 1.

200 The Aftermath of a Hepatic Artery Aneurysm: A Rare Etiology of Biliary Obstruction Abhishek Seth, MD1, Kunal Suryawala, MD2, Robby Rahim, MD2, Ankur Sheth, MD, FACG2, Moheb Boktor, MD2, Guillermo Sangster, MD2, Paul Jordan, MD, FACG2. 1. LSU Health Sciences Center and Overton Brooks VA Medical Center, Shreveport, LA; 2. Louisiana State University Health Sciences Center, Shreveport, LA.

[198B] Figure 2.

Hepatic artery aneurysms (HAA) constitute 14-20% of visceral artery aneurysms. Most of the HAA are asymptomatic. Although rare, obstructive jaundice due to external bile duct compression or rupture of the HAA into the biliary tree with clots occluding the lumen, has been reported. 56 year old white male with history of COPD and HTN presented to an outside hospital with complaints of yellowing of skin, eyes, right sided abdominal pain and dark urine for. Laboratory work revealed WBC 9000/ cu mm, total bilirubin 24 mg/dl, ALP 1104 U/L ,AST 200 U/L and ALT 236 U/L. CT abdomen and pelvis revealed intra and extra hepatic biliary dilatation with a hepatic artery aneurysm causing compression of the CBD. He was transferred to our hospital where he underwent an ERCP with cholangioscopy. This revealed a CBD stricture ~ 2-3 cm long at the level of cystic duct takeoff, with massive biliary dilation proximally. Biopsies were obtained and a plastic stent was deployed traversing the stricture. Biopsies revealed inflammation. CT angiography with 3 D reconstruction was obtained which confirmed location of fusiform hepatic artery aneurysm compressing the CBD. Patient had remarkable improvement in symptoms as well as hepatobiliary chemistries- AST 59 U/L, ALT 52 U/L, ALP 239 U/L and total bilirubin 2 mg/dl, two week following the procedure. He then underwent coil embolization of the hepatic artery. Stent grafting could not be attempted secondary to discrepancy in the size of proximal(10mm) and distal(5mm) entry into the aneurysm. Patient tolerated the procedure well and was later discharged. Management of obstructive jaundice secondary to HAA depends on clinical presentation. Biliary stenting prior to surgical management of aneurysm, is usually attempted in patients without hemobilia. However risk of the stent entering the aneurysm and precipitating major hemorrhage must be considered. In patients with HAA presenting with abdominal pain, obstructive jaundice and hemobilia (Quinke’s triad), biliary obstruction should be dealt with as part of the definitive excision of the aneurysm and repair of the damaged bile duct.

[198C] Figure 3.

199 A Rare Cause of Pancreatitis: Inferior Vena Cava Filter Migration Clara Tow, MD1, Aurada Cholapranee, MD2, Sammy Ho, MD1, Harmit Kalia, DO1. 1. Montefiore Medical Center, Bronx, NY; 2. Moses Montefiore Hospital, Allison Park, PA.

[200A] Figure 1.

Inferior vena cava (IVC) filters are often placed in patients with venous thromboembolism (VTE) who have an absolute contraindication to anticoagulation or continue to develop VTE despite anticoagula-



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[201A] Figure 1.

[200B] Figure 2.

[201B] Figure 2.

[200C] Figure 3.

201 Acute Pancreatitis and Multiple Organ Dysfunction Syndrome After Percutaneous Mechanical Thrombectomy: Case Report Nathaniel Ernstoff, MD1, Simi Singh, MD2, David L. Carr-Locke, MD, FACG3. 1. Mount Sinai Beth Israel, New York, NY; 2. Mount Sinai Beth Israel, New York, NY; 3. Mount Sinai Beth Israel Medical Center, New York, NY. Acute pancreatitis is most commonly caused by gallstones, alcohol and ERCP. Less common etiologies include trauma, drugs, and surgical procedures. We discuss a rare case of pancreatitis as a side effect of percutaneous mechanical thrombectomy. A 53 year old woman with a history of peripheral artery disease presented with acute leg ischemia. The patient underwent revascularization with the AngioJet Rheolytic Thrombectomy System. Post-procedure angiography showed improved flow, however, 2 hours afterwards she developed abdominal pain, nausea and vomiting. Physical exam revealed epigastric pain without jaundice, rash or bruising. Notable labs included lipase=10,110 U/L, ALP=99 U/L, AST=324 U/L, ALT=94 U/L, total bili=6.6 mg/ dL, direct bili=5.1 mg/dL, Cr=1.99 mg/dL (0.94 baseline), and Hgb=7.6 g/dL (12.9 baseline).


[201C] Figure 3.


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Abstracts CT abdomen without contrast showed edema and peripancreatic infiltration of the head and neck of the pancreas with fluid tracking towards the right paracolic gutter. She became hypotensive and tachycardic with worsening renal function. Lipase levels peaked at 11,323 U/L. ERCP revealed hematin and dark bile in the stomach, an edematous duodenum, and a normal major papilla. Sphincterotomy was performed, revealing black bilious fluid within the common bile duct (CBD). CBD and pancreatic duct stents were placed. Creatinine rose to 6.05 mg/dL in the setting of anuria, leading to hemodialysis. She subsequently developed acute respiratory distress syndrome, requiring intubation. Her recovery lasted 14 days, and after discharge she had 2 episodes of recurrent acute pancreatitis. This is the most severe case of pancreatitis reported after mechanical thrombectomy. A literature review found 10 prior incidents of pancreatitis after this procedure. These patients, like ours, had no history of pancreatitis, yet all developed symptoms within 4 days of the procedure. The proposed mechanism is hemolysis overwhelming the body’s ability to bind free hemoglobin via haptoglobin and hemopexin. Induction of an inflammatory cascade with leukocyte infiltration and neutrophil migration occurs. Another suggested mechanism is that renal injury during hemolysis further increases the risk for pancreatitis. Known side effects of mechanical thrombectomy are hemolysis, distal embolization, vessel perforation/ dissection, and thrombosis. Pancreatitis appears to be a rare but serious side effect that should be considered in patients who develop abdominal pain post-procedure.

202

[202B] Figure 2.

Amoxicillin-Clavulanic Acid Induced Pancreatitis: A Case Report Lyna M. Campo, MD1, Anas All Halak , MD 2, Raquel Olivo, MD2, Kinesh Changela, MD3, Andrea Culliford, MD4, Jay P. Babich, MD5. 1. St. Barnabas Hospital, SBH Health System, Englewood, NJ; 2. St. Barnabas Hospital, SBH Health System, Bronx, NY; 3. The Brooklyn Hospital Center, Brooklyn, NY; 4. St. Barnabas Hospital, SBH Health System, New York, NY; 5. St. Barnabas Hospital, SBH Health System, Teaneck, NJ. Introduction: Amoxicillin, a popular oral antibiotic for respiratory and cutaneous infections, generally well tolerated. However in rare cases it can result in adverse cutaneous, gastrointestinal and hematologic effects. Minimal data exists regarding amoxicillin induced pancreatitis. Case Report: A 42 year-old obese African-American woman with history of hypertension and hypothyroidism, presents to the emergency department with epigastric abdominal pain with radiation to the back three days after being started on amoxicillin-clavulanic acid for pharyngitis. Physical exam was significant for epigastric tenderness. The patient denied history of smoking, alcohol or illicit drug use, as well as travel history, personal or family history of pancreatic disorders. Laboratory studies demonstrated a mild leukocytosis, a mild transaminitis and increased serum lipase. Dyslipidemia or electrolyte abnormalities were not found. The only new medication was amoxicillin/clavulanic acid. Abdominal CT suggested acute pancreatitis. Ultrasound and MRCP were negative for gallstones, choledocholithiasis or biliary strictures. The patient was managed with IV fluids and, cessation of the amoxicillin, which resulted in significant improvement within 72 hours. Discussion: Drug-induced pancreatitis is a rare cause for acute pancreatitis; most of the cases result from gallstones or alcohol abuse. However, 525 different drugs are listed in the World Health Organization database as suspected causative agents of acute pancreatitis. Although, amoxicillin-clavulanic acid is not among them. The prevalence of drug-induced pancreatitis is still unclear because incidence has been documented only as case reports; this is why, evidence of causality is difficult to assess. The overall incidence probably ranges between 0.1 and 2% of cases. Causality is classified as definite if the symptoms followed the drug administration in a close temporal sequence and in a known response pattern. Furthermore, the symptoms have to improve upon cessation of the drug and re-appear after repeated exposure. After extensive review of the literature, there are no reports regarding Amoxicillin associated pancreatitis. In this case, the patient’s symptoms as well as her pancreatic enzymes improved with the cessation of the drug. Amoxicillin-clavulanic acid induced pancreatitis has rarely been reported in the literature; however it should be added to the “list” of medications felt to result in pancreatitis.

203 Biliary Bipolaris: A Rare Case of Disseminated Fungal Infection in the Biliary Tract Nathaniel Avila, MD1, Asha Kuruvilla, MD2, Meera Avila, MD1, Dishita Pandya, MBBS2, Nirav Thosani, MD2, Sheila Reddy, MD3. 1. University of Texas Health Science Center, Bellaire, TX; 2. University of Texas, Houston, TX; 3. University of Texas Health Science Center, Houston, TX. This is a case of a 39-year-old African American woman with no past medical history who presented with new onset seizures. Initial CT and MRI of the brain demonstrated bilateral temporal masses. Upon further questioning, the patient revealed she had a one week history of mild RUQ abdominal pain and laboratory tests showed an alkaline phosphatase of 1322, AST 96, ALT 236, and total Bilirubin of 1.3. Subsequent CT of the chest, abdomen, and pelvis demonstrated marked thickening of the CBD and CHD walls of up to 8 mm. ERCP was performed, with initial cholangiogram showing multiple irregular shaped filling defects within the entire biliary tree and CBD and CHD dilation of up to 10 mm. After biliary sphincterotomy was performed, large amounts of brown and green fragments, characteristic of mold, were seen exiting the bile duct and that were collected for culture. Choledochoscopy was then performed showing multiple fragments of mold fi lling the lumen of the CBD and CHD. The bile duct aspirate and CBD biopsies was positive for Bipolaris species. The patient then underwent resection of the right temporal lesion, with cranial biopsies revealing Bipolaris species infection of the brain as well. The patient was treated with IV ambisome and Voriconazole for a total of 6 months. Repeat ERCP two months later to remove a previously placed plastic stent showed near resolution of the biliary tract irregularities, with improvement in biliary dilation and normalization of liver function tests. A literature search suggest that this is the first case report of tissue proven Biloparis infection in the biliary tract in any patient type, immunocompromised and competent. Bipolaris species, are a group fungi commonly found in soil and plant material, and are present worldwide. Though they are recognized pathogens of plants, they rarely cause infections in animals and humans. When they have been present in human infection, they have typically been associated with immunosuppression sinusitis and allergic broncopulmonary disease. The literature suggest that amphotericin B alone or in combination with imidazoles is the recommend treatment. Due to the devastating consequences of disseminated Bipolaris, early diagnosis and treatment are essential.

[203A] Figure 1.

[202A] Figure 1.



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[203B] Figure 2.

[204A] Figure 1.

[203C] Figure 3.

204 Symptomatic Chronic Recurrent Benign Pneumoperotenium Treated With ERCP Brijesh Patel, MD1, Javier Nieves, MD2, Prasad Kulkarni, MD2. 1. University of South Florida, Department of Internal Medicine, Tampa, FL; 2. University of South Florida, Tampa, FL. Introduction: Pneumoperitoneum (PP), a dreaded surgical emergency requiring urgent intervention, may rarely be benign, chronic and recurrent. We present a case of chronic recurrent PP where an unusual final presentation led to therapeutic intervention and resolution. Case Report: This 85YOM visited ER over 12 months with recurrent PP. His most recent visit was for acute epigastric pain. Chart review revealed multiple ER visits during past 12 months for similar symptoms; the most recent being 48-hours prior. Each time, alarmed by the PP, he would be evaluated by surgical service, admitted for observation, and discharged after a stable course over the next 24-48 hours and with improving PP. Surgery had been deferred due to age and comorbidities. Initial CT this time confirmed moderate free epigastric and right sub-diaphragmatic intraperitoneal air, intrahepatic biliary dilation and extensive colonic diverticulosis without acute diverticulitis or oral contrast extravasation. Prior CTs had noted mid-small-bowel pneumatosis, small gas “dots” within peritoneal space and mesenteric fat and small para-pancreatic-head diverticulum; all with unclear significance. No H/o abdominal surgeries, recent abdominal/pelvic intervention. Upon admission patient did have abnormal liver tests for the first time compared to 2 days ago. Liver US revealed gallstones/sludge. Repeat CT-pancreas showed early acute cholecystitis. With concern for choledocholothiasis due to intra-hepatic biliary dilation on CT led to ERCP and sphincterotomy with MAC using CO2 insufflation; revealing only biliary sludge. Surgical service was on stand-by for emergency peritoneal decompression should PP deteriorate during ERCP. Positive blood cultures (E.coli) were treated with appropriate IV and PO antibiotics. PP has not recurred for over 2 years. This is a rare case of chronic, recurrent, benign PP complicated with E. coli bacteremia likely secondary to cholangitis. Discussion: A case of chronic, recurrent, benign PP that remained an enigma for over 12 months is presented. None of the postulated etiologies was ever confirmed. ERCP is generally contraindicated in presence of PP; but the last presentation with hepato-biliary features indicated a biliary etiology and performing simply an ERCP with CO2 insufflation with surgical service on standby, resolved the issue. Benign etiologies of PP do exist and their awareness may help avoid unnecessary surgical intervention.


[204B] Figure 2.

205 Cholecystectomy Clip Conundrum: An Atypical Migration of Cholecystectomy Clip and Its Management Celeste P. Pizza, MD, Kasra Adham, MD, Alan Brijbassie, MD. Virginia Tech Carilion School of Medicine, Roanoke, VA. Introduction: As it replaces conventional cholecystectomy, laparoscopic cholecystectomy complications have become increasingly recognized. Here, we describe an atypical migration of a cholecystectomy clip. Case Presentation: A 39-year-old female with symptomatic cholecystitis undergoes laparoscopic cholecystectomy complicated by a cystic remnant Strasberg Type A leak. ERCP with sphincterotomy and placement of a fully covered metal stent in a transpapillary fashion was performed for definite management. Interval ERCP to remove the stent defines leak resolution; however, a cholecystectomy clip was observed in close proximity to a common hepatic duct stricture at the level of the confluence (Figure 1).


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Abstracts A 59-year-old man presented with recurrent low-grade fevers, elevated alkaline phosphatase (AP) and gamma-glutamyl transpeptidase (GGT), without abdominal pain or jaundice. Ten years prior he underwent routine cholecystectomy for symptomatic cholelithiasis complicated by biliary leak requiring hepaticojejunostomy. He denied drug, herb, medication, or significant alcohol intake. Vital signs were stable and within normal limits. There was no scleral icterus. He had mild abdominal distension and a healed chevron scar. Liver and spleen margins were non-palpable and no gross evidence of ascites was noted. Lab work revealed elevation of AP ranging from 92-149 IU/L and an elevated GGT of 128 IU/L. Viral hepatitis serologies and anti-mitochondrial antibodies were negative. Hepatobiliary MRI showed peripheral intrahepatic duct dilatation, with beaded appearance, in the right and left lobes of the liver. There was a 4 cm hyperperfusion lesion with parenchymal edema in the anterolateral right lobe and a 2.5 cm hyperperfusion lesion in the lateral right lobe, consistent with cholangitis. The hepaticojejunostomy anastomosis was free of stenosis. He was diagnosed with intrahepatic cholangitis and started on ursodiol. Follow-up MRI three months later showed resolution of the previous hyperperfusion lesions in the right lobe of the liver. However, a new 1 cm focus of cholangitis with marked ring enhancement was seen in hepatic segment 5. A small bowel series showed reflux of enteric contrast into the biliary tree and the efferent roux limb was measured to be less than 20 cm. Thus, he was referred to hepatobiliary surgery for surgical lengthening of the efferent roux-en-y limb. While stasis from obstruction is the most common cause of cholangitis, our patient suffered recurrent reflux cholangitis due to altered surgical anatomy. An absent sphincter of Oddi as well as proximal location of the biliary tree to the enteroenteric anastomosis allowed passage of bowel contents to reflux under the pressure of motility. Although rare, reflux cholangitis is an important etiology to consider in the differential diagnosis of cholangitis in patients who had previous biliary reconstruction.

207 [205A] Figure 1.

Symptomatic Metastatic Cutaneous Melanoma of the Gallbladder: A Rare Case Report Dhruvan Patel, MD1, Aparna Basu, MD1, Aasim Mohammed, MD2, Vivek Mehta3, Steven Lichtenstein, DO4. 1. Mercy Catholic Medical Center, Philadelphia, PA; 2. Mercy Catholic Medical Center, Yeadon, PA; 3. Mercy Catholic Medical Center, Philadelphia, PA; 4. Mercy Health System, Penn Valley, PA. Introduction: Metastases of cutaneous melanoma to the gallbladder are unlikely and usually asymptomatic. Here, we report a rare case of symptomatic metastatic melanoma of the gall bladder. Case report: A 41 year old male admitted to the hospital with 3 weeks history of right upper quadrant (RUQ) abdominal pain, nausea, alternate bowel movements and 15 pounds of weight loss. He was recently diagnosed with stage IIC (T4N0M0) cutaneous melanoma of face 4 months prior to admission. He underwent excision of melanoma and was started on interferon therapy. His positron emission tomography (PET-CT) was negative for any metastatic lesion 3 months prior to admission. His physical examination revealed RUQ tenderness otherwise unremarkable. His WBC, amylase, lipase were normal. Liver function test revealed aspartate transaminase 62 U/L, alanine transaminase 96 U/L, alkaline phosphatase 76 U/L, and total bilirubin 0.3 mg/dL. An abdominal computed tomography and liver ultrasound showed 1.1X1 cm gallbladder lesion concerning for mass. Ultrasound guided gallbladder biopsy was attempted but it was unsuccessful. Patient underwent laparoscopic cholecystectomy with hepatic wedge resection. It revealed no evidence of gallbladder mass, intraoperatively or on back table inspection (image 1). Frozen section of gallbladder was also negative for tumor. Interestingly, pathology suggested metastatic melanoma of the gallbladder with positive V600K mutation. His symptoms were improved post-surgery. His 1 month follow up PET-CT scan was negative for any metastasis. Patient is scheduled for close outpatient follow up visit for subsequent PET-CT scan. Discussion: Melanoma tends to metastasize extensively with most common sites of metastases are liver, brain and lung. Although gallbladder involvement is seen in 4-20% of patients with metastatic melanoma as suggested by autopsy report, it is unlikely for metastatic gallbladder melanoma to present with symptoms. The most common presentations of symptomatic metastatic gallbladder melanoma are acute cholecystitis followed by jaundice, hemobilia, biliary fistula and intractable abdominal pain as seen in our patient. Despite advancement in chemotherapy and immunotherapy, the prognosis of metastatic melanoma to the gallbladder is very poor with a median survival of 6-9 months. Isolated, resectable gallbladder metastases can be treated with cholecystectomy and hepatic wedge resection, and can achieve longer survival as indicated in our patient.

[205B] Figure 2.

The stricture was subsequently treated with bilateral plastic stents across the right and left hepatic ducts bridging the area of luminal narrowing. Repeat ERCP in three months defines extrusion of the migrated cholecystectomy clip into the duodenal lumen (Figure 2) on balloon withdrawal. The biliary stricture was eventually resolved. Conclusion: This case highlights erosion of a cholecystectomy clip into the biliary tract with complications of stricture formation and migration. There is scant available literature regarding the optimal management of this complication.

206 Recurrent Focal Cholangitis Due to Intestinal Content Reflux Post-Hepaticojejunostomy David DiCaprio, DO, Andrew Nguyen, DO, Ilan Weisberg. Lenox Hill North Shore-LIJ Hospital System, New York, NY. Cholangitis is an infection of the biliary tract that primarily results from biliary stasis or obstruction. We present a rare case of recurrent cholangitis due to intestinal content reflux secondary to a short efferent roux limb after hepaticojejunostomy.


[207A] Figure 1.


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Conclusion: Our case emphasizes on close investigation of hepatobiliary lesion when the patient has a previous history of cutaneous malignant melanoma. Active screening and early detection is the key to achieve longer survival in malignant melanoma of the gallbladder.

208 Spontaneous Biloma: A Rare Complication of Acute Cholecystitis Bisharah S. Rizvi, MD1, Aarthi Rajkumar, MD2. 1. Canton Medical Education Foundation, Canton, OH; 2. Canton Medical Education Foundation, Canton , OH. Biloma is defined as an encapsulated collection of bile outside the biliary tree. Most cases are either iatrogenic following a biliary procedure or traumatic. Non-traumatic biloma or spontaneous biloma is a rare entity and occurs as a complication of choledocholithiasis, cholangiocarcinoma or rarely hepatic infarction. We report a case of spontaneous biloma as a complication of acute cholecystitis. A 66-year-old male presented to the emergency department (ED) with complains of nausea, vomiting and epigastric pain of five days duration. He had leukocytosis with mildly deranged liver enzymes. An Ultrasound (US) of the abdomen showed cholelithiasis without evidence of acute cholecystitis and he was discharged home on antiemetics. Four days later, he developed right upper quadrant pain with fever prompting another ED visit. This time he had significantly elevated transaminases and alkaline phosphatase with normal bilirubin. Repeat US showed a new loculated complex fluid collection at the inferior margin of the right hepatic lobe, again without evidence of acute cholecystitis. Computerized tomog-

raphy (CT) abdomen confirmed an 8.8 x 5.6 x 5.7 cm rim enhancing right subhepatic fluid collection. Percutaneous drainage drained 130 ml of golden yellow fluid, confirmed as bile by dipstick method. A hepatobiliary (HIDA) scan was done to investigate for any bilious leak that showed cystic duct obstruction suggesting acute cholecystitis but no leak. He underwent an open cholecystectomy with intra operative cholangiogram. No evidence of gall bladder perforation or biliary leak was noted however the gall bladder and cystic duct were markedly inflamed. Spontaneous biloma formation is extremely rare. The proposed mechanism is raised intraductal pressure caused by obstruction from a gallstone stone or a tumor leading to bile leak. Our patient initially presented with clinical features of cholelithiasis and mild transaminitis with no radiological signs of obstruction. Subsequently he developed a biloma, however no clear evidence of bile leak could be demonstrated radiologically or intraoperatively. The only inciting cause of biloma was the presence of acute cholecystitis. Biloma have the potential to get infected and early drainage is mandated. This leads us to postulate that a spontaneous biloma can occur as a complication of acute chloecystitis. So far only two cases of this rare complication of acute cholecystitis have been documented. Given the rarity of occurrence, one needs to keep a close watch or this entity may be overlooked.

209 Endoscopic Ultrasound-Guided Endoscopic Choledochoduodenostomy Using a Lumen-Apposing Covered Self-Expanding Metal Stent to Palliate Malignant Distal Biliary Obstruction Salman Nusrat, MD1, Aftab Ahmed, MD2, John Maple, DO1. 1. University of Oklahoma Health Sciences Center, Oklahoma City, OK; 2. Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK. Endoscopic retrograde cholangiopancreatography (ERCP) with biliary stent placement is the preferred strategy for the palliation of cholestasis in the setting of unresectable malignant distal biliary obstruction. Historically, failed ERCP in this setting has been variably managed, with percutaneous transhepatic drainage commonly utilized. We describe an effective and safe alternative to commonly utilized practices. A 77 year-old female presented to her local physician with 2 weeks of abdominal pain, vomiting, jaundice and 15 lbs weight loss. Laboratory evaluation was significant for a total bilirubin of 7.2 mg/dL. An abdominal CT scan demonstrated a hypoattenuating pancreatic genu mass with upstream dilation of both the bile duct and the pancreatic duct. Upon transfer to our medical center, an endoscopic ultrasound (EUS) with fine needle aspiration was performed, confirming CT findings and also demonstrating encasement of the portal vein and adenocarcinoma on cytology. During same-sedation ERCP, complete obstruction of the extrahepatic bile duct was noted. A low-inserting cystic duct joined immediately below the obstruction, and various angled guidewires always preferentially entered the cystic duct rather

[208A] Figure 1.

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[208B] Figure 2.


[209B] Figure 2.


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Abstracts 211 A Shocking Complication: Haemophilus Influenzae Sepsis After Extracorporeal Shock Wave Lithotripsy David DiCaprio, DO1, Anish Mammen, MD2, Gregory Haber, MD, FACG2. 1. Lenox Hill North Shore-LIJ Hospital System, New York, NY; 2. Lenox Hill Hospital, New York, NY.

[209C] Figure 3.

than traversing the malignant obstruction. It was elected to proceed with EUS-directed biliary drainage. The common hepatic duct was punctured across the wall of the duodenal bulb with a 19 g needle and needle cholangiography performed. A 0.035”x 450 cm hydrophilic tip wire was successfully passed into the left intrahepatics. A 4 mm x 4 cm dilating balloon was then used to dilate the tract. A 10 mm lumen apposing fully covered self expanding metal stent (Axios, Xlumena, Mountain View, CA) was placed across the choledochododuodenostomy under endoscopic, sonographic, and fluoroscopic guidance. A 10 mm x 4 cm dilating balloon was used to dilate the stent waist. Follow-up cholangiography confirmed excellent position and drainage. The patient’s liver function tests markedly improved following the procedure and she was discharged 3 days later in stable condition. Palliation of cholestasis is indicated for many patients presenting with malignant distal biliary obstruction. When ERCP fails, transhepatic and surgical biliary drainage are associated with significant morbidity. In this setting, EUS-directed biliary drainage methods including the creation of a choledochoduodenostomy using a lumen-apposing self expanding metal stent are safe and effective.

210 A Case of Cholangitis in a Burmese Immigrant to Arizona Shruti Mony, MD1, Mohit Pahuja, MD1, Abdul Nadir, MD2. 1. St. Joseph’s Hospital and Medical Center, Phoenix, AZ; 2. Maricopa Integrated Health System, Phoenix, AZ. Recurrent pyogenic cholangitis is typically seen in the Southeast Asian Population. We report a case of pyogenic cholangitis in a Burmese gentleman who migrated to USA a few years earlier. A 32- year-old male no underlying co-morbid conditions presented with epigastric pain, nausea, vomiting, anorexia and generalized weakness for two days. He complained of recurrent spells of these symptoms in the past. On examination he was tachypneic and tachycardic with epigastric tenderness, but no peritoneal signs. His labs showed normal WBC count with 90% neutrophils and total bilirubin elevated to 2.8. His blood cultures (2 of 2) grew gram negative bacteria which were pan sensitive. His CT abdomen with contrast showed an ill-defined 3.3x2.5cm region of abnormal enhancement at the confluence of right and left intrahepatic bile ducts. Both ERCP and MRCP showed multiple intrahepatic calculi with stricture in the common hepatic duct. A guidewire was passed through the common hepatic duct, but could not be passed into the left intrahepatic duct because of complete occlusion by a stone. Despite biliary sphincterotomy, and left hepatic stent placement, there was no adequate drainage. He underwent left hepatic resection, following which he dramatically improved and was discharged home in good condition. During his 8 week follow up, his stent was removed and he was doing well, with no recurrence of symptoms since surgery. The resected liver biopsy report, showed intraparenchymal biliary dilatation and numerous obstructing calculi, further justifying our diagnosis. A diagnosis of recurrent pyogenic cholangitis was made based on his demographic background, clinical presentation and radiological findings. This condition was first described in Chinese population in 1930 and has been described to be associated with infections including Clinorchis, Ascaris and liver flukes like Fascicola. The diagnosis of this condition is typically delayed and many clinical presentations including sepsis, fistula formation, cirrhosis, portal hypertension and cholangiocarcinoma have been described and high morbidity and mortality has been reported. Our case highlights that this condition can be seen in the USA among the immigrant population. A high index of suspicion among patients with typical symptoms should lead to prompt treatment including consideration of curative surgery as was accomplished in the described case.


Extracorporeal shock wave lithotripsy (ESWL) is a well established modality for management of urinary tract stones. It also plays an important role in the fragmentation of intraductal pancreatic stones, which are are often impacted and inaccessible for endoscopic removal. We present a case of non-typeable Haemophilus influenzae (NTHi) sepsis after pancreatic ESWL therapy without Endoscopic Retrograde Cholangiopancreatography (ERCP). A 62 year-old woman presented to the ED with severe abdominal pain. She had a history of type 2 diabetes that preceded the diagnosis of idiopathic chronic calcific pancreatitis 5 years ago. At that time, she had an ERCP with a stent placed in the pancreatic duct (PD) for 5 months to relieve an obstruction from a PD stone. She was pain free for 4 years until one month ago when she developed intermittent mild epigastric pain. She then had an ERCP which revealed a large pancreatic stone obstructing the PD, and was scheduled for ESWL. She received 2500 shockwaves delivered at max power with a dornier lithotripter with no immediate complications. Three days afterwards, she developed constant epigastric pain without radiation. She complained of subjective fevers, but no nausea, vomiting, or diarrhea. She had a pulse of 110 and a fever of 104°F. Her WBC count was 6.3 with 98% neutrophils. Amylase and lipase were normal. Liver enzymes were initially normal, but on day 2 the alkaline phosphatase spiked to 157, Total bilirubin to 1, direct bilirubin to 0.5, ALT to 107, and AST to 128, which all normalized by day 5. A non-contrast CT showed an atrophic pancreas with calcifications, but no acute findings. Abdominal ultrasound was negative for biliary pathology. She was given IV ciprofloxacin and flagyl, but continued to spike high fevers for two days. Blood cultures from admission grew pansensitive NTHi in 2/2 bottles and she was discharged on oral antibiotics. While antibiotic prophylaxis is not recommended for pancreatic ESWL or renal ESWL without UTI, it is recommended in gallstone ESWL to prevent the rare complication of cholangitis (evidence level III; recommendation level B). Our patient had sepsis from NTHi, which has been found to cause cholangitis in patients with diabetes and other significant comorbidities. Our case suggests that local irritation from ESWL may be enough to cause translocation of biliary flora. The prevalence of NTHi has increased since HiB vaccination. Due to fastidious growth requirements, laboratories may underestimate the prevalence of NTHi. ESWL is largely free of infectious complications, but this case highlights the importance of considering NTHi in patients with fever or prolonged pain after ESWL, whether or not there is intraluminal manipulation.

212 A Case of Post-transplant Lymphoproliferative Disorder (PTLD): Diffuse Large B-Cell Lymphoma (DLBCL) of the Jejunum Raj Shah, Richard Johnson. University of Missouri, Kansas City, MO. Introduction: G. lamblia filled pancreatic masses are a rarely reported entity. Furthermore, masses associated with cancer exist but only in a few case reports. Here we present a case of a G. lamblia filled pancreatic cystic mass in a patient with a recent history of T-cell, B-cell rich lymphoma. Methods: The authors performed a PubMed search using mesh terms of pancreas, mass, Giardia, and lymphoma. Case Description: A 53 year old gentleman status post 6 cycles of R-CHOP for T-Cell, B-Cell rich lymphoma (diagnosed: 11/13) presented to the ED for 1 week epigastric abdominal pain and nausea in 5/13. A CT abdomen found a 2.3 cm hypodense pancreatic cystic mass. FNA showed lymphocytes, reactive atypical epithelial cells, and numerous organisms consistent with Giardia lamblia. He was given metronidiazole 250 mg PO TID for 5 days. Discussion: Rare case reports have been found with Giardia lamblia in the pancreas. The pathologist indicated sheets of numerous Giardia in the sample making small bowel contamination less likely and G. lamblia aspirate from the pancreas more probable as the source. The authors hypothesize that this patient may have had chronic G. lamblia infection as a potential cause for the T-cell B-cell rich lymphoma manifestation. The patient reported travel to an area with possible exposure to G. lamblia 1 year prior to presentation for the lymphoma. During that time he had increasing abdominal pain, intermittent chronic diarrhea and inability to keep weight on. G. lamblia’s mechanism of actions have been hypothesized to involve, induction of pro-apoptotic factors, intestinal barrier dysfunction, upregulation of cell-cycle genes, and crypt hyperplasia. Conclusion: The mechanism of action of pancreatic masses filled with G. lamblia and the association of G. lamblia and cancer is still not fully understood. Further research must be done to help better understand these possible phenomena as it can help us better comprehend G. lamblia, its associations, and new cancer etiologies.

213 Retroperitoneal Abscess Presenting as an Incidental Finding Post Endoscopic Retrograde Cholangiopancreatography (ERCP) Amaninder Jeet Singh. Dhaliwal, MD1, Hernan Lopez-Morra, MD2, Taruna Bhatia, MD 3, Garen Derhartunian, MD4, Natasha Suleman, MD1, Alexander Vidershayn, MD1, Yitzchak Moshenyat, MD1. 1. NYU Lutheran Medical Center, Brooklyn, NY; 2. The Brooklyn Hospital Center, Brooklyn, NY; 3. Mount Sinai/The Brooklyn Hospital Center, Brooklyn, NY; 4. NYU Lutheran Medical Center, Glendale, CA. Background: ERCP is a well-recognized tool in the managment of choledocholithiasis. However, even with careful patient selection, complications happen. Among ERCP complications, perforation represents one of the most feared events at a rate of 0.5-2.1%. We report a case of 90-year-old female status post ERCP 3 weeks prior to admission, that presented with shortness of breath and was found to have an incidental retroperitoneal abscess on radiological imaging. Case Report: An 89-year-old female with past medical history of hypertension, presented with shortness of breath for four days. She underwent ERCP with sphincterotomy, mechanical lithotripsy and stent placement for choledocholithiasis. On admission, she was afebrile and tachycardic without abdominal pain. Physical examination revealed bilateral decreased breath sounds, coarse crackles and jugular venous distention. Laboratory values showed elevated liver enzymes (AST- 73 IU/L and


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ALT- 21 IU/L). Computed tomography (CT scan) of chest with contrast showed pulmonary emboli (PE) with moderate to large pericardial effusion with possible right heart strain. She was started on intravenous heparin drip for PE. Pericardiocentesis with pericardial biopsy was performed. Pericardial biopsy was positive for large B-cell lymphoma. Enhanced abdominal CT scan demonstrated an incidental finding of right-sided retroperitoneal abscess measuring 5.5 x 5.5 x 5.7 cm in dimension. Upper gastrointestinal series found no gross abnormalities of the stomach and duodenal bulb. One day after admission she developed a temperature of 100.8 F and was started on antibiotics. CT guided percutaneous drainage was performed with placement of right sided pigtail catheter. Gram stain and culture of fluid drained from retroperitoneal abscess did not grow any bacteria, since antibiotics were started prior to the draining of abscess. She completed six days course of antibiotics with complete resolution of symptoms. Discussion: Retroperitoneal abscess is a rare complication post ERCP most likely secondary to focal perforation and transmigration of bacteria. Patients could be asymptomatic or septic depending on the size of perforation and location of abscess. Early identification and treatment can lead to improved survival and better outcomes in patients with post ERCP complications.

[213C] Figure 3.

214 A United States Air Force Chaplain and His Atypical Presentation of Primary Biliary Cirrhosis Cassandra L. Craig, MD, Eric Plott, MD. Keesler AFB, Biloxi, MS.

[213A] Figure 1.

Military members are exposed to unique environments as a result of their active duty obligations, just as chaplains are. It is important to keep in mind the infectious diseases, environmental exposures, and chemical prophylaxis a chaplain in the United States Air Force (USAF) would be exposed to in their work. A previously healthy 57 year old active duty chaplain presented to clinic with complaints of disabling fatigue and low grade fevers having just returned from deployment to Eastern Africa. He was found to have an alanine aminotransferase (ALT) predominant elevation in liver function tests (LFTs) and was given an initial diagnosis of acute hepatitis of unknown etiology. He tested negative for Q-fever, was immune to Hepatitis A and B and had no evidence of Hepatitis C or E, Cytomegalovirus (CMV) or Epstein-Barr virus (EBV). Contemporaneously he was noted to have fluctuating titers of anti-mitochondrial antibodies (AMA) and anti-smooth muscle antibodies (ASMA). Initial liver biopsy revealed chronic biliary tract injury without ductopenia and previous parenchyma necroinflammatory injury. A second liver biopsy obtained eight months later was non-diagnostic. In the interim, his LFTs and antibody levels fluctuated while his fatigue improved. The patient was recently seen in gastroenterology (GI) clinic for routine follow up and found to have new elevations of LFTs and he was referred again for repeat biopsy. These results in conjunction with elevated AMA and alkaline phosphatase (AP) confirmed the diagnosis of primary biliary cirrhosis (PBC). The patient was started on therapy with prednisone, azathioprine, and ursodiol and will be followed up in GI clinic. Prevalence of primary biliary cirrhosis is reported as being 19 to 402 cases per million persons with the majority being female (90-95%). In a typical presentation of PBC, AP would be preferentially elevated. This patient had exposures to infectious diseases, antibiotics, antimalarial prophylaxis, analgesics, neuroleptics, and nonsteroidal anti-inflammatory drugs (NSAIDs) while deployed, all of which could lead to derangements in LFTs. It is unclear if his initial presentation was clouded by these exposures, however, his presentation to GI clinic was atypical and suggests the military population might represent a more difficult population to diagnose with PBC given their exposure risks.

215 Pancreatic Ductal Stent Placement for the Palliation of Pain in Patients With Pancreatic Adenocarcinoma, With and Without Pancreatic Ductal Dilatation Kavitha Nair, MD1, Parit Mekaroonkamol, MD2, Saurabh Chawla, MD2, Field Willingham, MD, MPH3. 1. Emory University School of Medicine, Atlanta, GA; 2. Emory University School of Medicine, Atlanta, GA; 3. Emory University, Atlanta, GA.

[213B] Figure 2.


Background: Endoscopic pancreatic duct stenting is commonly performed for pancreatic duct strictures and ductal dilatation. Though much less common than celiac plexus block, there are reports of the use of pancreatic duct stenting for the management of pain in patients with pancreatic cancer and pancreatic ductal dilatation. There are no published reports of pain relief with stenting in patients with pancreatic cancer without pancreatic ductal dilatation. Methods: A retrospective review was performed in two patients who underwent pancreatic duct stenting prior to a diagnosis of pancreatic carcinoma. Results: Two patients were evaluated for chronic abdominal pain. The first patient, was a 76 year-old male, with no significant past medical history who presented with greater than 6 months of worsening epigastric abdominal pain and a 22 pound weight loss. At the time of presentation, 2 computed tomography scans and magnetic resonance imaging had revealed pancreas divisum and pancreatic ductal dilatation without a pancreatic mass lesion. The second patient was a 41-year-old male with no significant past medical history who presented with chronic upper abdominal pain. His imaging had revealed an ill-defined retroperitoneal mass surrounding the proximal superior mesenteric artery (SMA). An EUS and biopsy had been negative for malignancy. The main pancreatic duct was not dilatated, and there was no intrahepatic biliary ductal dilatation. Both patients underwent ERCP with pancreatic duct stent placement (via the minor papilla and major papilla, respectively). Both patients experienced complete relief of


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Abstracts their pain and their stents were subsequently removed. A diagnosis of adenocarcinoma was subsequently established in both patients by EUS and CT guided biopsy respectively. Conclusion: Relative to celiac plexus block, pancreatic duct stenting is much less commonly used in the palliation of pain in pancreatic adenocarcinoma. In two patients initially with chronic pain but without a diagnosis of malignancy, pancreatic ductal stenting provided complete relief, both in the presence and in the absence of pancreatic ductal dilatation. Further investigation may help determine the role of stent placement as compared to other interventions in patients with and without dilatation of the main pancreatic duct.

216 A Rare and Elusive Cause of Gastrointestinal Bleeding: A Case of Hemosuccus Pancreaticus Shawn L. Shah, Bharat Maraj, Timothy B. Gardner, MD, MS. Dartmouth-Hitchcock Medical Center, Lebanon, NH. Hemosuccus pancreaticus is an exceedingly rare condition that results from bleeding from the ampulla of Vater via the pancreatic duct. Currently, there are less than 100 cases of hemosuccus pancreaticus that have been reported in the English literature. We report a case of a 53-year-old male with cerebral palsy and chronic pancreatitis who presented with a one-day history of severe epigastric pain along with hematemesis and hematochezia. Abdominal and pelvis computed tomography showed, in addition to acute on chronic pancreatitis, a heterogeneous fluid collection in the tail of the pancreas with numerous foci of extra-luminal and extra-cavitary air, concerning for an infectious process or fistula. An esophagogastroduodenoscopy and colonoscopy performed the following day revealed no active source of bleeding. An endoscopic retrograde cholangiopancreatography was then performed given the aforementioned fluid collection, and revealed blood extruding from the ampulla of Vater, suggestive of hemosuccus pancreaticus. The pancreatic duct was then cannulated, resulting in copious bright red blood from the rectum. The patient became hemodynamically unstable and an emergent mesenteric arteriography was performed with vascular occlusion of the proximal splenic artery. The patient was ultimately discharged on hospital day 5 with no further episodes of bleeding. Hemosuccus pancreaticus is a rare cause of upper gastrointestinal bleeding in patients with chronic pancreatitis, pancreatic pseudocysts, and pancreatic tumors. Prompt recognition and intervention, either by embolization or surgery, can lead to control of this potentially life-threatening bleed.

nied with dehydration without the elevation of hepatobilially and pancreatic enzyme, inflammation, and anemia. In the endoscopic ultrasound (EUS), the rupture of pseudoaneurysm in duodenal mucosa was suspected because the communication between cyst and duodenal vessel was assumed. After the embolization with coil by angiography, the cyst was decreased once at least. Five month after the first admission, he visited emergency room with nausea and frequent vomiting. The CT showed the recurrence of duodenal stenosis with dilatation of the stomach. Duodenal submucosal cyst was observed and duodenal lumen was almost occulted. Endoscopic aspiration was performed by EUS and bile with high levels of amylase was obtained. Endoscopic nasal drainage tube was placed to the cyst. Although the communication between main bile duct and duodenal cyst could not be detected by enhancement of drainage tube and endoscopic retrograde cholangiopancreatgraphy (ERCP), the character of fluid aspirated by drainage tube suggested choledochal cyst which is formed intermittently. Discussion: Choledochal cyst is classified five types according to Todani classification. Type III cyst which is characterized by their intraduodenal location at the pancreaticobiliary junction comprise 1% to 4%. Common presentations are abdominal pain and jaundice associated with cholangitis and pancreatitis. This case is very rare because type III choledochal cyst is found for the first time with the symptom of frequent vomiting by duodenal occlusion without any cholangitis or pancreatitis. Since 10-30% of choledochal cyst is reported to develop biliary malignancies, the precise diagnosis and close follow up of choledochal cyst is supposed to be important when the duodenal submucosal cyst is observed.

218 Endoscopic Ultrasound-Guided, Needle-Based Probe Confocal Laser Endomicroscopy (nCLE) of Intrapancreatic Accessory Spleen: Case Report and Literature Review Jose M. Nieto, DO, FACG1, Amanda B. Bastidas, MD2, David Holloman, MD3, Ali Lankarani, MD4. 1. Borland Groover Clinic, Jacksonville, FL; 2. Universidad de Especialidades Espiritu Santo, Jacksonville, FL; 3. Baptist Medical Center, Jacksonville, FL; 4. Borland Groover Clinic, St. Johns, FL. Introduction: Accessory spleens are often incidental findings on imaging and usually present as a solid mass at splenic hilum or other organs such as pancreas. Most patients with accessory spleens are asymptomatic however abdominal pain has been associated with an accessory spleen. Intrapancreatic accessory spleen (IPAS) can mimic a pancreatic neuroendocrine tumor (NET) on imaging studies and therefore posing a diagnostic dilemma. We present a case of IPAS in which the concomitant use of nCLE and fine needle aspiration (FNA) helped make the diagnosis. A 24 year old female referred for EUS for a pancreatic mass on CT scan. She presented with abdominal pain and during the workup a 3cm x 2.9cm round hypervascular hypodense mass in the tail of the pancreas was found. Her past medical history is significant for second degree relative with pancreatic cancer. Patient has a past medical history of Thrombotic Thrombocytopenic Purpura (TTP) and she underwent splenectomy 5 years ago for profound thrombocytopenia. On EUS a 2.8cm x 2.9cm round homogenous hypoechoic mass in pancreatic tail was identified. Initially the mass was punctured using a 19-G needle that was pre-loaded with AQ-Flex 19 probe inside the needle before puncture in lieu of the stylet. Fluorescein (2.5mL of 10 % fluorescein sodium) was injected simultaneously with probe insertion. Numerous thick white bands with floating small black particles inside the bands suggestive of network of blood vessels and floating Erythrocytes. Interrogation of the mass did not identify any finger-like papillary projections, crypt-like structures or dark aggregates of cells which is seen in a villous structure or neoplastic cells. Then 4 passes using a 22 G FNA needle was performed with onsite pathology and endomicroscopy review supported the final diagnosis of IPAS. Discussion: Accessory spleen is a rare entity which can be seen in the splenic hilum or at the tail of the pancreas. In 3000 autopsies reported by Halpert et al, 364 accessory spleens were found in which 17%

[216A] Figure 1.

217 Choledochal Cyst with Duodenal Occlusion; A Rare Case Report Seiichiro Fukuhara1, Takahisa Shiraishi1, Naofumi Kamioka1, Akihiko Ikura2, Yuu Aoki1, Ken Teramoto1, Toshihiko Higashizawa2, Yukishige Okamura2. 1. Sano Kousei General Hospital, Gastroenterology and Hepatology, Tochigi, Japan; 2. Sano Kousei General Hospital, Gastroenterology and Hepatology, Sano, Japan. Introduction: Choledochal cyst is a congenital anomaly defined as dilatation of the extrahepatic bile duct usually associated with pancreaticobiliary maljunction. Majority of choledochal cyst cases are diagnosed in infants and young children within the first decade of life. It is unusual to be found without any abnormality of hepatobiliary and pancreatic enzyme in blood test. Case report: The patient is a 69 year-old male with hyperlipidemia and diabetes who visited our hospital by right upper quadrant pain and frequent vomiting. The computer tomography (CT) showed notable gastric dilatation with duodenal stenosis. After the admission, huge duodenal submucosal cyst was observed by upper endoscopic examination. The blood exam revealed mild renal dysfunction accompa-


[218A] Figure 1.


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[218B] Figure 2.

[219A] Figure 1.


were IPAS. Accessory spleens can be acquired entities (splenosis) which is the auto transplantation of splenic tissue in abnormal locations as a result of trauma or post splenectomy. This is the first case that incorporates real-time endomicroscopy and onsite pathology to diagnose IPAS. Patients with IPAS may undergo distal pancreatectomy because they mimic a hypervascular NET on CT and MRI scans. Onsite pathology and endomicroscopy review increases the diagnostic accuracy for differentiating between IPAS and pancreatic NET. In patients with a hypervascular mass in the tail of pancreas addition of real time nCLE to traditional FNA can increase the diagnosis yield of EUS and potentially prevent unnecessary surgery.

219 Diffuse Involvement of Mixed-Type IPMN Kevin B. Patel, MD, Peter J. Sargon, MD, Jennafer Ottenheimer, MPH, PA-C, Smita Patel, MD, A. Aziz Aadam, MD. Rush University Medical Center, Chicago, IL. Introduction: The malignant potential of intraductal papillary mucinous neoplasm (IPMN) of the pancreas is associated with involvement of the main pancreatic duct. We present a case of a multi-cystic IPMN involving the main pancreatic duct and its side branches. Case: A 72-year-old male with a medical history of stroke and tobacco use presented with a 3-week history of abdominal pain, along with unintentional weight loss of 40 lbs over the last year. A CT scan


[219C] Figure 3.


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Abstracts showed a grossly abnormal pancreas with a multi-macrocystic mass centered at the head of the pancreas, measuring approximately 5.7 cm x 7.0 cm. The extrahepatic and intrahepatic bile ducts demonstrated marked dilatation. Laboratory evaluation was significant for total bilirubin 3.8 mg/dL, alkaline phosphatase 758 U/L, AST 79 U/L and ALT 107 U/L. The patient underwent EUS showing multi-cystic replacement of the majority of the pancreas parenchyma. The pancreatic duct was dilated to 12 mm in the head of the pancreas. The common bile duct was dilated to 17 mm and abruptly terminated in the head of the pancreas due to the obstructing cyst. Cyst aspirate was performed and sent for analysis. Cytology of the cystic fluid showed acute inflammatory cells and proteinaceous debris, suggestive of a pseudocyst. The fluid amylase and CEA were elevated to 10,205 U/L and >1500 ng/mL, respectively. Serum CA 19-9 was elevated to 230 U/mL. These findings are consistent with a mixed-type IPMN, which has a similar risk for malignancy as a main-duct IPMN. According to the Fukuoka guidelines, this patient had high-risk stigmata of malignancy including obstructive jaundice and main pancreatic duct > 10 mm. Therefore, he underwent a total pancreatectomy with pathology revealing invasive mucinous carcinoma arising in the background of extensive IPMN. The surgical margins were free of involvement, and he is being treated with adjuvant chemotherapy. Discussion: Multi-cystic lesions of the pancreas can often appear as pseudocysts, but may in fact represent mixed-type IPMN. Most IPMNs are solitary, but 5-10% involve the entire gland. Further evaluation of these lesions is essential, as mixed-type IPMN carries a similar risk of malignancy as main-duct IPMN.

220 A Unique Cause of Painless Jaundice Caroline R. Jouhourian, MD, Moises Guelrud, MD. Tufts Medical Center, Boston, MA. Background: Kaposi sarcoma (KS) is a virally transmitted vascular tumor associated with the human herpes virus 8 (HHV-8). Although having four epidemiologic forms, KS is often associated with AIDS. Due to the advent of antiretroviral therapy, the incidence of AIDS related KS has declined to 10%. Despite

[220C] Figure 2.

this decline, KS remains the most common HIV associated gastrointestinal (GI) malignancy with our knowledge limited to case reports. AIDS related KS often presents with cutaneous lesions but in 25% of patients manifests in the visceral organs. GI involvement typically presents with asymptomatic or bleeding mucosal lesions predominantly in the stomach and duodenum. Biliary tract involvement has been seldomly reported and usually occurs with pancreatic and hepatic infiltration. We present a unique case of AIDS related KS presenting with painless jaundice due to ampullary involvement and discuss the management of the patient. Case: A 28 year old cachectic male with AIDS, not on therapy, presented with complaints of fatigue and painless jaundice. Blood work revealed a transaminitis in the 300 IU/L range, an alkaline phosphatase of 384 IU/L, and a total bilirubin of 5.2 mg/dL. Concern for AIDS cholangiopathy prompted an endoscopic retrograde cholangiopancreatography (ERCP) which revealed a normal cholangiogram, however an abnormal appearing ampulla was noted and thus biopsied (picture 1). A plastic biliary stent was subsequently placed. Pathology revealed a Kaposi sarcoma (picture 2). He was started on HAART therapy and alpha interferon with doxorubicin with subsequent regression of the tumor (picture 3) and amelioration of his liver function test. Conclusion: KS is an AIDS defining disease. With our increased understanding of HIV and advancement in treatment, the incidence of KS has dramatically declined. GI manifestations of KS are even rarer with seldom, if little, biliary involvement. Our case highlights a unique presentation of painless jaundice in an HIV patient that stresses the need for consideration on a differential. Additionally, we describe non-surgical management of the lesion.

[220A] Figure 1.

221 An Unusual Presentation of a Mediastinal Pseudocyst Mindy W. Lee1, Srinivas G. Gunturu, MD2, Sammy Ho, MD1. 1. Montefiore Medical Center, Bronx, NY; 2. Montefiore Medical Cente-Wakefield, Bronx, NY.

[220B] Figure 2.


Pancreatic pseudocysts can present in atypical locations. This case highlights the diagnostic and therapeutic challenges associated with mediastinal pseudocysts. A 50- year-old man presented with a 3-day history of dyspnea and chest pain. He had a history of congestive heart failure, recurrent pleural effusions, a prior episode of pulmonary embolism and chronic alcoholic pancreatitis. On arrival, he was hypoxic and hypotensive. Chest radiograph showed a large left pleural effusion. Thoracentesis removed 2000cc of cloudy fluid with stabilization of respiratory status. Pleural fluid analysis showed an amylase level of >7500 U/L and a lipase level of 22149 U/L. CT showed a large lobulated cystic mass measured 10.2 X 8.5 X 17.8 cm from the pancreatic head, extending superiorly into the mediastinum with a thin communicating tract extending superiorly from the pancreatic duct. ERCP with pancreatic sphincterotomy was performed; a 7Fr X 15cm transpapillary stent was placed into the pseudocyst. Patient symptomatically improved. Repeat CT 5 days later showed marked decrease in pseudocyst size. Repeat CT at 10 weeks showed complete resolution of the pseudocyst and pleural effusion. Transpapillary stent was then removed without complications. Atypical pancreatic pseudocysts can represent a diagnostic and therapeutic challenge. Atypical locations can include liver, spleen, kidneys and mediastinum. The most common cause of pancreatic pseudocysts is acute or chronic alcohol induced pancreatitis. Mediastinal pseudocysts present most commonly with abdominal pain, followed by dyspnea from direct space occupation or recurrent pleural effusions, and compressive symptoms i.e. dysphagia. It has been reported that between 54% and 90% of mediastinal pseudocysts have an associated pleural effusion. Therapeutic modality depends on the presence and identification of fistula, ductal anatomy and experienced interventionist. Endoscopically, EUS- guided drainage and ERCP have shown to be > 90% effective in the treatment of mediastinal pseudocysts. This case report demonstrated a successful treatment of a mediastinal pseudocyst using a transpapillary stent.


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present in the early postoperative period, late-onset pseudoaneurysms do occur, though much more rarely. We report a case of massive lower gastrointestinal hemorrhage in a 58-year-old female with a history of enteric-drained pancreatic transplant and donor duodenum anastomosis to recipient jejunum. This transplant occurred 7 years prior but 1 year prior the pancreatic graft failed as insulin-dependent diabetes mellitus recurred. Around the same time, a small bowel obstruction occurred requiring a small bowel resection with primary anastomosis. The bleeding episode began with the patient initially presenting in hypovolemic shock from hematochezia and an acute hemoglobin drop to 5.5 g/dL. Upper endoscopy was unremarkable, and colonoscopy revealed blood within the colon and the terminal ileum but no source could be identified. An abdominal angiogram and tagged RBC study were also unable to identify a source of gastrointestinal hemorrhage. CT angiogram of the abdomen revealed a mid-right common iliac artery pseudoaneurysm at the failed pancreatic graft site. Deployment of a covered stent across this vascular structure resulted in controlling the active extravasation into the small bowel lumen. Follow-up abdominal CT showed an excluded thrombosed pseudoaneurysm. In summary, we report this case to emphasize the diagnostic challenges associated with identifying this rare but life-threatening and at times late-onset complication of enteric-drained pancreatic transplant.

223 Peripheral Intrahepatic Biliary Stones Removed Using a Hybrid Percutaneous and Endoscopic Approach Peter J. Sargon, MD, Jennafer Ottenheimer, MPH, PA-C, A. Aziz Aadam, MD. Rush University Medical Center, Chicago, IL.

[221A] Figure 1.

Introduction: Intrahepatic biliary stones pose a challenge to endoscopic removal with low rates of success with treatment and high recurrence rates. Therefore, at this point, surgical resection of the affected lobe has a primary role in the treatment of hepatolithiasis. However, alternative treatment options should be considered in patients in whom surgery is not an option. Case Report: A 57 year-old male with a history of HBV cirrhosis who underwent a liver transplant 11 years ago presented with fever and abnormal liver enzymes. He was found to have E. Coli bacteremia with abnormal ultrasound and MR imaging of the abdomen significant for left intrahepatic biliary dilatation and left intrahepatic calculi with presence of microabscesses. Given his history of liver tranplantation, surgical resection was not an option. Interventional radiology performed a percutaneous transhepatic cholangiogram with placement of an internal-external biliary drainage catheter. Eight weeks later the patient underwent a hybrid percutaneous and endoscopic procedure. To address the biliary stones. A guidewire was inserted into the existing drainage catheter and exchanged for a 12 Fr sheath. Cholangioscopy using the Spyglass (Boston Scientific, Natick, MA) platform was performed through the sheath. Multiple biliary stones were visualized within the left hepatic duct. Electrohydraulic lithotripsy was performed using irrigation with 0.9 normal saline. All visualized stones were fragmented into sand like particles. The fragments were flushed distally into the small bowel. Subsequent cholangiogram confirmed clearance of all stones. The patient is now six months post-procedure and doing well without recurrence. Conclusion: Hepatolithiasis typically poses a clinical challenge often requiring surgery. Our case illustrates a minimally invasive hybrid approach utilizing interventional radiology techniques along with direct cholangioscopy to allow complete fragmentation and clearance of hepatolithiasis.

224 Is There an Association of Pancreatic Cancer With Sarcoidosis? Praneet Wander, MD1, Adedapo Iluyomade1, Arunpreet Kahlon2, Aakash Aggarwal1. 1. Mount Sinai St. Luke’s Roosevelt Hospital Center, New York, NY; 2. SUNY upstate Medical University, Syracuse, NY.

[221B] Figure 2.

222 Graft Pseudoaneurysm Hemorrhage in a Patient With a History of an Enteric-Drained Pancreatic Transplant: A Case Report Marielle Reataza, MD1, Farid Jalali, MD1, Jason B. Samarasena, MD1, C. Gregory Albers, MD, FACG2. 1. University of California Irvine, Orange, CA; 2. University of California Irvine Medical Center, Orange, CA.

Sarcoidosis is a chronic granulomatous disease, usually affecting the lungs and intrathoracic lymph nodes. It has been reported to have association with certain malignancie. We describe a case of pancreatic mucinous adenocarcinoma, found to have sarcoidosis on autopsy. 67 year old Caucasian male with past medical history significant for Chronic Obstructive Pulmonary Disease, Diabetes mellitus Type II, coronary artery disease and hypothyroidism presented to his primary care physician with 20 lbs weight loss over a period of one year. Laboratory findings showed abnormal liver function tests with ALT, AST, Alkaline phosphatase of >200U/L, >200U/L, >1200 U/L respectively, Bilirubin direct- 5mg/dl, total 7mg/dl, Albumin 2g/dl. Thyroid function and diabetes were well controlled. CT abdomen revealed a mass in pancreatic head along with peripancreatic lymph node enlargement suspicious for neoplasm. Endoscopic ultrasonographically guided biopsy was positive for mucinous pancreatic adenocarcinoma. Patient suffered from acute cholangitis and pancreatitis as a result from intervention into his biliary system. He developed sepsis and was hospitalized. A thoracic CT scan showed incidental finding of hilar and mediastinal lymph node enlargement. Few months later he died as a result of complications from pancreatic adenocarcinoma. An autopsy was requested by the family which revealed non-caseating granulomatous inflammation of hilar and mediastinal lymph nodes consistent with sarcoidosis. Sarcoidosis associated with malignancy is termed as sarcoid-like reaction(SLR) and is seen in lymph nodes draining primary tumors and extranodal sites. They do not usually have classical sarcoidosis clinical features and lab findings. Immuno-histologically, SLR has B cell positive granulomas compared to B cell negative in sarcoidosis. These occur as part of T cell-mediated response to antigenic factors shed by tumor cells or released during tumor necrosis, which is carried to lymph nodes and cause “hypersensitivity-like” reaction producing non-caseating granulomas. SLR has been described to occur with lung, skin cancer and lymphomas. We describe a rare case of sarcoidosis/SLR associated with pancreatic mucinous adenocarcinoma. Literature on sarcoidosis and SLR with pancreatic cancer is scarce, although isolated cases have been reported. This provides a diagnostic riddle to evaluate lymphadenopathy with pancreatic malignancy before considering staging and deciding management options.

Graft pseudoaneurysm is a rare but life-threatening complication in patients who have undergone pancreatic transplantation. While most of the reported post-pancreatic transplantation pseudoaneurysms



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Abstracts 225 Plate-like Atelectasis Mimics Pneumoperitoneum in Patient With Acute Gangrenous Cholecystitis: A Very Diagnostic Challenge

right hemidiaphragm from plain film. If the clinical presentation is not typical for hollow organ perforation, computed tomography is indicated to avoid unnecessary exploratory laparotomy. References: [1]. Westcott JL, Cole S. Plate atelectasis. Radiology. 1985;155(1):1-9. [2]. Mc CJ. Radiographic signs of acute suppurative cholecystitis. California medicine. 1959;90(2):139-43.

Narisorn Lakananurak. King Chulalongkorn Memorial Hospital, Bangkok, Thailand. Purpose: Though plate-like atelectasis can occur in patient with acute cholecystitis, it is normally in linear shape and easily to differentiate from pneumoperitoneum. We present a case with convex platelike atelectasis at lower lung zone that looks very similar to free air under right hemidiaphragm. It is very difficult to differential diagnosis from hollow organ perforation that need emergency surgical management. Case: A 81-year-old man was admitted to King Chulalongkorn Memorial Hospital with a 1-day history of right upper quadrant abdominal pain and high grade fever. His past medical history was significant for diabetes mellitus, hypertension, dyslipidemia and asymptomatic gallstone. On physical examination, his vital signs were as follow: body temperature 38.9 °C, blood pressure 140/80 mmHg, and pulse rate 110 beats per minute. Abdominal examination revealed diminished bowel sound, moderate distension and tenderness with voluntary guarding at right upper quadrant without rebound tenderness. The initial laboratory showed leukocytosis with neutrophil predomination and normal liver function test. The acute abdominal series was done and suspected free air under right hemidiaphragm. (figure 1) The computed tomography of the abdomen showed convex platelike atelectasis at right lower lung zone without pneumoperitoneum. The gallbladder was distended with cystic duct obstruction from a large gallstone. (figure 2) After 1 day of empirical antibiotic with ceftriaxone and metronidazole, his symptom was deteriorated with sign of peritonitis at right upper quadrant. Laparotomy was done and revealed acute gangrenous cholecystitis without perforation of gallbladder. His condition dramatically improved after cholecystectomy and he was discharged from the hospital 3 days later. Discussion : Plate-like atelectasis is usually band-like and frequently perpendicular to a pleural surface. It is usually seen in patients with low lung volumes due to hypoventilation, rather than bronchial obstruction. (1) In acute cholecystitis, plate-like atelectasis of right lung base can be seen around 4% from plain radiography. (2) We reported a very rare case of convex plate-like atelectasis that mimics free air below

226 Recurrent Pyogenic Liver Abscesses Secondary to Retained Surgical Metal Coil Within the Bile Duct Jennafer Ottenheimer, MPH, PA-C, Peter J. Sargon, MD, Shubha Singh, A. Aziz Aadam, MD. Rush University Medical Center, Chicago, IL. Introduction: Recurrent pyogenic abscesses are typically caused by bile stasis or stone formation proximal to biliary strictures leading to recurrent episodes of cholangitis. The Southeast Asian population is affected at a higher rate than others with an epidemiologic association with biliary parasites, which are endemic to the area. However, there is no conclusive evidence supporting the role of these infections in the pathogenesis of recurrent pyogenic cholangitis. We present a unique case of iatrogenic recurrent pyogenic cholangitis. Case Report: A 53 year-old female with a history of recurrent hepatic abscesses presented to our hospital with jaundice. She had a strong history of autoimmune disease including mixed connective tissue disease, dermatomyositis, and Hashimoto’s thyroiditis. Her past surgical history was significant for cholecystectomy and common bile duct exploration. Abnormal labs included elevated WBC 23.5 k/ mcL and elevated liver enzymes including AST 96 U/L, ALT 47 U/L, ALP 268 U/L, and total bilirubin 21.7 mg/dL. MRI abdomen was significant for multiple abscesses within the left lobe of the liver with largest measuring 3.7 cm x 2.1 cm with bile ducts seen leading to the abscess, suggesting possible communication with the biliary tree. Intra and extrahepatic biliary ductal dilatation was visualized with a 9 mm filling defect within the distal common bile duct. ERCP was performed for further evaluation. Cholangiogram was abnormal with multiple fi lling defects within the CBD as well as a metal coil moving freely within the bile duct. Biliary sphincterotomy and multiple balloon sweeps were performed with extraction of sludge and stones. The metal coil was brought down to the ampulla and removed with rat-tooth forceps. Two straight plastic biliary stents were placed side-by-side individually under fluoroscopic guidance. Excellent biliary drainage was subsequently noted. We identified the metal coil as a surgical item that was retained in the patient’s bile duct after her cholecystectomy with common bile duct exploration. Subsequently, the patient was treated with antibiotics and is now doing well s/p repeat ERCP with removal of previously placed biliary stents and without recurrence of hepatic abscesses. Conclusion: The incidence of retained surgical items varies from 1:1000-1500 to 1:5500-18670. The majority of patients with retained surgical items are symptomatic with abdominal pain being the most common complaint. Our patient was unique and unfortunate in that she developed recurrent pyogenic abscesses from the retained surgical metal coil.

227 Endoscopic Ultrasound-Guided Gastrojejunostomy With Use of Lumen-Apposing Covered Metal Stent (LACMS) for Treatment of Afferent Loop Syndrome Jose M. Nieto, DO, FACG1, Kelli Hathaway, BSN1, Ali Lankarani, MD2. 1. Borland Groover Clinic, Jacksonville, FL; 2. Borland Groover Clinic, St. Johns, FL. Introduction: Afferent loop syndrome (ALS) is a complication that can occur after abdominal surgery causing obstruction to the afferent jejunal loop. ALS occurs when something traps the flow of bile up to and past the surgical anastomosis into the digestive system. The accumulation of bile acid and pancreatic juice causes pressure and occlusion in the afferent limb. Common causes of ALS may be twisting or kinking of the afferent loop, scar tissue, ulceration, or cancer. The incidence of patients developing ALS after a

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Whipple procedure may be as high as 13%. A patient with ALS is most likely to present with symptoms of cholangitis, abdominal pain, nausea, fullness after eating and sudden vomiting of bilious fluid (Pannala et al). ALS can be lethal if not treated promptly. The most common treatment for ALS is surgery. This is the first case reported using a cold AXIOS stent for the treatment of ALS. Case Description: The patient is a fifty-one year old male who has a history of pancreatic adenocarcinoma, chronic pancreatitis and post Whipple procedure in August 2013. The patient presents with severe abdominal pain and nausea. Afferent loop obstruction was confirmed on CT. A percutaneous internal-external drain was placed but unsuccessful in treatment. Endoscopic ultrasound revealed severe stenosis of the pancreatoduodectomy afferent limb anastomosis. A novel technique using EUS guided cold AXIOS under fluoroscopy guidance was performed. A 10 mm x 15 mm AXIOS (LACMS) was placed creating a gastro-jejunal anastomosis with decompression of the afferent jejunal limb. Thirty day follow up showed decompression of the afferent limb and proper stent placement. Discussion: Diagnosis of ALS is most often made by abdominal ultrasound, CT, or chlangiography (Yao, et al). Prior to endoscopic and percutaneous techniques, the most common treatment of ALS was surgery. The most commonly used non-surgical treatment of ALS is the percutaneous approach. This case presents the treatment of ALS using a novel endoscopic technique with placement of a cold AXIOS (LACMS) stent for the creation of a gastro-jejunal anastamosis for decompression of the afferent limb. Evidence has shown the endoscopic approach to be an effective treatment for ALS and have less procedure-related complications than other alternatives (Burdick, et al).

Case Report: A 58 year old male with no significant past medical history had a CT of the abdomen performed at an outside hospital after sustaining a fall. In addition to a rib fracture, a 2 cm mass was visualized in the head of the pancreas. A follow up MRI confirmed a 1.8 cm enhancing lesion in the pancreaticoduodenal groove. The patient was referred for endoscopic ultrasound (EUS). Standard upper endoscopy was first performed revealing a subepithelial lesion in the second portion of the duodenum. During EUS, a round well-demarcated, 2 cm hypoechoic mass was visualized in the periampullary region. The pancreas parenchyma was normal throughout the pancreas. The common bile duct and pancreatic duct were normal in caliber and tapered normally to the ampulla. EUS guided fine needle biopsy was performed and histology demonstrated spindle cell proliferation and immunohistochemistry was positive for DOG-1, CD117, CD34, and SMA, consistent with a GIST. The patient is currently awaiting surgery for planned wedge resection. Conclusion: Duodenal GISTS are rare, accounting for 3-5% of GISTS and are especially uncommon in the periampullary region. Our case illustrates the importance of EUS with fine needle biopsy which determined the pancreas was not involved and also confirmed the diagnosis of GIST based on immunohistochemistry, allowing the patient to undergo a less invasive surgical option.

229 Choledochal Cyst Complicated With Pancreatic Adenocarcinoma in an Adult Sridivya Parvataneni1, Dhara Chaudhari1, Puneet Goenka2, Mark Young, MD1. 1. East Tennessee State University, Johnson City, TN; 2. East Tennessee State University, Johnson City , TN.

228 Periampullary GIST Masquerading as a Pancreas Mass Jennafer Ottenheimer, MPH, PA-C, Peter J. Sargon, MD, A. Aziz Aadam, MD. Rush University Medical Center, Chicago, IL.

Introduction: Choledochal cyst is a rare disease of the biliary tract. Though diagnosis of a choledochal cyst is often made during childhood, 25% of patients are seen as adults. We present an adult patient who presented with obstructive jaundice and found to have pancreatic adenocarcinoma and type III choledochal cyst.

Introduction: Gastrointestinal stromal tumors (GISTs) rarely affect the periampullary region, with only a few anecdotal cases reported in the literature.

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Abstracts insulin or heparin along with fenofibrates. A 34 year old obese Hispanic female with past medical history of hyperlipidemia (HPL) presented to the emergency room with a chief complaint of 3 days history of progressively worsening severe epigastric pain radiating to her lower back, associated with nausea and vomiting. She had no prior similar episodes. Her personal, family, medication and social history was unremarkable except occasional alcohol drinking of the standard one to two drinks every month, but prior to this ER visit she reported drinking more than 3 standard drinks per day for the past 2 days. Relevant laboratory tests revealed mild hyponatremia of 130 mEq/L, lipase of 1039 U/L, with a normal calcium, blood glucose (BG) and liver function tests, but the serum was abnormally milky white in appearance. The lipid panel revealed triglycerides (TG) > 3000 mg/dl. An abdominal ultrasound showed non-obstructive cholelithiasis with a common bile duct size of 7 mm. She was managed conservatively with AP treatment guidelines, but due to severe hypertriglyceridemia (SHTG) and symptoms she underwent one session of plasmapheresis with albumin replacement. The TG subsequently trended down to 349 mg/dl and she was advanced on a low fat diet and Fenofibrate. Follow-up TG after 1 month was 80 mg/dl. HTGP is clinically evident when levels are > 1000mg/dl and is classified as SHTG and very severe HTG for levels > 2000 mg/dl. The goal of the treatment is lowering the TG levels to < 250 mg/dl and identifying the underlying cause. Patients with HTGP have higher chances of recurrent AP than pancreatitis from other causes. There is evidence of improvement in symptoms as well as lowering TG levels with IV insulin in patients with HTGP and marked hyperglycemia, but in patients with normal BG levels treatment of HTGP is not very well defined. Our patient was treated with plasmapheresis leading to a significant improvement in her TG levels, clinical and laboratory parameters in a relatively short time leading to a shorter hospital stay. Currently there are no guidelines for the use of plasmapheresis in treatment of HTGP. Plasmapheresis seems to be an effective method for the treatment of HTGP and an important area of future research, especially in patients with severe AP and normal BG levels.

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232 Gallbladder Agenesis With Refractory Choledocholithiasis

Case: 81 year old male with newly diagnosed diabetes mellitus presented to hospital with weight loss and yellow discoloration over the last 4 weeks. Patient was found to have total bilirubin 3.3 g/dl, alkaline phosphates 847 IU/L, and minimal elevation of aspartate and alanine transaminase. Magnetic resonant imagining was concerning for pancreatic mass (figure 1) and endoscopic ultrasound revealed a mass lesion in pancreatic head which was suspicious for malignancy on biopsy. Endoscopic retrograde cholangiography (ERCP) revealed cystic dilatation of the ampulla consistent with a type III choledochal cyst (figure 2). The guidewire was placed into the pancreatic duct. The papillotome was repositioned, and placed into the bile duct/cystic portion. Attempted placement of the wire into a narrowed segment proximal to the cyst after multiple attempts were unsuccessful and further filling revealed a stricture in the bile duct. Patient underwent Roux-en-Y choledochojejunostomy. The surgery revealed type III choledochal cyst and pancreatic head adenocarcinoma by surgical biopsy. Patient is currently doing well with normalization of laboratory values. Discussion: Type III Choledochal cyst is a pediatric diagnosis. The age of presentation and the association of pancreatic head mass with type III cyst are unique in our case. The other key point is that inability of imaging to discover the cyst poses high need for clinical suspicion.

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Jamie Tjaden, MD, Kevin Patel, MD, Peter J. Sargon, MD, Jennafer Ottenheimer, MPH, PA-C, A. Aziz Aadam, MD. Rush University Medical Center, Chicago, IL. Introduction: Congenital agenesis of the gallbladder is a rare anomaly which is usually asymptomatic and found incidentally. Case Report: A 63 year-old female presented with jaundice and right upper quadrant abdominal pain with nausea and vomiting. Her liver enzymes were elevated in a mixed cholestatic and hepatocellular pattern. An abdominal ultrasound failed to adequately visualize the gallbladder attributed to the patient’s obesity, but a structure adjacent to the duodenum with a small calcification was presumed to be a contracted gallbladder with small stones. There was lack of extrahepatic bile duct dilation. Based on these findings an endoscopic ultrasound (EUS) was done demonstrating a dilated common bile duct to 13 mm along with extensive choledocholithiasis. An ERCP revealed numerous large stones within the common bile duct up to 15 mm in size. Sphincterotomy with balloon sweep was performed, however two large stones 15 mm in size could not be extracted. One week later, ERCP with mechanical lithotripsy (ML) was done with partial stone extraction. A repeat ERCP was performed utilizing electrohydraulic lithotripsy (EHL), resulting in reduction of the common bile duct stones by 30-50%. Another ERCP six weeks later utilizing ML was repeated, but the stones remained impacted in the common bile duct. Due to the patient’s refractory choledocholithiasis despite ML and EHL, the decision was made to perform external shock wave lithotripsy (ESWL). ESWL was successfully performed with complete fragmentation of the remaining stones. A final ERCP was done successfully extracting all the stone fragments. The patient was

Infective Portal Vein Thrombosis: A Rare Complication of Pancreatitis Hussein Al-Hamid1, Wuttiporn Manatsathit, MD2, Leonard Johnson, MD3, Mohammed Barawi, MD3. 1. Providence Hospital, Southfield, MI; 2. Albert Einstein, Grosse Pointe Woods, MI; 3. St. John Hospital and Medical Center, Grosse Pointe Woods, MI. Introduction: “Pylephlebitis” or infective suppurative thrombosis of the portal vein is a rare condition with a 30-80% mortality rate. Most cases are associated with intra-abdominal sepsis. Diverticulitis and appendicitis are the primary foci in most reported cases. Only 5% of cases are associated with pancreatitis. Case: A 38-year-old African American female with recent history of alcoholic pancreatitis complicated by pseudocyst status post endoscopic retrograde cholangiopancreatography (ERCP) with pseudocyst drainage presented with acute abdominal pain, fevers, nausea and vomiting. Physical examination revealed normal heart rate and blood pressure. Abdominal exam was significant for severe epigastric tenderness and palpable liver margin. Laboratory values included WBC 10.5, hematocrit 23.6, lipase 31, alkaline phosphatase 144 and normal hepatic transaminases. Contrast enhanced computerized tomography scan of the abdomen showed acute portal vein thrombosis with multiple low-density lesions within the liver suggestive of abscesses. Blood cultures grew the anaerobic bacteria Eubacterium aerofaciens. The diagnosis of infective suppurative thrombosis of the portal vein was rendered. Parenteral antibiotics and anticoagulation were initiated. CT-guided drainage of the largest liver abscess was performed and cultures grew Streptococcus viridans. She showed progressive clinical improvement and she was successfully transitioned to outpatient care. Discussion: Portal vein pylephlebitis is very rare and usually presents with nonspecific clinical and laboratory findings. Pancreatitis is an uncommon etiology. Hepatic abscesses can complicate severe cases. The prothrombotic effect of the underlying infectious or inflammatory process is the main proposed mechanism. The early recognition and management of pylephlebitis with antibiotics and anticoagulation play significant role in outcome.

231 Plasmapheresis in Treatment of Severe Hypertriglyceridemia Induced Acute Pancreatitis Nayla Ahmed, MD, Bhavtosh Dedania, MD, Sravanthi Madala, MD. University of Connecticut Health Center, Farmington, CT. Hypertriglyceridemia induced pancreatitis (HTGP) is the third most common causes of acute pancreatitis (AP) after alcohol and gallstones. The commonly used treatment for HTGP is either intravenous (IV)


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referred for laparascopic cholecystectomy, however during surgery it became apparent that the patient had congenital agenesis of the gallbladder. Conclusion: In agenesis of the gallbladder, 25-50% of patients will develop stones in the common bile duct. The increased frequency of choledocholithiasis in patients with gallbladder agenesis has been hypothesized to be a result of hypertonic muscular retrograde contraction of the sphincter of Oddi. This results in biliary dyskinesia leading to common duct dilatation, biliary stasis, and gallstone formation2. Although agenesis of the gallbladder is a rare finding, patients with agenesis of the gallbladder are at increased risk of developing de novo choledocholithiasis which may be challenging to extract and require unconventional methods.

233 Ampullary Gangliocytic Paraganglioma Treated With Endoscopic Mucosal Resection Kartik Sampath, MD, Sarah Hyder, MD, Arief Suriawinata, MD, Timothy B. Gardner, MD, MS, Stuart R. Gordon, MD. Dartmouth-Hitchcock Medical Center, Lebanon, NH. Introduction: Gangliocytic paragangliomas (GPs) are rare submucosal neuroendocrine tumors, consisting of epitheliod, spindle and ganglion cells. Ninety percent of these tumors are located in the periampullary portion of the duodenum, and occasionally in the esophagus, jejunum and pancreas. The differential includes gastrointestinal stromal tumors (GISTs) and ampullary adenomas. The clinical presentation varies and includes gastrointestinal bleeding, abdominal pain, jaundice and pancreatitis. These lesions can be asymptomatic and incidentally found during endoscopy. Case Report: 51 year-old male presented initially to an outside medical center with 2 weeks of periumbilical pain. Physical exam noted moderate midepigastric tenderness. Laboratory values were normal. Abdominal ultrasound noted a hypoechoic mass surrounding the pancreatic head, no pancreatic and biliary dilation noted. Abdominal contrast computerized tomography revealed a 2 cm solid homogenous mass in the proximal duodenum. Upper endoscopy (EGD) revealed an ampullary mass; biopsies suggested an adenoma with low grade dysplasia. The patient elected for endoscopic resection and was referred to our institution. An ERCP revealed a 2 cm ampullary mass that was resected via snare electrocautery. A temporary pancreatic duct stent was placed for pancreatitis prevention and a biliary sphincterotomy was performed to facilitate post-procedural biliary drainage. Microscopic and immunohistochemical tissue analysis revealed epithelioid, spindle and ganglionic cells staining positive for synaptophysin, S-100, neuron specific enolase (NSE), and somatostatin consistent with a gangliocytic paraganglioma. Resection margins were negative. Discussion: GPs carry inherent malignant potential with documented cases of both regional lymph node and distant metastases. Previous case series note metastasis rates of seven percent. Current first line management is endoscopic mucosal resection as reported here. GP recurrence post-resection is exceedingly rare. Surgical pancreatoduodenectomy is often performed if endoscopic resection is not possible or positive margins are observed. Radiotherapy is now being utilized as adjuvant therapy for patients with regional metastasis. Chemotherapy has not been formally investigated. As more cases of GPs are reported, oncologic management of advanced lesions and post-resection surveillance strategies will need to be further investigated and defined.

234 Endoscopic Ultrasound (EUS)-Guided Fiducial Placement for Stereotactic Body Radiotherapy (SBRT): First Global Experience With a New 22-Gauge “Pre-loaded” EUS Fiducial Needle Shivangi Kothari, MD1, Truptesh Kothari, MD, MS1, Guobao Wang, MD2, Tamas A. Gonda, MD3, Francis G. Gress, MD4, Vivek Kaul, MD, FACG1. 1. University of Rochester Medical Center, Rochester, NY; 2. Sun Yat-Sen University Cancer Center, Rochester, NY; 3. Columbia University Medical Center, New York, NY; 4. New York Presbyterian Hospital/Columbia University Medical Center, New York, NY.

Objective: To assess the feasibility, safety & efficacy of a new 22-gauge “pre-loaded” EUS fiducial needle in patients referred for image guided radiotherapy at two tertiary referral centers. Design: Patients were initially selected for SBRT based on clinical presentation and after multidisciplinary tumor board review. These patients were then referred for EUS guided fiducial placement at 2 tertiary referral centers. Ten consecutive, eligible patients underwent EUS guided fiducial placement using a new 22-gauge “pre-loaded” EUS fiducial needle between 4/2014-05/2015 (see Table 1 for details). All patients received intra-procedural antibiotics. Data was retrospectively reviewed per medical records. Results: Patient & procedure details are listed in Table 1. Mean patient age was 57 yrs; 70% were males. EUS-guided fiducial placement was successful in all 10 patients. All patients underwent successful SBRT. SBRT was defined “optimal” in 9/10 patients (per feedback from radiation oncology). Average fiducial placement time (time from first fiducial placed to last fiducial placed) was 7.2 min. There were no infections, complications or deaths related to the procedure. All procedures were performed on an outpatient basis and patients were discharged home after an uneventful procedure & recovery. Conclusion: EUS-guided fiducial placement using the new 22-gauge “pre-loaded” needle is safe, effective and very efficient. Successful deployment was achieved in all 9 patients; optimal SBRT was achieved in 9/10 patients. This series represents the first global experience with this new pre-loaded EUS fiducial needle. The pre-loaded nature of the needle simplifies the procedure, reduces overall procedure time and eliminates potential needle-stick exposure for ancillary staff. Further experience with this needle will clarify its role and impact in interventional EUS.

235 Rare Case of Acute Pancreatitis With Normal Lipase Level Anugayathri Jawahar, MD1, Aparna Basu, MD2, Junad Chowdhury, MD3, Dhruvan Patel, MD2, Sandhya Vunnam, MD4. 1. Mercy Catholic Medical Center, Chicago, IL; 2. Mercy Catholic Medical Center, Philadelphia, PA; 3. Mercy Catholic Medical Center, Darby, PA; 4. Mercy Catholic Medical Center, Willingboro, NJ. Introduction: Acute pancreatitis can be diagnosed with one of the following criteria: clinical symptoms of pancreatitis, radiological findings and/or elevated serological markers for pancreatitis. However, there is very limited literature on acute pancreatitis with normal lipase level. Case description: 64 yo female with h/o hypertension and chronic back pain, presented with acute onset severe non-radiating epigastric pain, nausea and vomiting. She was not a smoker but drinks 4-5 glasses of hard liquor once every week. Significant examination findings: BP 153/100 mmHg, HR irregularly irregular, severe epigastric tenderness with no guarding or rigidity. Significant lab results included: lipase 30 U/L, calcium level 9.9 mg/dl, WBC count 17500 thou/uL, glucose 132 mg/ dl, total bilirubin 1.7 mg/dl, direct bilirubin 0.5 mg/dl, normal transaminases. The liver function test normalized on day 2. CT abdomen and pelvis with IV contrast: acute edematous pancreatitis with extensive atherosclerotic plaques with 30% narrowing in the proximal SMA and no gall stones. IgG713 mg/dl, IgG4- 45.9 mg/dl (normal). On admission in the ED, she was also found to be in atrial fibrillation with RVR (175/min) and further tests for causes of atrial fibrillation revealed elevated free T4 level- 3.44 and suppressed TSH- 0.01- primary hyperthyroidism. She had no symptoms of hyperthyroidism except for minimal weight loss. She was improved with conservative management and was discharged. Discussion: There are very few cases of acute pancreatitis with normal lipase level in literature. Lipase level has 55-100% sensitivity and 94-100% negative predictive value in the diagnosis of acute pancreatitis. Whereas contrast enhanced CT scan has 92% sensitivity and 100% specificity in diagnosing pancreatitis. Autoimmune pancreatitis should be a consideration in patients with normal lipase level and checking IgG4 level can be of value. When negative in such patients like our patient, clinical and imaging findings can suffice the diagnosis of acute pancreatitis.

Fiducial guided SBRT has been approved for the treatment of various malignancies. Stereotactic radiosurgery system delivers radiation with high precision using real-time image guidance. Radiographic markers (gold fiducials) implanted in the tumor are used as reference points by the system to target the radiation beams. Fiducials have been placed intra-operatively, percutaneously or using a re-loadable EUS needle. We describe the first experience using a new 22-gauge “pre-loaded” EUS Fiducial needle (4 fiducials pre-loaded per needle).

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Abstracts 236 Acute Idiopathic Pancreatitis With Normal Lipase: Case Report and Literature Review Estela Mogrovejo, MD1, Mihajlo Gjeorgjievski, MD2, Borko Nojkov, MD3. 1. William Beaumont Hospital, Royal Oak, MI; 2. Department of Internal Medicine, Beaumont Health, Royal Oak, MI; 3. William Beaumont Hospital, Royal Oak , MI. Introduction: Serum lipase level is considered a highly reliable test to rule out acute pancreatitis. Few previous cases of clinically proven acute pancreatitis, with normal lipase, have been reported in the setting of alcohol intake, gallstone, trauma, hypertriglyceridemia and medications. No prior case of acute idiopathic pancreatitis with normal lipase has been reported. Case: A 21-year-old woman presented to the emergency room with one-day history of severe, acute onset, epigastric pain. The pain was sharp, radiating to the back, and associated with nausea and vomiting. The patient had a similar episode several months prior. Review of systems was negative. There was no recent trauma. She had no significant past medical or surgical history. Patient quit smoking 2 years prior, did not use any alcohol or illicit drugs, nor was consuming any medications, including over the counter and herbal supplements. Family history was negative for hypertriglyceridemia, autoimmune and pancreatic/gallbladder related diseases. Physical examination was positive only for tenderness in the epigastric area. Laboratory studies revealed unremarkable complete blood count, comperhensive metabolic panel, amylase (46, nl=20-104 U/L) and lipase (46, nl=7-60 U/L). A CT scan of the abdomen and pelvis with contrast done the day of admission showed moderate peripancreatic and mesenteric inflammatory changes consistent with acute pancreatitis, without evidence of gallstones or cholelithiasis. Lipid panel and immunoglobulin-G4 level were normal and MRCP confirmed the CT scan findings. Patient was treated supportively with intravenous fluids and analgesics. Amylase and lipase levels remained normal throughout the hospital stay. Patient was discharged on day 7 with complete resolution of symptoms. Discussion: According to the ACG guidelines the diagnosis of acute pancreatitis requires 2 of the following: 1) characteristic abdominal pain 2) serum amylase and/or lipase more than 3 times the upper limit of normal; or 3) CT scan findings compatible with acute pancreatitis. Serum lipase rises within a few hours of symptoms onset in acute pancreatitis and it has a negative predictive value that approaches 100%. A normal serum lipase level in the setting of acute pancreatitis is an extremely rare occurrence. Conclusion: This report shows that acute pancreatitis with normal amylase and lipase levels can occur and, in appropriate clinical setting, abdominal imaging should be obtained to confi rm the diagnosis.

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Review of systems were positive for intermittent epigastric/right upper quadrant sharp pain and 20lb weight loss. His blood glucose (BG) was undetectable in ER, which was treated symptomatically and the patient was admitted for further work up. He had no prior diagnosis of diabetes mellitus. A CT of the abdomen revealed a mass at the head of the pancreas measuring 6.5 x 5.6 cm with central necrosis and innumerable hypo-dense lesions in the liver, the largest measuring 6.8 cm in the right lobe and 4.2 cm in the left lobe. Proinsulin and chromogranin A levels were elevated at 65.7 pmol/L and 2531 ng/L and undetectable sulfonylurea levels. Biopsy of liver mass revealed tumor cells with immunereactivity for chromogranin, synaptophysin and insulin, with a mitotic index of 5 mitoses/10 hpf and a Ki-67 index of 20%. These findings were consistent with a metastatic insulin producing grade 2 PNET. An octreotide scan showed uptake in the liver and the head of the pancreas. Interestingly, surgical resection was deferred given the extent of his lesions. He was managed conservatively with octreotide, diazoxide and two cycles of TACE with doxorubicin, and everolimus leading to progressive regression of the tumor. Insulinomas are rare indolent PNETs with a yearly incidence of 4 cases per million. Though infrequent but when they do metastasize, PNETs have a tendency to spread primarily to the liver. The current gold standard treatment for such metastatic PNETs regardless of the size, grade or extent of metastasis is surgical resection. In patients with extensive metastases, surgical resection may not be an option and TACE could be an alternative effective option. There is insufficient data compar-

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Role of ERCP SpyGlass Electrohydraulic Lithotripsy in Patients With Chronic Pancreatitis and Pancreatic Duct Calculi Causing Duct Obstruction: An Updated Case Series Laura Hamad, DO1, Sagarika Sinha, DO2, Hazem Tabbaa, DO3, Alyssa Kaleta4, Lara Dakhoul, MD5, Hafiz Muhammad Sharjeel Arshad, MD5, Faizan Khan6, Rasha Issa, MD7, Kamran Ayub, MD8, Taylor Alridge, MMS, PA-C9. 1. Franciscan St. James Hospital, Darien, IL; 2. Franciscan St. James Health, Orland Park , IL; 3. Franciscan St. James Health, Lemont, IL; 4. Advocate Lutheran General Hospital, Park Ridge, IL; 5. University of Illinois at Chicago/Advocate Christ Medical Center, Oak Lawn, IL; 6. Franciscan St. James hospital, Richton Park, IL; 7. Advocate Christ Medical Center/UIC Internal Medicine, Bridgeview , IL; 8. Silver Cross Hospital, Oak Brook, IL; 9. Southwest Gastroenterology, Minooka, IL. ERCP with SpyGlass cholangioscopy and Electrohydraulic Lithotripsy (EHL) is an established treatment for large common bile duct stones. However, the role of SpyGlass EHL in treating patients with pancreatic duct calculi has yet to be well studied. The current management of pancreatic duct stones consists of extracorporeal shock wave lithotripsy (ESWL) or surgical intervention. The aim is to study the safety and efficacy of SpyGlass EHL in patients with pancreatic duct calculi In patients with chronic pancreatitis and pancreatic duct stones, we performed ERCP with SpyGlass pancreatoscopy and EHL in an attempt to break the calculi into smaller fragments in order to relieve the pancreatic duct obstruction. Consecutive patients with pancreatic duct stones were included in the study. Pancreatic duct stents were placed following lithotripsy in all patients. The stents were later removed at a four-six week interval after the procedure. ERCP with SpyGlass EHL was performed in ten patients with chronic pancreatitis and stones. Four patients were relieved of their obstruction after only one procedure. Four patients required two procedures and one patient required three procedures. ERCP with SpyGlass EHL was successful in relieving the main pancreatic duct obstruction in seven patients. The remaining three patients were referred to a multidisciplinary pancreas team for ESWL therapy. Two of these patients required surgery to relieve the obstruction and one is undergoing surgical evaluation. One patient received Puestow’s procedure while the other received Berger’s operation. Two patients had enough pain following the ERCP and EHL treatment and required overnight hospitalization. One patient had mild pancreatitis. No other complications were reported. ERCP with EHL appears to be a safe and effective therapeutic procedure in the majority of patients with chronic pancreatitis and pancreatic duct calculi. Even larger studies are needed to validate the results of our pilot study.

[238B] Figure 2.

238 Pancreatic Neuroendocrine Tumor With Liver Metastases: To Resect or Not to Resect? Sravanthi Madala, MD, Bhavtosh Dedania, MD, Nayla Ahmed, MD. University of Connecticut Health Center, Farmington, CT. To understand the gold standard treatment for metastatic Pancreatic Neuroendocrine tumor (PNET). Various modalities like excision of the tumor and/or resection of only the affected lobe of liver or transarterial chemoembolization (TACE) are the alternative treatment options. A 30 year old African American incarcerated male with no past medical history was brought in to the ER with multiple syncopal episodes over the past 1 month, which was preceded by physical exertion.


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ing the efficacy of surgical resection v/s TACE and medical management as a primary treatment for metastatic PNETs. There exists little evidence to guide optimal clinical practice. Such cases warrant exploration of therapies such as TACE as a treatment that can preserve quality of life and provide clinical benefit.

239 Immunoglobulin G4-Related Disease: A Case of Autoimmune Pancreatitis With Pulmonary Tuberculosis as Proposed Catalyst Jamie Skrove, DO1, Fiorella Calderon Sandoval, MD2, Bruce Le, DO3, Javier Sobrado, MD3, Seth Rosen, MD4. 1. Nova Southeastern University-Larkin Hospital, Cutler Bay, FL; 2. Universidad de Ciencias Medicas, Cartago, Costa Rica; 3. Nova Southeastern University-Larkin Hospital, Miami, FL; 4. Gastro Health, Kendall, FL. Immunoglobulin G4-related disease (IgG4-RD) is an immune-mediated condition that often affects multiple organ systems and may present as lymphadenopathy, autoimmune pancreatitis (AIP), salivary gland disease, orbital disease, IgG4-related sclerosing cholangitis, thyroid disease, and/or retroperitoneal fibrosis. 60-90% of patients with IgG4-RD have multisystem involvement. The condition is composed of several disorders that share similar pathologic, serologic, and clinical features. All manifestations share characteristics such as tumor-like swelling of involved organs, a lymphoplasmacytic infiltrate enriched in IgG4(+) plasma cells, and fibrosis with a “storiform” pattern. Elevated serum IgG4 levels are found in 60-70% of patients. Although the exact pathogenesis for IgG4-RD is unclear, it is speculated that IgG4 antibodies respond in a down-regulatory pattern secondary to another primary process. A 59 year old male patient with a past medical history of diabetes mellitus and hypertension presented with the complaint of left upper quadrant abdominal pain without radiation, nausea, vomiting, or jaundice. Physical exam was remarkable only for epigastric pain with palpation. Chest radiograph showed a cavitary lesion in the right apex with chest CT confirming presence of nodules. Lab data showed positive quantiferon gold, elevated lipase, amylase and IgG4. Abdominal MRI showed “sausage” configuration of the pancreas and findings suggestive of IgG4 related cholangitis. The patient’s condition improved after initiating therapy with Prednisolone and Isoniazid. This patient’s case illustrates AIP in association with an asymptomatic and incidental finding of pulmonary tuberculosis in a patient with no identifiable risk factors. Genetic, immunologic, and molecular mimicry associations with AIP have been hypothesized, however an exact etiology of AIP is still quite ambiguous. Infectious agents play an important role in the development of autoimmune disease in general, with H. pylori recently hypothesized to induce AIP via molecular mimicry. Guernari et al proposed that in genetically predisposed individuals, human and microbial antigens can be a trigger for the onset of AIP with the host immune response targeting human carbonic anyhydrase II. In a literature review, Kawano et al, Imai et al, and Salahuddin et al reported cases of various IgG4 related diseases with an association to tuberculosis. Although many autoimmune triggers exist for AIP, this patient showed a high index of suspicion that M. tuberculosis is the suspected catalyst for the AIP, leading to an autoimmune response versus humoral immunity reaction causing an acute attack on this patient’s pancreas supported by elevated IgG4 levels.

of cholangitis. The disease is found almost exclusively in people who originate or have lived in Southeast Asia. Case: A 26-year old Mexican female with a past medical history of Clonorchis infection was transferred from an outside hospital with nausea, jaundice, and pruritus. The patient initially was diagnosed with Clonorchiasis in 2011 when she presented with sub-acute RUQ pain following cholecystectomy. ERCP performed on that admission directly visualized liver flukes that were confirmed on duodenal aspirate to be Clonorchis. She completed anti-helmintic treatment, but continued to have pain. Three weeks prior to her transfer, the patient had worsening of her RUQ pain. She was found to have choledocholelithiasis, for which an ERCP was performed with stone extraction and biliary stent placement. The patient had some improvement in her symptoms, however three days prior to transfer, she developed jaundice and pruritus requiring re-admission. Repeat ERCP showed recurrent biliary stones/debris as well as possible proximal intrahepatic sclerosis. Upon transfer to our institution, the patient was afebrile, jaundiced, and abdominal exam revealed RUQ tenderness without evidence of rebound, guarding, or hepatomegaly. Laboratory data revealed a normal WBC count without eosinophilia; a Bilirubin of 13.3 mg/dL with direct component of 9.6 mg/dL, and an elevated Alkaline phosphatase of 198 IU/L. The patient’s aminotransferase levels were within normal limits. MRCP performed showed significant peripheral intrahepatic biliary ductal dilatation with sparing of the central intrahepatic ducts and extrahepatic ducts. Repeat ERCP and cholangioscopy showed multiple intrahepatic filling defects from large pigmented stones. The extrahepatic ducts appeared normal. A biliary stent was placed. Duodenal aspirates and biliary washings were obtained and were subsequently negative for parasitic infection. Subsequently, the patient’s symptoms improved. She underwent repeat ERCP with cholangioscopy with successful. Recurrent Pyogenic Cholangitis remains a relatively rare disease of western civilization. Immigration patterns from endemic areas have increased disease prevalence slightly, although no such travel existed in this patient. Despite a fairly strong epidemiologic association for Clonorchiasis, no proven pathogenic mechanism has been elucidated. It is hypothesized that parasitic infection leads to a strong and persistent inflammatory response resulting in biliary stricture formation with intrahepatic stone formation.

240 Choledochal Cyst With Intestinal Metaplasia Presenting as an Unusual Case of Recurrent Cholangitis Rabail Chaudhry, MD, Jennifer Lamberth, MD, Steve Bynon, MD, Sadhna Dhingra, MD, Nirav Thosani, MD. University of Texas, Houston, TX. This is the case of a 64 year old African-American female with a history of recurrent cholangitis and choledolithiasis requiring repeated Endoscopic retrograde cholangiopancreatography (ERCP) procedures. She presented to our institution with severe abdominal pain. She underwent multiple prior ERCPs at outside institution which showed fusiform dilation of biliary tree with recurrent choledocholithiasis. During ERCP at our institution she was noted to have fusiform dilation of biliary tree with very low cystic duct take off marked by very thick cystic duct insertion wall. Single operator cholangioscopy confirmed thick cystic duct insertion wall and spy bite biopsies of thick septum at cystic duct insertion showed inflammatin with intestinal metaplasia. She underwent hepaticojejunostomy with excision of the biliary tree was performed without post-surgical complications. Final pathology revealed cholechocal cyst with focal intestinal metaplasia within biliary mucosa. Choledochal cysts are rare congenital anomalies involving intra- or extrahepatic ducts1-3 with an incidence of 1 in 100,000 – 150,000 in western countries but a remarkably high incidence of 1 in 1,000 in Asia8. Etiology of choledocal cysts remains unclear; however the most popular theory proposed by Babbitt’s4 which attributes the cyst formation to abnormal pancreaticobiliary duct junction (APBDJ). This allows pancreatic fluids to flow into the bile duct causing inflammation and weakness of the duct wall leading to cyst formation. cyst formation. In our present case the cyst represents the category type 1A. There is a strongIn our present case the cyst represents the category type 1A. There is a strong association of malignancy with type I and type IV cysts9, however all types are resected despite histo-pathology findings to prevent malignant transformation. Amongst the various laparotomy vs laparoscopic surgical approaches, Roux-enY, Hepaticojejunostomy, and complete cyst resection are currently the procedure of choice. This case highlights potential stepwise progression to cholangiocarcinoma with intestinal metaplasia as intermediate step.

[241A] Figure 1.

241 Recurrent Pyogenic Cholangitis: An Unusual Presentation of a Young Female with History of Clonorchiasis Originating From a Non-Endemic Area James R. Penn, MD1, Angela Hira, DO2, Amy Tilara, MD2, Mark Bramwit, MD2, Swati Pawa, MD2. 1. Rutgers Robert Wood Johnson Medical School, Piscataway, NJ; 2. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ. Recurrent Pyogenic Cholangitis is characterized by intrabiliary pigment stone formation and biliary stricturing, which ultimately leads to biliary obstruction that is complicated by recurrent bouts


[241B] Figure 2.


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Abstracts 242 Rare Case of Chemotherapy Resistant Pancreatic B Cell Lymphoma Vinshi N. Khan, MD, Hamid Ehsan, MD, Mohammed Nabeel, MD. Union Memorial Hospital, Baltimore, MD. A 58 year-old male presented with a 10- day history of diarrhea and abdominal pain. His stool was lightcolored and the urine was darker than usual. He had an unintentional weight loss of 30 pounds over the past several months. Finally, he also reported sweats with shaking chills, headache, and generalized weakness. On exam, he appeared well nourished and had stable vital signs, mild scleral icterus, moist oral mucosa, and mildly icteric subglossal mucosa. His neck was supple, with palpable right posterior cervical lymph node, that was 2- 3 cm in size, firm, mobile, non tender to touch. The abdomen was mildly tender on deep palpation in epigastrium with no palpable masses. The spleen was palpable 3 cm below the left costal margin; liver edge was not palpable. Laboratory tests showed hemoglobin of 10.6, elevated alkaline phosphate 248, aspartate transaminase(AST) 95, alanine transaminase (ALT) 64, positive HIV-1 Antibody, CD4 count of 146, and HIV RNA load of 48,635. Computed Tomography (CT) of abdomen/pelvis showed physiologically distended gallbladder, mild intra- and extrahepatic biliary dilatation, and splenomegaly with possible venous collaterals in the splenic hilum. It did not show any evidence of peripancreatic infl am-

[242C] Figure 3.

mation or fluid collection.Patient underwent an MRCP (Magnetic Resonance Cholangiopancreatography), which showed a large mass in the portahepatis/ pancreatic head region (3.7/5.9/5 cm) causing common bile duct obstruction. Additional masses were seen within pancreatic body/tail. An ERCP (Endoscopic Retrograde Cholangiopancreatography) with biopsy was undertaken which revealed a high- grade B cell lymphoma.Immunohistochemical stain was strongly positive for CD 20 in the tumor cell. It was also tested positive for CD45, CD79a and Ki-67, amarker that shows increased proliferative rate. Patient subsequently underwent placement of a common bile duct stent, chemotherapy with R-CHOP, and initiation of HAART. He later had undetectable HIV RNA viral load by PCR and completed six cycles of chemotherapy (R-CHOP). Follow up PET (Positron Emission Tomography) scan and CT abdomen/pelvis showed no response to chemotherapy, with enlargement of pancreatic mass, additional pancreatic lesions, peritoneal masses, and hepatic involvement. He then underwent palliative radiation therapy. Though there was progressive decline of CD4 count from 146 to 11, the HIV RNA remained undetectable. A liver biopsy was done to rule out any other malignancies, which was again found to be CD20 positive, further consolidating the diagnosis of high grade B-cell lymphoma.

[242A] Figure 1.

243 Pancreatic Elastofibromatosis: First Case Report Abhinav Goyal, MD1, Deepanshu Jain, MD1, Shahid Hussain, MD, PhD2, Shailender Singh, MD, PhD2. 1. Albert Einstein Medical Center, Philadelphia, PA; 2. University of Nebraska Medical Center, Omaha, NE.

[242B] Figure 2.


Introduction: Elastofibroma is a benign tumor identified by the presence of characteristic elastinophilic fibers. It was originally described as a subscapular connective tissue tumor. Over the years, it has been seen to involve other musculoskeletal sites like ischial tuberosity, greater trochanter and deltoid. It has been rarely described in GI tract (stomach and colon) as case reports but to our knowledge has never been described in pancreas. Case report: 45-year-old female with history of joint pains (HLA B27 positive, seronegative inflammatory arthritis) presented with intermittent abdominal pain of few years duration. Routine physical exam and serum chemistry were unremarkable. CT scan of abdomen revealed 1.4 by 1.4 cm hypodense lesion in the pancreatic neck, anterior to portal confluence, with no vascular involvement. Another 6 mm nodule located adjacent to it was seen, and was thought to represent a lobulation vs. a new lesion. No peri-pancreatic lymphadenopathy was seen. Subsequently, endoscopic ultrasound (EUS) was done which showed a 2.5 x 1.2 cm hypoechoic mass in the neck of pancreas (Figure 1). FNA of the pancreatic mass was non-diagnostic. Repeat EUS-FNA was reported negative for malignancy. But, since appearance of the lesion was concerning for malignancy, surgical resection was performed with central pancreatectomy. Histopathology of the resected specimen showed three well demarcated nodules of hypocellular collagen with abundant elastic fibers (highlighted by a Verhoeff ’s Van Gieson or VVG stain), and admixed bland spindle to stellate cells without necrosis or mitotic activity. Immunostaining of spindle cells was negative for epithelial membrane antigen (EMA), H-caldesmon, pankeratin, CD117, S100, desmin, and beta catenin nuclear stain. Hence, a diagnosis of pancreatic elastofibroma was made. Discussion: Elastofibroma is a relatively uncommon benign tumor classically found in the musculoskeletal system. It is characterized by abnormal accumulation of elastin fibers, pathogenesis of which is unclear. Treatment is not needed unless symptomatic and surgical resection is the preferred therapeutic option. It has been rarely reported in GI tract but never in the pancreas. This case adds another entity to the differential diagnosis of pancreatic mass lesions.


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[243A] Figure 1.

[245A] Figure 1.

244 A Case of Cholangiocarcinoma Diagnosed by Skin Biopsy Neema Saraiya, MD, Venkatesan Ranganathan, MD, Nikhil Shastri, MD. University of Illinois at Chicago, Chicago, IL. A 72-year-old man presented to an outside hospital with abdominal pain, jaundice, and a 30 lb weight loss. CT showed choledocholithiasis and suspected cholecystitis. He underwent endoscopic retrograde cholangiopancreatography (ERCP) which revealed stones in the common bile duct (CBD). Sphincterotomy and stone extraction with stent placement was performed. A laparoscopic cholecystectomy was done, revealing a hydropic gallbladder (GB) that was pierced open, suctioned and subsequently removed in an endobag. A JP drain was left in the GB bed and pulled through a port site. The patient’s jaundice did not improve and he was transferred to another facility where endoscopic ultrasound demonstrated a hilar mass with an associated CBD stricture. An ERCP with brush and biopsy of the CBD stricture was also done, and cytology returned showing only atypia. Both procedures were repeated two weeks later and results were again negative. In the interim, the patient underwent skin biopsy of an enlarging subcutaneous nodule located at a previous surgical port site and the results returned as metastatic adenocarcinoma. A GI pathologist re-examined the GB specimen obtained during the laparoscopic cholecystectomy and noted that there was evidence of cholangiocarcinoma (CCA) within the GB wall. CCA carries a dismal prognosis when detected in an advanced stage and early diagnosis is a challenge. The prevalence of incidental GB carcinoma is between 1% and 2% of all cholecystectomies performed with some studies reporting an incidence as high as 7.4%. Removal of unsuspected GB carcinoma laparoscopically can lead to seeding of tumor cells into the abdominal wall. Incidence of port site recurrence after laparoscopic cholecystectomy for unsuspected GB cancer can be as high as 14%. Intraoperative GB perforation can raise this rate of recurrence to 40%. Recurrences usually occur 6 to 16 months after the operation as was seen in this case. There are several proposed mechanisms of port site recurrence, the most popular of which include: direct wound contamination from laparoscopic instruments; the bile itself containing exfoliated tumor cells which can spread with bile spillage; and also, whether insufflation of the peritoneum can enhance wound metastases. In this case, JP drain placement along with GB perforation may also have been a route of seeding. Physicians should be aware of the risk of tumor seeding when CCA is a possibility in order to avoid the acceleration of metastatic disease.

245 Rosuvastatin-Induced Pancreatitis Michael Itidiare, DO, MBS1, Abdul Rahman, MD1, R. Swami Nathan, MD, FACG2, Sunya Ashraf , MD3. 1. Hackensack University Medical Center-MSH, Montclair , NJ; 2. Hackensack University Medical CenterMSH, Verona, NJ; 3. Hackensack University Medical Center-MSH, Bloomfield , NJ. Acute pancreatitis (AP) is a debilitating condition with significant morbidity and mortality. The most common causes of AP are gallstones and alcoholism and the mechanisms of inciting inflammation are understood. However there is a subset of AP occurring 1.4-2% annually that is attributed to commonly prescribed medications. In light of this rarity, we report a case that highlights AP secondary to rosuvastatin exposure. This is a 73-year-old female with a past medical history significant for hyperlipidemia who presented to the ED with persistent, nonradiating abdominal pain accompanied with nausea for one week. On physical exam, vitals were stable and she had mild epigastric tenderness with no peritoneal signs. Initial laboratory data was unremarkable with the exception of elevated lipase at 1156U/L. Follow up abdominal CT showed peri-pancreatic edema suggestive of AP. Patient was thereafter admitted and treated with aggressive hydration. Initially, no clear etiology was found for patient’s pancreatitis as patient denied alcohol use, recent viral illness, trauma, or abdominal biliary tract procedures. Patient had additional work up which revealed normal serum calcium, an unremarkable lipid panel, and abdominal ultrasound which revealed a contracted gallbladder without stones. On further review of patient’s


medication list, it was found that she started taking rosuvastatin about ten days ago. Rosuvastatin was thereafter held on admission. Patient had resolution of her pancreatitis and was discharged without rosuvastatin. Drug induced pancreatitis is often difficult to diagnose. Almost a quarter of these patients are often misdiagnosed as idiopathic pancreatitis before attributing medication as the cause. Of the several medications that may cause pancreatitis, statin induced pancreatitis has become increasingly common. There have been several case reports of statin induced pancreatitis, and they have been associated with the use of simvastatin, pravastatin, fluvastatin, and more recently atorvastatin. However, there have been very few reported cases of rosuvastatin induced pancreatitis. In light of increasing use of rosuvastatin, our case highlights the importance of recognizing rosuvastatin as a cause for pancreatitis. It is important for clinicians to be aware of the association of rosuvastatin and AP, as the complications associated with AP can be debilitating and possibly fatal if missed.

246 Bile Peritonitis After Percutaneous Liver Biopsy and Persistent Bile Leak Aaron Goodwin, MD1, Jason Lewis, MD2, David Iannitti, MD3. 1. Carolinas Medical Center, Department of Internal Medicine, Charlotte, NC; 2. Carolinas Medical Center, Department of Internal Medicine, Division of Gastroenterology, Charlotte, NC; 3. Carolinas Medical Center, Department of Surgery, Division of Hepatobiliary Pancreatic Surgery, Charlotte, NC. A 40 year old man with a past medical history significant for obesity, dyslipidemia, and long standing low back pain underwent percutaneous liver biopsy (PLB) for persistently elevated LFT. Immediately following biopsy the patient experienced significant abdominal pain and urgent CT scan demonstrated only trace hemorrhage along liver edge. Twenty-four hours later the patient presented to an outside emergency department for persistent abdominal pain and nausea. Vital signs were stable with initial studies were only significant for mildly elevated LFT. Repeat imaging showed mild to moderate “ascites”. Diagnostic paracentesis yielded 100 mL of brownish-green fluid with a total fluid bilirubin of 51 consistent with bilious ascites. ERCP with stent placement was attempted but was unsuccessful due to inability to cannulate the ampulla. He was subsequently transferred to our institution where repeat ERCP demonstrated extravasation of contrast from a peripheral biliary branch of the right hepatic system. Biliary sphincterotomy with placement of a 10F x 7cm biliary stent was performed. Surgical consultation was obtained given the degree of bile seen in the abdomen on imaging. The following day laparoscopic evaluation showed friable and inflammatory adhesions throughout the abdomen with removal of 2L of bile tinged fluid. Inspection of the liver showed severe fatty changes and a puncture site on the right lateral liver. Puncture site was closed using intracorporeal suturing and knot tying techniques with no visible bile emanating from the liver after suture ligation. Post-operative course was unremarkable and the patient improved over several days with resolution of abdominal pain and decreasing output from abdominal drains. Four weeks after initial ERCP, repeat ERCP showed complete resolution of previously seen hepatic bile leak. Complication rates from PLB are very rare with multiple studies citing major complication rates 1% or less with bile leak rates occurring less than 0.001%. Once treated conservatively with drainage and supportive care, standard care now requires a multidisciplinary approach with endoscopic and surgical interplay. Endoscopic treatment involves biliary stenting with or without sphincterotomy to allow for biliary tree decompression with repeat endoscopy and stent extraction 4-6 weeks later. Laparoscopy allows for better evacuation and irrigation of the peritoneum with direct repair of amenable lesions as in this case. As exemplified by this patient, post PLB bile leak and subsequent bile peritonitis though extremely rare can be successfully managed through a skilled multidisciplinary approach.


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Abstracts

[247A] Figure 1.

[246A] Figure 1.

[247B] Figure 2.

[246B] Figure 2.

247

consistent with an abscess. Three weeks later EUS/ERCP confirmed complete resolution of cystic mass and normalization of CA 19-9 to 40 IU. Results: Pancreatic malignancy is devastating disease with abysmal survival rates. Surgery is the only cure in carefully selected patients. In a healthy patient with pancreatic mass that highly suggests malignancy EUS guided biopsy is not necessary before surgey. However in our case EUS with biopsy was critical to secure the correct diagnosis, which turned out to be an isolated pyogenic collection in the head of the pancreas. Pancreatic infection is usually a complication of pancreatitis. Isolated pancreatic abscesses are rare and usually due to infection with tuberculosis. Infections without obvious sources are particularly common among patients with diabetes mellitus,. and some experts believe that diabetes mellitus is an important risk factor for abscesses without other etiologies. Discussion: EUS guided biopsy is crucial tool for diagnosis and staging of pancreatic cystic lesions. Pancreatic infection is a rare etiology and should be considered in differential of pancreatic cysts mimicking malignancy, especially in diabetic patients.

Pancreatic Abscess Mimicking Carcinoma of the Pancreas Oleg Shulik. Seton Hall University, Wood Ridge, NJ. Introduction: 67 year-old asian male with history of diabetes presented with new onset of jaundice associated with fatigue anorexia and weight loss for 2 weeks. Patient denied fever or chills and had no abdominal pain complaints. Vitals signs where stable. White cell count, lipase where normal, however CA 19-9 was 1732 IU and liver function tests suggested obstructive jaundice with Total bilirubin 7.2 gm/dL direct bilirubin 6.9 gm/dL and elevated transaminases. CT abdomen followed by MRCP demonstrated dilated biliary tree and 2.5 cm cystic mass in the head of the pancreas compressing the CBD. Therapeutic ERCP was attempted and demonstrated 3 cm long smooth tapering CBD stricture consistent with extrinsic compression from pancreatic lession in the head of the pancreas. Surgical evaluation concluded that patient is operable, pancreatic mass is without vascular invasion, good acces on imaging, thus Whipple surgery was initially reccomended. To complete the staging EUS with FNA was persued a week later. It revealed slightly smaller cystic lesion in the head of the pancreas that was surprisingly easly aspirated in whole. Pathology results revealed inflammatory cells and bacteria


248 Endoscopic Ultrasound-Guided, Needle-based Confocal Laser Endomicroscopy in the Diagnosis of Cystic Pancreatic Neuroendocrine Tumor: Emerging Imaging Criteria From Surgical Pathologic Correlation in Two Cases Takeshi Tsujino, MD, PhD1, Jason Samarasena, MD2, Kenneth Chang, MD2. 1. University of California Irvine, Irvine, CA; 2. University of California Irvine, Orange, CA. Introduction: Cystic pancreatic neuroendocrine tumors (NETs) are relatively rare, with the reported incidence of < 10% of resected pancreatic cystic lesions. Preoperative diagnosis of cystic pancreatic NET remains challenging. Needle-based confocal laser endomicroscopy (nCLE) during EUS guided fine needle aspiration (EUS-FNA) has been shown to be useful in other pancreatic cystic neoplasms (ex Intraductal papillary mucinous neoplasia or IPMN). However, the utility of EUS-guided nCLE in


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revealed well-differentiated pancreatic NET. nCLE images corresponded well to histological images (Fig 2). [Case2] A 71-year-old male with diabetes presented for evaluation of a pancreatic tail lesion seen on CT during investigation of abdominal pain. EUS demonstrated a 21X16 mm unilocular cystic lesion in the pancreatic tail with partial wall thickening. On nCLE, a high density of dark cord-like structures was observed. Distal pancreatectomy was performed and histology revealed a pancreatic NET. Conclusion: EUS-guided nCLE images correlated well with surgical pathology in 2 cases of cystic pancreatic NET. A high density of dark thick cord-like structures or dark nest-like structures may be important diagnostic criteria. If these criteria are prospectively validated, nCLE may play a role in the diagnosis of cystic pancreatic neuroendocrine tumors.

249 Extranodal, Diffuse, Large B-Cell Lymphoma Diagnosed by Ampullary Mass Biopsy From ERCP for Ascending Cholangitis: An Atypical Case Presentation Dominic M. Colella, DO, Bruce Le, DO, Cristina Marin, MD, Javier Sobrado, MD. Nova Southeastern University-Larkin Hospital, Miami, FL.

[248A] Figure 1.

Diffuse large B cell lymphoma (DLBCL) is a histological subtype of non-Hodgkin lymphoma (NHL) that accounts for approximately 25% of all NHL cases. DLBCL usually presents as a rapidly enlarging mass, most commonly nodal enlargement in the neck or axilla. Systemic B-symptoms are often reported, including night sweats, fever, and weight loss. Extranodal disease has been reported in up to 30% of cases, and the diagnosis of DLBCL is most commonly made with excisional lymph node biopsy. A 73-year-old female patient with a history of anemia presented with the complaint of painless jaundice, abdominal pain, subjective fevers, and recent weight loss. Physical exam was remarkable for jaundice and mild sclera icterus. Lab data was positive for a HGB of 7.5, WBC of 18.4, ALT of 73, AST of 57, ALKP of 786, TBILI of 3.7, DBILI of 3.2, LDH of 247, lipase of 859, Fe of 27, TIBC of 202, and ferritin of 722. Antibiotic therapy was initiated. US abdomen showed marked intra- and extra-hepatic biliary dilation, gallbladder distention, and abrupt termination of the common bile duct in the pancreatic head, most likely due to pancreatic head mass. CT scan confirmed biliary dilation most likely due to pancreatic adenocarcinoma (AC) with extensive peritoneal metastases or lymph nodes. The patient’s CA 19-9 level was 8894. An ERCP with sphincterotomy, stent placement, and cytology brushing with ampullary biopsy revealed an ampullary mass, a 1.5 cm dilated intrahepatic biliary tract, and a 5 cm distal and mid-common bile duct stricture beginning at the ampulla. A PET-CT scan was positive for abnormal uptake in posterior mediastinal, right axillary, right cardiophrenic, mesentery, and retroperitoneum lymph nodes, as well as in the right lobe of the liver and the head and tail of the pancreas. Cytology brushing revealed atypical cells and ampullary biopsy revealed DLBCL. Further management was recommended per hem-onc. This case of DLBCL was very unique, as her presenting symptoms of painless jaundice, abdominal pain, subjective fevers, and recent weight loss were not typical initial symptoms of DLBCL. No rapidly enlargement mass or nodal enlargement of the neck and axilla was present. Her symptoms could have been explained solely by her ascending cholangitis. It was also remarkable how the clinical presentation resembled that of a pancreatic AC but was actually due to a DLBCL with significant distant metastasis. This less common extranodal presentation would not have been expected given her complaints, as additional symptoms or a diagnosis would have presumably been previously suspected. Lastly, the majority of DLBCL diagnoses are made with excisional lymph node biopsy, but this case’s diagnosis was interestingly made from an ampullary mass biopsy from an ERCP for ascending cholangitis.

250 IgG4-Related Multiorgan Disease: A GI Perspective Parth J. Parekh, MD1, Monika Kowalczyk, MD2. 1. Tulane University School of Medicine, Gretna, LA; 2. Tulane University School of Medicine, Division of Gastroenterology, New Orleans, LA.

[248B] Figure 2.

the diagnosis of cystic pancreatic NET has not been reported, and imaging criteria based on surgical pathologic correlation has not been established. Methods: Under EUS guidance, the pancreatic cystic lesion was punctured with a 19-gauge FNA needle. After confirmation of cyst entry, fluorescein was injected intravenously. The nCLE probe was then advanced through the needle into the cyst, and the cyst wall was carefully imaged. Results: [Case 1] A 65 year-old-male presented for rapid enlargement over one year of a known pancreatic cystic neoplasm. On EUS, a 23X22 mm unilocular cystic lesion was seen in the pancreatic tail. There was no evidence of wall thickening or mural nodules. nCLE demonstrated a high density of dark thick cord-like structures or dark nest-like structures (Fig 1 ). There was no evidence of papillary projections, dark rings, or a superficial vasculature network, suggesting IPMN or serous cystadenoma, respectively. Laparoscopic distal pancreatectomy was performed. Histology of the resected specimen


IgG4-related disease is a chronic fibro-inflammatory disease considered to be of autoimmune origin. Autoimmune pancreatitis was the first defined manifestation of IgG4-related disease, with histopathology considered the gold standard for diagnosis. In recent years, the disease spectrum has expanded to include many autoimmune disease processes once thought to be individual disease entities. A 67-year-old male was referred to GI clinic for further evaluation of chronic pancreatitis, intermittent watery diarrhea, and dysphagia. In clinic, physical exam revealed lacrimal duct involvement and sialadenitis. Imaging performed to further evaluate recurrent pancreatitis revealed retroperitoneal fibrosis and diffuse fatty infiltration of the liver. Biopsy of the lacrimal duct revealed Immunohistochemical stains for IgG 4 (>50 /HPF) with IgG-positive plasma cells predominating and a ratio of IgG4:IgG >50%, consistent with IgG4- mediated autoimmune sclerosing sialadenitis. Here we present the various presentations of IgG-4 disease particularly gastrointestinal manifestations, review the relevant up to date literature, present treatment options, and discuss differing hypothesis for entities that may be part of the IgG-4 spectrum, ie IgG4 esophagitis, IgG-4 hepatopathy and lymphoplasmacytic gastritis as seen in our patient.

251 An Uncommon Diagnosis Mimicking Peritoneal Carcinomatosis Joseph Salhab, DO1, Bruce Le, DO2, Javier Sobrado, MD2, Cristina Marin, MD2. 1. Nova Southeastern University-Larkin Hospital, Tampa, FL; 2. Nova Southeastern University-Larkin Hospital, Miami, FL. Peritoneal carcinomatosis is a term that characterizes the presence of extensive metastasis inside the peritoneal cavity, usually spread from a near-by primary malignancy. This diagnosis is associated with a grim prognosis, indicating intraperitoneal seeding or haematogenous dissemination from several types of tumors, including gastric, ovarian, pancreatic and colorectal cancers. There are, however, multiple


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Abstracts non-neoplastic disease processes that can imitate peritoneal carcinomatosis on high-grade imaging. Our case presentation illustrates a rare and benign differential diagnosis in a patient who exhibited findings suspicious for peritoneal metastases with malignant ascites. A 79 year-old male with a PMH of DM, COPD, and BPH presented to the ER with the chief complaint of abdominal pain, distention, nausea, and malaise. He admits that the abdominal pain has been intermittent over the past 3 months and increasing severity. He admitted to a laparoscopic robotic singlesite cholecystectomy performed 7 months prior to this admission. A colonoscopy and endoscopy 1 year prior to this admission was normal. Abdominal CT demonstrated ascites and seven enhancing peritoneal lesions resembling implants. Abdominal MRI confirmed the findings. Paracentesis removed 2500ml of clear fluid, but cytology was non-diagnostic. A diagnostic laparoscopy found a 1.5cm abdominal wall nodule that was adherent to the anterior abdominal wall; no other peritoneal implants could be visualized. The liver appeared normal and there were no other gross abnormalities. Pathology of the lesion demonstrated granulomatous inflammation with fibrosis, with pigmented material resembling bile or a gallstone. Follow-up with the patient 2 weeks later demonstrated resolution of the ascites and abdominal pain. This case represents an extremely uncommon etiology of findings that were initially suspicious for peritoneal metastases. After thorough literature review, an explanation for this finding includes the spillage of bile during his laparoscopic cholecystectomy, which triggered an inflammatory response to the bile deposits trapped inside the peritoneum, mimicking the nodular implants of peritoneal carcinomatosis seen on computed tomography and magnetic resonance imaging. However, it is unclear why this occured in this patient specifically. Lingering questions include the possibility of genetic predisposition, the possibility of infection leading to an abnormal immune response resulting in granuloma formation, and the possibility of an existing disease such as Wegener’s granulomatosis which lead to these findings. To conclude, a vast array of disease processes, including benign pathology, can mimic peritoneal carcinomatosis on imaging; thus, obtaining biopsies with appropriate histopathology and microbiology is vital in clenching the final diagnosis.

[252B] Figure 2.

252 Pancreatic Hamartoma: A Mimicker of Pancreatic Adenocarcinoma Omar Shahbaz, MS, MD, Mitesh Patel, MD, FACG. MedStar Washington Hospital Center, Washington, DC. The term ‘hamartoma’ refers to a disorganized benign growth of cells and tissue normally found in an anatomic area. While the most common site is the lung, one rare site of hamartomatous growth is the pancreas. Since approximately 80-90% of primary tumors the pancreas are due to adenocarcinoma, pancreatic hamartoma can present a pre-operative diagnostic dilemma. We present the case of a 62 year old female with a past medical history of coronary artery disease and hypertension who presented with epigastric abdominal pain for 3-4 months duration. Pain was described as vague, moderate intensity, intermittent, crampy, and generalized. She had nausea without vomiting but denied post-prandial discomfort or change in bowel movement. The patient’s complete blood count, basic metabolic panel, liver function tests and lipase were unremarkable. A CT scan of her abdomen showed a low density focus within the pancreatic uncinate process suspicious for malignancy. An MRI of the abdomen subsequently revealed a 14mm hypoenhancing lesion at the junction of the head and uncinate process of the pancreas with imaging characteristics worrisome for pancreatic carcinoma. No evidence of metastatic disease was noted. She underwent EUS showing an oval mass in uncinate process of the pancreas predominantly hypoechoic and heterogenous measuring 14mm x10mm. No evidence of vascular invasion was seen. FNA performed showed clusters of epithelial cells and rare cluster of ductal epithelial cells with mild atypia. No definitive evidence of malignancy. CEA and CA 19-9 levels were normal. After an informed discussion with the patient indicating there was a high likelihood of pancreatic malignancy, she elected to undergo a Whipple procedure. Surgical pathology showed a circumscribed lesion composed of disorderly well differentiated pancreatic acinar, islet, and ductal cells with fibrous stroma consistent with pancreatic hamartoma. Pancreatic hamartomas are extremely rare, with less than twenty cases reported in the literature. Since they share many radiological features with pancreatic adenocarcinoma, diagnostic difficulties are typically resolved after operative resection and histopathological examination. The literature shows that all reported cases underwent surgical resection. The present study demonstrates that less common pancreatic lesions like hamartoma should be considered in the differential diagnosis and surgery can represent overtreatment since hamartomas generally have a benign course.


[252C] Figure 3.

253 A Case of IgG4-Related Disease: A Unique Presentation of a Rare Entity Kirat Gill, MD1, Justin Reynolds, MD1, Anita Kohli, MD, MS1, Ann Moore, NP2, Ashley Hepner, ANP1, Robert Gish , MD1, Richard Manch, MD, MHA, FACG1. 1. Division of Hepatology, St. Joseph’s Hospital and Medical Center, Creighton University Medical School, Phoenix, AZ; 2. St. Joseph’s Hospital and Medical Center, Phoenix, AZ. IgG4-related disease is a rare, systemic fibroinflammatory condition characterized by lymphoplasmacytic infiltrates and often times elevated serum IgG4 levels. Multiple organs are implicated in the disease and although the pathogenesis is not entirely understood, genetic risk factors and autoimmune dysregulation have been associated. Pathology from biopsied lesions is varied and can range from a dense lymphoplasmacytic infiltrate to fibrosis. Currently, there are limited reports of IgG4-related disease in the literature. A 69 year-old female with a past medical history significant for salivary gland tumor (s/p resection and radiation), rheumatoid arthritis (on Methotrexate), alcohol use (2-3 glasses of wine for several years) presented to hepatology clinic for evaluation of elevated liver function tests noted on routine blood work. ALP was 367 IU/L, ALT 162 IU/L and AST 67 IU/L. CA 19-9 was also elevated to 45 U/mL, however MRI and EUS were unremarkable. Liver biopsy showed portal fibrosis, lymphocytic, neutrophilic and eosinophilic portal and lobular hepatitis with bile ductular proliferation. After an unrevealing extensive workup for other causes of abnormal liver tests, it was thought the abnormal tests and biopsy finding may be secondary to ethanol abuse and methotrexate. Over the subsequent year, the patient continued to have elevated liver function tests, a thirty-five pound weight loss, jaundice and pruritus. MRI of the abdomen revealed an infiltrating peri-choledochal, peripancreatic, porta hepatic and retroperitoneal soft tissue mass, narrowing the common bile duct and multiple enlarged retroperitoneal and pericardial lymph nodes. EUS showed an irregular, 2.3 x 2.3 cm, poorly defined area within the region of the head of the pancreas, dilation of the pancreatic duct and distal common bile duct stricture. Biopsies were not performed, and cytology from FNA revealed only benign pancreatic acini. IgG4 levels were ordered to evaluate for IgG4 related autoimmune pancreatitis/sclerosing cholangitis and were elevated to 125 mg/dL. Given the elevated IgG4, and multiple organ dysfunction, a presumed diagnosis of IgG4-related


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disease was made. Although glucocorticosteroids are the mainstay of therapy, the patient has not since returned to clinic. IgG4-related disease is a rare yet potentially treatable entity that can mimic primary organ disease or malignancy, yet should always remain in the differential diagnosis. Close follow up and cognizance of this disease entity is critical as a lag in treatment can have significant implications.

254 Choledochal Cyst With Autosomal Dominant Polycystic Kidney Disease: It Is Far More Rare Than You Think! Hemant R. Mutneja, Mary J. Atten, MD, FACG, Bashar M. Attar, MD, PhD, FACG, Meron Teshome. Cook County Health and Hospital Systems, Chicago, IL. Introduction: Renal fibropolycystic disease is often associated with polycystic liver disease and Caroli’s intrahepatic biliary dilatation. However, its association with choledochal cysts has rarely been reported. We describe the case of a young female with this uncommon association. Case presentation: A 34 year old female with a recent diagnosis of Autosomal Dominant Polycystic Kidney Disease presented with right flank pain, vomiting and subjective fevers of 1 week duration. Physical exam was notable for high grade fever (102.6F) with mild right lumbar region tenderness on abdominal examination. Labs revealed mild leukocytosis (14,000 per cubic millimeter). CT of the abdomen revealed massively enlarged bilateral kidneys with innumerable cysts, with concern for overlying cyst infection at the right inferior pole. She was started on antibiotics for probable cyst infection. Incidentally discovered on the CT were ectatic intrahepatic and periportal bile ducts without any gall stones or distention of the gall bladder. Liver function tests were within normal limits. MRCP revealed fusiform dilatation of the common hepatic duct and proximal common bile duct (consistent with a type 1 choledochal cyst) with a simple cyst in the lateral segment of the left hepatic lobe. After being treated for renal cyst infection, the patient was discharged with surgical clinical follow up. She has been offered surgery given the possible risks of cholangitis and/or malignancy and is currently being planned for surgical resection of the choledochal cyst. Discussion: Only a handful of cases describing the association of choledochal cysts and ADPKD have been reported in the past. In contrast, the association of choledochal cysts with autosomal recessive polycystic kidney disease is relatively stronger. The etiology for development of choledochal cysts in association with fibrocystic kidney disease may not be pancreatobiliary maljunction, as has been hypothesized in other causes of biliary cysts. Malformation of the ductal biliary plate is the most likely etiology of the choledochal cyst in this case. Regardless of the etiology for formation of the choledochal cyst, surgical excision to prevent future complications remains the best treatment modality.

255 The Mysterious E. Coli Amrita Dhillon, MMBS, Arunpreet Kahlon, MBBS, Arundeep Kahlon, MBBS, Hegazy Housam. SUNY Upstate Medical University, Syracuse, NY. Introduction: Gram negative bacilli cause about a quarter to half of all blood stream infections with urinary tract being the most frequent source. Infections of gastrointestinal tract, biliary tract, and skin or soft tissues are less frequent sources. E. coli is the predominant organism in cases of community onset gram negative bacteremia. We present an interesting case of E.coli bacteremia with atypical presentation of GI tract origin. Case: A 56 year male with history of hypertension, obesity, presented to the ER with 3 day h/o malaise, fatigue, fevers and chills. He denied h/o headache, abdominal pain, nausea, vomiting, diarrhea or sick contacts. On examination he was tachycardic and febrile. Scleral icterus was noted, he was alert but oriented to person only. Labs showed WBC 15000/uL, BUN/Creatinine, 24/1.3, total bilirubin 3.4, direct bilirubin 2.2 mg/dl, AST 568, ALT 161 and normal ALP. CT head showed no acute intracranial process. Ultrasound abdomen showed hepatic steatosis with gall bladder sludge. Patient was empirically started on broad-spectrum antibiotics. Blood cultures grew E.coli, urine and CSF cultures were sterile. Patient underwent imaging to look for source of bacteremia. A CT abdomen showed right hepatic lobe fluid density consistent with simple cyst and cholelithiasis without evidence of cholecystitis. Patient responded well to the antibiotics with improvement in mental status, along with improvement in renal function and LFTs . The fever and WBCs also trended down but patient persisted to have a left shift and intermittent low-grade fevers therefore an IR guided drainage of the hepatic cyst was done and small amount of fluid was aspirated. MRCP could not be obtained due to patient’s claustrophobia. An ERCP was done which showed distal CBD inflammatory stricture and sludge, which was relived with endoscopic biliary sphincterotomy. The ERCP findings were suggestive of passage of a CBD stone. The liver cyst fluid cultures were positive for E.coli. The patient likely had ascending cholangitis due to CBD obstruction with eventual passage of the CBD stone, and it also lead to a liver phlegmon. Patient’s white count and temperature normalized. Patient was treated with 4 weeks of IV antibiotics followed by elective cholecystectomy. Discussion: Biliary tract infections are a common cause of bacteremia and are associated with a reported 30-day mortality of 10 %. Cholangitis should be considered in the differential diagnosis oin a septic patient, as only a third of patient present with typical features of right upper quadrant pain, fever and jaundice. There should be a low threshold to investigate the biliary tract, as delay in decompression increase the emergent operative mortality rate (17-40%) and increases the incidence of life threatening complications of septic shock, hepatic abscess and liver failure.

256 Extramedullary Hematopoiesis Presenting as Acute on Chronic Cholecystitis Zaid Tafesh, MD, Carl V. Crawford, Jr., MD. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY. A 55-year-old man with a history of JAK-2 heterozygous myelofibrosis presented with 2 weeks of abdominal pain, nausea, and fever. Work up prior to this admission included a CT scan revealing inflammatory


changes of the pancreas, gallbladder and duodenal wall. He represented with persistent symptoms, a wbc count of 14.4K/ul, alkaline phosphatase of 156 IU/L, and normal transaminases, bilirubin, amylase, and lipase. An ultrasound revealed gallbladder sludge and gallstones with diffuse wall thickening and pericholecystic fluid. An MR/MRCP revealed acute pancreatitis, common and cyst duct mural thickening, cholelithiasis, and chronic portal vein thrombosis. He underwent a cholecystectomy and his pathology was consistent with acute on chronic cholecystitis with evidence of extramedullary hematopoiesis associated with primary myelofibrosis within the gallbladder. Myelofibrosis is characterized by bone marrow fibrosis in the setting of ineffective erythropoiesis. Extramedullary hematopoiesis serves as a source of ectopic blood cellular components. It is most common in the spleen and can be complicated by portal vein thrombosis, consistent with our patient’s initial presentation. Other common sites include the liver, lymph nodes, or serosa, among others. The presence of extramedullary hematopoiesis in the gallbladder has been reported only four times in the literature. In all cases, patients had undergone cholecystectomy for a clinical picture of cholecystitis. In our patient, abdominal pain led to the diagnosis of acute cholecystitis that ultimately resulted in the rare identification of extramedullary hematopoiesis in this organ. Given that all reported cases were identified in symptomatic patients, it is possible that the prevalence of myeloid metaplasia in the gallbladder of asymptotic patients is underreported. Whether the process of extramedullary hematopoiesis directly resulted in an inflammation of the gallbladder remains unclear, but its recognition exclusively in the presence of a clinical picture consistent with cholecystitis makes it a likely culprit. The presence of pancreatitis in our patient also raises the suspicion for the possibility extramedullary hematopoiesis in the pancreas or common bile duct. In conclusion, we present the fifth reported case of myeloid metaplasia in the gallbladder, which serves as a reminder to clinicians that patients with myelofibrosis are at risk for complications in the hepatobiliary tree including cholecystitis.

257 Anomalous Junction of the Pancreaticobiliary Ductal System With a Long Common Channel in a Patient With Chromosome 14 Translocation Causing Recurrent Acute and Chronic Pancreatitis Omar Shahbaz, MS, MD1, Faryal Mirza, MD1, Kelley Shirron, CPNP-PC2, Jaime Wolfe, MD2, John Snyder, MD2, R. Martin Bashir, MD, FACG1. 1. MedStar Washington Hospital Center, Washington, DC; 2. Children’s National Health System, Washington, DC. The pancreatic duct (PD) and common bile duct (CBD) normally join with a short (4-5mm) common channel into the duodenum. Rarely, anomalous junctions can occur outside the duodenum where they are no longer influenced by the sphincter of Boyden. One such anomaly is the ‘long common channel’ in which the PD inserts into the CBD outside the duodenum and a common channel over 15mm enters the duodenum. These cases are associated with higher incidence of chronic pancreatitis as both bile and pancreatic juices are allowed to reflux into the opposing channel. We present the case of a two year and 3 month old toddler with a past medical history of chromosome 14 translocation (Turner Syndrome variant), agenesis of the corpus callosum, possible optic nerve atrophy, s/p Nissen procedure x2 and gastric tube dependence who presented to the hospital with abdominal pain. Of note, she had recurrent bouts of biliary pancreatitis as well as pancreatitis of unclear etiology. Her symptoms began at 20 months of age when she was jaundiced and underwent MRCP demonstrating gallbladder sludge, and biliary stenosis. She subsequently underwent laparoscopic cholecystectomy but continued to develop recurrent bouts of pancreatitis. Endoscopic cholangiopancreatography (ERCP) demonstrated diffuse irregularity with dilatation (6mm) and beading of the main ventral pancreatic duct in the head of the pancreas and tortuosity with clubbing of the side branches. Also noted was a long 20mm common channel with the pancreatic duct entering the common bile duct (CBD) 2cm above the ampulla. At ERCP, filling of the pancreatic duct was noted upon injecting contrast in the distal CBD. This anatomic variation with an anomalous high entry of the pancreatic duct into the CBD with clear bile reflux into the pancreatic duct was the likely etiology of the patient’s recurrent acute on chronic pancreatitis. A 5 french/5cm pigtail stent was endoscopically placed into the pancreatic duct, preventing reflux of bile into the pancreatic duct. This was subsequently changed 2 weeks later. Post-stenting, no recurrent bouts of pancreatitis were noted and the patient did not require hospital readmission. She subsequently underwent laparoscopic choledochoduodenostomy without incident. She remains thriving at this time without further episodes of pancreatitis since surgery. This is the first reported case of an anomalous long common channel in a toddler with a chromosome 14 translocation. Further, it is the first case to successfully treat a long common channel endoscopically with a pancreatic stent, and surgically with choledochoduodenostomy. The development of severe chronic pancreatitis in this case in an unfortunate sequela of the persistent bile reflux through this anomaly.

258 A Case of Pancreatic Adenosquamous Carcinoma Obstructing the Common Bile and Pancreatic Ducts, Duodenum, and Gastric Outlet Yahya Kurdi, MD, MS1, Joshua R. Peck, MD2, Rachel Roth3, Darwin L. Conwell, MD, MS4. 1. Akron General Medical Center, Akron, OH; 2. Section of Hepatology, Division of Gastroenterology, Hepatology, & Nutrition, The Ohio State University Wexner Medical Center, Galloway, OH; 3. The Ohio State University Wexner Medical Center, Columbus, OH; 4. Division of Gastroenterology, Hepatology, and Nutrition, Department of Internal Medicine, The Ohio State University, Columbus, OH. A 76-year old Caucasian female was admitted for a 6 week-history of nausea, vomiting, abdominal pain, and a 20-pound weight loss. No tobacco or alcohol consumption and no previous history of pancreatic disease or familial pancreatic cancer were reported. Vital signs were within normal. Physical exam was notable for epigastric tenderness. Serum lipase, alkaline phosphatase, and cancer antigen 19-9 were elevated. Other routine laboratory test results were non-contributory. Contrast-enhanced computed tomography (CECT) of the abdomen and pelvis showed a 2.7 by 3.5 cm heterogeneously enhancing mass in the head of the pancreas causing obstruction of the common bile duct (CBD) and stomach and nearly occluding the portal vein at the confluence. EUS identified an irregular, hypo-echoic mass in the pancreatic head measuring 40 by 35 mm in maximal cross-sectional diameter with intact interference between the mass and the adjacent structures suggesting lack of invasion. Several peritumoral malignant, appearing lymph nodes were also identified by EUS. The pancreatic


| OCTOBER 2015

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Abstracts duct and CBD were dilated at 4 and 20 mm in diameter respectively. EUS-FNA biopsy was performed using a 22-gauge Wilson-Cook EchoTip biopsy needle via a transduodenal approach. Cytological and immunohistochemistry (IHC) staining showed the presence of two components of cells; adenocarcinoma and squamous carcinoma. Based on clinical exam, CECT, EUS-FNA biopsy, and IHC staining, a diagnosis of locoregional PASC was made. Pancreatic cancer is the fourth leading cause of cancer deaths in the USA. PASC is rare, more aggressive, and makes only 0.5 % of pancreatic cancer. This is a rare case of PASC obstructing multiple

gastrointestinal and hepatobiliary sites and presenting without jaundice or significant elevation in bilirubin. The combination of CECT with EUS seems to produce the highest accuracy for staging and diagnosing pancreatic neoplasm and for assessing the respectability of the tumor. Cytology and IHC staining of collected EUS-FNA biopsies showed a dual population of malignant glandular cells with intracellular mucin production as well as pleomorphic squamous cells making greater than 30 % of malignant cells; meeting histological criteria of PASC. The application of the CECT/EUS-FNA modality helped characterize the tumor resectability in our patient. In a locoregional PASC, tumor resectability is the strongest independent predictor of to survival. The patient underwent surgical tumor resection successfully and will be followed up.

259 Is It Really a Malignancy? A Case of Chronic Pancreatitis With Vitamin D Deficiency Masquerading as Malignancy Ashref Mohamed 1, Kenneth Nugent2. 1. Texas Tech University Health Sciences Center, Lubbock, TX; 2. Texas Tech University Health Science Center, Lubbock, TX. Chronic pancreatitis is longstanding inflammation of the pancreas that causes scarring and damage to the organ which eventually leads to alteration in its structure and function. Chronic pancreatitis can

[258A] Figure 1.

[258B] Figure 2.

[259A] Figure 1.

[258C] Figure 3.



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D levels and if low, then PTH levels. We can cut back on malignancy workup and save lot on financial burden in Health Care.

260 Renal Cell Carcinoma Presenting as an Ampullary Mass: A Case Report and Review of Literature Syed Hasan, MD1, Toseef Javaid, MD1, Nauman Siddiqui, MD2, Ali Nawras, MD, FACG3. 1. University of Toledo, Toledo, OH; 2. University Of Toledo Medical Center, Toledo, OH; 3. University of Toledo Medical Center, Toledo, OH. Introduction: Renal cell carcinoma accounts for 3-4% of all malignancies and is often treatable by surgical nephrectomy. Despite this, up to 50% of patients have recurrences with distant metastases, though metastasis to the ampulla of Vater is exceedingly rare. To our knowledge this is the 12th case of renal cell carcinoma with metastasis to the ampulla. Amongst the typical findings are bleeding and jaundice. Most patients with ampullary metastasis have been previously diagnosed with RCC. Case: This is a case of a 60 year old female patient with a past medical history significant for renal cell carcinoma status post right nephrectomy and chemotherapy. On a previous CT she was noted to have pancreatic a mass that was compressing the common bile duct. She presented to the hospital with low back pain, fatigue, jaundice and a 2 week history of nausea and vomiting. Endoscopic retrograde cholangiopancreatogram (ERCP) and endoscopic ultrasound (EUS) revealed a large ampullary mass causing biliary obstruction with multiple large subcarinal, celiac, and paraduodenal lymph nodes, the largest of which was 42mm X 36mm. Fine needle aspirates of the ampullary mass and subcarinal lymph nodes, all of which revealed metastatic renal cell carcinoma. A biliary stent was placed and over the course of the next day the patients biliary obstruction was relieved. Conclusion: Ampullary metastasis should be considered amongst the causes of biliary obstruction in patients with a history of renal cell carcinoma. Early diagnosis and excision of the tumor can help to improve the patients outcome.

[259B] Figure 2.

cause severe vitamin D deficiency, which could be significant, causing secondary hyperparathyroidism and bone lesions. Clinicians should be aware of the causes of bone lesion found incidentally. Most common differential for a patient with Bone lesion is malignancy. Other causes not uncommon but to be considered as seen in our patient are vitamin D deficiency secondary to causes such as chronic pancreatitis. 49 year-old African American inmate presented to our hospital, as a transfer from outside facility with a concern of metastatic cancer after bone scan showed evidence of osteoplastic lesions in the humeri and ribs. Patient has history of significant weight loss, night sweats, generalized weakness and bone pain over a course of one year. He also has a history of rib fracture secondary to simple fall. He reported a history of heavy alcohol abuse before he was incarcerated in prison in 1995. On Physical exam he looked cachectic, clinically anemic. Chest was clear to auscultation with chest wall tenderness . Abdomen is soft with no organomegally. Rectal exam was negative. His admission labs were remarkable for Calcium 5.9 mg/dl, Vitamin D level was undetectable. His HIV serology was negative. Repeated bone scan shows pathologic radio tracer uptake in the ribs and pubic bones. Malignancy work up including CT scan chest, abdomen and pelvis was unremarkable. Tumor markers including PSA were negative. Pancreas was noted to be atrophic with calcification in the abdominal CT scan. On further questioning, patient gave history of chronic abdominal pain and diarrheal episodes. We ordered PTH . It was 1590 pg/ml . It was concluded that his clinical manifestation is related to severe pancreatitis with subsequent malabsorption syndrome and severe vitamin D deficiency which have led to what’s called brown tumors of the bone with pathological fracture. Patient then was started on pancreatic enzymes replacement, Vitamin D and calcium. We are reporting a rare presentation of chronic pancreatitis. Clinical manifestation such bone pain, fractures, and weight loss with bone lesions in bone scan could be misleading of cancer diagnosis and could lead to ordering complex and expensive tests . Clinician should be alert to the late and severe presentation of chronic pancreatitis causing vitamin D deficiency with subsequent secondary hyperparathyroidism leading to Brown tumors particularly in patient who have dark skin, prisoners with limited sun exposure such as in our patient. These patients will benefit with simple lab tests such as vitamin

[260]

261 Systemic Amyloidosis Presenting as an Ampullary Mass With the Double Duct Sign Andrew Korson, MD1, Kirsten Threlkeld, MD1, Matthew M. Yeh, MD, PhD2, Bryan L. Balmadrid, MD3. 1. University of Washington, Seattle, WA; 2. University of Washington, Department of Pathology, Seattle, WA; 3. University of Washington, Division of Gastroenterology, Seattle, WA. A 60 year old man with a history of Hepatitis C, intravenous drug use and end stage renal disease undergoing hemodialysis presented to our hospital with fever, confusion and severe, episodic left lower quadrant (LLQ) “dull” abdominal pain with sharp “twinges” worsened by meals and associated with anorexia and early satiety. Physical examination was remarkable for LLQ abdominal pain without rebound or guarding. Laboratory studies including liver biochemical tests, and CBC were normal. CT of the abdomen revealed a 10mm polypoid mass at the ampulla of vater with prominence of the pancreatic and common bile ducts measuring 4mm and 8mm respectively, the “double duct sign”, concerning for pancreatobilliary malignancy. EGD revealed a 10mm ampulla with irregular polypoid characteristics, and a 3mm duodenal polyp with thickened duodenal folds (figure 1). Endoscopic ultrasound demonstrated mild dilation of the pancreatic duct measuring 5mm in the body and head of the pancreas with normal pancreatic echotexture without cysts, masses or calcifications. The common bile duct was dilated, measuring 8 mm without choledocholithiasis or sludge (figure 2). Histological examination of the periampullary mass and duodenal polyps showed slightly polypoid and denuded mucosa with blunted villi, and gastric foveolar metaplasia. Surprisingly, abundant eosinophilic and amorphous material was identified within the lamina propria, between the crypts, and within blood vessels. The material appeared “salmon-colored” under routine

Table 1. Literature Review

Patient

Age

Gender

Diagnosis prior to Ampullary Metastasis

Side of Tumor

Staging of RCC at Diagnosis

Time from Nephrectomy

Symptoms

Outcome

1

50

M

No

R

N/A

N/A

Jaundice, Fever, Malaise, fatigue, GI Bleed, Weight Loss

Pancreatoduodenectomy (curative 5yrs)

2

77

M

Yes (w/nephrectomy)

R

T2N0M0

3 YRS

Jaundice

Sunitinib, Endoscopic Excision with APC for palliation. Died of metastatic disease (1.5ys)

3

78

F

Yes (w/nephrectomy)

L

STAGE 2

10 YRS

Pruritis, Melena, Weight Loss

Pancreatoduodenectomy (curative 2.5yrs)

4

53

M

Yes (w/nephrectomy)

R

STAGE 3

8 YRS

Melena, Weight Loss

Megace, Transduodenal resection with Pancreatoduodenectomy and retroperitoneal lymph node resection (curative 6.5yrs)

5

64

M

Yes (w/nephrectomy)

L

N/A

11 YRS

Malais, SOB, Fatigue

Megace, surgical resection. Died of Pulmonary Embolism post-operatively

6

70

M

Yes (w/nephrectomy)

L

STAGE 3

12 YRS

Weakness, melena

Pancreatoduodenectomy

7

52

M

Yes (w/nephrectomy)

R&L

1B

10 YRS AND 4 YRS

Weight Loss, Anemia, Malabsorption, Steatorrhea


8

78

F

Yes (w/nephrectomy)

R

N/A

16 YRS

Anemia, Weight Loss, Melena, Upper GI Bleed


9

68

F

Yes (w/nephrectomy)

L

N/A

6.5 YRS

Upper GI Bleed, Epigastric Pain


10

75

M

Yes (w/nephrectomy)

L

N/A

17.5 YRS

Upper GI Bleed

Unknown

11

55

F

Yes (w/nephrectomy)

L

1

2 YRS

Obstructive Jaundice

Died of Metastatic Disease

12 Our Case

60

F

Yes (w/nephrectomy)

R

4

4 MONTHS

Fatigue, Jaundice, Nausea, Vomiting, Anemia



| OCTOBER 2015

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Abstracts HPI: An 87 year old male with diagnosis of Prostate Cancer(CR) was started on chemotherapy with docetaxel and prednisone, following the 1st cycle he developed melena, secondary to prednisone induced gastritis. Prednisone was discontinued and Docetaxel dose was reduced by 20%, he tolerated cycles 2 and 3 well and received 4th cycle a day prior to presentation. Within few hours of the infusion, he began to experience epigastric discomfort which progressed to an intense stabbing epigastric pain, following which he presented to our facility. On PE, there was guarding with excruciatingly tender left upper quadrant and diminished bowel sounds. CT abdomen showed mesentric edema, increased density and stranding adjacent to the pancrease, consistent with acute pancreatitis. Lab studies showed amylase, 1482 U/L; lipase, 10279 U/L & normal calcium, bilirubin, and triglyceride levels. The patient was hospitalized, and given IVF with analgesics. By the following day, he reported significantly less pain and tolerated a liquid diet. By day 3, amylase and lipase levels reduced significantly(307 and 416 U/L, respectively). He was able to tolerate a solid diet by day 5 and was discharged home (graph.1). The patient received no further chemotherapy as he decided to pursue hospice care due to reduced performance status. Discussion: The patient’s clinical and lab presentation was consistent with acute pancreatitis. His home medications included Omeprazole and HCTZ, which have previously been reported to cause pancreatitis, but the patient had tolerated these medications for a period of time without any adverse effects. Re-administering Docetaxel to determine definite causality was not feasible due to the severity of his presentation. Based on the adverse drug reaction probability scale, by Naranjo et al; there was possible cause, while as per the WHO-UMC causality criteria; Docetaxel was the probable cause of acute pancreatitis in this patient.

[261A] Figure 1.

[262A]

Table 1. Amylase levels(U/l)

Lipase levels(/l)

Day 1

1482

10,279

Day 3

307

416

Day 5

260

[261B] Figure 2.

light microscopy and the sections were stained with Congo Red and demonstrated apple-green birefringence under polarized light, consistent with amyloid deposition (figure 1). Systemic amyloidosis encompasses a group of disorders arising from the extracellular deposition of insoluble polymeric protein fibrils which disrupt the structure and function of tissue. Gastrointestinal manifestations of amyloidosis are protean, ranging from nausea, abdominal pain, and malabsorptive diarrhea to pseudo-obstruction, bleeding and perforation. While primary AL amyloidosis is the most common form, and can present polypoid intraluminal masses, the amyloid material is typically found within the muscularis mucosa, submucosa and muscularis propria. In contrast, amyloid deposits seen in AA amyloidosis are found in the lamina propria as in the present case. To our knowledge, this is the first case report of systemic amyloidosis with duodenal involvement presenting as an ampullary lesion causing papillary stenosis with an enlarged pancreatic and common bile duct. The case highlights the protean manifestations of amyloidosis and emphasizes the importance of a broad differential diagnosis when evaluating polypoid masses in the upper gastrointestinal tract. n/a: form will not allow submission without entering a table, please do not publish this table.

[262A] Figure 1.

262 Docetaxel-Induced Acute Pancreatitis Vijayalekshmi Nair, MBBS1, Naveen Gnanabakthan, MD1, Dinesh John, MD, CPHQ2. 1. SUNY Upstate University Hospital, Syracuse, NY; 2. VA hospital, Upstate Medical University, Syracuse, NY. Introduction: Docetaxel is a taxane derivative that has been FDA approved for 5 key cancers including prostate cancer. It has been well established and widely used for around 20 years, with known side effects. We are reporting a case of acute pancreatitis induced by Docetaxel, a very rare side effect that has been reported only once previously.


[262B] Figure 2.


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Pancreatitis is an infrequent, but potentially critical complication of chemotherapy. On review of literature, pancreatitis has previously been reported with multiple chemotherapeutic agents. It is possible that diagnosis of pancreatitis may be missed in patients with milder symptoms, as nausea,vomiting and abdominal pain are frequently assumed to be secondary to chemotherapy. A high index of suspicion is required to make an accurate diagnosis of chemotherapy related pancreatitis in patients with similar clinical presentation.

263 Pancreatic Cancer: The Great Masquerader Arunpreet Kahlon, MBBS1, Praneet Wander, MD2, Dhruv Lowe, MD1, Wajihuddin Syed, MBBS1, Amrita Dhillon, MMBS1, Fatme Allam1. 1. SUNY Upstate Medical University, Syracuse, NY; 2. Mount Sinai St. Luke’s Roosevelt Hospital Center, New York, NY. Pancreatic malignancy is one of the most lethal cancers of human body. Survival rates are improving but are still very poor with 1 year survival rate of 20% and 5 year survival rate of around 6%. Catching the tumor at an early stage is the key for a favourable outcome. We describe a case of pancreatic cancer where the pancreatic cancers ability to hide itself proved to be more than the diagnostic resources available. Case: A 76 year old male with past medical history of coronary artery disease, diabetes mellitus, and hypothyroidism presented to his primary care office with decreased appetite, weakness and tiredness. He was found to have 60 pounds weight loss in 1 year. He was also having generalized pruiritis, dark urine and whitish colored stools. His laboratory findings were significant for abnormal liver function tests with AST, ALT, alkaline phosphatase, albumin, Bilirubin total and direct of 200 units/L , 250 Units/L ,1200 international units/L, 0.8 g/dl ,5 mg/dl and 4 mg/dl respectively. A CT scan of abdomen showed a periampullary mass in the pancreatic head and dilated common bile duct (CBD) and hepatic ducts. Patient was sent to hospital for endoscopic retrograde cholangio-pancreatography(ERCP) and further evaluation of the mass. ERCP revealed no stone or biliary sludge and a stent was placed in the CBD to drain the bile. Two EUS guided biopsy of the periampullary mass was obtained on separate occasions showed benign cellular elements both times. A CA 19-9 level was elevated. Positron emission tomography (PET) scan came back negative for any intra-abdominal malignancy. Patient eventually developed acute cholangitis and pneumonia and was admitted to intensive care unit. A surgical consult for biopsy of pancreatic mass was considered but due to his low albumin levels and co-morbidities, he was considered a poor surgical candidate. He died few weeks later and an autopsy done showed mucinous adenocarcinoma of pancreatic head with surrounding fibrous tissue. Discussion: Periampullary mass in pancreas seen on abdominal imaging is 90% of time malignant. Accuracy of EUS guided fine needle aspiration biopsy is between 75 to 95%. PET scans are 85 to 90% accurate in diagnosing a pancreatic cancer. Our case is a rare scenario where pancreatic cancer escaped 2 EUS guided biopsies and a PET scan. Autopsy showed adenocarcinoma surrounded with fibrous tissue revealing aggressiveness of this cancer. This case provides a great learning point that pancreatic cancer can evade all diagnostic modalities and prompt surgical intervention should be sought for diagnosis if patient is a candidate.

264 Littoral Cell Angioma of the Spleen Krishna Venkata, MD, Ronak Patel, Rehan Sarmad, Mohsen Hasanin, Kannan Thanikachalam. University of Alabama Birmingham Montgomery Campus, Montgomery, AL. Littoral Cell Angioma (LCA) of the spleen is a rare benign vascular tumor arising from littoral cells which are flattened endothelial cells with phagocytic and hematopoietic properties lining vascular sinuses of lymph nodes, spleen and liver. Less than 100 cases have been reported in the literature. A 66-year-old man presented with melena and fatigue. He was anemic (Hb 4.4gm/dL) and thrombocytopenic (Platelet 49k/μL) on admission. EGD showed polyps and an arteriovenous malformation in 2nd part of duodenum. Biopsy was negative for dysplasia while that of gastric mucosa was positive for H. pylori. Further investigation revealed that 7 years ago, when being evaluated for blunt trauma, CT showed an enlarged spleen with multiple low attenuated lesions in the spleen that were worrisome for either lymphoma or metastases. At that time his Hb was 10.8gm/dL, MCV 71 fl, platelets 71k/μL and his peripheral blood smear revealed microcytic anemia, schistocytes, reticulocytes, and thrombocytopenia. Splenic biopsy showed scattered small cystic spaces lined with tall endothelial cells, negative for CD 34, positive for CD 68 and vimentin, findings consistent with the diagnosis of LCA. As the patient was asymptomatic, he was discharged and advised to follow-up with hematology. He was lost to follow-up and presented to ER with anemia and thrombocytopenia- most common presenting features of LCA. Primary tumors of the spleen are rare when lymphoid and hematologic tumors are excluded. LCA should be considered in the differential diagnosis of multinodular spleen, especially in the presence of anemia, thrombocytopenia and absence of associated adenopathy. While fever, fatigue, weight loss, early satiety maybe presenting symptoms, most patients are asymptomatic and detected incidentally, as in our case. In advanced cases, splenic rupture and hemo-peritoneum can occur. On CT with contrast during the portal venous phase multiple small ovoid areas of hypoattenuation are seen in the spleen. Metastatic disease, lymphoma, sarcoidosis, Kaposi’s sarcoma, microabscess formation due to infectious etiology may mimic LCA. Ultrasound guided biopsy with histopathology and immune histochemical studies (positive for CD31, CD68, CD163, CD21, Factor VIII antigen, and negative for CD34 and CD8) can confirm the diagnosis. Definitive treatment for LCA is splenectomy but close clinical follow up and surveillance is recommended due to the association with visceral cancers and malignant lymphoma in recent case reports.

265 Hemodynamic Instability Secondary to Inferior Vena Cava Compression: A Rare Complication of Massive Walled-off Pancreatic Necrosis Toseef Javaid, MD1, Nauman Siddiqui, MD2, Syed Hasan, MD1, Jamal Saleh, MD2, Arunkumar Baskara, MD3, Ali Nawras, MD, FACG4. 1. University of Toledo, Toledo, OH; 2. University Of Toledo Medical Center, Toledo, OH; 3. University Of Toledo Medical Center, Perrysburg, OH; 4. University of Toledo Medical Center, Toledo, OH. Severe acute pancreatitis has significant morbidity and mortality and is often complicated by pancreatic necrosis. Walled-off pancreatic necrosis (WOPN) may form as a sequelae of acute pancreatitis over the following weeks. Most uncomplicated acute pancreatic fluid collections are managed conservatively unless symptomatic or infected. We present a rare complication of WOPN causing IVC compression leading to shock requiring emergent intervention.

[265A] Figure 1.



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Abstracts A 56 year old male with a history of alcoholism presented with right lower quadrant abdominal pain and a significant elevation of amylase and lipase. Initial CT scan showed moderate necrosis at the head of the pancreas with a moderate fluid collection in the right half of the abdominal cavity. MRCP showed a dilated main pancreatic duct proximally with distal tapering towards the tail of the pancreas and stone in the main pancreatic duct. Despite a week of conservative treatment with fluids, bowel rest and pain control, the patient continued to have worsening abdominal pain. A repeat CT scan showed an interval increase in fluid collection compared to prior exam. At this time, endoscopic intervention was deferred as pancreatic necrosis was not walled off. However, the patient developed progressively worsening abdominal distention over the following week followed by sudden onset respiratory distress and hemodynamic instability on 18th day from initial presentation. The patient was transferred to the intensive care unit and CT scan showed a massive walled-off pancreatic necrosis causing compression of inferior vena (image 1 a & b) and right hydronephrosis (image1c) with large amount of necrotic fluid in right retronephric space displacing right kidney anteriorly. An emergent CT guided percutaneous drainage was performed with significant improvement in fluid collection (image 2) and patient’s vital signs and respiratory distress over next 24hours. Fluid output from percutaneous drain slowly decreased over next few days as the patient continued to recover. Compression of IVC by a large walled-off pancreatic necrosis is a rare potential cause of hemodynamic instability in a patient with severe acute pancreatitis.

266 Autoimmune Pancreatitis Resolved Without Any Steroid Trial Suzan Ebrahimi1, Amir Taefi, MD2, Won Cho, MD2. 1. Washington Hospital Center, Chevy Chase, MD; 2. MedStar Washington Hospital Center, Washington, DC. Back ground: Autoimmune pancreatitis is a benign fibroinflammatory disease of the pancreas of probable autoimmune origin, which includes 2 different phenotypes: type 1 (lymphoplasmacytic sclerosing pancreatitis) and type 2 (idiopathic duct-centric pancreatitis). Its clinical presentation as obstructive jaundice in patients with a pancreatic mass is common and therefore it must be included in the differential diagnosis of pancreatic neoplasia. Autoimmune pancreatitis (AIP) and its histopathological features typically respond dramatically to steroid therapy. Case report: A 74-year-old male with uncontrolled type II Diabetes Mellitus, essential hypertension presented to medicine clinic complaining of weight loss and jaundice. Patient lost about 5 pounds over 3 months. Review of systems is unremarkable. Routine work up revealed elevated LFT’s (AST, ALT, Alk phos) and patient was hospitalized for further evaluation. MRCP was performed which revealed a pancreatic head mass with parapancreatic lymph nodes involvement suggestive of malignancy. CA 19-9 and CEA were normal. EUS with FNA biopsy did not reveal evidence of malignancy. ERCP with biliary stent and cytologic brushing was then performed. The CBD cytologic brushing failed to show malignant cells. Patient’s hepatitis panel, workup for connective tissue disease, serum ceruloplasmin and autoimmune hepatitis were all normal except elevated IGG. Considering absence of malignancy, elevated IGG and advanced imaging, a diagnosis of autoimmune pancreatitis was made. Without any steroid trial, repeat imaging showed significant improvement in the pancreatic inflammation. Patient gained weight, and LFT became normal. Conclusion: One of the main features of autoimmune pancreatitis is its dramatic response to steroid therapy, without the need for surgical treatment. Our case was unique given the fact that without using steroid; repeat imaging showed no mass or inflammation in the head of the pancreas.

[267A] Figure 1.

267 Endoscopic Resection of Early Ampullary Carcinoma in Medically Frail Patients Hassaan A. Zia, MD1, George Salem, MD2, Khadija Chaudrey, MD3, John Maple, DO2. 1. Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK; 2. University of Oklahoma Health Sciences Center, Oklahoma City, OK; 3. Digestive Diseases and Nutrition Division, University of Oklahoma Health Sciences Center, Oklahoma City, OK. Introduction: There is scarcity of data for the role and outcomes of Endoscopic Ampullectomy for ampullary carcinomas. While pancreaticoduodenectomy (PD) is the primary surgical approach for ampullary carcinoma, age and medical comorbidities may limit its use. We report two cases of endoscopic resection of early ampullary carcinomas. Case 1: An 82 year-old male presented elsewhere with jaundice and biliary dilatation on abdominal ultrasound. Endoscopic Retrograde Cholangiopancreaticography (ERCP) revealed a fungating, mildly ulcerated, friable ampullary mass. Forceps biopsies revealed a tubulovillous adenoma with high grade dysplasia. Upon referral to our center, endoscopic ultrasound (EUS) identified a 2.5 cm ampullary mass, staged T1N0M0. Owing to patient and surgeon’s refusal to pursue PD, endoscopic ampullectomy was requested. At ERCP, the ampullary mass was resected en bloc with a 27 mm oval polypectomy snare using ERBE Endocut current (ERBE USA, Marietta, GA). Histopathology demonstrated mucinous adenocarcinoma arising in a tubulovillous adenoma, not involving the resection margins. On a 4 month surveillance ERCP, an 8 mm sessile polyp at the ampullectomy site was resected, consistent with tubular adenoma on histopathology. A 10 month surveillance ERCP, showed no gross or histopathologic evidence of residual or recurrent neoplasia at ampullectomy scar site. A primary care clinic visit 2.5 years later remained reassuring. Case 2: A 72 year-old male with history of COPD and peptic ulcer disease status-post partial gastrectomy presented with abdominal pain, diarrhea and raised alkaline phosphatase levels. Computerized tomography of the abdomen showed intra- and extrahepatic biliary dilatation. At EUS a 2.8 cm polypoid ampullary mass was identified (image 1), staged T1N0M0. Forceps biopsies demonstrated tubular adenoma. At subsequent ERCP the ampullary lesion was completely resected en bloc using a polypectomy snare with ERBE Endocut current (image 2). Histopathology showed a low grade ampullary adenocarcinoma extending to the surgical margins with no lymphovascular invasion. Owing to chronic lung disease, surgical consultation was deferred, patient now awaits a planned surveillance ERCP. Conclusion: Endoscopic ampullectomy has decreased associated morbidity and mortality compared to local or radical surgical resections and may deserve consideration in aged and medically unfit patients. This remains an area for further interest and investigation.


[267B] Figure 2.

268 Post Cholecystectomy Bile Leak From the Duct of Luschka in a Patient With Marfan’s Syndrome Zainab Shahnawaz1, Muhammad O. Arif, MD2, Ajoy Roy, MD3. 1. Upstate Medical University, Camillus, NY; 2. SUNY Upstate Medical University, Syracuse, NY; 3. Upstate Medical University, Syracuse, NY. Marfan’s syndrome is a rare connective tissue disorder and has been associated with poor post-surgical wound healing. It has been associated with increased incidence of Cholelithiasis as compared to the general population. There is no literature regarding post-cholecystectomy complications in patients with Marfan’s syndrome. We present a 29 year old female with Marfan’s syndrome and a history of aortic dissection with aortic valve rupture and replacement with prosthesis. She was diagnosed with gallstone pancreatitis and Choledocholithiasis. Endoscopic retrograde cholangiogram showed a 20 mm stone in the common bile duct. Multiple endoscopic procedures were needed to accomplish removal of the large stone and these included papillotomy, stenting and mechanical lithotripsy. Laparoscopic cholecystectomy was attempted which had to be converted to laparotomy due to extensive scarring around the gallbladder. Intraoperatively, a bile leak was noted which on cholangiogram was found to be from a severed accessory Duct of Luschka. The leak was closed with suturing. Two weeks post-surgery, the patient developed right upper quadrant abdominal pain. Imaging showed a fluid collection in the gallbladder fossa. Nuclear hepatobiliary (HIDA) scan did not show a bile leak. Percutaneous drainage of the fluid collection was performed and 40 cc of green colored fluid was aspirated, analysis of which did not reveal any


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[269A] Figure 1.

[268A] Figure 1.

[269B] Figure 2.

[268B] Figure 2.

evidence of infection. After two weeks, she presented with severe chest pain radiating to the back. Her WBC count was increased at 21,000 and CT imaging at this time showed a larger fluid collection in the gallbladder fossa. Repeat HIDA scan did not show a bile leak. She underwent repeat percutaneous drainage and 20 cc of purulent material was aspirated. She was treated with antibiotics and discharged from the hospital. Follow up CT showed significant reduction in the size of the fluid collection. To our knowledge, this is the first reported case of post cholecystectomy bile leak in a patient with Marfan’s syndrome which was from injury to the Duct of Luschka. Intraoperative ligation of the duct with suturing failed to control the leak leading to a Biloma and subsequent abscess. This may have been a result of poor wound healing around the suture. In patients with connective tissue disorders such as Marfan’s syndrome, Endoscopic therapy of post-cholecystectomy bile leaks with trans-papillary biliary stenting may be considered.

269 A Rare and Fatal Case of ST-Segment Elevation Myocardial Infarction and Pancreatitis Geoffrey You, MD1, Julia Shor, MD2, Francesco Pontoriero, DO3, Christine Fanning, MD3. 1. Rutgers Robert Wood Johnson Medical School, Newark, NJ; 2. Rutgers Robert Wood Johnson University Hospital, Highland Park, NJ; 3. Rutgers Robert Wood Johnson University Hospital, New Brunswick, NJ. Introduction: Acute pancreatitis, while generally a local process, can cause widespread systemic effects. Although the cardiac manifestations of acute pancreatitis are usually limited to arrhythmias and nonspe-


cific ST changes, it is rarely associated with true ST-segment elevation myocardial infarctions (STEMIs). We present the first reported case of acute pancreatitis complicated by STEMI and fatal hemorrhagic necrosis of the pancreas. Case Report: A 68 year old male presented with severe abdominal pain radiating to his chest and back after a fatty meal. Initial evaluation was notable for an EKG with 1.5-2mm ST-elevations in the inferolateral leads as well as lipase >2,450 U/L. Acute coronary syndrome protocol was immediately activated and the patient was given loading dose clopidogrel prior to undergoing cardiac catheterization. He was found to have 100% occlusion of the mid left circumflex artery for which a bare metal stent was placed. The patient was kept on integrilin drip for the next 12 hours, as well as daily aspirin, clopidogrel, and statin therapy. His chest pain quickly resolved, however the abdominal pain persisted and he was treated in the CCU with bowel rest, IV fluids, and pain control for pancreatitis. It was thought that the cause of pancreatitis was likely of biliary etiology, however, ERCP was deferred in light of patient’s cardiac status. Over the next two days, the patient’s condition rapidly deteriorated with multisystem organ failure requiring initiation of hemodialysis and mechanical ventilation. On day 3 of hospitalization, he became bradycardic and asystolic, and expired despite resuscitation with ACLS protocol. An autopsy revealed extensive necrosis and hemorrhage of the entire pancreas. Discussion: While the presentation of acute pancreatitis can mimic that of acute STEMI, it is rare to have the two entities coexist with less than 10 case reports in the current literature. However, this represents the first case of acute pancreatitis complicated by myocardial infarction (MI) and fatal hemorrhagic necrosis of the pancreas following stenting and antiplatelet therapy. At present, management of MI in the setting of acute pancreatitis remains undefined due to a paucity of cases. Although pancreatitis is not a contraindication to antiplatelet therapy, in the setting of a concurrent STEMI it may be reasonable to consider balloon angioplasty as an alternative to stenting and dual antiplatelet therapy in order to avoid the risk of a fatal complication of hemorrhagic pancreas.


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Abstracts 270

271

An Unusual Cause of Hemobilia

Mirrizi Syndrome in a 28-Year-Old Gentleman With Sickle Cell Disease

Rohit Sharda, MD, Andrew Scanga, MD. Vanderbilt University, Nashville, TN.

Jacek Mysior, MD1, Venkata Gourineni, MD2, Jay Krishnakurup, MD3, Caroline S. Loeser, MD4. 1. Bridgeport Hospital/Yale University School of Medicine, New Haven, CT; 2. Bridgeport Hospital/Yale University School of Medicine, Milford, CT; 3. Bridgeport Hospital/Yale University School of Medicine, Bridgeport, CT; 4. Bridgeport Hospital/Yale University School of Medicine, Bridgeport, CT.

Introduction: Patient is a 65-year-old Caucasian woman with NASH cirrhosis complicated by transfusion-dependent GI bleeding, GAVE, and a recent history of TIPS placement 9 months prior to admission who presented electively for recurrent GAVE ablation. Over the preceding year, the patient had reportedly received more than 170 U of packed RBCs due to ongoing, intermittent episodes of bleeding. Extensive prior endoscopic evaluation, including EGD, enteroscopy, and colonoscopy, revealed portal hypertensive gastropathy and changes consistent with GAVE, but no active bleeding lesions had previously been described. As such, given presumed GAVE-related bleeding, the patient had undergone regularly scheduled GAVE ablations with temporary hemostasis, but no permanent cessation of bleeding. On this occasion, endoscopic evaluation of the antrum once again revealed GAVE, which was ablated. However, upon entering the duodenum, a gush of blood was seen emanating from the major papilla, which was confirmed via direct visualization using a duodenoscope. This had never previously been described on any of her prior endoscopies. Given recent history of TIPS placement, patient was sent for angiography, where she was found to have a hepatic artery pseudoaneurysm. She underwent coil embolization with occlusion of the right anterior segmental artery, preservation of the right posterior segmental artery and no flow into the pseudoaneurysm. Discussion: Hepatic artery pseudoaneurysm leading to hemobilia is an uncommon complication of TIPS placement (less than 5% of cases), particularly when occurring in such a delayed fashion. Hemobilia may occur in the setting of traumatic liver injury, iatrogenic liver procedures (surgery, biopsies, percutaneous transhepatic cholangiography), or pancreatic ductal hemorrhage (hemosuccus pancreaticus). In the setting of TIPS, placement of the shunt can lead to an abnormal fistulous communication between intrahepatic bile ducts and branches of the hepatic artery, with resultant blood loss manifesting as hemobilia. While initial endoscopic evaluation can raise suspicion for hemobilia, diagnosis and treatment are best accomplished via IR-guided transarterial embolization. Surgical intervention is also possible, but carries a much higher morbidity and mortality. Outcome: Following embolization of her hepatic artery pseudoaneurysm, our patient stabilized and did relatively well for a brief time period. Unfortunately, due to multiple infectious complications and progressive deterioration of her liver function, she was eventually transitioned to hospice care several months after this presentation.

Patient is a 28 year old African gentleman from Ghana with sickle cell disease, anemia, malaria, and chronic indirect bilirubinemia, with one previous sickle cell crisis in the setting of acute malarial infection. who presented to the hospital with 3 days of bilateral upper quadrant abdominal pain associated with nausea and vomiting. Review of systems was positive for dark urine, headache and decreased appetite. On examination, he was afebrile, with a regular heart rate and rhythm and normal respiratory rate. He was jaundiced and had right upper quadrant fullness, tenderness, and guarding. There was no abdominal rigidity. The remainder of the examination was normal. Laboratory evaluation revealed normal kidney function, elevated bilirubin to 31. 7 mg/dl with direct bilirubin of 27 mg/dl,ALP 239 u/L., AST 200 u/L, ALT 94 u/L, hemoglobin 7.1 g/dl,lipase 23 u/L, INR 1.2, and ferritin 122. Ultrasound of the abdomen showed intrahepatic biliary duct dilatation and common biliary duct (CBD) measuring 10mm with enlarged gallbladder and multiple echogenic shadowing stones and gallbladder thickness measuring 5mm. Subsequent magnetic resonance imaging revealed a 1.4 cm stone in the neck of the cystic duct protruding into the CBD with no stones in the CBD. Patient underwent an endoscopic retrograde cholangiopancreatogram with stent placement in the CBD followed by a open cholecystectomy that revealed xanthogranulomatous cholecystitis and pigmented cholelithiasis. The patient’s hyperbilirubinemia improved and returned to his baseline indirect predominance. Conclusion: Mirrizzi syndrome should remain in the differential in young patients with sickle cell disease due to increased risk of long standing pigmented gallstones.

272 Biliary Obstruction and Ascending Cholangitis Caused by an Atypical Human Parasite: Fascioliasis Faryal Mirza, MD1, Suzan Ebrahimi2, R. Martin Bashir, MD, FACG1. 1. MedStar Washington Hospital Center, Washington, DC; 2. Washington Hospital Center, Chevy Chase, MD. Fascioliasis a zoonotic infection effecting ruminants such as sheep and goats and is caused by Fasciola Hepatica or Fasciola Gigantica. F. Hepatica has worldwide distribution while F. Gigantica is prevalent in tropics. Fascioliasis occurs in the United States in domesticated herbivorous pets, but is very uncommon in humans, with only a few human cases reported to date. We report a common presentation of a very uncommon infection in humans, diagnosed by ERCP. A 63-year-old African American female originally from Ethiopia presented with two weeks of right upper quadrant pain, fever, lethargy and jaundice. Laboratory assessment was remarkable for elevated transaminases, ALP, hyperbilirubinemia and marked leukocytosis with eosinophilia. Abdominal sonogram revealed a distended gallbladder with diffuse biliary ductal dilation. CT (A/P) demonstrated dilated biliary tree with acalculous cholecystits. MRCP revealed intra and extra hepatic biliary dilation without calculi. ERCP demonstrated biliary sludge and cholangitis with a large amount of viscous, purulent drainage noted after sphincterotomy. Bile aspirate and culture for ova/parasite revealed intestinal flukes, specifically F Hepatica. Patient was successfully treated with nitazoxanide, and subsequently developed an upper gastrointestinal bleed, which required transfusion. An EGD was performed revealing gastric and duodenal ulcerations with marginal biopsies demonstrating marked eosinophilia. In conclusion, diagnosing fascioliasis in a timely manner prevents the acute phase of infection from becoming chronic. Typically, fascioliasis is diagnosed by multiple modalities such as stool or duodenal aspirate for presence of ova/ parasites, commonly in its early stage. Although not conventionally used to diagnose fasciola infections, ERCP with biliary aspiration can be diagnostic and therapeutic to alleviate patient’s symptoms of biliary obstruction. Therefore, ERCP should be considered as diagnostic modality in management of parasitosis. We report this case to emphasize the importance of having fascioliasis in a differential diagnosis of patients presenting with biliary obstruction, eosinophilia and vague abdominal symptoms.

[270A] Figure 1.

273 EUS-guided Endoscopic Transduodenal Necrosectomy in a Patient With Sleeve Gastrectomy Avik Sarkar, MD1, Ragui Sadek, MD2, Matthew Lissauer, MD1, Amy Tilara, MD1, Swati Pawa, MD1. 1. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ; 2. Advanced Surgical & Bariatrics of NJ, Somerset, NJ.

[270B] Figure 2.


Walled-off pancreatic fluid collections (PFC) occur after an acute attack of pancreatitis in approximately 10 percent of cases. Decompression of the collection is advocated when specific indications are met, such as pain, gastric outlet or biliary obstruction, fluid leakage, fistulization, weight loss and infection. Endoscopic drainage has been widely adopted as the primary approach for symptomatic walled-off PFC. Difficulty can arise in cases of altered gastric anatomy, as the procedure requires an adequate amount of space to maneuver. We present the first case of a patient with sleeve gastrectomy who underwent successful endoscopic transduodenal necrosectomy (TDN). 40 year old woman with history of morbid obesity status post sleeve gastrectomy in 2009 with intermittent post-prandial RUQ abdominal pain was found to have symptomatic gallstone disease. Patient’s course was complicated by severe necrotizing gallstone pancreatitis and further complicated by symptomatic walled off pancreatic necrosis (WOPN). Imaging at 8 weeks revealed 10.8 x 7.6 cm fluid collection with portions of solid components seen in the body and tail of the pancreas. The decision was made to attempt endoscopic necrosectomy. EGD revealed a tubular gastric body and antrum, with extrinsic compression in the antrum and duodenal bulb from the pancreatic cyst. Duodenal bulb was selected as the preferred fistula site due to sleeve gastrectomy. The patient underwent successful TDN with placement of three 10Fr pigtail stents. Patient had symptomatic improvement and was discharged to outpatient follow-up. Although the transgastric approach is preferred for walled-off PFC, usually due to more favorable location, as well as the comfort level of endoscopists, there is no definite evidence that transgastric drainage


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is superior to transduodenal drainage. The duodenal approach was used in our patient as sleeve gastrectomy involves removal of the stomach body and a large portion of the antrum producing a high pressure system inside the stomach which may lead to inadequate drainage. Additionally, intervention adjacent to the staple line may predispose to anastomotic leak and break down of the staple line. One prior case has been reported of a patient with sleeve gastrectomy undergoing laparoscopic cyst-gastrostomy after aborted endoscopic cyst-gastrostomy due to limited working space and the inability to visualize the posterior aspect of the stomach. Although laparoscopic cyst-gastrostomy is an acceptable approach for these patients, randomized trials have demonstrated equal efficacy between endoscopic and surgical luminal pancreatic pseudocyst drainage, with endoscopic treatment associated with shorter hospital stays and lower cost. This case illustrates the feasibility of endoscopic necrosectomy in patients with altered gastric anatomy.

274 Sclerosing Cholangitis in an Adult Patient With Langerhans’s Cell Histiocytosis Muslim Atiq, MD, Lokesh Jha, Michael Keppen. Sanford University of South Dakota School of Medicine, Sioux Falls, SD.

[273A] Figure 1.

Background: Sclerosing cholangitis is an extremely rare complication of Langerhans cell histiocytosis in adults with only 15 cases reported in literature. We report a case of Langerhan’s cell histiocytosis with sclerosing cholangitis in an adult with excellent clinical response to cladribine-based chemotherapy. Case History: 71 years old female with history of Langerhans’s cell histiocytosis and breast cancer presented to us with itching and jaundice. Laboratory studies were pertinent for abnormal liver function tests (LFTs); bilirubin of 2.7 mg/dL, Alkaline Phosphatase 990 IU/L, Aspartate Aminotransferase 91 IU/L, Alanine Aminotransferase 106 IU/L. One year ago, patient initially presented with generalized skin eruption. She also started to have symptoms of polyuria and polydipsia suggestive of diabetes insipidus. PETCT showed focal FDG uptake pituitary gland; no PET bony metastases were noted. A clinical diagnosis of Langerhan’s histiocytosis was made. She was treated symptomatically with Desmopression for symptoms of polyuria and polydipsia. At this time, her labs were extensively reviewed. MRI abdomen showed no biliary ductal dilatation. Changes consistent with fatty liver were noted on MRI. A skin biopsy showed compact parakeratosis overlying an epidermis with acanthosis and spongiosis with a dense infiltrate of Langerhans cells within the superficial dermis. EUS revealed distal bile duct wall thickening without focal mass lesions. FNA from bile duct wall was negative for malignancy. ERCP revealed dominant strictures involving distal bile duct and common hepatic duct. Cholangiogram demonstrated multiple focal irregularities involving the intra-hepatic ducts. Serial balloon dilatation of the biliary strictures involving main duct was performed. Bile duct brushings were performed. Stent was not placed. No atypical cells were seen on brushing cytology. There was no significant improvement in LFTs after ERCP. Patient was then treated with cladribine-based chemotherapy. LFTs improved to baseline with significant improvement in bilirubin (0/9 mg/dL) and Alkaline Phosphatase (490 mg/dL). Conclusion: Sclerosing Cholangitis should be considered in patients with Langerhans’s Cell histiocytosis presenting with jaundice and abnormal LFTs. MRI may not demonstrate changes suggestive of Sclerosing Cholangitis, and an ERCP may be needed for diagnostic evaluation. Cladribine-based chemotherapy may provide beneficial response in this subset of patients.

275 The Great Chameleon: Eosinophilic Gastroenteritis Presenting as Recurrent Acute Pancreatitis

[273B] Figure 2.

Krishna Venkata, MD, Radha Varanasi, Ronak Patel, Mohsen Hasanin, Ashwini Sharma, Wickliffe Many. University of Alabama Birmingham Montgomery Campus, Montgomery, AL. Recurrent acute pancreatitis secondary to eosinophilic gastroenteritis (EGE) is a rare entity and less than 15 cases are described in literature. We present a case of EGE causing recurrent acute pancreatitis in a HIV patient coexisting with H. pylori and to our knowledge, this is the first case report of its kind.

[273C] Figure 3.


[274A] Figure 1.


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Abstracts A 39 year old female with recurrent acute pancreatitis, upto twice a month for 3 years, was readmitted with abdominal pain, nausea and vomiting. Past history includes HIV (CD 4 < 5 cells/μL) diagnosed months after her first pancreatitis admission and weight loss. She denied any alcohol or tobacco use. Examination revealed epigastric tenderness. Laboratory findings included WBC of 2500/μL (N37%, L11%, M8%, B1%, E20%), protein of 7.0 g/dL, albumin of 2.8 g/dL, lipase of 1427 unit/L, triglycerides of 76 mg/dL. Celiac disease and autoimmune pancreatitis workup was negative. Stool fat was grossly abnormal. Serum IgE was >5000 IU/mL. HAART therapy was adjusted for the possibility of medication induced pancreatitis, which failed to resolve her symptoms. CT abdomen/pelvis, MRCP, EGD, EUS, were normal. Despite cholecystectomy, she continued to be symptomatic. A repeat EGD with multiple biopsies from esophagus to duodenum revealed extensive eosinophilic infiltration in esophagus (80 eosinophils/HPF) and duodenum (120 eosinophils/HPF). Gastric biopsy was positive for H. pylori. Stool and duodenal aspirate for O & P were negative. All her symptoms resolved along with a 43 lbs weight gain, once treated with prednisone and quadruple therapy for H.pylori. Follow up EGD with biopsies showed decreased eosinophil count (20 eosinophils/HPF). Since then, patient has not been admitted for any further episodes of acute pancreatitis. EGE, first described by Kaijser, is characterized by eosinophilic infiltration of the bowel wall. Exact incidence is still unclear although atleast 300 cases have been reported in the literature. It can involve any part of the gastrointestinal tract . Stomach and duodenum are the most common sites involved. There are three disease patterns: mucosal, sub-mucosal, serosal. Mucosal disease, which is what our patient had, is the most common and is accompanied by protein-losing enteropathy, bleeding, and malabsorption. Diagnosis is based on four crtieria: the presence of recurrent gastrointestinal symptoms, eosinophilic infiltration of the GI tract, exclusion of parasitic disease, and absence of other systemic involvement. Management includes dietary therapy and oral prednisone (20- 40 mg/dL) for 4 weeks. Life time risk of developing acute pancreatitis in individuals with EGE is about 1-2%. EGE should be considered in patients with recurrent acute pancreatitis with negative workup and peripheral eosinophilia.

presentation to pancreatic cancer makes for a significant diagnostic challenge and significantly alters therapy. Case: A 67 year old African American male presented with two weeks of painless jaundice, darkening urine, and light-colored stools. Patient denied abdominal pain, fevers, chills, night sweats, or significant weight loss. Laboratory studies revealed a total bilirubin of 12.6 mg/dl, elevated alkaline phosphatase (435 IU/L), normal serum transaminases, elevated IgG levels (2990 mg/dl). Abdominal CT revealed a soft tissue mass in the proximal common bile duct causing intrahepatic biliary ductal dilatation concerning for cholangiocarcinoma. The pancreas was not diffusely enlarged. ERCP revealed diffusely dilated intrahepatic bile ducts without beading, a tight stricture within the distal common hepatic duct,

276 Copycat Pancreatitis: A Case of Autoimmune Pancreatitis and the Importance of Early Diagnosis Adil S. Zahiruddin, MD, Andrew Caruso, MD. Baylor College of Medicine, Houston, TX. Learning Objective: Autoimmune pancreatitis (AIP) is an IgG4 associated disease (systemic fibroinflammatory disorder) that has pancreatic and extrapancreatic manifestations. The similarity in clinical

[276A] Figure 1.

[276B] Figure 2.

[276C] Figure 3.



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and midcommon bile duct approximately 1 cm in length. Biliary sphincterotomy was performed with common bile duct biopsies and a plastic biliary stent placed with prompt drainage of bile and contrast. An EUS revealed heterogeneous and edematous pancreatic head parenchyma with no discrete mass. There was heterogeneous and hypoechoic circumferential thickening of the mid and distal common bile duct. Several core needle biopsies of the pancreatic head revealed a dense lymphoblastic infiltrate organized in a storiform pattern with obliterative phlebitis and negative for malignant cells. Prednisone therapy was initiated (40mg/day for six weeks with a subsequent slow taper). At discharge, the total bilirubin decreased to 3.6 mg/dl with improvement in symptoms. Serum IgG4 subclass antibodies were not elevated. Patient underwent biliary stent exchange ten months later with a fully covered metal stent to improve chances of eliminating the stricture and provide more time in between procedures. Patient remains asymptomatic. Discussion: AIP was first recognized as a distinct form of chronic pancreatitis in 1995. Obstructive jaundice is the most common presenting symptoms. For physicians, it is crucial to recognize this disease as the presentation is very similar to that of malignancy. In contrast to malignancy, AIP responds dramatically to steroids. Studies have shown that about one third of patients undergoing pancreatic resection for possible cancer were ultimately found to have benign disease with the characteristic lymphoplasmacytic infiltrate of AIP. Furthermore, about 30% of patients with autoimmune pancreatitis relapse. Recognition of autoimmune pancreatitis is crucial in both prognosis and defining therapeutic options.

277 Giant Pancreatic Pseudocyst With Mediastinal Extension and Large Pleural Effusion Damodar Pandey, MD, Anand Kumar, Kamran Zahid, MD, Hilary Hertan, MD, FACG. Montefiore Medical Cente-Wakefield, Bronx, NY. Instruction: Pancreatic pseudocyst is a known complication of acute or chronic pancreatitis but its mediastinal extension is very rare. We report a case of mediastinal pseudocyst (MP) associated with chronic pancreatitis successfully treated with ERCP guided stent placement and drainage. Case: A 50 year old man with history of chronic pancreatitis and recurrent DVT was admitted with worsening shortness of breath, upper abdominal and chest pain, and weight loss. Chest X-ray showed a large left pleural effusion and globular cardiac silhouette. 1.7 L of cloudy fluid was drained via thoracentesis. Pleural fluid analysis showed amylase > 7500 U/L and lipase 22 k U/L raising suspicion of pancreatico-pleural fistula. CT scan with contrast demonstrated a large lobulated cystic mass measuring about 17 x 10 x 8 cm with a thin communicating tract from the pancreatic head extending superiorly into the mediastinum, bilateral pleural effusions and mass effect on left atrium causing passive hepatic congestion. Transpapillary drainage of the MP was planned. ERCP guided sphincterotomy and CBD stenting was done to gain preferential access into pancreatic duct (PD). A fistula communicating PD and pseudocyst was revealed. The fistula was dilated with a hurricane balloon and a 7Fr 15cm stent was placed. White debris from pseudocyst drained into the duodenum. Follow up CT scan after 2 weeks showed complete resolution of the MP and stents were then removed. Discussion: Mediastinal pseudocysts are thought to be caused by rupture of the pancreatic duct posteriorly into the retroperitoneal space and subsequent tracking of the fluid, via diaphragmatic openings for esophagus and aorta, into mediastinum. Majority of patients present with symptoms of mass effect including abdominal, chest or back pain, dyspnea, dysphagia and weight loss. Though pleural effusion is common in MP it is secondary to lymphatic obstruction from peri-cystic inflammation, as opposed to a pancreatico-pleural fistula as seen in our patient. CT scan is the investigation of choice. Spontaneous regression of MP is rare. Management depends on the presence of symptoms, location and size of the pseudocyst and available expertise. EUS guided transgastric drainage with deployment of a stent is highly successful. Surgery should be considered in case of associated infection, obstruction, rupture, or hemorrhage. ERCP is helpful in defining the ductal anatomy and ERCP guided stent placement via

[277A] Figure 1.


[277B] Figure 2.

pancreatic duct to the pseudocyst cavity may be the management of choice if the pseudocyst is found to communicate with the PD, as in our case.

CLINICAL VIGNETTES/CASE REPORTS - COLON

278 Olgivie Syndrome After Knee Replacement Surgery Eduardo A. Rodriguez, MD1, Frederick Williams, MD2. 1. University of Miami Palm Beach Campus, West Palm Beach, FL; 2. University of Miami Palm Beach Campus, Atlantis, FL. Acute colonic pseudo-obstruction often has a benign prognosis if treated appropriately. If the diagnosis is missed, it can easily complicate and lead to several complication such as perforation, sepsis and death. The following case illustrates the importance of early diagnosis and treatment of acute abdominal pain in the setting of recent surgery and electrolyte abnormality. 61 year old male patient with history of bilateral knee osteoarthritis and left knee replacement surgery three weeks prior to the presentation, was admitted complaining of right knee pain not well controlled with oral oxycodon for the last three days. Vital signs were within normal limits. Right knee was not erythematous nor warm, tenderness was not elicited on palpation and rest of joint examination was unremarkable. Patient was admitted for medical management of arthralgia. He was given intravenous (IV) morphine 1 mg every 4 hours conditional to pain and home dose of scheduled oral oxycodon. During the following two days, patient started to complain of progressive abdominal distention and loose stools, no pain. Abdominal exam revealed a distended abdomen and hyperdynamic bowel sounds without elicited tenderness, rebound or guarding. He presented as well with hypokalemia of 2.6 mEq/dL and an abdominal x ray done revealed a colon diameter of 11 cm. No pneumoperitoneum, obstructions or air fluid levels. CT of the abdomen described it as moderate air distended colon. All narcotics were stopped, no food was given by mouth, IV fluids and IV potassium chloride were started and a rectal tube was placed. After 48 hours, abdominal x ray showed colonic diameter of 15 cm, without symptoms reported by the patient. Later that day he underwent decompressive colonoscopy and repeat abdominal x ray demonstrated a colon diameter of 12 cm. During the following days, diet was advanced without any nausea or vomiting. IV NSAIDs were started in order to help patient´s knee pain. He was able to start physical therapy and by the day of discharge, his abdomen was no longer distended, patient was having normal bowel movements and abdominal x ray revealed a colon diameter within normal limits. Olgivie Syndrome or acute pseudo-obstruction has been associated with orthopedic surgeries in about 7% of the cases, however for our patient it was multifactorial as he had also been taking high doses of narcotics and had been presenting with diarrhea, leading to hypokalemia. Supportive care with removal of potential precipitants is the initial management, provided there is no pain or extreme colonic distension (>12 cm). If clinical deterioration is present or conservative approach has failed, other therapies such as neostigmine or colonic decompression should be considered.


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280

Crystal-Associated Colitis With Ulceration Leading to Hematochezia and Abdominal Pain

A Rare Case of Idiopathic Colonic Varices in a Young Male

Meeta Desai, MD1, Nancy Khov, MD2, Zhaohai Yang, MD, PhD2, Aaron J. Reiprich, DO3, Abraham Mathew, MD, MSc1, John M. Levenick, MD2. 1. Penn State Milton S. Hershey Medical Center, Hershey, PA; 2. Penn State Hershey Medical Center, Hershey, PA; 3. Pinnacle Health, Mechanicsburg, PA.

Samina Afreen, MD1, Mohammed Younis, MD2, Rahul Nayani, MD, MPH3, Andrew Sanderson, MD, DM4. 1. Howard University Hospital, Department of Internal Medicine, Falls Church, VA; 2. Howard University Hospital, Department of Internal Medicine, Silver Spring, MD; 3. Howard University Hospital, Falls Church, VA; 4. Howard University, Washington, DC.

Colitis induced by chemical crystals is rare and can pose a diagnostic challenge. This is a report of a patient who presented with recurrent hematochezia and acute blood loss anemia. A 45-year-old female presented with a three-month history of intermittent abdominal cramping and hematochezia. She is on hemodialysis and has type 2 diabetes mellitus, ischemic cardiomyopathy, peripheral vascular disease, and endometrial carcinoma treated with radiation and surgery. Her initial hospitalization with abdominal pain was attributed to radiation colitis. During her second hospitalization, she had recurrent rectal bleeding and tested positive for C. difficile. She presented a third time to the same hospital and was treated for pneumonia, however, due to ongoing rectal bleeding a colonoscopy was done and revealed pancolitis. She was given prednisone and mesalamine for presumptive ulcerative colitis and transferred to a tertiary care hospital for surgical evaluation given her persistent bleeding. Upon presentation the patient was hemodynamically stable without evidence of peritonitis. Her hemoglobin was 8.0 g/dL, hematocrit 24.7%, platelets 32 K/uL, and stool was negative for C. difficile toxin. No significant colonic thickening was noted on a contrast CT of the abdomen. Colonoscopy revealed a normal terminal ileum, partially healing linear ulcerations at the flexures and transverse and sigmoid colon, and radiation changes in the lower colon (figure 1). Ischemic colitis on top of radiation colitis was considered. Biopsies showed acute inflammation associated with fragments of crystal material (figure 2). Both sevelamer and cholestyramine were discontinued and the patient’s hematochezia resolved. Crystal induced colitis is a rare cause of hematochezia. Sevelamer, cholestyramine, and sodium polystyrene sulfonate are all ion-exchange resins that have been reported as causes of rectal bleeding. If crystal-induced colitis is found, all potentially contributing medications should be stopped. In our patient, discontinuation of both sevelamer and cholestyramine led to resolution of her pain and hematochezia, suggesting a relationship between these medications and her crystal-induced mucosal-injury.

Less than 35 cases of idiopathic colonic varices have been reported in the English medical literature. Bleeding idiopathic colonic varices are even rarer. We present the case of a young male with bloody diarrhea whose colonoscopy showed colonic varices which even after thorough investigation did not reveal an identifiable etiology. A 32 year old Hispanic male presented with multiple episodes of painless bloody diarrhea, occurring intermittently for the last 10 years. The patient did not drink alcohol, but smoked 4-5 cigarettes/day. He did not have any other past medical history. On physical exam, pale conjunctiva was the only significant finding. Stool studies were positive for fecal WBC but negative for cultures, C. diff, ova, parasites and cysts. Hb was 6.5, with normal WBC, platelets and LFTs. Colonoscopy 3 years ago had revealed prominent vasculature throughout the colon. There were three inflammatory polyps. Random colonic biopsies showed benign colonic mucosa. Colonoscopy done this admission revealed varices in the rectosigmoid junction, sigmoid colon and hepatic flexure and AVM in the sigmoid colon, while no active bleeding was noted. CT of abdomen and pelvis with contrast showed unremarkable liver, spleen, pancreas with patent celiac trunk, superior and inferior mesenteric artery. Doppler ultrasound of abdomen showed fatty liver with no evidence of biliary dilatation and normal duplex Doppler flow patterns in the main portal vein, hepatic vein branches, abdominal aorta, IMA, SMA and visualized portions of IVC. Mesenteric angiography, which is the gold standard test to evaluate colonic varices, could not be done in this patient as he left against medical advice. Secondary colonic varices are caused by portal hypertension usually due to liver cirrhosis or portal vein thrombosis. Our patient did not have any signs of portal hypertension and the imaging studies revealed patent intra-abdominal blood vessels. Previous studies have indicated a familial component to idiopathic varices. The hypothesis that these might be the result of congenital vascular anomalies is supported in this patient by him also having an AVM in the sigmoid colon. Knowledge of these varices will avoid the risk of causing hemorrhage by doing a biopsy when they are mistakenly identified as polyps or tumors.

[279A] Figure 1.

[280A] Figure 1.

281 Amebic Colitis in a Post Liver Transplant Patient Steve Serrao, MD, MPH1, Vincent Kao, DO, MS2, Lydia Aye, DO3. 1. Loma Linda University Health, Loma Linda, CA; 2. Loma Linda University Medical Center, Loma Linda, CA; 3. Loma Linda University, Redlands, CA.

[279B] Figure 2.


A 63-year-old Hispanic male, presented with two week history of blood tinged diarrhea, abdominal cramping, and decreased appetite. He had been discharged from the hospital one month prior for liver transplant for hepatocellular carcinoma. Prior to the transplant he had visited Mexico where he ate an unrestricted diet including seafood and pork. He also had contact with roosters, chicken, pigeon, cats, goats and horses. He was on immunosuppressive agents, Tacrolimus, with a normal level of 17.6 ng/mL and Prednisone with Valganciclovir, Clotrimazole and Trimethoprim Sulfamethoxazole. He was admitted and managed with intravenous fluid and electrolyte resuscitation. Stool studies were negative for Clostridium difficile, Shiga Toxin 1 and 2, Salmonella, Shigella, Campylobacter, E.coli 0157 and ova and parasites. He was referred for colonoscopy which demonstrated the presence of non-hemorrhagic ulcers throughout the colon starting from the rectum and ending in the cecum (Figure 1). There


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[281A] Figure 1.

[282A] Figure 1.

[281B] Figure 2.

was no active bleeding and there were patchy areas of normal appearing mucosa. Multiple biopsies were taken from the bases and the edges of the ulcers and of normal mucosa. Histological exam of biopsies (Figure 2) showed benign colonic mucosa with ulceration, and granulation tissue with accompanying necroinflammtory debris. Scattered among the mucosa, were amebic organisms consistent with Entamoeba histolytica showing foamy cytoplasm with ingested red blood cells and eccentric nucleus. Entamoeba antibody titer was found to be positive, and further work up including Toxoplasmosis IgG and IgM, Cysticercosis Trypanosoma Cruzi, Brucella and Bartonella antibody titer were negative. Patient was treated and subsequently discharged on Metronidazole, for the duration of six weeks. No changes were made to the immunosuppression therapy. In 1875, Losch first described the trophozites of Ameba coli in the feces of a Russian woodcutter with fatal diarrhea. Acquired via the oral-fecal, oral-anal and oral-genital routes, this parasite was named E.Histolytica for its ability to lyse tissues. Though not seen in our patient, amebic liver abscess is the most common manifestation of invasive amebiasis. Other organs can also be involved, including pleuropulmonary, cardiac, cerebral, renal, genitourinary, peritoneal, and cutaneous sites. Intestinal amebic infections are relatively rare in the Unites States. For individuals infected with a single GI parasite, E. histolytica accounts for 1% of cases. This case confirms that prior travel to endemic areas is a significant risk factor for intestinal parasitic infections. This case also highlights the importance of a thorough dietary, travel and exposure history, prior to and after starting immunosuppression in an organ transplant recipient.

[282B] Figure 2.

282 Ipilimumab-Induced Colitis Syed Amer, MBBS1, Jennifer L. Horsley-Silva, MD2, Jessica Noelting, MD2, Shabana F. Pasha, MD3, Christine O. Menias, MD2, Dora Lam-Himlin, MD4. 1. Division of Internal Medicine, Mayo Clinic, Phoenix, AZ; 2. Mayo Clinic, Phoenix, AZ; 3. Division of Gastroenterology and Hepatology, Mayo Clinic Arizona, Phoenix, AZ; 4. Mayo Clinic, Scottsdale, AZ. A seventy-seven year old man with a history of metastatic melanoma, on chemotherapy with ipilimumab presented with a chief complaint of abdominal pain and diarrhea. His symptoms began six weeks after


[282C] Figure 3.


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Abstracts initiation of ipilimumab. He described the diarrhea as watery, non-bloody bowel movements occurring 3-4 times a day. A CT of his abdomen revealed a diffusely dilated colon with pericolonic stranding and distention of the transverse colon (Image 1). Initially, he was treated with antibiotics, ciprofloxacin and metronidazole without improvement. Stool studies for infectious etiologies including Clostridium difficile were negative. A flexible sigmoidoscopy was performed that showed an area of moderately congested, edematous mucosa with exudates involving the rectum, sigmoid and descending colon (Image 2), biopsies of which revealed changes consistent with ipilimumab colitis (Image 3). Ipilimumab was discontinued high dose dexamethasone was administered. Within one week, the diarrhea improved and the patient was discharged on tapering doses of steroids. Ipilimumab is an immunomodulating agent used in the treatment of metastatic melanoma. It acts by inhibiting cytotoxic T-lymphocyte antigen 4 (CTLA 4), which typically works to down-regulate the T-cell response and protects self-antigens from recognition by the immune system. Because the T-cells are no longer down-regulated by this antigen, they are permitted to proliferate, thereby helping to prevent melanoma tumor evasion. As a result of the up-regulation of the immune system, numerous immunemediated adverse effects have been reported including colitis, dermatitis, hepatitis and rarely hypophysitis. Patients usually experience colitis approximately 6 to 7 weeks after initiation of the medication; however, patients can still develop symptoms within the first several weeks. Typically, colitis in these patients is treated with high-dose steroids and most eventually improve. For cases refractory to corticosteroid therapy, other immunosuppressants such as infliximab can be used. In conclusion, ipilimumab-related diarrhea is among the most common adverse effects observed with use of this drug. Left unrecognized or untreated, it can rapidly escalate in severity and become lifethreatening. Prompt recognition and treatment, including exclusion of other etiologies, are important for successful management.

[283B] Figure 2.

283 A Rare Case of Acute Abdomen Secondary to Omental Infarction Mimicking Acute Ascending Colitis Mustafa Musleh, MD1, Bhoompally Reddy, MD2, Salma Akram, MD3. 1. Wright State University, Miamisburg, OH; 2. Dayton VA Medical Center, Dayron, OH; 3. Wright State University/Dayton VAMC, Department of Gastroenterology, Dayton, OH. Introduction: Omental infarction is a very rare cause of acute abdominal pain that is often misdiagnosed pre-operatively. We report a case of acute abdominal pain secondary to omental infarction that presented resembling acute colitis. Case Description: A 23 year old white male present to the Emergency Department with severe, sharp, right sided abdominal pain of 2 days duration. He also had vomiting and diarrhea for 2 days prior to the pain onset. On exam he was afebrile, and his vital signs were normal. Abdomen was tender to palpation with guarding and rebound tenderness in the right mid abdomen, and bowel sounds were hypoactive. Initial labs revealed normal complete blood count and comprehensive chemistry panel. C-reactive protein (CRP) was 116 mg/dl [0-8 mg/dl]. CT abdomen showed fat stranding thickening of the right lateral soft tissue extending from the tip of the liver inferiorly adjacent to the ascending colon. Patient was admitted to hospital and had a colonoscopy and ileoscopy which were normal. Patient’s pain and abdominal tenderness continued to worsen, a repeat CT scan of the abdomen with contrast was done on hospital day 3 showed worsening inflammatory stranding in the right colic gutter. He underwent a diagnostic laparoscopy which showed an inflammatory omental mass for which partial omentectomy was performed. Pathology evaluation confirmed acute and chronic inflammation and necrosis consistent with omental infarction. Discussion: Omental infarction is a rare cause of acute abdominal pain that can mimic multiple pathologies that often require surgery. It is usually caused by torsion of the greater omentum that compromises blood supply leading to inflammation and necrosis. Omental torsion can be secondary to underlying abdominal pathologies like tumors, cysts, or adhesions. Primary torsion is more common though, often predisposed by trauma, hyperperistalsis and obesity. Omental infarction can be clinically indistinguishable from acute appendicitis, also it can mimic cholecystitis, right sided diverticulitis and rarely colitis. CT scan often suggest the diagnosis by showing a fat stranding and inflammatory changes with minimal or no bowel wall thickening. Although CT can be accurate, it often fail to exclude other causes that usually require surgery. In our patient, clinical presentation and imaging initially suggested ascending colitis. Worsening abdominal exam and CT findings were concerning, and surgery was indicated to make diagnosis. Omental infarction usually follows a benign course and on rare occasions complications such as omental abscess have been reported. Conservative

[283C] Figure 3.

management should be adequate in the majority of the cases, however, most of the reported cases indicate that surgical intervention is often necessary to establish diagnosis.

284 Primary Amyloidosis and Hematochezia: An Unexpected Discovery Cari Sorrell, MD1, Charles Brady , MD2, Nicole D. Riddle, MD1. 1. University of Texas Health Science Center, San Antonio, TX; 2. Division of Gastroenterology, University of Texas Health Science Center, San Antonio, TX.

[283A] Figure 1.


Introduction: Primary amyloidosis is a rare entity with only 1200 to 3200 new cases reported each year. Clinically apparent gastrointestinal (GI) involvement with the disease is seen even less frequently; quoted as low as 1% in some reviews. The disease is due to extra-cellular deposition of fibril-forming monoclonal immunoglobulin light-chains that can affect any organ system, including the GI tract, presenting as GI bleeding, diarrhea, or other symptomatology. We present here a rare case of primary amyloidosis presenting with an isolated episode of hematochezia and chronic diarrhea. Case Report: A 59 year-old female with history of thyroid cancer and primary (AL) amyloidosis on renal biopsy for hypoalbunemia as well as a bone marrow biopsy consistent with plasma cell myeloma presented with an episode of hematochezia. For one-month prior, she had chronic diarrhea with ten to twelve episodes of loose, liquid, non-bloody stools daily that are only minimally improved with loperamide. These symptoms had not changed until one day prior to presentation, when she experienced a single episode of hemaotchezia when wiping prompting her to seek medical care. Physical exam was unremarkable. Her infectious diarrheal stool work-up was negative as well as a normal red blood cell count. A CAT scan of the abdomen demonstrated wall edema and thickening of the descending colon, sigmoid colon and rectum. Based on these findings, a colonoscopy was performed for further evaluation during which, there were multiple areas of protuberant, sub mucosal hematomas mixed with small mucosal hemorrhages scattered throughout the colon concerning for visible vessels versus vascular infiltration of amyloid. Multiple biopsies of these affected areas demonstrated changes consistent with ulcer formation and a Congo red stain showing apple green birefringence in walls of several small vessels consistent with amyloid deposition in these vessels and thus amyloid involvement of the colon.


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Discussion: Gastrointestinal manifestations are uncommon in primary amyloidosis with biopsy diagnosed disease and clinically apparent disease occurring in only 8% and 1% respectively in one retrospective review. However, gastrointestinal bleeding or diarrhea can occur as a presenting symptom in patients with amyloidosis. This may be caused by ischemia, infarction, and ulceration or from generalized oozing without an observed source. The clinical suspicion for amyloid involvement of the colon in a patient presenting with diarrhea and scant hematochezia is usually low even with a previous diagnosis of renal amyloid involvement given the rarity of such findings, however, we present here a case of this unexpected discovery.

285 Evidence Supporting Seeds, Nuts, or Popcorn as a Cause of Diverticulitis? A Rare Case of an Ingested Foreign Body Causing Diverticulitis Jennifer Thompson, MD1, Joshua Wu2, Melvin Lau, MD3. 1. Texas A&M School of Medicine, Round Rock, TX; 2. Ross University School of Medicine, Round Rock, TX; 3. Baylor Scott and White Healthcare, Round Rock, TX. A 71 year-old male presented to the hospital with a one day history of left lower abdominal pain and bright red blood per rectum. He had a fifty-year history of smokeless tobacco use and no prior colonoscopy. Physical exam revealed an afebrile man with stable vital signs and mild tenderness in the left lower quadrant. Computed tomography of the abdomen and pelvis revealed uncomplicated sigmoid diverticulitis. His hospital course was complicated with a drop in hemoglobin from 12.7 gm/dL to 7.6 gm/ dL resulting in two units of packed red blood cells. Following transfusion his hemoglobin improved and his symptoms resolved with antibiotics. The patient was subsequently discharged with instructions to return for colonoscopy in 4 weeks. During colonoscopy a cylindrical foreign body was found embedded between two adjacent diverticula in the sigmoid colon. The colonoscope was unable to move proximal to the foreign body and the procedure was aborted in fear of colonic perforation. After surgical consultation, repeat colonoscopy was performed the following day in the operative room with concomitant laparoscopy. Careful removal of the foreign body with large grasping forceps was successfully utilized in removal of the foreign body without any complications. Upon removal, the foreign body was identified as a 39 mm tobacco stem. After recovery, the patient admitted to chewing tobacco and must have inadvertently swallowed a tobacco stem. This case is highly unusual in that most foreign body pass through the colon, and even if they were to become lodged, it is not typically found in a diverticulum. What is even more unusual is the development of diverticulitis afterwards, especially after the association between high residue foods and diverticulitis had been debunked by the long-term study of the effects of nuts, popcorn or corn on diverticulosis. Perhaps, like most early legends, there is a small grain of truth in the beginning.

286 The Lost Buckyballs Leigh B. Lurie, MD1, Moshe Rubin, MD2, Sang Kim, MD2, Suma Kamath, MD2. 1. New York Hospital Queens/Weill Cornell Medical College, Long Island City, NY; 2. New York Hospital Queens/Weill Cornell Medical College, Flushing, NY. A 15 year old female with no past medical history presented to the emergency department after ingesting two Buckyballs she was using to create a mock tongue piercing. She was asymptomatic at presentation. On exam her abdomen was soft, nontender, and nondistended. Abdominal xray was obtained which showed 2 radiopaque objects in the upper abdomen. Repeat xray showed the objects in the lower abdomen. The patient underwent bowel prep and was taken for colonoscopy. The colon and terminal ileum were normal without visualization of the Buckyballs. A repeat abdominal xray showed the objects in the right lower quadrant. A retrograde double balloon enteroscopy was then performed. The enteroscope was advanced 150 cm into the small bowel without visualization of the Buckyballs. Fluoroscopy was then used to confirm the location of the Buckyballs in the right lower quadrant. The enteroscope was reduced under fluoroscopy until the tip of the scope was at the site of the Buckyballs. This placed the enteroscope in the cecum at the appendiceal orifice. The enteroscope was then passed into the appendix. The Buckyballs were found wedged in the tip of the appendix. A 0.035 Boston Scientific Dreamwire™ was advanced beyond the balls into the appendix. Attempts were made using a 9mm/12mm Boston Scientific Extractor™ Pro RX Balloon, a Cook® Memory Soft Wire Basket, a US Endoscopy Talon™, and an EndoGator®. All of these attempts were unsuccessful at removing the Buckyballs. The patient was taken for laparoscopic appendectomy. The patient recovered without complication.

[286A] Figure 1.

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[287A] Figure 1.

[286C] Figure 3.

Magnetic foreign body ingestion is most common in the pediatric population (1). The ingestion of two or more magnetic foreign bodies pose the highest risk to patients as the force between two magnets can trap a portion of bowel causing necrosis with fistula formation, perforation, obstruction, volvulus, or peritonitis (2). It is recommended that each magnetic foreign body that is ingested be removed endoscopically if in reach. If not in endoscopic reach it is recommended that the foreign bodies be removed surgically (3). Foreign bodies in the appendix are a well documented occurrence, however, this is the first documented case of a magnetic foreign body in the appendix. Unfortunately the Buckyballs were unable to be removed endoscopically in this patient, but the prompt identification of the Buckyballs by enteroscopy prevented appendiceal necrosis and perforation.

287 Septic Phlebitis: A Dangerous Complication of Diverticulitis Monica Cespedes, MD1, Aixa Dones-Rodriguez, MD2, Karen Torres-Gonzalez, MD3. 1. San Juan City Hospital/Internal Medicine Program, Carolina, Puerto Rico; 2. San Juan City Hospital/Internal Medicine Program, Gurabo, Puerto Rico; 3. San Juan City Hospital/Internal Medicine Program, San Juan, Puerto Rico. Colonic diverticulitis is an inflammation of the colon due to microperforation of a diverticulum, a sac-like protrusion of the colonic wall. This digestive tract disease is most common among the elderly people and affects predominantly the distal portion of the colon (sigmoid and descending). Pericolonic abscess, fistula formation, perforation, luminal obstruction, and peritonitis are well-known complications of diverticulitis. One of the most rare fistulas is enterovascular, which is a communication between a blood vessel and adjacent bowel. An uncommon complication and threatening condition of perforated diverticula is septic phlebitis, in which perforation spreads to the mesentery and erodes a blood vessel. We report a case of septic phlebitis due to enterovascular fistula. This is the case of a 79 year-old female, Latin American, past medical history of diverticulosis, arterial hypertension, and lumbar disk herniation who presented with low back pain, abdominal pain, fever, and nausea; she was treated symptomatically and discharged home from a hospital of the metropolitan area. She returned due to persistence of symptoms and multiple episodes of bright red blood per rectum. On examination, patient was acutely ill with positive digital rectal exam for blood. She was admitted and placed NPO with high dose of proton pump inhibitors plus antibiotic therapy. Abdominopelvic CT scan with IV contrast was performed which showed acute sigmoid diverticulitis with abscess formation, nodular liver appearance, and left portal vein thrombosis. Blood cultures were done and showed anaerobic gram-negative bacilli consistent with Porphyromonas spp. During hospitalization, patient developed septic shock and acute respiratory failure that required vasopressor therapy and intubation, respectively. Abdominopelvic CT with PO and IV contrast was repeated which showed portal venous thrombosis with sigmoid/inferior mesenteric vein fistula. Bowel rest was given and total parenteral nutrition was started. Patient was given intravenous fluids and broadspectrum antibiotics; end colectomy with Hartmann’s pouch and partial colectomy was done with significant improvement of symptoms. Patient was discharged home to complete physical therapy rehabilitation. Septic phlebitis of the inferior mesenteric vein is an unusual complication of diverticular disease. History, physical examination, and radiographic imaging are helpful in identifying this entity. Prompt radiologic imaging is detrimental to the diagnosis, treatment, and management of abdominal pathology. Surgical intervention in a rapidly manner can be lifesaving. Early diagnosis and treatment should be emergent due to high-risk mortality from this complication.

[287B] Figure 2.

[287C] Figure 3.



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288 Colonic Dieulafoy Lesion Raymond Pashun, MD1, Yecheskel Schneider, MD2, Monica Saumoy, MD1, David W. Wan, MD1, Sonal Kumar, MD, MPH3. 1. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, Brooklyn, NY; 3. Weill Cornell Medical College, New York, NY. A 76 year old man with hepatitis C cirrhosis complicated by hepatocellular carcinoma treated with embolization and ablation, ESRD on dialysis, diabetes, hypertension, and MGUS is admitted with shortness of breath for one week and chronic abdominal pain progressively worsening for several months. On admission, the patient denied bright red blood per rectum but then had a bloody bowel movement during evaluation. The patient became hypotensive to systolic blood pressures of 70 mmHg and found to have anemia with a hemoglobin of 6.8 g/dL. He received blood products, octreotide, nexium, and neosynephrine drips and admitted to the MICU. Emergent upper endoscopy showed portal hypertensive gastropathy and two small antral erosions in the stomach with bleeding that were cauterized. Flexible sigmoidoscopy revealed blood and clots in rectum but no bleeding source was identified. He was started on ceftriaxone for SBP prophylaxis. The patient continued to have hematochezia and subsequent colonoscopy showed blood throughout the colon, sparing the terminal ileum. A single site of bleeding was located 50 cm from the rectum suggestive of colonic dieulafoy where argon plasma coagulation and two hemostatic clips were successfully used for hemostasis. Following colonoscopy, his hemoglobin downtrended slowly despite normal stools and negative CT scan. The patient was weaned off pressor support and required no further transfusions. He developed septic shock of unclear etiology and despite aggressive treatment the patient expired. The Dieulafoy lesion is described as a tortuous, large-calibre arteriole protruding through a small defect in the mucosa. It represents only 1-2% of all gastrointestinal bleeds, but can result in massive and recurrent bleeding. Typically Dieulafoy lesions are localized to the stomach in 71% of cases whereas only 2% are found in the colon. These lesions can then be managed by epinephrine injection, thermal anticoagulation, or hemostatic clipping. Hemostatic clipping is more successful in achieving permanent hemostasis when compared to epinephrine injection; however, if the anatomy does not allow for accurate placement of hemoclips it may result in continued hemorrhage. Thus, it is important for clinicians to not only assume hematochezia is from a diverticular source, and maintain a high index of suspicion for the presence of Dieulafoy lesions in lower gastrointestinal bleeds to reduce the mortality associated with it.

[289B] Figure 2.

289 Common Presentaion of an Uncommon Disease: Juvenille Polyposis Syndrome Belen Tesfaye1, Firew Wubiee, MD, MS2, Adeyinka O. Laiyemo, MD, MPH3, Angesom Kibreab, MD1. 1. Howard University Hospital, Washington , DC; 2. Howard University Hospital, Washington, DC; 3. Division of Gastroenterology, Department of Medicine, Howard University College of Medicine, Washington, DC. Introduction: JPS (Juvenile Polyposis syndrome) is an autosomal-dominantly inherited rare condition where multiple juvenile polyps are found in the GI tract. Most patients develop symptoms in the first two decades of life .The average age at diagnosis is 18.5 years but may be later. Rectal bleeding with anemia is the most common presenting symptom, followed by abdominal pain, diarrhea, passage of tissue per rectum, and intussusception. SMAD 4 and BMPR1A mutation is found in up to 60% of patients. Clinical criteria for diagnosis include at least five juvenile polyps in the colorectum, juvenile polyps in other parts of the GI tract or any number of juvenile polyps in a person with a known family history of juvenile polyps. Patients with JPS have high risk for colon cancer and an increased risk for gastric, duodenal, and pancreatic cancers. Juvenile polyps are characterized by cystic spaces filled with mucin. Microscopically, there is abundant lamina propria with benign but often elongated and cystically dilated glands and lack of a smooth muscle core which differentiates it from other hamartomatous polyps such as in peutz jeghers. Management is removal of the polyps endoscopically or surgically followed by surveillance with EGD/ Colonoscopy every 1-3 yrs starting from age 12-15.

[289C] Figure 3.

Case presentaion: We present a case of a 28 year old African American female who presented with hematochezia , normocytic anemia and weight loss. She has no family history of polyposis syndrome or colon cancer. She had a normal EGD and Colonoscopy showed a 7cm by 8 cm fleshy looking, polypoid lesion in the sigmoid colon. Biopsy was inconclusive. Patient opted for surgery over endoscopic resection and she had sigmoidectomy. Pathology was consistent with Juvenile polyposis syndrome. Patient got referred for genetic testing and counseling. Conclusion: A high degree of suspicion is required in a young patient with hematochezia and anemia despite absence of family history. Early diagnosis and endoscopic surveillance prevent patients from developing colon cancer and helps in identifying and screening at risk family members.

290 Synchronous Squamous Carcinoma of Anus and Adenocarcinoma of the Rectum: Third Case in World Literature Nirmal S. Mann, MD, MS, PhD, DSc, MACG1, Virmeet Singh, MD2. 1. University of California Davis School of Medicine, Sacramento, CA; 2. VA Medical Center, Sacramento, CA.

[289A] Figure 1.


Synchronous and metachronous adenocarcinoma of the colon are well described.The incidence of such colon cancers is reported to be 5--10%.However synchronoius squamous carcinoma (SCC) of anus with adenocarcinoma of the rectum is very rare. Only two such cases have been reported before(W V Med J


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Abstracts 1992;88:9-10, Rev Med Chir Soc Med Nat lasi 2004;108:797--799.).We report the the third such case.A 64 year old man had a history of bright red rectal bleeding daily for one yeart. It was ascribed to hemoohoids. The patient had no h/o nausea,vomiting,hematemesis or melena.There was no abdominasl pain and no h/o weight loss.The patient had no F.H of colon cancer and had undergone no colonoscopy before.He did not drink alcohol but smoked 0.5 pack cig daily for 20 years.He had obsrtuctive sleep apnea.On physical exam he was found to be obese;otherwise the physical exam was unremarkable. The Hb was 13.5,hematocrit 42.1 RDW 14.2.The CEA was 2.5 (reference range 0-3).Comprehensive metabolic panel including liver tests were normal.On colonoscopy a 3 mm cecal polyp was found to be a serrated lesion.At 12 cms from the anal verge in the rectum an ulcerated mass 2.5 cm was biopsied which showed adenocarcinoma of rectum.Another 2.0 cm ulcerated mass at the anorectal junction on biopsy showed SCC of the Anus.A CT of the thorax ,abdomen & pelvis showed rectal wall thickening with prominent perirectal lymph nodes;there were no visceral or bony metastasesThe patient is undergoing chemoradiation with plan to perform low anterior resection for adenocarcinoma of the rectum. This is the third case of this kind in the world literature.The previous two reported cases were also men 64 year and 75 years old,both presenting with rectal bleeding & wt. loss.the prognosis in such cases is worse compared to those with synchronous or metachronous adenocarcinoma of the colon.

291 Segmental Colitis of Cecum Associated With Cecal Diverticulosis: The First Case Nirmal S. Mann, MD, MS, PhD, DSc, MACG1, Sital Singh, MD2. 1. University of California Davis School of Medicine, Sacramento, CA; 2. University of California Davis School of Medicione, Sacramento, CA.

[292B] Figure 2. Segmental colitis associated with diverticulosis (SCAD) is an uncommon but well-established clinicoendoscopic entity( Hepato-Gastroenterology 2012;59:2119--2121.Colorectal Dis 2010 ;12:464--470). Endoscopically it shows hyperemia,friability of the mucosa and microulceration of the folds between colonic diverticula( Crescent Fold Disease).It may cause abdominal pain,diarrhea and rectal bleeding. It should be diffrerntiated from acute diverticulitis. It is usually localized to the sigmoid and descending colon.We report the first case of segmental colitis restricted to the cecum associated with cecal diverticulosis.A 63 year old man underwent screening colonoscopy. he had history of vague RLQ pain off and on for one year.There was no history of nausea,vomiting,hematemesis,melena or hematochezia. He had histiry of osteoarthritis of the hips,COPD,essential hypertension and tobacco abuse.He did not drink alcohol;there was no significant family history. CBC and comprehensive metabolic panel was normal.The physical examination was unremarkable. On colonoscopy he was foiund to have uncomplicated diverticulosis of the sigmoid and descending colon. He had mutiple diverticula in the cecum. The triangular fold in the cecum and the Ileo-cecal valve showed masrked hyperemia,friability and micro-ulceration (Crescent Fold Disease).The ostia of cecal diverticula were normal.The biopsy from the cecal fold showed acute inflammation.

292 A Rare Case of Voluminous Diarrhea Secondary to Intestinal Involvement of Acute Myeloid Leukemia Robert B. Cooper, II., DO , James Lennon, DO , Jonathan Okman , MD. Lankenau Medical Center, Wynnewood, PA. Gastrointestinal involvement is a rare manifestation of Acute Myeloid Leukemia (AML). We present a case of a 76-year old African American female with a past medical history of hypertension and chronic kidney disease (baseline creatinine of 1.3 mg/dL) who presented to the emergency department with chief complaint of voluminous, watery diarrhea over the course of five days. The diarrhea was frequent, occurring more than 10 times per 24 hour period, large volume, watery, non-bloody, and with nocturnal symptoms. There was no association between her diarrhea with oral intake. She also had symptoms of lethargy and shortness of breath. Upon presentation her vital signs were significant for a fever of 101F orally, HR 141 bpm, BP 105/59 mmHg. Her physical examination was significant for tachycardia without murmurs. Lungs were clear to auscultation. Abdominal examination revealed a soft abdomen,

[292C] Figure 3.

non-tender to palpation with hyperactive bowel sounds, no rebound or guarding. Non-contrast CT scan of her head, chest, abdomen, and pelvis showed no signs of bowel wall thickening, however, the liver was enlarged to 22cm in craniocaudal length. Initial laboratory evaluation revealed the patient to have acute on chronic renal failure with a creatinine of 3.3 mg/dL, bicarbonate 10 mEq/L, uric acid 11 mg/dL, phosphorous 5.4 mg/dL, and a white blood cell count of 126,000 of which 78% were blasts. Stool studies were unremarkable. In the emergency department her mental status deteriorated and she became increasingly lethargic and hypotensive. She was diagnosed with acute blast crisis of Acute Myeloid Leukemia (AML) and Tumor Lysis Syndrome (TLS) and was transferred to the Intensive Care Unit on vasopressor medications. Her hospital course was complicated, secondary to her overwhelming disease which, on autopsy, was confirmed to have invaded nearly every tissue in her body including her liver, colon, and small intestine (images 1-3). We found this case interesting because of the unique presentation of diarrhea and the multi-organ system involvement of this stereotypically hematological disease. Gastrointestinal involvement is not a frequent initial manifestation of AML. When involved, the mouth, rectum, and anal canal are the most commonly affected sites that lead to patient symptoms. This patient’s voluminous diarrhea prompting medical evaluation was secondary to the leukemic invasion of the small intestine and colon.

293 Squamous Cell Carcinoma of the Rectum Ayah Oglat, MD1, Pascale White2, David W. Wan, MD3, Charles Maltz, MD, PhD3. 1. Houston Methodist Hospital, Houston, TX; 2. New York-Presbyterian/Weill Cornell Medical Center, New York, NY; 3. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY.

[292A] Figure 1.


A 61 year-old-woman from the Dominican Republic with history of breast cancer treated with chemotherapy, radiation and left radical mastectomy (1995) was admitted with first time onset of 3 episodes of BRBPR. She denied fever, nausea or vomiting, abdominal pain, change in bowel habits, melena and weight loss. For the past month, she had been taking daily ibuprofen (2-4 pills) for right leg pain and


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denied taking anticoagulants. On admission, her vitals were stable. No external hemorrhoids noted on rectal exam and she was guaiac positive. Her labs are significant for hemoglobin of 12.4, which dropped to 11.2 with no further bleeding during hospitalization, elevated transaminases (AST 119, ALT 226) and alkaline phosphatase 147. She was kept NPO, given IV fluids and proton pump inhibitors. RUQ ultrasound and hepatitis panel were negative. Colonoscopy showed a mass 10cm from anal verge and biopsy showed invasive squamous cell carcinoma. Carcinoembryonic antigen was normal. MRI of the abdomen showed a multiloculated hypoenhancing mass arising from the right anterior wall of the rectum displacing the uterus anterolaterally into the left hemipelvis. Additionally, a metastatic right pelvic sidewall lymph node was seen. CT of the chest without obvious metastases. Since malignancy was found in one lymph node, surgical and oncology teams recommended radiation and chemotherapy before and after surgical resection. Patient was offered treatment at New York Presbyterian Hospital but she decided to have further treatment in the Dominican Republic. Rectal Squamous cell carcinoma is a rare malignancy with incidence approximately 0.10 to 0.25 per 1000 colorectal cancer. It usually presents during advanced stage disease with nonspecific symptoms. It is diagnosed with endoscopic examination and the appearance can range from a polyp to an ulcerated obstructing mass. Biopsy with Immunohistochemistry with cytokeratins staining proved useful in characterizing these lesions. Trans-rectal endoscopic ultrasound, endorectal MRI and CT are used staging of the tumor and evaluation for regional and distant metastasis. There is lack of randomized studies indicating the most appropriate therapy due to the infrequency in which rectal squamous cell carcinoma cases are encountered. Treatment mainly involves surgery secondary to the often late stage of presentation. References: [1]. Dyson T, Draganov PV. Squamous cell cancer of the rectum. World J Gastroenterol. 2009 Sep;15(35): 4380–4386. doi:10.3748/wjg.15.4380. Epub 2009 Sep 21.

[295A] Figure 1.

294 A Rare Case of a Poorly Differentiated Neuroendocrine Rectal Tumor With Shared CLL Histology Daniel Bodek, DO1, Thomas Park, MD, MHS2, Nitasha Bhatia, MD3, Mubdiul Ali Imtiaz, MD3, Shanthi Srinivas, MD2. 1. Rutgers New Jersey Medical School, Hoboken, NJ; 2. VA New Jersey Health Care System, East Orange, NJ; 3. Rutgers New Jersey Medical School, Newark, NJ. Introduction: Poorly differentiated neuroendocrine tumors (PDNETs) are rarely found in the GI tract1. Also uncommon is CLL infiltration of the GI tract. We report a rare case of a patient presenting with a rectal tumor that included both CLL and PDNET histology. Case Report: A 56 year old male with a history of CLL in remission presented with the complaint of 3 weeks of foul smelling diarrhea with blood spotting, bloating, and anorexia. The patient was taken for a colonoscopy, during which a 4cm friable, fungating mass was visualized on the right side of the distal rectum near the anal verge. A biopsy was performed which showed co-existing poorly differentiated neuroendocrine carcinoma and CLL. It was was strongly reactive for chromogranin and synaptophysin. It was also positive for CD5, CD20, and CD23. A CT scan revealed liver masses and extensive lymphadenopathy. Liver biopsy revealed PDNET histology. The patient was started on his first cycle of cisplatin and etoposide. Discussion: PDNETs comprise far less than 1% of GI malignancies. They are usually metastasized at discovery and may present similarly to adenocarcinomas. They are diagnosed by biopsy and histologic examination, demonstrating high mitotic rates and necrosis1. Untreated, survival is 6 months, in comparison to treatment with a regimen of etoposide and cisplatin, which offered an average survival of 15 months. In localized disease, adjuvant chemoradiation with surgery is recommended3. Management strategies for PDNETs rely on experience with small cell lung cancer therapies due to their rarity2. As for CLL, it is uncommon to see in GI tract biopsies unless it has converted to a diffuse large cell lymphoma. The prevalence of GI involvement in asymptomatic CLL patients based on autopsy studies is estimated at 7-13%3. On review of the literature, no case of co-existing CLL and PDNET was found. However, there are reports of increased rates of secondary malignancies in CLL patients, which may be related to immunological dysfunction or the effects of chemotherapy4. References: [1] Bezerra, J, et al. Neuroendocrine Tumors: Poorly Differentiated Neuroendocrine Tumors. 157-170. Totowa, NJ, USA: Humana Press, 2011. [2] Lalani, M., et al. Uncommon Presentations of Some Common Malignancies: Case 3. JCO. Feb 20, 2005;23(6):1315-131. [3] Mitry E, et al. Treatment of poorly differentiated neuroendocrine tumours with etoposide and cisplatin. BJC. Dec 1999;81(8):1351-5. [4] Morton L, et al. Second malignancy risks after non-Hodgkin’s lymphoma and chronic lymphocytic leukemia: Differences by lymphoma subtype. JCO. 2010; 28(33):4935–4944.

[295B] Figure 2.

295 Cecal Bascule or “Seesaw Cecum”: A Late Complication of Gastric Bypass Surgery Sunita Upreti1, M. Cornelious Musara, MD2. 1. Trinity School Of Medicine, Towson, MD; 2. Antares Surgical Solutions, Glen Burnie, MD. Intestinal obstruction is an increasingly common condition in inpatient population, majority of which are due to small bowel pathologies. Large bowel obstructions are far less common with obstructing tumors and acute diverticulitis accounting for 90% of all causes. A much less common condition is colonic volvulus which can present with signs and symptoms of obstruction and often warrants surgical intervention. Here we discuss a case of Cecal Bascule which is a rare anatomical variance of cecal volvulus. There are few published case reports of Cecal volvulus in patients who have undergone laparoscopic gastric bypass surgery but a cecal bascule as its late complication has never been reported before. A 52 year old female, who underwent a laparoscopic gastric bypass surgery four years ago presented with intermittent abdominal colic and constipation for two weeks. Examination revealed, distended abdomen with hypoactive bowel sounds. Plain Xray showed a dilated large bowel on the left side suggesting a sigmoid volvulus. Conservative treatment failed to improve the symptoms and she underwent a contrast enhanced CT scan which revealed markedly dilated cecum which crossed the midline extending to the left side of the abdomen. A definitive diagnosis of Cecal volvulus was made and the patient underwent an exploratory laparotomy. Intraoperatively, however, there was no torsion of the colon or twisted mesentery, but the cecum was hugely dilated to >12cm and anteriorly folded on the ascending colon like a flap-valve, a classic presentation of cecal bascule. The patient then underwent


[295C] Figure 3.


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Abstracts a right hemicolectomy with an uncomplicated postoperative recovery. Cecal bascule differs to the classical volvulus as it is not an axial torsion. It occurs when the cecum folds itself in cephalad direction and intermittently obstructs the cecal outflow to the ascending colon by creating a crease in between, like a seesaw. During embryogenesis, abnormal fusion of right colonic mesentery to the lateral wall causes malfixation of the cecum. This predisposes the cecum to move freely especially during operative manipulation. It remains unclear whether gastric bypass surgery is an etiological factor in the development of cecal bascule. But based on a few published reports, it was hypothesized that the rapid weight loss resulting in lengthening of the mesocolon may predispose the cecum to move freely. This case highlights the importance of considering rare diagnoses in evaluating causes of intestinal obstruction especially in post-gastric bypass patients.

296 Idiopathic Myointimal Hyperplasia of the Mesenteric Veins (IMHMV): A Challenging Case of Colitis in a Young Man Mark A. Gromski, MD1, Michael Sinnott, MB, BCh, BAO2, Monika Fischer, MD, MS3. 1. Indiana University School of Medicine, Indianapolis, IN; 2. Indiana University, Indianapolis, IN; 3. Department of Medicine, Indiana University, Indianapolis, IN. A 25 year-old male presented for evaluation of six weeks of diarrhea and abdominal pain. He had progressive worsening of abdominal pain, poor oral intake, weight loss (30 pounds) and 10-20 daily bowel movements that were predominantly mucous and blood. Initial work-up at an outside hospital revealed wall thickening of the descending colon to the rectum on CT scan and two flexible sigmoidoscopies with diffuse congestive erythema, ulceration and necrosis from the sigmoid colon to rectum. Upon referral to our medical center, work-up included a repeated flexible sigmoidoscopy that showed an area of congested, friable, dusky mucosa with overlying exudate in the recto-sigmoid colon, which appeared ischemic. Endoscopic biopsies were most consistent with ischemic colitis, with no evidence of CMV. Extensive infectious work-up (C. difficile, stool culture, ova and parasites, CMV, syphilis, HSV, gonorrhea, chlamydia) and clotting factors all were normal. CT angiography showed normal mesenteric vasculature. A diagnosis of IMHMV was suspected, and the patient underwent a laparoscopic sigmoid colectomy with end colostomy and mucous fistula. Gross sectioning revealed multiple blood vessels with thickened vessel walls. Microscopic examination revealed occlusive vasculopathy with prominent intimal hyperplasia of small to medium-sized mesenteric veins with abscess, necrosis and serositis, confirming the diagnosis of idiopathic myointimal hyperplasia of the mesenteric veins (IMHMV). IMHMV is a rare cause of colitis that afflicts predominantly men of young to middle age. It has been reported in sixteen published reports in the literature. The presentation is nonspecific, with abdominal pain, diarrhea, hematochezia and mucous in stool. The clinical presentation alone can lead to a diagnostic dilemma, as many components are similar to other causes of colitis. It is often mistaken initially for inflammatory bowel disease given the demographic of the patient, yet endoscopic appearance can suggest ischemia and biopsies are frequently more consistent with ischemic colitis than inflammatory bowel disease. Generally, it requires pathological evaluation of a surgical resection specimen to confirm the diagnosis. Six months after his operation, our patient is doing well. His symptoms have resolved completely. A subsequent endoscopic evaluation was essentially normal with rectal biopsies showing mild architectural distortion. He is currently being considered for take-down of his colostomy, which has never been reported in the literature before.

tinged urine negative for constipation, diarrhea, or weight loss. In the ED pt was tachycardic HR at 110, afebrile and normotensive, Physical exam revealed tenderness to deep palpation of the epigastrium as well as bright red blood on rectal examination, vaginal exam revealed a laceration with minute bleeding. Gastric lavage did not reveal any blood, UA positive for RBC. CBC revealed a HG of 9.2 from a baseline of 12, HCT of 26.8 from 35 MCV 123, Vit B12 and folate wnl, Iron panel normal other than ferritin of 1826. LFT showed transaminases with AST 418 ALT 212 with an anion gap 14 (which resolved in 48 hours) remainder of Lab where unremarkable. Imaging such as Ct abdomen pelvis, MRCP, MRI where unremarkable. OBGYN where consulted performed an EB and applied pressure to the laceration and stopped the bleeding. GI was consulted and performed an EGD and colonoscopy. EGD revealed gastritis, duodenitis, and a hiatal hernia, colonoscopy revealed multiple mucosal ulceration and clip was placed over pigmented ulcer, remainder of exam wnl. Biopsies of endometrium where unremarkable and egd colon only showed evidence of chronic inflammation. Pt continued to have bleeding per rectum and had 4 more sigmoidoscopies to stop the bleeding via clips. Heme/ Onc was consulted and performed a bone marrow biopsy which was unremarkable. Further hx from family members revealed that although her BMI was 20 she had a very poor diet, eating rice and very little of food. Vit C level was checked and was found to be zero. Her symptoms improved after starting vit C supplementation. Pt has not yet had a followup sigmoidoscopy. Scurvy is result of vit C deficiency/ Ascorbic acid. Vit C is a water soluble vitamin found mainly in fruits and vegetables. Other than having anti-oxidant properties Vit C is a cofactor required in hydroxylation of proline and lysine in synthesizing collagen. Deficiency of such will result in easy bleeding. Recommendations for male adults is 90mg/day and females 75mg/day, during pregnancy 85 and 125 during breastfeeding. One should always remeber that rare historic disease can still occur to this date. References: Pailhous S1 et al. Scurvy, an old disease still in the news: Two case reportsArch Pediatr. 2015 Jan;22(1):63-5. [2] Talarico, et al. Do you remember scurvy? Clin Ter. 2014 Sep-Oct;165(5):253-6. [3] Blee, et al. Hemorrhage associated with vitamin C deficiency in surgical patients. Surgery. 2002 Apr131(4):408-12.

[297B] Figure 2.

297 Ascorbic Acid Deficiency Resulting in Bleeding Per Rectum Rahman Nakshabendi, MD1, Andrew C. Berry, DO2, Ozdemir Kanar, MD1, Bilkisu Gaye, MPH, MD1, Matthew Clark, MD3, James Scolapio, MD3, Silvio DeMelo, MD3, Amie Deutch, MD3, Emely Eid, MD3. 1. University of Florida Health College of Medicine, Jacksonville, FL; 2. Department of Medicine, University of South Alabama, Muskego, WI; 3. University of Florida Health College of Medicine, Division of Gastroenterology, Jacksonville, FL. We present a 43YO WF 2yr post-menopausal with no pertinent pmhx presents to the hospital with chief complaint of epigastric discomfort accompanied with nausea and vomiting with bright red blood per rectum of 3 days duration. Of the above mentioned complaints the BRBPR has been going on for the last 2 years intermittently but has increased in frequency over the last month. ROS was only positive for pink

[297C] Figure 3.

[297A] Figure 1.



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298 Pointing Towards Colonoscopy: A Case Series Review of Sharp Foreign Body Removal via Colonoscopy Melissa Hershman, MD, RN, BSN1, Steven Shamah, MD2, Michael Glick, MD, PNS, CNSC1. 1. North Shore-LIJ Lenox Hill Hospital, New York, NY; 2. North Shore-LIJ Lenox Hill Hospital, New York , NY. Background: Accidental and intentional ingestion of foreign bodies occur commonly. While a majority of objects pass spontaneously, sharp objects in particular uniquely warrant urgent upper endoscopy for retrieval based on reported perforation rates of 35%. To date, there is limited evidence to validate colonoscopy as the treatment modality for objects failing to progress through the colon. This report aims to demonstrate that colonoscopy can be safely utilized as a means of retrieving sharp objects after distal migration. Case 1: A 25-year-old female seamstress presented after accidental ingestion of a 4cm-sewing pin. Physical examination and routine laboratory investigations were unremarkable. CT imaging

[298C] Figure 3.

[298A] Figure 1.

demonstrated a foreign object just beyond the Ligament of Treitz, and so, endoscopy was deemed of low utility and high risk. The patient was followed with serial abdominal examination and X-ray imaging, which showed migration of the pin into the proximal ascending colon on day 3. The pin was successfully extracted during colonoscopy by securing the sharp end with hot biopsy forceps and pulling the foreign body hood forward over the entire pin. Reassessment of the sigmoid following removal revealed intact colonic mucosa with no evidence of abrasions, tearing or perforation. Case 2: A 23-year-old female presented with concern for glass ingestion after alcohol consumption. A 3.4 curvilinear opacity was identified on X-ray, after which upper endoscopy failed to distinguish the foreign body, likely due to distal migration. The patient remained hemodynamically stable and was followed with serial Abdominal X-ray. Between hospital day 2 and 4 the object failed to advance, prompting the decision for removal via colonoscopy. The glass was identified in the mid ascending colon and retrieved using Roth Basket. Follow up X-ray showed absence of the object with no evidence of free air or perforation. Conclusions: Sharp object retrieval via colonoscopy shares common features to the upper endoscopy approach including use of a protector hood or overtube to shield gastric mucosa, and slow retrieval by endoscopic forceps, nets or polypectomy snares. Our case series demonstrates that careful monitoring with serial X-rays and physical examination allows for the supervised passage of sharp objects into the colon, at which point when poor migration is noted, it is both safe and effective to remove these objects by colonoscopy.

299 An Incidental Finding of Rectal Carcinoid Tumor Sudha Pandit1, Mitchell Basel, MD2. 1. Louisiana Health Science Center, Bossier City, LA; 2. LSU Health Sciences Center and Overton Brooks VA Medical Center, Shreveport, LA. Adenocarcinoma is the most common malignancy found in the rectum. However, the incidence of rectal carcinoid has been rising after implementation of screening colonoscopy. The rectum is the second most common anatomic site for carcinoid tumor. Embryologically, rectal carcinoids are hindgut tumors which are non secretory. Hence, they rarely present with carcinoid syndrome even in patients with metastatic disease. A recent systematic review of rectal carcinoid by McDermott et.al was unable to perform a metaanalysis on optimal treatment strategies for localized and widespread disease due to the wide variety of data recorded from various sources. Our aim is to make physicians aware that the rectal carcinoid is becoming a common diagnosis thus clinicians should have current knowledge of classification, management and treatment options available. A 62-year-old African American male with a significant past medical history of hypertension and tobacco abuse presented to the gastrointestinal (GI) lab for colorectal cancer screening colonoscopy. Patient had no specific GI complaints and a 10-point review of symptoms was unremarkable except for decreased exercise tolerance. Physical examination was unremarkable including digital rectal exam. During colonoscopy, a 7-10 mm firm polypoid submucosal lesion was noted in distal rectum and was resected using an electrocautery snare and ERBE endocut current. Histologic evaluation of the resected polyp demonstrated a well-differentiated neuroendocrine neoplasm that stained positive for chromogramin, synaptophysin, and Ki-67 proliferation marker. Patient underwent repeat colonoscopy about a month later. Biopsy obtained from previous polypectomy site was negative for carcinoid tumor cells. The rectal carcinoid classification, management and treatment options have been defined based on the size and aggressiveness of the lesion. As there is no defined TNM system classification, there is no homogenous data available yet on how to manage rectal carcinoid. Treatment strategy is based on tumor size, radiologic testing and surveillance examination including use of rectal EUS.

[298B] Figure 2.



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[299A] Figure 1.

300 An Unordinary Recurrence of Urothelial Bladder Carcinoma in the Colon Presenting as Hematochezia Michael Krzyzak, MD1, Youssef El Douaihy, MD2, Iskandar Barakat , MD2, Wei Xue, MD2, Frank Gress, MD3, Liliane Deeb , MD4. 1. Staten Island University Hospital, Brooklyn, NY; 2. Staten Island University Hospital, Staten Island, NY; 3. New York Presbyterian Hospital/Columbia University Medical Center, New York, NY; 4. Staten Island University Hospital/NorthShore LIJ Health System, Staten Island, NY. The conventional route of recurrence and metastasis in primary urothelial cell carcinoma of the bladder is through lymphatics and hematogenous system with regional lymph nodes, lungs, liver, brain and bone being the most commonly involved sites. Invasive urothelial cancers could also spread locoregionally to surrounding organs including female genital tract, prostate and gastrointestinal tract especially colo-rectum. However, recurrence of this cancer inside the colon in the absence of locoregional invasion, and after achieving complete long-term remission is extremely unusual. A review of the literature revealed a single case reported by Yang et al. of an urothelial cancer recurrence in the colon with mixed urothelial/colonic malignant pathology [1]. Herein we report the second case, to our knowledge, of an urothelial cell bladder carcinoma that recurred inside the colon in the form of a mass causing hematochezia, which on pathology and immunohistostaining proved to be primarily of urothelial rather than colonic origin.

[300A] Figure 1.


67 year old male heavy smoker with stage III (T3a, N0, M0) transitional cell carcinoma of the bladder had undergone radical cystectomy, neo-bladder reconstruction and adjuvant chemotherapy following initial diagnosis. He poved repetitively to have no evidence of disease until he presented 4 years later with intermittent hematochezia and anemia. Colonoscopy revealed a fungating, ulcerated mass in the sigmoid colon suggestive of a primary colon cancer (fig1). Pathology disclosed high grade/poorly differentiated carcinoma invading the colonic mucosa that surprisingly favored an urothelial origin. Upon further immunostaining, final diagnosis of a metastatic high-grade urothelial carcinoma was confirmed by positive cytokeratin (CK) 7 stain (specific for urothelial cells) and negative villin and CDX2 stains that are both specific for gastrointestinal differentiation (fig2). CT scan of abdomen and pelvis, and PET scan did not reveal any other sites of cancer recurrence. Patient received a tailored chemotherapy and responded appropriately.. This case illustrates a rare kind of recurrence of urothelial cancer in the form of a colonic mass resembling primary colon cancer. This unordinary way of recurrence could pose a clinico-pathological diagnostic challenge in distinguishing this disease treated basically with chemotherapy, from a primary colon cancer managed primarily by surgical resection. Immunohistochemical stains are essential for an accurate diagnosis. Heightened awareness is of utmost importance in such patients with history of urothelial cancer in order to appropriately tailor further treatment strategies that differ between primary and secondary colonic tumors.. Reference: 1- Yang MH, et al. CEA-producing urothelial cell carcinoma with metastasis presenting as a rectal adenocarcinoma. Kaohsiung J Med Sci. 2012;28(11):624-627.

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301 CVID-Induced Diarrhea: A Rare Cause of Chronic Diarrhea Umair Sohail, MD1, Ashraf Almashhrawi, MD2, Rubayat Rahman, MD, MPH2, Imran Ashraf, MD2, Douglas Nguyen, MD3, Matthew Bechtold, MD, FACG2. 1. Division of Gastroenterology/Hepatology, University of Missouri, Columbia, MO; 2. University of Missouri, Columbia, MO; 3. University of California Irvine, Anaheim Hills, CA. Introduction: Common variable immunodeficiency (CVID) is a primary immunodeficiency disorder characterized by impaired B-cell differentiation with defective immunoglobulin production. We report a case of chronic non-infectious diarrhea associated with CVID. Case: A 59 years-old female with history of rheumatoid arthritis, recurrent sinus infections, recurrent urinary tract infections, and hypothyroidism was referred to gastroenterology clinic for chronic diarrhea and fecal incontinence for several months. She had several bowel movements a day which she described as soft to loose with occasional abdominal pain. No systemic symptoms of fever, chills, hematochezia, melena, or weight loss. Her physical examination including vital signs was unremarkable. Her CBC, BMP, celiac panel, TSH, and stool studies were unremarkable. Her EGD and colonoscopy was unremarkable. She was empirically treated with rifaximin for bacterial overgrowth with recurrence of her symptoms after stopping the antibiotics. She was started on loperamide and dicyclomine on as needed basis with improvement in her symptoms. For her fecal incontinence, anorectal manometry with balloon defecography revealing low sphincter pressures, intact neurological reflexes, and prolonged balloon expulsion time. She also underwent rectal ultrasound which showed possible defect at the internal and external anal sphincters. She was managed conservatively. Due to her history of recurrent sinus infection, urinary tract infections, she was referred to immunology for evaluation of immune deficiency. She was diagnosed with CVID. She was started on treatment for CVID. Soon after treatment initiation, her diarrhea resolved. Discussion: CVID is a primary immune deficiency characterized by low levels of antibodies (IgG, IgA, IgM), normal or decreased B-cell numbers, or impaired antibody response to infections. Gastrointestinal manifestations, including malabsorption, diarrhea, and weight loss, are the most common presentation. Mild watery diarrhea can be seen in up to 20% of patients with CVID and 10% have been reported to have severe enteropathy. Treatment of CVID by steroids or other immunosuppressive agents generally improves the GI symptoms. Therefore, immunodeficiency should be kept in mind in patient with chronic non-infectious diarrhea, even in the absence of recurrent infections.

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[302B] Figure 2.

Discussion: The reported prevalence of IS varies between 2.5% to 16% and occurs more commonly among homosexual males and patients with low socioeconomic status. A significant number of patients are HIV positive, but there is no link between the degree of immunodeficiency and the severity of disease. The methods of transmission are suspected to be fecal-oral or sexual contact. It remains to be confirmed whether intestinal spirochetes are pathogenic or commensal organisms, as majority of cases are asymptomatic. On colonoscopy, the mucosa can appear normal, erythematous or edematous. The hallmark histological feature includes a 3-μm basophilic fringe on the intestinal mucosal epithelium. IS has been reported in all parts of the colon, including the appendix and rectum. We found these organisms on random biopsies of the colon, including the right side which has not been frequently reported. Metronidazole is the antibiotic of choice for treatment of symptomatic IS, other options include tetracycline, ceftriaxone and meropenem. For asymptomatic IS, watchful waiting is preferred.

A Case of Colonic Spirochetosis: An Enigma Unravelled Muhammad I. Ahmad, MD1, Mamoun Younes, MD2, Andrew W. Dupont, MD2. 1. University of Texas Health Science Center, Houston, TX, Tuvalu; 2. University of Texas Health Science Center, Houston, TX. Introduction: Spirochaetaceae encompass a small group of gram-negative bacilli that cause infestation and infections in humans, mainly in the large intestine. In the US most cases of intestinal spirochetosis (IS) are caused by Brachyspira aalborgi. The previously reported cases of IS have been diagnosed in biopsies of left colon or with stool studies. Case Report: A 42 year-old male without significant past medical history presented with chronic abdominal pain and bloating for the past 23 years. He described the pain as diffuse and colicky, which worsened with food intake and was relieved after a bowel movement. He also had intermittent episodes of diarrhea and tenesmus. Physical examination revealed a BMI of 33 kg/m2 and his abdomen had no abnormal findings. He had previously visited several physicians with same complaints and previous serological work up for Celiac disease had been negative with no final established diagnosis and incomplete relief from symptomatic therapy. EGD and colonoscopy were subsequently performed, which were grossly unremarkable with normal-appearing mucosa throughout. Random biopsies were obtained from the stomach, duodenum and colon. Histopathology results from both the right and left colon biopsies showed intestinal spirochetosis, which was clearly evident on routine H&E stain as well as on PAS stain with diastase (Figures 1 & 2). Patient was prescribed 2 weeks of oral metronidazole.

303 Barium Impaction: A Rare Cause of Bowel Obstruction Carmine Catalano, MD1, Rafael A. Ching Companioni, MD2, Melik Tiba2, Loveleen Sidhu3, Aaron Walfish, MD3. 1. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), East Rockaway, NY; 2. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), Elmhurst, NY; 3. Elmhurst Hospital Center, Elmhurst, NY. Barium enema is a special x-ray of the colon and rectum. Barium is not water soluble and becomes inspissated in the colon when water is absorbed. Rarely, the thickened barium can cause an obstruction in the gastrointestinal tract. In most cases medical management will not suffice and endoscopic or surgical intervention is required to ameliorate the obstruction. We report a case of barium impaction of the cecum that occurred sixteen days after a barium enema but more interestingly two days following bowel surgery for an ileostomy reversal. The obstruction resolved without endoscopic or surgical intervention but rather conservative management alone. A 36-year-old male with no significant medical history was admitted for sigmoid diverticulitis that was complicated by perforation. Exploratory laparotomy with sigmoid resection and primary anastomosis with a loop ileostomy was performed. Six weeks later a diagnostic colonoscopy was performed prior to the reversal of the ileostomy. The procedure was aborted secondary to an incomplete bowel preparation. The patient refused a second colonoscopy so a barium enema was performed which revealed a patent sigmoid anastomosis. Fourteen days later the patient was taken for surgery to reverse the loop ileostomy. On postoperative day 2 the patient complained of intermittent, crampy abdominal pain, nausea, and vomiting. The patient was febrile but vital signs were otherwise unremarkable. Physical examination revealed a tender, distended abdomen that was tympanic with hyperactive bowel sound. Laboratory studies revealed a leukocytosis and hypokalemia. X-ray of the abdomen (see Image 1) and computed tomography of the abdomen and pelvis displayed a 7.0 centimeter barium concretion in the cecum causing obstruction of the colon with dilated loops of small bowel. Emergent colonoscopy with removal of the barium was not performed for concern of perforation. The patient was treated conservatively with laxatives and tap water enemas in an effort to loosen the concretion. Two days later the patient defecated the barium and a repeat abdominal radiograph showed resolution of the obstruction. Barium impaction is a rare complication and cecal impaction is exceedingly rare. Although it has been historically described in other parts of the colon there are only three reported cases of barium impaction in the cecum. This may be due to the wider diameter of the cecum. What makes our case even more interesting is that the obstruction presented greater than two weeks after the Barium enema and two days after bowel surgery for the ileostomy reversal. We believe that a post-operative ileus likely contributed to the impaction and that in these cases conservative bowel preparations alone may lead to resolution of the obstruction.

[302A] Figure 1.



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[304B] Figure 2.

305 Mucocele of the Appendix: A Rare Disease

[303A] Figure 1.

304 Triple Primary Cancer in Iron Deficiency Anemia Steven Shamah, MD1, Samit Datta, MD2, Arun Swaminath, MD3. 1. North Shore-LIJ Lenox Hill Hospital, New York , NY; 2. North Shore-LIJ Lenox Hill Hospital, New York, NY; 3. Lenox Hill Hospital, New York, NY. GI malignancy is a common finding in patients that presents with Iron Deficiency anemia. Furthermore, multiple primary malignancies are very uncommon. Current colon cancer guidelines stop screening for patients after the age of 85. In this case, we present a functional, independent 88 year old female who presented with symptomatic iron deficiency anemia. Patient was up-to-date with all screening and presented with a hemoglobin of 7 (down from baseline 11-12) and was recommended for EGD and colonoscopy. EGD revealed 3cm mass with pathology showing high grade dysplasia. Colonoscopy represented 4cm mass with pathology consistent with invasive colorectal adenocarcinoma. Staging CT also detected a mass in the right adnexa. Multiple primary malignancies with three or more tumors are extremely rare. This case report highlights the need to re-address current screening guidelines for the increasingly functional elderly population.

Aakash Aggarwal, MBBS1, Badal Kalamkar2. 1. Mount Sinai St. Luke’s Roosevelt Hospital Center, Hartford, CT; 2. Baystate Medical Center, East Longmeadow, MA. Introduction: Mucocele of the appendix is caused by a retention cyst, mucosal hyperplasia, mucinous cystadenoma or mucinous cystadenocarcinoma. It is extremely rare, found in 0.2-0.3% of resected appendices in the United States. Early diagnosis is rare due to absent or nonspecific symptoms like right lower quadrant abdominal pain, gastrointestinal bleeding, intestinal obstruction, genitourinary symptoms or acute abdomen. Early diagnosis and resection are important since some appendiceal mucoceles are malignant and may lead to peritoneal dissemination and the clinical syndrome of pseudomyxoma peritonei. Case report: A 74-year-old male presented with intermittent right lower quadrant abdominal pain and hematochezia for 4-6 weeks. He had no pertinent abdominal symptoms including nausea, vomiting, bloating, diarrhea or constipation or weight loss. Routine laboratory testing showed microcytic anemia. He had a colonoscopy 5 years ago which was normal. Repeat colonoscopy showed a protuberant mass at appendiceal orifi ce which was firm on palpation with biopsy forceps. Biopsy of the lesion showed mild infl ammatory changes. With the above described endoscopic appearance of the lesion, clinical suspicion for mucocele was high, hence CT scan was obtained. CT scan showed low attenuation, well-defined 2.5-cm mass, with no signs of infl ammation suggestive of mucocele of the appendix. Patient underwent surgery for ileo-caecal resection. Histopathology of the surgical specimen was reported as mucinous cystadenoma of appendix. On 3-month follow-up, patient is doing well and his anemia is resolving. Discussion: Appendiceal mucoceles may be recognized at colonoscopy as an extrinsic or submucosal lesion with smooth indentation into the caecal lumen. Appearance of the appendiceal orifi ce in the center of the mound has been labeled as the “volcano sign.” Highly suggestive endoscopic fi nding is that of a glossy, rounded, balloon-shaped mass protruding from the appendiceal orifi ce and moving in and out with respiration. Th is case highlights the importance of endoscopic appearance of appendiceal mucocele which can be missed on a biopsy. Further imaging is warranted when mucocele of appendix is suspected on colonoscopy. Recognition at colonoscopy is important as it enables accurate diagnosis of this rare clinical entity. Surgical excision of the tumor without rupture is of paramount importance because rupture of the lesion causes pseudomyxoma peritonei. Survival is excellent aft er standard appendectomy of retention cysts, mucosal hyperplasia, or cystadenoma.

306 Clostridium difficile Infection Can Mask Diagnosis of Other GI Infections in Immunocompromised Patients: A Tale of Co-existing Bacteria and Fungus Naga Saranya Addepally, Jagpal Singh Klair, MD, Mayank Pahwa, Mohit Girotra, Daniel K. Brown. University of Arkansas for Medical Sciences, Little Rock, AR.

[304A] Figure 1.


Introducton: Clostridium difficile infection (CDI) can occur commonly in immunocompromised patients. However, lack of response to treatment should alert physicians to actively re-investigate for presence of other co-existing GI infections, which our interesting case alludes to. Case presentation: A 55 year-old man with HIV (CD4 43/mm3) and hepatitis-C presented with RLQ pain with fever & intermittent bloody diarrhea for 2-week. Outside hospital work-up (abdominal CT & stool studies) was unremarkable, except for (+) Clostridium difficile antigen. Patient was started on PO Vancomycin, to which he initially responded but was later re-admitted with worsening pain and persistent bloody stools. Repeat CT revealed concentric bowel wall thickening/edema in cecum/ascending colon along with lymphadenopathy. Antibiotics were restarted for assumed recalcitrant CDI, but after 21 days of unsuccessful therapy, transferred to us. Colonoscopy divulged inflamed, edematous and friable appearing cecum/ascending colon, with multiple discrete punched out ulcers through out the colon.


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Biopsies were consistent with histoplasmosis. Patient had no co-existent pulmonary lesions or other sites of dissemination. He responded well to liposomal amphotericin B. Discussion: Histoplasma can be identified in the GI tract of 70-90% patients with disseminated disease, but only 3-12% of those are symptomatic. Typical endoscopic lesions are patchy or continuous superficial-deep ulcerations, accompanied by diffuse mucosal erythema, and rarely as polypoid masses causing obstruction, or annular constricting ulcers leading to strictures, mimicking malignancy or IBD. Serum/ urine serological antigen is useful for diagnosis (+ in >90% patients with disseminated disease) but may be falsely negative in patients with localized GI involvement. Hence, biopsy is warranted for appropriate diagnosis. Pathology suggests abundant inflammatory infiltrate and multiple intracellular ovoid-spherical narrow based budding yeast cells, visualized better with methanamine silver stain. Patients with less severe disease may be treated with itraconazole, but amphotericin-B is merited in moderate-severe disease. Disseminated histoplasmosis carries high mortality (~80%), hence early identification and treatment is necessary. Summary: Co-infection with common nosocomial bugs like Clostridium difficile may masquerade the underlying histoplasmosis, hence high index of suspicion is quintessential, especially in immunocompromised patients.

NSAIDs). Similarly, terminal ileum causes are CD, IBD, medication induced, or secondary to autoimmune causes. Colonic lymphocytosis may be secondary to autoimmune diseases such as Hashimoto’s thyroiditis, drug-induced, or CD. Concomitant occurrence of lymphocytosis in the stomach, small bowel (duodenal and ileum), and colon is exceedingly rare. Our patient responded well to prednisone therapy and was successfully switched to budesonide therapy.

307 Chronic Inflammatory Diarrhea in Severe Hypogammaglobinemia Associated With Good Syndrome Naga Saranya Addepally, Jagpal Singh Klair, MD, Arjun Vaid, Shyam Dang. University of Arkansas for Medical Sciences, Little Rock, AR. Introduction: Good syndrome is characterized by triad of thymoma, immunodeficiency and hypogammaglobulinemia. This acquired Immunodeficiency usually manifests in late adulthood and affects both cell mediated and humoral immune system. Immunodeficiency in these patients puts them at risk for recurrent sino-pulmonary infections and opportunistic infections. Case presentation: A 50-year-old gentleman with history of incidental thymoma (status post thymectomy) was admitted to the hospital with chronic diarrhea. He reports having 8-15 loose stools everyday for preceding eight years along with significant unintentional weight loss of 100 pounds in last one year. Stools were described as loose in consistency accompanied by abdominal cramps. Diarrhea would wake him up from sleep and at times patient had experienced urge incontinence. Patient would have diarrhea despite fasting. Extensive laboratory workup to rule out infectious etiology, fat malabsorption, and celiac disease was negative. Colonoscopic exam was normal with random right and left sided biopsies showing mild focal active colitis. Terminal ileum was normal. Trial of steroids and oral mesalamine failed to improve symptoms. After multidisciplinary evaluation considering history of thymoma, chronic diarrhea and recurrent pulmonary infectious, we suspected Good syndrome. Serum quantitative immunoglobulins and was found to be extremely low- IgG 320, IgA. Discussion: The initial presentation of Good syndrome can be varied. Some patients present with pressure like symptoms from thymoma while some present with recurrent infections and thymoma is incidentally found on imaging. Chronic diarrhea is presenting symptom in 50% of patients resulting from patchy inflammation, recurrent infections or malabsorption secondary to villous atrophy. Diagnosis of GS needs a high clinical suspicion. When suspected, immunologic investigations including quantified immunoglobulins and flow-cytometric analysis of B and T cell subsets should be considered. Thymectomy should be considered in patients with thymoma. However, it is ineffective in reverting back immune deficiency, might even worsen hypogammaglobulinemia. IVIG can be given to patients with hypogammaglobulinemia suffering from recurrent pulmonary infections or chronic diarrhea. In our patient, diarrhea responded promptly to administration of IVIG. Summary: Good Syndrome is an uncommon cause of chronic diarrhea. Diagnosis can be challenging and needs high clinical suspicion as thymoma and onset of immunodeficiency can occur at different time periods. Prognosis in Good Syndrome is thought to be worse than other immunodeficiencies and have 40-50% mortality rate.

[308A] Figure 1.

[308B] Figure 2.

308 Concomitant Lymphocytic Gastritis, Enteritis, and Colitis Vikas Pabby, MD, MPH1, Sahar Samaha, MD2. 1. University of California Los Angeles, Porter Ranch, CA; 2. Miraca Life Sciences, LS, Phoenix, AZ. A sixty-two year old male with a past history of hypertension, hypothyroidism, hypogonadism, and recent right renal cell carcinoma presented with a history of diarrhea present since the 2 months ago. The diarrhea was 4-8 times per day, watery, and without blood. He had reported weight loss of twenty-five pounds since the onset of the diarrhea. The patient denied abdominal pain, nausea / vomiting, fevers, arthralgias, rash, mouth sores, or eye redness. There was no family history of inflammatory bowel disease (IBD) or autoimmune. C-reactive protein was not elevated at 1.21. The tissue transglutaminase antibody was negative. Esophagogogastroduodenostomy (EGD) showed erythema throughout the entire examined stomach and a 2 cm hiatal hernia. The esophagus and duodenum were otherwise normal. Colonoscopy showed sigmoid diverticulosis, internal hemorrhoids, and two sub-centimeter polyps in the sigmoid colon. Biopsies from the stomach, duodenum, terminal ileum, and random colon (right and left) showed significant intra-epithelial lymphocytic infiltrate with severe villous blunting of the duodenum, and terminal ileum. There was no evidence of collagenous gastritis or colitis. The patient was started on prednisone 40 mg per day, which resulted in resolution of diarrhea with one formed bowel movement per day and stabilization of the weight. Tapering prednisone to 20 mg caused recurrent diarrhea. The patient was transitioned to budesonide 9 mg orally per day and was able to come off the prednisone. Increased numbers of intra-epithelial lymphocytes can be found in the esophagus, stomach, small intestine, and colon in a variety of clinical circumstances. In the stomach, it is important to exclude celiac disease (CD) and H. pylori gastritis prior to making the diagnosis of lymphocytic gastritis. In our patient, serologic workup for CD was negative. In the duodenum, causes of lymphocytosis may be secondary to CD, autoimmune enteropathy, common variable immune deficiency, or medication induced (i.e


[308C] Figure 3. VOLUME 110 | SUPPLEMENT 1

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Recurrent Rectal Bleeding in a Patient With Angiosarcoma of the Colon

Kayexalate-Induced Bowel Necrosis: A Rare Complication From a Common Drug

Nayna Riyat, MD1, Ruchi Bhatia, MD2, Jinping Lai, MD, PhD3, Jill Elwing, MD4. 1. Saint Louis University School of Medicine, Department of Internal Medicine, Saint Louis, MO; 2. Saint Louis University School of Medicine, Division of Gastroenterology and Hepatology, Saint Louis, MO; 3. Saint Louis University School of Medicine, Department of Pathology, Saint Louis, MO; 4. John Cochran VA Medical Center and Washington University School of Medicine, Division of Gastroenterology, Saint Louis, MO.

Marjan Islam, MD, Dovid Moradi, MD, Supreeti Behuria, MD. Mount Sinai Beth Israel, New York, NY

Angiosarcoma is a rare, aggressive malignant endothelial-cell tumor of vascular or lymphatic origin that occurs most commonly in the skin and soft tissues, and accounts for less than 1% of all soft tissue sarcomas. Colorectal angiosarcomas account for less than 0.001% of all colorectal cancers and are associated with a poor prognosis. We describe a case of colon angiosarcoma presenting as recurrent rectal bleeding. A 75 year old male with atrial fibrillation on warfarin presented for evaluation of melena and orthostasis for 2 days. Laboratory evaluation revealed a hemoglobin of 3.9 g/dL and an INR of 11. EGD showed Barrett’s esophagus. Colonoscopy revealed diverticulosis, but was limited due to tortuosity with difficulty advancing the scope past the transverse colon. Capsule endoscopy revealed a single, small non-bleeding arteriovenous malformation. Symptoms resolved and he was discharged with instructions to discontinue warfarin. Shortly post-discharge, he presented with large volume hematochezia. Advanced endoscopic colonoscopy showed a 2.5 cm cecal mass and 1.5 cm ascending colon mass. Biopsy revealed moderate pleomorphism and immunohistochemistry positive for CK-7, vimentin, factor VIII, and CD 31, consistent with angiosarcoma (Figure 1). A right hemicolectomy was performed, with histopathology revealing poorly differentiated neoplasia with pleomorphic epithelioid and focal spindle cell morphology. Colon angiosarcoma is a rare colonic neoplasm. A review by Sherid, et al. described 30 cases, and we have found 4 additional cases described since then, including our patient. Of the 30 patients, the median age of primary colon angiosarcoma was 61.5 years and 58% occurred in females. Angiosarcomas have a 5-year survival of approximately 35%; however, colonic angiosarcomas rapidly progress to death in a median time of 4 months. Our case shows the typical pattern of angiosarcoma with pleomorphic epithelioid endothelial cells, spindle cells, and mitotic bodies. Immunohistochemistry is crucial for proper diagnosis, with angiosarcoma expressing CD 31, CD 34, von Willebrand factor, and VEGF. Surgery is essential for treatment of colon angiosarcoma. The role of adjuvant chemotherapy has been described with unclear results, and warrants further investigation.

Case Presentation: A 71 year-old female with a history of chronic kidney disease (CKD) presented with worsening shortness of breath and cough for 1 week. She was admitted for COPD exacerbation precipitated by pneumonia, and improved with antibiotics and a short course of steroids. On hospital day 8, she was noted to be hyperkalemic with a potassium of 5.5mmol/L, and was treated with a dose of 15g/30mL of kayexalate. Within hours, she developed severe nausea and vomiting with abdominal pain. Abdominal x-ray and CT scan showed a markedly dilated, stool filled transverse and descending colon. Her condition quickly deteriorated, prompting an emergent exploratory laparotomy. She was found to have a cecal perforation with ischemic and hemorrhagic bowel, requiring subtotal colectomy with end ileostomy. Pathology later revealed diffuse mucosal necrosis with dark purple crystals present, implicating kayexalate-induced bowel necrosis as the cause. The patient had an uncomplicated post-operative period and was discharged on day 14, with an end-ileostomy. Discussion: Our case highlights a rare but devastating complication from a very common drug. While the precise mechanism remains unclear, kayexalate-induced bowel necrosis has been linked to renin and angiotensin-mediated mesenteric vasoconstriction and consequent intestinal ischemia. Sorbitol, a common medium for kayexalate, has also been implicated, disrupting the mechanisms that regulate cell volume through its effects as a high osmotic load. Additionally, increased osmolarity has been shown to cause local vascular shunting, further exacerbating ischemia. Systematic reviews of the reported cases have found that predisposing risk factors include CKD, the post-operative period, and solid organ transplants. While bowel necrosis is indeed exceedingly rare, it is a life threatening and potentially catastrophic condition, warranting acknowledgement of the risks involved when administrating kayexalate. We hope our case demonstrates the importance of remaining judicious in its use, particularly in patients with chronic kidney disease.

[309A] Figure 1.

310 [311A] Figure 1.

A Case Report of Familial Adenomatous Polyposis 1

2

3

John C. Marston , Ahmad Armoghan Yousuf. Awan, MD , Jacob m. Feagans, MD . 1. Louisiana State University Health Sciences Center, Metairie , LA; 2. Howard University Hospital, Rawalpindi, Pakistan; 3. Hattiesburg Clinic, Hattiesburg, MS. Introduction: The purpose of this case is to recognize the proximal manifestations of FAP, understand its genetics and pathogenesis, and discuss the treatment options and surveillance recommendations. Case: A 65-year-old woman with known FAP status post proctocolectomy was referred to gastroenterology clinic with newer onset symptoms including epigastric pain and dyspepsia. Appetite was normal and she denied nausea, vomiting, and diarrhea. History was negative for bleeding or weight loss. Examination was normal except for a healthy and functioning ostomy. Upper endoscopy revealed a suspicious group of lesions in the distal duodenum. Biopsy contained tissue with tubulovillous adenomas with areas of high-grade epithelial dysplasia (HGD). Due to the high risk for malignancy the patient was transferred to tertiary care setting for surgical evaluation. She subsequently underwent pancreaticoduodenectomy (PD) with a relatively uneventful recovery. She is currently followed by oncology and undergoing periodic endoscopic surveillance. Discussion: FAP is a hereditary cancer syndrome characterized by an autosomal dominant mutation in the APC gene, leading to the development of hundreds to thousands of polyps in the colon and rectum beginning in adolescence, and greatly increased colorectal cancer risk. FAP may present with abdominal pain, rectal bleeding, constipation, or diarrhea. Initial diagnosis is made by colonoscopy, and confirmed by genetic testing. The primary goal in treatment of FAP is the colorectal cancer prevention. Prophylactic proctocolectomy is the treatment of choice with options for ileorectal or ileoanal anastomosis depending on rectal involvement. Annual rectal or ileoanal pouch screening is recommended; ileostomy screening is recommended biannually. Screening for thyroid malignancy is recommended annually. Gastroduodenal screening is recommended every 6 months to 4 years based on Spigelman score. Duodenal polyposis is a significant concern in post-colectomy FAP patients. Advanced stage polyposis is correlated with increased risk of HGD, and development of invasive adenocarcinoma. Endoscopic resection or PD is indicated when HGD is present. Spigelman score greater than 8 indicates stage III polyposis and is the best predictor of HGD development.Spigelman score increases annually in many FAP patients, with stage IV polyposis present in 42.9% by age 60 and 50% by age 70, so close follow up is necessary for timely detection of HGD and prevention of malignancy.


[311B] Figure 2.


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313 Turning off the Faucet: Novel Therapy for Lymphocytic Colitis Nicklesh Singh, MD, Anish Patel, DO. Carl R. Darnall Army Medical Center, Ft. Hood, TX.

[311C] Figure 3.

312 Abdominal Pain and Diarrhea: Mitotic Arrest in the Colon Divyanshoo Kohli, MD1, Andy Ngo, MD2, George Smallfield, III., MD, MSPH3. 1. Virginia Commonwealth University, Richmond, VA; 2. Virginia Commonwealth University, Pathology, Richmond, VA; 3. Virginia Commonwealth University, Division of Gastroenterology, Richmond, VA. A 45 year old male was referred to our center after he had presented to another provider with abdominal pain and diarrhea. The pain had been present for over a year, was present diffusely throughout the abdomen and crampy in nature. It lasted for about 1-2 hours before gradually improving. He described 7-8 loose bowel movements with occasional hematochezia and a 6 kilogram loss of weight over 2 months. The patient was allergic to shellfish, had no family history of colorectal cancer and had a 20 year pack year smoking history. His co-morbid illnesses include migraine headaches, diabetes mellitus, GERD and gout for which he took Amitriptyline, Ibuprofen, Omeprazole and Colchicine. A physical examination was unremarkable as was the rectal examination. CT angiography did not reveal bowel ischemia or any other finding. Stool studies for ova, parasites, pathological bacteria, elastase and fat were unrevealing. Esophagogastroduodenoscopy and colonoscopy do not show any structural or mucosal abnormality to explain the diarrhea or abdominal pain. The biopsy of the normal appearing colonic mucosa showed increased and often abnormal mitotic figures and epithelial pseudo-stratification. This ‘mitotic arrest’ occurs by the inhibition of microtubule formation. The patient was taking colchicine for gout which is known to interfere with cell cycle by binding to tubulin. Colchicine toxicity also explained the crampy abdominal pain and diarrhea in the patient. Colchicine toxicity is associated with distinct morphologic changes, seen as metaphase mitoses, epithelial pseudo-stratification, and loss of polarity. Isolated case reports have described metaphasic mitotic figures in the mucosa of the colon and the liver in patients with colchicine toxicity. Colchicine has been used for the management of chronic constipation because it causes an acceleration of the colonic transit time and significantly increases the number of bowel movements. Colchicine is rapidly absorbed from the gastrointestinal tract, metabolized in the liver, and excreted in bile, feces and urine after enterohepatic circulation. The extended exposure to the gastrointestinal mucosa may explain the prominent gastrointestinal symptoms of generalized crampy abdominal pain associated with defecation. The patient was taken off colchicine and a follow-up colonoscopy was performed. The mucosal biopsies showed very few mitotic figures. The patient remains asymptomatic on follow-up.

Background: Microscopic colitis, in particular, lymphocytic colitis is a relatively common cause of chronic diarrhea. The incidence of lymphocytic colitis is reported up to 63.7 per 100,000 person-years. Unfortunately, limited pharmacologic interventions are available with durable remission. We present a case of lymphocytic colitis refractory to conventional therapy with efficacy with budesonide MMX therapy. Case Presentation: A 60-year-old Caucasian retired Army service member presented to a civilian Gastroenterology clinic with complaint of chronic diarrhea. He had an associated history of GERD and hemochromatosis. He reported having up to 6-8 liquid bowel movements per day with Bristol 5-6 consistency for over 4 months. He reported having associated mild weight loss of 10 pounds. He reported no exacerbation of symptoms with lactose products and/or gluten-containing products. He underwent a colonoscopy with reports demonstrating a normal mucosal appearance but with random biopsies consistent with lymphocytic colitis. He was initially discontinued on esomeprazole therapy and started on loperamide with no improvement in symptoms after 4 weeks. He was started on bismuth subsalicylate for another 4 weeks with minimal to no response. He attempted a short course of oral prednisone therapy but was intolerant due to significant side effects including headaches and migraines. He underwent an EGD and repeat colonoscopy for second opinion evaluation. Random duodenal biopsies were negative for enteritis (to include celiac) and repeat colonic biopsies with persistent lymphocytic colitis but negative for infectious agents and/or inflammatory bowel disease (Figures 1,2). All specimens were reviewed by a gastro-pathologist. Patient was started on budesonide MMX therapy daily for 2 months. He noted complete resolution of symptoms with normalization of bowels within 1 week of therapy. He remained asymptomatic at followup 3 months after therapy completion. Discussion: Lymphocytic colitis is a common colonic disorder associated with chronic watery diarrhea. When medication side effects and food-related diarrhea is eliminated, pharmacological options are limited with short rates of durable remission. Budesonide MMX is a novel therapy option due to its formulation and colonic delivery design allowing high rates of colonic penetration with minimal systemic absorption.

[313A] Figure 1.

[312A] Figure 1. [313B] Figure 2.



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314 Hepatic Abscess: An Uncommon Presentation of Adenocarcinoma of the Appendix Viveksandeep Thoguluva Chandrasekar, Kunal Chawla, Gaurav Khullar, Sekou Rawlins, MD. SUNY Upstate Medical University, Syracuse, NY. Introduction: Hepatic abscesses are the most common type of abscesses accounting for 48% of the visceral abscesses. They are most commonly associated with intra-abdominal infections leading to peritonitis, hepatobiliary diseases and pancreatitis. We report a rare presentation of hepatic abscess caused by adenocarcinoma of the appendix. Case: 57 year old male was referred to the hospital with a 6 week history of fatigue, fever, chills and 15 lb weight loss. Outpatient workup with CT thorax revealed multiple liver masses. Physical examination was unremarkable and vitals stable. Laboratory workup revealed a WBC count of 10.8x103/microliter with a predominance of neutrophils and LFTs within normal limits. CT abdomen and pelvis revealed multiple right hepatic lobe rim-enhancing lesions, largest measuring 5.3x6.4x4.5 cm. An IR guided 12 Fr drain was placed and he was started on broad spectrum antibiotic. Gram stain revealed few WBCs however cultures were negative and FNA did not reveal malignancy. Antibiotics were switched to Levofloxacin and metronidazole to provide gram negative and Entamoeba coverage. Serology for Entamoeba histolytica and Echinococcus granulosus were negative. Patient reported colonoscopy 3 months ago during which an 8 cm tubulo-villous adenoma was removed from the sigmoid colon with difficulty. A repeat CT was done revealing an interval decrease in the size of the abscess and a tubular density within the appendix measuring 4.1x4.9x1.8. Colonoscopy was performed and revealed an occluded appendiceal orifice. Laparoscopic appendectomy with hemicolectomy was performed. Biopsy revealed moderately differentiated adenocarcinoma of the appendix with invasion into the muscularis propria with clear margins. The specimen was negative for K-RAS and MMR mutations. As there was no evidence of metastasis, it was staged T2N0M0, Stage 1 cancer and surgery was considered curative without need for chemotherapy. Imaging performed 3 weeks and 4 months after the surgery revealed continued decrease in size of hepatic collections. At last follow-up, the patient was doing well with no new symptoms with removal of drain. Discussion: Studies report that colorectal malignancy can rarely present as a hepatic abscess. This may be due to luminal obstruction leading to inflammation and infection causing portal septicemia leading to abscess. Clinicians should also look for occult malignancies in the colon and appendix in addition to infections as a part of workup.

[314C] Figure 3.

315 The Occupational Hazards of Being a Lumberjack Clara Tow, MD, Joann Kwah, MD. Montefiore Medical Center, Bronx, NY.

[314A] Figure 1.

A 40-year-old man visiting from Guyana was admitted to the hospital with 2 weeks of worsening abdominal pain associated with non-bloody diarrhea, fevers, and weight loss. His exam was notable for mild epigastric and left-sided abdominal tenderness. Laboratory studies revealed anemia (hemoglobin 7.2 g/ dL), leukopenia (3.6 k/uL), thrombocytosis (744 k/uL), hypoalbuminemia (2.5 g/dL), and hyponatremia (124 mEq/L). Chest x-ray was normal. Computed tomography of the abdomen and pelvis showed segmental areas of mural thickening throughout the colon that was highly concerning for Crohn’s disease. Inflammatory markers, however, were only mildly elevated. The patient underwent a flexible sigmoidoscopy, which found numerous large, annular, almost completely circumferential clean-based ulcers with heaped up edges in the sigmoid colon and rectum. Microscopic exam demonstrated active granulomatous colitis with scattered small fungal yeasts approximately 2-4 um consistent with histoplasmosis. His urine histoplasma antigen was negative. Subsequent HIV testing was positive with a CD4 count of 193 cells/uL. The patient was started on antiretroviral therapy and itraconazole 200mg twice daily by mouth and is scheduled for outpatient gastrointestinal follow-up. Histoplasmosis, a fungal infection caused by the inhalation of Histoplasma capsulatum, is most commonly found in North and Central America. The patient’s exposure to bird dropping- and bat guanocontaminated soil while working as a lumberjack in Guyana and his HIV infection made him particularly susceptible to developing this rare presentation of histoplasmosis. While 75 percent of individuals infected are immunocompetent, gastrointestinal involvement, particularly in the rectum, is a rare manifestation of this disease and should raise suspicion for an immunocompromised state. This case illustrates the ability of histoplasmosis to mimic inflammatory bowel disease in the immunocompromised patient. The urine histoplasma antigen has a sensitivity of 93 percent but for this patient was negative despite a diagnostic biopsy. Such findings likely indicate that he has focally disseminated disease, which will more often produce negative urine antigen results.

316 Recognizing the Acquired Chilaiditi Syndrome and Managing It With Novel Therapy Noa Krugliak Cleveland, MD, Abraham Dachman, MD, Mark Siegler, MD, David T. Rubin, MD. University of Chicago Medicine, Chicago, IL.

[314B] Figure 2.


Introduction: The rare finding of colonic interposition between the liver and the right hemidiaphragm (Chilaiditi sign) may present as a syndrome with mild to severe gastrointestinal symptoms including abdominal pain, constipation, bowel obstruction, volvulus or even ischemic bowel. We describe a patient who developed Chilaiditi syndrome over time, and describe our management using a novel therapy. Case Description: An 84 year-old female with history of obesity and hypothyroidism presented with months of intermittent right upper abdominal discomfort, worse for the past 10 days. The symptoms were unrelated to food intake or bowel movements, but better when lying down. She had a history of abdominal discomfort evaluated with an unremarkable CT of the abdomen 9 years ago. At that time, those symptoms were distinctly different from her current presentation. Her physical examination was unremarkable, and she was diagnosed with idiopathic constipation and dyspepsia, for which she received PEG cathartics and esomeprazole. There was no improvement in her symptoms, and a plain abdominal radiograph followed by a contrast enhanced CT of the abdomen were performed. The CT showed a new finding of interposition of the transverse colon under the right hemidiaphragm (See Figures.) consistent with Chilaiditi sign, which was thought to be contributing to her symptoms. She then received a stronger purgative bowel regimen for several weeks, but her discomfort persisted. We therefore prescribed gabapentin, 100 mg twice daily. After 2 weeks the combination of laxatives and gabapentin provided significant improvement in her symptoms. In 3 month follow-up, her improvement continues.


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Discussion: This is a case of acquired Chilaiditi syndrome, with the added and serendipitous benefit of serial imaging demonstrating the evolution (over years) of the interposition of colon and liver. Chilaiditi syndrome is rare (estimated 0.25-0.28% of the general population) and can be confused for colonic inertia, IBS or dyspepsia. When the diagnosis does not necessitate more urgent surgical intervention, management is usually conservative and includes stool softeners and in more severe cases, bed rest or NG decompression. In this patient, our initial conservative management failed to relieve her symptoms, so we added management for presumed chronic pain syndrome with gabapentin, which achieved symptomatic improvement. When evaluating patients with abdominal pain, clinicians should be aware of the Chilaiditi syndrome and its variant manifestations, as well as traditional and novel treatment strategies.

case of one of the youngest adults with primary SmCC of the Colon and the first one with concomitant diagnosis of Autosomal Recessive Polycystic Kidney Disease (ARPKD). Case description: This is the case of a 24 year old Caucasian man with ARPKD status post kidney transplant and Chronic Antibody-Mediated Rejection (AMR) on monthly IVIG treatment who presented with rectal bleeding for 1 week associated with constipation and abdominal pain. Physical exam was consistent with severe conjunctival pallor. Lab work showed anemia with hemoglobin of 6.2 g/dL. Colonoscopy revealed a large ulcerated mass at the hepatic flexure. Staging CAT scans and MRI showed hepatic metastases. Histopathology confirmed poorly differentiated Neuroendocrine SmCC with lympho-vascular invasion and tumor cells positive for Cytokeratin, Chromogranin, CD56 and TTF-1. Right hemicolectomy was performed and chemotherapy with Etoposide and Carboplatin was initiated. Disease course was complicated by septic shock secondary to perforated hollow viscus requiring emergent laparotomy and surgical repair. Thereafter, he was discharged in a stable condition and is now due for his third cycle of chemotherapy, about 4 months from the time of initial diagnosis. Discussion: SmCC of the colon has an incidence of less than 1% among colorectal cancers. At the time of diagnosis, it is common to find metastases with a 3-year survival rate less than 15%. Although, immunosuppression and ARPKD gene, PKHD1, have been implicated in an increased risk of colorectal adenocarcinomas, there is scant evidence correlating colorectal SmCC with such risk factors. American Society of Transplantation recommends annual FOBT and sigmoidoscopy every 5 years in renal transplant recipients from the age of 50 years with no recommendation to begin screening at an earlier age. Hence, it is important to identify potential associations to develop preventive strategies to reduce mortality from GI malignancies post transplant. We believe, this case report may provide a sense of clinical vigilance and research direction to facilitate the identification of key factors in the pathogenesis of this rare but fatal entity. Furthermore, it may provide supporting evidence for revising screening recommendations for high risk individuals.

[316A] Figure 1.

[317A] Figure 1.

[316B] Figure 2.

317 Neuroendocrine Small Cell Carcinoma of the Colon in a Young Man With Autosomal Recessive Polycystic Kidney Disease Khwaja F. Haq, MD1, Rahul Sao, MD2, Nancy Gupta, MD3, Muhammad Ali Khan, MD4, Dhruv Mehta, MD2, Nisha Sharma, MD2, Sachin Sule, MD2, Tyson H. Collazo, MD5, Ashley N. Maranino, MD2, Brad M. Dworkin, MD, FACG2. 1. New York Medical College/Westchester Medical Center, Woodbury, NY; 2. New York Medical College/Westchester Medical Center, Valhalla, NY; 3. Westchester Medical Center at New York Medical College, Valhalla, NY; 4. University of Tennessee Health Science Center, Memphis, TN; 5. New York Medical College/Westchester Medical Center, Bronx, NY. Introduction: Small Cell Carcinoma (SmCC) of the colon is a rare but aggressive neoplasm. Previously, it has been reported in the middle aged and the elderly. Here, to the best of our knowledge, we report the


[317B] Figure 2.


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[317C] Figure 3. [318B] Figure 2.

318 Endoscopic Evaluation of a Malignant Coloduodenal Fistula Krysta Johns-Harris, MD, MPH1, Akiva J. Marcus, MD, PhD2, Daniel Berkowitz, MD, MD, FACG3. 1. Montefiore Medical Center, Bronx, NY; 2. Digestive Disease Center of the Palm Beaches, Boca Raton, FL; 3. Montefiore Medical Center, White Plains, NY. An 83 year-old man presented to the ED with 5 days of fever, decreased oral intake and non-bloody diarrhea. He denied abdominal pain, nausea and vomiting. Labs showed a leukocytosis of 17,000, Hgb of 7.1, heme positive stool and Plesiomonas shigelloides bacteremia. An esophagoduodenoscopy was grossly normal and showed no etiology for GI bleeding. A colonoscopy 2 days later revealed a large, circumferential, obstructing, ulcerating mass in the hepatic flexure. Biopsies showed adenocarcinoma. A PET/CT showed possible invasion of the colonic mass into the duodenum. A push-enteroscopy using a pediatric colonoscope showed a normal upper GI tract and proximal jejunum but on withdrawal, postbulbar narrowing was seen along with an ulcerating, circumferential tumor and a central lumen which was a fistula between the duodenum and the colon. Advancing the scope through the fistula revealed the proximal edge of the tumor at the hepatic flexure and a stool-filled ascending colon. Given the advanced disease, the patient and family opted for no further treatment. Discussion: This case describes a patient who had an adenocarcinoma of the hepatic flexure with a fistula to the duodenum. Coloduodenal fistulas are rare. They are usually due to malignant tumors, mostly of the colon but also with carcinomas of the gallbladder and duodenum. Some occur as a result of benign disease such as Crohn›s disease and Peptic ulcer disease. There have been rare reports of idiopathic coloduodenal fistulas. The most common symptoms of such fistulas are diarrhea, weight loss and stercoraceous or fecaloid vomiting. Treatment is surgical.

[318C] Figure 3.

319 Mantle Cell Lymphoma Involving the Gastrointestinal Tract in a Patient on Tofacitinib for Rheumatoid Arthritis Abbas Rupawala, MD1, Curuchi Anand, MD2. 1. University of Massachusetts Medical School, Worcester, MA; 2. St. Vincent Hospital, Worcester, MA.

[318A] Figure 1.


Introduction: Tofacitinib is a Janus Kinase 1 and 3 inhibitor that is approved for the treatment of Rheumatoid arthritis (RA) in United States. The medication is also under investigation for treatment of Crohn’s disease and Ulcerative Colitis (UC). Most common side effects associated with the drug include nasopharyngitis, URTIs, headache and diarrhea. More serious side effects include severe infections and malignancies including Lymphoma. We present a case of a patient on Tofactinib for treatment of RA who developed Mantle cell lymphoma affecting the lower gastrointestinal tract. Case presentation: Patient is an 81 year old male with history of polyarticular RA affecting the hands that was diagnosed in 2012. Patient was subsequently tried on various medications including combination therapy with Methotrexate and Infliximab, Certolizumab and Tocilizumab without significant benefit and was finally started on Tofacitinib in September 2013. Patient experienced substantial improvement on Tofacitinib and was able to get off steroids. He started experiencing diarrhea after being on treatment for about 15 months. The severity of diarrhea increased over the next three months to 4-5 large bowel movements a day with urgency, incontinence and occasional blood. A colonoscopy in 2012 showed diverticulosis and internal hemorrhoids. Stool studies ruled out infections including Clostridium difficile. He underwent colonoscopy to the terminal ileum that showed patchy inflammation characterized by friability, ulceration involving the rectum, distal sigmoid, ascending colon and terminal ileum. Biopsies of involved areas showed a dense lymphoid infiltrate composed of a relatively monomorphic population of small to medium sized lymphoid cells with hyperchromatic nuclei. Immunoperoxidase staining was consistent with Mantle cell lymphoma. Discussion: Mantle cell lymphoma is a rare type of Non Hodgkin’s lymphoma and involvement of the gastrointestinal tract is common. An analysis of malignancies associated with Tofacitinib use in patients with RA found 12 cases of lymphoma with one case of Mantle cell lymphoma in 5671 patients on the


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medication. This case represents the second case of the same to the best of our knowledge. The clinical presentation and mucosal appearance was suggestive of inflammatory bowel disease. Since Tofacitinib may be available for treatment of Ulcerative colitis in the future, it would be important to be aware of this possible association.

320 Klippel-Trenaunay Syndrome of the Rectosigmoid Colon Presenting as Severe Anemia Eula Tetangco, MD1, Hafiz Muhammad Sharjeel Arshad, MD1, Rogelio Silva, MD2. 1. University of Illinois at Chicago/Advocate Christ Medical Center, Oak Lawn, IL; 2. Advocate Christ Medical Center, Oak Lawn, IL. Klippel-Trenaunay syndrome (KTS) is a rare congenital malformation defined by a triad of vascular and lymphatic malformations, soft tissue and bone hypertrophy, and atypical varicosities. Visceral involvement is uncommon but can be a significant source of morbidity and mortality. A 23-year old female with Klippel-Trenaunay syndrome was evaluated for abdominal pain and anemia. She denied fever, melena, and hematochezia. She had presented three years prior for anemia attributed to menorrhagia. Physical exam revealed a soft, slightly distended abdomen with mild right lower quadrant tenderness. Laboratory evaluation showed hemoglobin of 5.7 g/dL, unremarkable hepatic chemistries, and platelet count of 189,000/mcL with no evidence of coagulopathy. CT scan of the abdomen and pelvis demonstrated eccentric mural thickening of the rectosigmoid colon and perirectal inflammation. Esophagogastroduodenoscopy showed minor antral gastritis. Colonoscopy revealed diffuse venous congestion circumferentially extending from the mid-sigmoid to the rectum, multiple large varicosities, and purplish discoloration of the entire mucosa, with prominent internal hemorrhoids. With no active bleeding, she was treated conservatively with iron replacement and blood transfusion. She was advised tertiary evaluation for possible rectosigmoid resection. Patients with KTS have prominent external abnormalities. Visceral manifestations are lesser known but can lead to life-threatening complications from blood loss and anemia. Gastrointestinal involvement often goes unrecognized in asymptomatic patients. Bleeding is uncommon, presenting in 6 of 588 cases in the largest KTS study to date. Distal colon and rectum are involved in 1-12.5% of cases. Endoscopic therapies have a limited role due to the extensive nature of the disease. A conservative approach with iron replacement may be taken for non-significant bleeding. In cases of life-threatening bleeding, surgical resection has been effective. Visceral angiography aids in defining extent of disease prior to surgery. Angiographic embolization and clipping has been utilized emergently as a bridge to surgery, and to reduce risk of intraoperative bleeding. This case emphasizes that KTS may have vascular malformations beyond the classic triad. Gastrointestinal involvement may present without symptoms, and resection of the affected segment has been shown to control bleeding.

[320C] Figure 3.

321 Osseous Metaplasia in an Exceedingly Rare Location Richard Yeh, MD1, Simi Singh, MD2, Jason Bratcher, MD3. 1. Mount Sinai Beth Israel, New York City, NY; 2. Mount Sinai Beth Israel, New York , NY; 3. Mount Sinai Beth Israel Medical Center, New York, NY. Introduction: Osseous metaplasia (heterotopic bone formation) is a very rare phenomenon in the gastrointestinal tract. Ossification has been described in regions of the GI tract from the esophagus to the rectum. Bone formation in the GI tract has been associated with both benign and malignant neoplasms. The process through which this occurs in the GI tract is poorly understood. We present a seemingly benign presentation of bone metaplasia associated with a hyperplastic polyp in the appendiceal orifice. Case Presentation: A 60-year-old woman with a distant episode of idiopathic thrombocytopenic purpura and a family history of multiple myeloma in several first and second degree relatives presented for her first screening colonoscopy. She denied any constitutional symptoms, such as abdominal pain or change in bowel habits. The physical exam was normal. The colonoscopy was performed without any complications and revealed 3 sessile polyps located in the recto-sigmoid colon, descending colon and transverse colon, respectively. These were removed with a hot snare. A nodule was noted on the appendiceal orifice, which was biopsied. Pathology revealed a hyperplastic polyp in the recto-sigmoid colon and tubular adenomas in the transverse and descending colon. The biopsied nodule on the appendiceal orifice, however, revealed a hyperplastic polyp with heterotopic bone formation of the stroma. Discussion: Various mechanisms for heterotopic bone formation in the GI tract have been hypothesized. Bone Morphogenic Proteins are known to play an important role as a cytokine in the pathogenesis and pathophysiology of osseous metaplasia. A commonly cited possible mechanism includes inflammation and injury leading to activation of stromal fibroblasts and their differentiation into osteoblasts. Some theorize that mucinous stromal infiltration may also trigger metaplastic bone foci. More recently, it has been suggested that tumor cells can induce proliferation of local mesenchymal tissue and differentiation of mesenchymal cells to osteoblasts. Osseous metaplasia is more common with age, however, it has been described in patients as young as 6 years old. Ossification in benign polyps is thought to have no clinical significance and is likely an insignificant finding in our patient. In patients with malignancy, the presence of osseous metaplasia does not seem to affect outcome. However, in pre-malignant conditions such as esophageal metaplasia, the significance of osseous metaplasia remains to be seen.

[320A] Figure 1.

[321A] Figure 1. [320B] Figure 2. The American Journal of GASTROENTEROLOGY


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322 Synchronous Gastric and Diffuse Colonic MALT Lymphoma in a Patient With Strongyliodes Infection: A Causal or Incidental Association Obada Subei, MD1, Ismail Zahir, MD2, Cynthia Liu, MD, PhD3, Soren Gandhi, MD4. 1. New York University Woodhull Medical Center, Ridgewood, NY; 2. New York University Woodhull Medical Center, Brooklyn, NY; 3. New York University Langone Medical Center, New York, NY; 4. New York University Woodhull Medical Center, New York, NY. Mucosa-associated lymphoid tissue (MALT) lymphomas are well known and when occurring in the gastrointestinal tract, specifically the stomach, there is a well established association with Helicobacter pylori. Colorectal MALT lymphomas are very rare and usually present with a protruding mass, polyps or ulceration. Of those rare cases, only a few have been found synchronously with gastric MALT lymphomas. There are reports of colorectal MALT lymphomas regressing after antibiotic treatment of H. pylori in the stomach even when the organism is absent, suggesting other etiologies. We report a rare case of colorectal MALT lymphoma presenting as a diffuse colonic infiltration, occurring synchronously with gastric MALT lymphoma in the presence of H. pylori and Strongyloides stercoralis. A healthy 60 y/o male complaining of alternating constipation and diarrhea with intermittent hematochezia underwent a diagnostic colonoscopy which revealed a diffuse friable, nodular and erythematous mucosa visible throughout the colon (Figure 1). Biopsies showed sheets of CD10 small angulated B lymphocytes with atypical BCL2 expression overrunning scattered lymphoid follicles, histologically compatible with MALT lymphoma (Figure 2). His evaluation included a stool ova and parasites analysis that revealed Strongyliodes stercoralis. He was subsequently treated with two doses of Ivermectin and a repeat stool analysis confirmed eradication. The patient’s diarrhea had improved and a repeat colonoscopy two months later revealed less erythema and friability of the colonic mucosa, however biopsies were still consistent with MALT lymphoma. Subsequently an EGD revealed MALT lymphoma with H. pylori, which was treated with a standard antibiotic regimen and a stool antigen test one month later confirmed eradication. Ten months after treatment with confirmed eradication of both Strongyliodes and H. pylori, a repeat EGD was normal with no evidence of MALT and a repeat colonoscopy revealed normal mucosa (Figure 3), but biopsies still revealed residual atypical lymphocytes consistent with MALT. In reviewing the literature, MALT lymphoma of the colon presenting as a diffuse infiltration occurring synchronously with MALT lymphoma of the stomach in the presence of both H. pylori and Strongyliodes has never been reported. Although there was complete eradication of MALT lymphoma in his stomach, the MALT lymphoma of the colon still persisted despite being asymptomatic. It has been reported that Strongyliodes stercolis is associated with rare T-cell lymphomas in the GI tract raising the question whether or not Strongyliodes is a causative etiology or an incidental finding in this patient. This case illustrates the complexity in managing a patient with a rare presentation in an otherwise rare disease.

[322C] Figure 3.

323 Extramedullary Involvement of Sigmoid Colon With Acute Lymphocytic Leukemia Abdulfatah Issak, MD1, Sangeeta Agrawal, MD, FACG2. 1. Wright State University, Dayton, OH; 2. Dayton VA Medical Center, Wright State University, Dayton, OH.


Introduction: Gastrointestinal involvement with leukemia ranges from 5.7% to 13% and can be as high as 20% in cases of ALL. Leukemic infiltration into multiple organs is generally observed late in the course of the disease. However, leukemic infiltration into sigmoid colon is relatively rare. The stomach, ileum, and proximal colon are the most commonly involved sites, whereas the duodenum and distal colon were less commonly affected. We report a case of ALL with sigmoid infiltration in a patient evaluated for profuse diarrhea. Case Report: 61 year old male with recurrent Philadelphia Chromosome-positive (Ph+) ALL was being treated with Imatinib + Doxorubicin (DOX), Vincristine (VCR), and Dexamethasone (Hyper-CVAD) that alternated with high-dose Methotrexate (MTX) and Cytarabine (Ara-C). The patient’s course of treatment was complicated by chronic osteomyelitis of the spine secondary to E. coli. He then developed sepsis and acute diarrhea with alteration in antibiotics to include Vancomycin and Piperacillin/Tazobactam. Clostridium difficile toxin was identified and the antimicrobials were changed to metronidazole and cefuroxime PO. The diarrhea persisted and oral Vancomycin was started. The patient continued to have voluminous non bloody diarrhea despite treatment and repeat C. difficile toxin test being negative.


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A flexible sigmoidoscopy was performed which revealed a 1 cm pedunculated sigmoid polyp which was biopsied. Random sigmoid colon biopsies were also obtained. On pathology, the sigmoid colon polyp biopsy was found to be a tubular adenoma with high-grade dysplasia. The random sigmoid colon biopsies showed a few small foci of mild, nonspecific active colitis. In these areas, atypical mononuclear cells were noted. An immunohistochemical stain for CD34 highlighted a few cells in these areas suggestive of infiltration from the patient’s ALL. With continued ALL treatment, in addition to Imodium BID, patient’s diarrhea improved significantly, Discussion: Diarrhea secondary to leukemic infiltration of the colon can be the first presenting symptom of leukemia or it can be a complication of a patient with known leukemia, as it was described here. While chemotherapy with ARA-C is associated with gastro enteric complications, such as abdominal pain, diarrhea and melena, this patient had no such characteristics except diarrhea. Finding on the immunohistochemical stain also minimized such consideration. Cases of leukemic infiltration into the colon have increased in number likely from improved diagnostic methods and better survival in leukemia patients. This case highlights the importance of high index of suspicion for gastrointestinal infiltration of leukemia in patients presenting with unusual symptoms.

324 Initial Diagnosis of a Common Hematological Malignancy in a Screening Colonoscopy Timothy Ritter, MD1, Mahsa Sorouri2, Fayez G. Seif, MD3, Chris Fourment, MD1, Donna J. Lager, MD2, Cory A. Roberts, MD2, Matthew Lewin, MD2. 1. Texas Digestive Disease Consultants, Southlake, TX; 2. ProPath, Dallas, TX; 3. Texas Digestive Disease Consultants, Mesquite, TX. Extra-medullary (EM) manifestations of chronic lymphocytic leukemia (CLL) are relatively rare. Previous reports of EM-CLL suggest that the skin, CNS, and GI tract are the most commonly affected sites. In the majority of EM-CLL cases, EM involvement by CLL is only discovered after a primary diagnosis of CLL is made. GI involvement in CLL is generally associated with advanced stages of the disease in which the disease has transformed into large B cell lymphoma (i.e. Richter syndrome). Here we report a case of colonic involvement by CLL in a 50-year-old man who presented for a screening colonoscopy. This case is unique as the patient neither had a previous diagnosis of CLL nor experienced any of the associated symptoms. An asymptomatic 50-year-old man presented for his first screening colonoscopy. His past medical history was unremarkable except for prior squamous cell and basal cell skin carcinomas. Colonoscopy revealed grade 1 internal hemorrhoids and a 5 mm non-bleeding sessile polyp in the transverse colon which was resected for histological evaluation. Review of the specimen demonstrated multiple lymphoid aggregates composed of CD20 (+), CD5 (+), CD23 (+), LEF1 (+), Cyclin D1 (-) cells, which is consistent with involvement by CLL/small lymphocytic lymphoma (SLL). Blood counts were essentially normal, and no evidence of lymphoma or other pathologic abnormalities were found in the upper GI tract. A CT scan of the chest, abdomen, and pelvis revealed a small degree of lymphadenopathy above and below the diaphragm. The patient was diagnosed with stage IIIAE CLL/SLL. Further immunohistochemical analysis of the colon specimen indicated that the neoplastic cells did not express ZAP-70. Expression of ZAP-70 by the neoplastic cells is a reliable indication of the unmutated IgVH status in these cells. Considering that the unmutated IgVH status in the neoplastic cells is associated with a more aggressive clinical course of CLL, lack of ZAP-70 expression suggested an indolent course of disease. Immediate treatment was deferred, as the watch-and-wait approach is often the standard of care for low-risk CLL patients. This case is remarkable for at least two reasons: it demonstrates that the possibility of GI involvement in CLL should not be reserved only for later stages of the disease, and it emphasizes the need for the pathologists to remain vigilant for immunophenotype suspicious lymphoid aggregates even in the absence of a known CLL/SLL diagnosis.

325 Fecal Microbiota Transplant for Severe Complicated Clostridium difficile Infection via a Loop Ileostomy: A Novel Administration Route

326 Resolution After Rupture: The Case of a Rare Colonic Non-neoplastic Submucosal Cyst Peter Chung, MD1, Anjali Basil, MD2, Keshav Pandey, MD1, Jaroslav Zivny, MD1. 1. University of Massachusetts Medical Center, Worcester, MA; 2. UMass Memorial Health Care, Worcester, MA. Enteric duplication cysts are a rare phenomenon that can occur throughout the gastrointestinal tract. Thought to arise in early embryological development, they are usually discovered in the pediatric population and are uncommon in adults. In the pediatric literature, incidence of duplication cysts is 6.8% in the colon. In our search, we found only 16 reported cases of adult colonic duplication cysts. These cysts either arise from the submucosal layer or extrinsic to the intestinal wall. In adults, cysts are asymptomatic and found incidentally on endoscopy or imaging, with radiological findings either nonspecific or absent. To date, characterization and management of asymptomatic colonic duplication cysts is not well established. We present a case of an incidental benign cystic lesion found at the hepatic flexure during a screening colonoscopy, which we decided to follow with serial Endoscopic Ultrasound (EUS), subsequently ruptured following biopsy, and resolved. 50-year-old previously healthy female underwent a screening colonoscopy. A 2.2 cm cystic structure was found at the hepatic flexure. Subsequent endoscopic ultrasound (EUS) of the lesion revealed it to be anechoic, compressible, and fluid-filled. It was without any worrisome features of inflammation, granulation or ulceration. However, it was discovered to have a septation, with an intact layer of muscularis, and without communication to the colonic lumen. Biopsy resulted benign colonic mucosa. CT abdomen/ pelvis showed no extrinsic cause or abnormality. The next surveillance EUS (2 years from diagnosis) was again unchanged. However deeper biopsies of the area taken with forceps resulted in unroofing of the cyst and draining of clear fluid. Visualization through the opening showed a normal cystic wall appearance. Patient tolerated the procedure well and had no clinical symptoms of perforation or abdominal pain. Patient returned again for a colonoscopy at the 5 year mark which showed that the cyst had completely disappeared. A surveillance colonoscopy will be done in 5 years without need for further EUS given the cyst had resolved. To date there is no standardized way of evaluating colonic submucosal lesions. We present a case of a rare duplication cyst of the colon that was successfully characterized and monitored with endoscopic ultrasound. Our management suggests EUS can be successful in characterizing colonic cysts, and drainage may be a feasible treatment option for benign symptomatic cysts. Certainly, more studies are needed to understand, characterize, and manage submucosal colonic cysts.

327 Rare Case of a Colocolonic Intussusception Due to Giant Lipoma Amilcar Morales, MD1, Lindsay Jones Barnes, MD2. 1. Walter Reed National Military Medical Center, Mclean, VA; 2. Fort Belvoir Community Hospital, Fort Belvoir, VA. Adult bowel intussusceptions are rare and represent 1% of all bowel obstructions in this population. Malignancies are the most common cause of lead point for colo-colonic intussusceptions. We present a rare case of a colo-colonic intussusception due to a benign, 7 cm lipoma. 56 y/o male with unremarkable past medical history presents to the emergency department complaining of a one month history of progressive left lower quadrant crampy abdominal pain with sudden development of constipation, two events of hematochezia and no systemic symptoms. No family history of GI malignancies and no previous screening colonoscopy. His initial laboratory work up was unremarkable including hemoglobin of 13.6 g/dl. A CT abdomen/pelvis with IV and oral contrast was performed and showed a 7.1 by 3.8 cm teardrop shaped fat density mass located in the descending/sigmoid colon with evidence of intussusception (image 1). A colonoscopy was performed showing a larger pedunculated mass with a thick stalk and an ulcerated surface (image 2 and 3). Due to his clinical presentation and size of the mass the patient underwent a left colectomy. Pathology evaluation of the mass showed a tumor involving the submucosa with evidence of mature adipocytes consistent with a giant lipoma. Bowel intussusceptions account for 1% of all adult bowel obstructions. Colo-colonic intussusceptions, due to giant lipomas (lesions over 4 cm), are rare with around 50 cases reported in the last decade.

Rashid Syed, MD1, Usman Rahim, MD2, Felicia Humphrey, MD2, Arnab Ray, MD2. 1. Ochsner Medical Center, Metairie, LA; 2. Ochsner Medical Center, New Orleans, LA. Introduction: Clostridium difficile infection (CDI) is the most common cause of infectious diarrhea in healthcare settings. High cure rates of CDI with fecal microbiota transplantation (FMT) have been reported (88 to 100%). Successful delivery of donor fecal material has been described via nasogastric duodenal tube, colonoscopy, physician administered retention enemas and self-administered enemas. To our knowledge there has been no reported case of successful FMT for CDI via a loop ileostomy. Case Report: A 57-year-old women with past medical history of hypertension and type II diabetes mellitus developed diarrhea related to CDI after a hospitalization for pneumonia that had required antibiotics. She was successfully treated with oral vancomycin and intravenous flagyl. Two months later she re-developed diarrhea and was diagnosed with severe complicated CDI. On this second presentation her WBC count was 87 k/uL and a CT abdomen showed pan-colitis. She developed septic shock with multi-organ system failure. She required pressor support, mechanical ventilation and intermittent hemodialysis. She was treated with oral and rectal vancomycin, intravenous flagyl and oral pro-biotics. When she failed to respond, a laparoscopy was done to create a loop ileostomy. She was given vancomycin solution through the ileostomy for about 10 days. She showed some clinical response to this aggressive antibiotic therapy with declining leukocytosis and pressor requirement but remained critically ill and continued to have diarrhea. At this point it was decided to perform a FMT. All her antibiotics were stopped for a 24-hour period prior to instillation of 250 mL of open biome donor feces into her ileostomy. All antibiotics were held for another week after the FMT. Her diarrhea completely resolved. Her subsequent hospital course was complicated by candidal fungemia, multiple drug resistant Pseudomonas aeruginosa empyema and bilateral femoral deep venous thrombosis but she remained free from recurrence of CDI. Two repeat PCR’s for C. difficile approximately one and two month after FMT via loop ileostomy remained negative. She has now been discharged from the hospital and is doing well. Conclusion: This is the first ever reported case of successful cure of recurrent severe complicated CDI with FMT through a loop ileostomy. This report demonstrates the versatility of routes through which a successful FMT can be performed.


[327A] Figure 1.


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Abstracts white light, was seen at the distal sigmoid colon. This polyp was completely excised by hot snare polypectomy. The polyp was retrieved and sent for histologic examination. Immunohistochemical stain S100 highlighted the ganglion and spindle cells, supporting the diagnosis of ganglioneuroma. This unique finding highlights an unexpected case of an asymptomatic, solitary polypoid colonic ganglioneuroma. Ganglioneuromas are most often found in constellation syndromes such as multiple endocrine neoplasia type IIB (MEN-IIB), Von Recklinghausen’s disease, and Cowden Syndrome. However, for a solitary colonic ganglioneuroma to be found in an asymptomatic individual, especially in an adult male; this is an exceedingly rare presentation for a rare tumor.

[327B] Figure 2.

[328A] Figure 1.

[327C] Figure 3.

[328B] Figure 2. The diagnosis is usually made with a radiologic study, with CT scan being the recommended modality. Asymptomatic large lipomas can be successfully removed by endoloop in a grab and let go technique. For symptomatic lesions, including intussusception, the therapy of choice is surgery. However, in the last few years several case reports have shown the possibility of endoscopic resection (unroofing/electrocautery) using endoscopic ultrasound and lifting techniques with good success and low complication rates. We present a rare case of a colo-colonic intussusception with a giant lipoma. As in our case, these lesions tend to lose the classic well-delineated sub mucosal bulging, making it hard to differentiate between a benign lipoma and malignancy. As we continue to improve our endoscopic technics and equipment, endoscopic resections could be feasible even in the symptomatic lesions. If endoscopic resection is contemplated, surgical support should be available in case of a perforation or major bleeding.

328 A Colonic Polypoid Ganglioneuroma: An Unexpected Finding on a Screening Colonoscopy Simran Arora, MD1, Tarek Abu-Rajab Tamimi, MD2. 1. University of Missouri, Kansas City, MO; 2. University of Missouri/Truman Medical Center, Kansas City, MO. Introduction: Ganglioneuromas are benign peripheral neuroblastic tumors of the neuroectodermal family composed of mature ganglion cells, schwann cells, and supporting cells. They can occur anywhere along the sympathetic chain, most commonly in the mediastinum, retroperitoneum, and adrenal glands. They most often occur in the pediatric population in association with genetic syndromes with 60% being diagnosed before age 20, and occur most often in females. Case Description: A 56 year old African-American male with Diabetes Mellitus and chronic HCV infection underwent first average-risk screening colonoscopy. The colonoscopy was completed to the cecum with good bowel preparation. A 7 mm sessile polyp, which was not characteristically adenomatous under


[328C] Figure 3.


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329 Antiphospholipid Syndrome Presenting as Thrombotic Acute Mesenteric Ischemia of an Anomalous Inferior Mesenteric Vein Obada Subei, MD1, Virendra Tewari, MD2, Gulam M. Khan, MD, MS3. 1. New York University Woodhull Medical Center, Ridgewood, NY; 2. New York University Woodhull Medical Center, Elmsford, NY; 3. New York University Woodhull Medical Center, Brooklyn, NY. Introduction: Thrombosis of the splanchnic circulationis an uncommon manifestation ofAntiphospholipid Syndrome (APS); a rare site of which is the Inferior Mesenteric Vein (IMV). The rarest etiology of Acute Mesenteric Ischemia (AMI) is thrombosis of the venous supply (2-5%). We present a case of a patient found to have APS presenting with AMI of the left colon secondary to thrombosis of an anomalous IMV. Case Report: A 76 y/o female presented with bright red blood per rectum, mild abdominal pain and tenderness with no rigidity or guarding. Investigations revealed nonspecific rectal and distal sigmoid inflammatory process on non-contrast CT. A flexible sigmoidoscopy revealed multiple ulcers in the rectum and sigmoid colon, with congested mucosa and exudates. Proximally the descending colon mucosa gradually normalized in appearance with a clear marginal zone which was suspicious for an ischemic etiology (Figure1). An abdominal angiogram revealed multiple filling defects in a dilated IMV abnormally draining into the Superior Mesenteric Vein (SMV) with significant wall thickening of the left colon (Figure 2). Intravenous heparin drip was initiated. A rapid improvement in symptoms was observed. An anti-phospholipid antibody panel showed an increase in IgA anti β2- glycoprotein, confirming APS. The patient was bridged to Rivaroxiban. A re-evaluation after six months revealed no recurrence of symptoms. A follow up Colonoscopy showed normal mucosa of the colon with complete resolution of mucosal ischemic changes (Figure3). Discussion: APS presented itself with thrombosis in the least common location within the splanchnic circulation in our patient. The most common site of all- cause splanchnic thrombosis is the SMV (50 to 82%) and rarely involves the IMV (14%). Our patient has an anomaly by which the IMV drains into the SMV (normally drains into the splenic vein) which may explain the rarity of the location of her thrombosis and left colonic pathology. The early detection of our patient’s thrombosis and early intervention with anticoagulation therapy was essential in avoiding bowel wall necrosis and the need for surgical intervention. Our experience with managing this patient highlights the benefits of maintaining a high level of suspicion for thrombosis of the splanchnic circulation in patients presenting with abdominal pain and blood per rectum.

[329C] Figure 3.

330 That’s Not Just a Headache: A Rare Presentation of Metastatic Colon Cancer Lara Jones1, Michael Richins, DO, MBA2. 1. University of North Texas Health Science Center, Fort Worth, TX; 2. Plaza Medical Center/ University of North Texas Health Science Center, Fort Worth, TX. Among patients with colorectal cancer, metastatic brain lesions are rarely discovered. The paucity of this scenario decreases the clinical suspicion to search for colon cancer once a brain lesion is discovered. We report of case of metastatic colon adenocarcinoma discovered in the midst of the evaluation of a headache. A 57-year-old man with a history of smoking and coronary heart disease presented to the Emergency Department with a constant headache for two weeks, which was relieved by steroids and pain medication. The intensity and nature of his headache necessitated a cranial computerized tomography (CT) scan that revealed tumors in the cerebellum. Magnetic Resonance Angiogram showed three lesions, with the largest documented as 2.9 cm. He then had a CT of the chest, abdomen, and pelvis searching for other lesions. The CT chest revealed left hilar lymphadenopathy and consolidation of the left lower lobe. The abdomen and pelvis was unremarkable. The patient received a posterior fossa craniectomy with resection of the right cerebellar masses, which was found to be adenocarcinoma, consistent with metastatic

[329A] Figure 1.

[329B] Figure 2.


[330A] Figure 1.


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colorectal cancer. Gastroenterology was consulted and performed a colonoscopy which revealed a polypoid 6 centimeter circumferential partially-obstructing mass in the sigmoid colon. He was eventually discharged and treated with neoadjuvant chemotherapy and radiation. During that time, a diagnostic laparoscopy was performed for ablation and biopsy of liver metastasis, as well as resection of colonic and pulmonary lesions. This case demonstrates the possibility of colorectal adenocarcinoma metastasizing to unusual sites. Prolonged survival of patients with cancer increases the likelihood of uncommon metastasis. Thus, clinicians should keep an open differential diagnosis when masses in the brain parenchyma are discovered.

331 Primary Linitis Plastica Due to Transitional Cell Carcinoma of the Rectum Brian T. Moy, DO1, Haleh Vaziri, MD2. 1. Department of Medicine, University of Connecticut Health Center, Hartford, CT; 2. Division of Gastroenterology and Hepatology, University of Connecticut Health Center, Farmington, CT. Introduction: Transitional cell carcinoma is one of the rare tumors of the alimentary tract accounting for 2% of all anorectal cancers. Rectal linitis plastica is characterized by wall thickening of the rectum making it inelastic, rigid, and constricted. Here we report a rare case of primary linitis plastica due to transitional cell carcinoma of the rectum. Case Report: A 52-year-old male with no past medical history presented with rectal bleeding and decreased stool caliber for 2 months. He also reported dysuria, polyuria, nocturia, and hematospermia for the past several weeks. He denied any history of melena or weight loss. He had a routine screening colonoscopy done two years prior which was normal (Fig. 1). He denied any family history of GI tract

[331C] Figure 3.

cancers. He reported no history of high risk sexual behavior and did not smoke. On rectal exam he was found to have bright red blood, a firm enlarged prostate, and a palpable rectal mass. Flexible sigmoidoscopy was performed which showed a very stiff rectum with edematous and erythematous mucosa causing narrowing of the rectum consistent with linitis plastica (Fig. 2,3). The rectum was not distensible and no mass was seen. Rectal biopsies were consistent with transitional cell carcinoma. The cells were positive for p63, AE1/3, and negative for CK7, CK20, chromogranin, synaptophysin, and villin supporting this diagnosis. Computed tomography (CT) of the pelvis showed 2 large pelvic masses with one encasing the rectum and the other causing mass effect on the left ureter without tissue invasion into the ureter. The chest, abdomen, and bladder were normal on CT scan. Cystoscopy was performed to rule out primary transitional cell carcinoma of the bladder which was normal. Patient was started on chemotherapy with gemcitabine 1250 mg/m2 and cisplatin 70 mg/m2. His future treatment plan will depend on his response to the initial chemotherapy. Discussion: Ano-rectal transitional cell carcinoma usually presents with a perianal mass with or without pruritus, pain, or bleeding. It usually originates where columnar tissue transitions into squamous epithelium at the dentate line, but can also be found isolated in the distal part of the rectum. There are approximately 40 reported cases of primary transitional cell carcinoma of the rectum originating from interrupted embryologic entodermal cloacal vestiges. Metastatic transitional cell carcinoma of the rectum can occur through submucosal or lymphatic spread from the urinary tract causing secondary rectal linitis plastica. Our patient is unusual because he had primary linitis plastica from transitional cell carcinoma of the rectum without bladder involvement. Although very rare, a normal recent colonoscopy does not exclude the possibility of a malignant rectal pathology in patients with abnormal colorectal symptoms.

[331A] Figure 1.



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Diffuse Large B-Cell Lymphoma of Recto-Sigmoid Colon

A Case of Successful Treatment of Refractory Clostridium difficile Colitis With Fecal Microbiota Transplantation in a Critically Ill Patient

Diana A. Whitehead, MD1, Prabhjot Kaur, MD2, Arifa Toor, MD2. 1. Dartmouth-Hitchcock Medical Center, New London, NH; 2. Dartmouth-Hitchcock Medical Center, Lebanon, NH. Primary colorectal lymphoma (PCL) is a rare malignancy accounting for 3% of all GI lymphomas and 0.1-0.5% of all colorectal malignancies. The most frequent colonic location is the cecum followed by the rectum and ascending colon. Although several cases of PCL have been reported in the literature the recto-sigmoid junction as an origin has rarely been reported. We present a rare case of diffuse large B- cell lymphoma (DLBCL) in a patient presenting with anemia, weight loss and change in bowel habits. A 79 year old male with a past medical history significant for adenocarcinoma of the prostate status post (s/p) radiation, coronary artery disease s/p CABG, chronic kidney disease admitted to Dartmouth Hitchcock Medical Center (DHMC) with complaints 30 pound weight loss, intermittent lower abdominal pain with alternating diarrhea and constipation. Of note, one month prior to admission, he underwent colonoscopy at an outside hospital due to changes in his bowel habits. Biopsies taken at the time revealed non-specific acute inflammation thought to be related to ischemic colitis. During his admission at DHMC he underwent CT scan abdomen and pelvis which revealed thickening of the recto-sigmoid colon. Subsequent colonoscopy showed a colonic mucosa characterized by circumferential ulcerations with mucopurulent exudate that extended from rectum to sigmoid colon (Figure1). The appearance was suggestive of ischemic colitis, but rectal involvement seemed atypical. Biopsies taken were stained for hematoxylin and eosin and immunohistochemistry to reveal diffuse DLBCL of the colon. A PET-CT scan showed hypermetabolic activity involving lung, kidney, sigmoid and rectum. This was consistent with stage IVB DLBCL with extra-nodal involvement and 4 year survival of 40-50%. The patient underwent treatment with R-CHOP (Rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) however did not tolerate treatment due to worsening kidney and functional decline. He was transitioned to hospice care per family wishes and died one month later. The most common histological subtype of colorectal lymphoma is DLCBL. The etiology of DLBCL is unknown. Patient may present with variety of clinical symptoms that include abdominal pain, anorexia, weight loss, fatigue, anemia, fever, constipation and/or diarrhea. However, due to the nonspecific presentation diagnosis maybe delayed as seen in our patient. One should consider PCL in patient presenting with the above symptoms or with risk factors including HIV, organ transplant, inflammatory bowel disease and immunosuppressant agents. Endoscopists should think of a broader differential diagnosis when proctitis or colitis is seen during colonoscopy. Biopsies should be taken and reviewed by an expert GI pathologist.

Shannon J. Morales, MD1, Sabeen Medvedev1, Alice Lee, MD1, Mark Mattar, MD2. 1. MedStar Georgetown University Hospital, Washington, DC; 2. Georgetown University Hospital, Washington, DC. Introduction: Stool transplantation has proved to be an effective treatment for recurrent, refractory or severe Clostridium difficile (C. difficile) colitis. As recurrent C. difficile is associated with limited fecal microbial diversity, fecal microbiota transplantation (FMT) is gaining acceptance. Herein, we report a case of successful FMT treatment of refractory C. difficile in a critically ill patient. Case Report: A 72 year-old male nursing home resident with a history of chronic respiratory failure status post tracheostomy and percutaneous endoscopic gastrostomy (PEG) tube placement, and chronic kidney disease was admitted to an outside hospital ICU for respiratory distress and severe diarrhea. He was found to have bacteremia for which he was treated with broad-spectrum IV antibiotics, fungemia for which he was treated with antifungals, C. difficile colitis for which he was treated with oral vancomycin (250mg QID), and acute kidney injury requiring initiation of hemodialysis. After 10 days, the patient remained critically ill with refractory C. difficile colitis as evidenced by persistent and frequent diarrhea, and was transferred to our hospital for further management. Upon arrival, the patient was somnolent with a soft, mildly distended and non-tender abdomen. Initial testing showed a leukocytosis of 15, metabolic acidosis with respiratory compensation and creatinine of 3.2. On the day of transfer, FMT was performed with two administrations of 50cc of OpenBiome slurry via the patient’s PEG tube 20 minutes apart. Oral vancomycin was continued. Forty hours later, FMT was repeated due to continued diarrhea. The patient’s diarrhea rapidly resolved following this second FMT treatment (Figure). Repeat C. difficile stool antigen testing, 7 days after the first FMT, was negative. Discussion: We report successful treatment of refractory and severe C. difficile colitis with FMT. Our patient’s frequent exposure to antibiotics likely led to disruption of normal colonic flora causing colonization and overgrowth of C. difficile. FMT was indicated after failure of oral vancomycin, and the preexisting PEG tube allowed for low-risk introduction of fecal microbiota into the stomach, leading to rapid resolution of diarrhea and negative repeat testing after the second FMT. Conclusion: In cases of recurrent, refractory, or severe C. difficile colitis, FMT should be an early consideration. FMT should be performed at centers with experience and training.


334 A Dramatic Case of Incidental Ischemic Colitis Discovered at a Surveillance Colonoscopy Ashirf Al-Ghanoudi, MD, MPH1, Mohd Amer Alsamman, MD1, Alan Putrus, MD2, Francis Edeani , MD1, Joshua Max, MD1. 1. Good Samaritan Hospital, Cincinnati , OH; 2. Trihealth-Good Samaritan Hospital, Cincinnati, OH.

[332B] Figure 2.


Case presentation: A 72-year-old white male with a history of partial left colectomy eight years prior for invasive adenocarcinoma presented for surveillance colonoscopy. The patient reported alternating constipation and loose stools as well as occasional anal leakage. The patient consumed a bowel prep consisting of four liters of polyethylene glycol (PEG-3350, NaCl, NaHCO3, and KCl) prior to the colonoscopy. Due to a court appearance earlier in the day, the patient started the prep on the morning of his colonoscopy and was still drinking the bowel prep in the lobby of the surgical center upon arrival for his colonoscopy. Colonoscopy showed a confluent, ulcerated circumferential lesion spanning nine cm in the sigmoid colon, distal to the prior anastomosis (Figure 1A). A CT abdomen the same day demonstrated a long segment of severe colon wall thickening involving the sigmoid colon with stranding in the pericolonic fat (Figure 2). Colonic biopsies were consistent with acute ischemic colitis. The patient’s clinical course was benign. Outpatient surgical referral was arranged and repeat colonoscopy to evaluate for healing and rule out malignancy was recommended. The patient returned for a repeat colonoscopy five weeks later, prior to which he was instructed to drink the same bowel prep slowly and stay well-hydrated. Repeat colonoscopy showed significant healing of the prior severe sigmoid colitis, with some residual edema and superficial ulceration (Figure 1B). Biopsies reveled benign ulceration without evidence of ischemic injury or invasive malignancy.


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Abstracts Discussion: We present the case of a 72-year-old male who suffered an episode of ischemic colitis after bowel preparation for a surveillance colonoscopy. Ischemic colitis results from a reduction in colonic perfusion, leading to temporary, non-gangrenous colonic inflammation. The process resolves without any long-term complications in the majority of patients. Ischemic colitis is the most common form of gastrointestinal ischemia and has been reported with large doses of bisacodyl. While our patient did not take bisacodyl as part of his bowel preparation, he had known atherosclerotic vascular disease, which is a risk factor for ischemic colitis. We hypothesize that, in the setting of atherosclerosis, our patient’s poor oral intake surrounding his rapid bowel prep and chronic low-grade dehydration related to alcohol abuse resulted in ischemic colitis.

[335A] Figure 1.

[334A] Figure 1.

[334B] Figure 2.

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[335B] Figure 2.

Ipilimumab Enterocolitis: An Unusual Case of Colonic Perforation and Death Vikesh Khanijow, MD1, Shreya Chablaney1, Showkat Bashir, MD1, Marie L. Borum, MD, EdD, MPH, FACG2. 1. George Washington University, Washington, DC; 2. George Washington University, Washington, DC. Ipilimumab, a humanized monoclonal antibody to anti-cytotoxic T-lymphocyte associated antigen 4 (CTLA-4), is approved for treatment of melanoma and undergoing clinical trials for other malignancies. Immunological adverse effects due to T cell activation and proliferation have been described. Gastrointestinal side effects include abdominal pain, rectal bleeding, and diarrhea. While there have been reports of enterocolitis, we report an unusual case of multiple colonic perforations occurring three weeks after ipilimumab administration. A 63-year-old male with hormone-refractory metastatic prostate cancer received ipilimumab in a phase II clinical trial. Three weeks following ipilimumab administration, he developed fever, abdominal pain and bloody bowel movements. Stool studies were negative. Abdominal CT revealed pancolitis. Sigmoidoscopy showed mucosal friability with biopsies demonstrating focal active colitis without chronicity, ischemic injury or viral infection. Steroids and mesalamine were administered for suspected ipilimumab enterocolitis. Bowel movements improved and he was discharged on prednisone. One week later, he was re-admitted with abdominal pain and persistent diarrhea. Labs were notable for a leukocytosis and negative stool studies. He received intravenous steroids with improvement. Following a sigmoidoscopy to assess his status prior to discharge, he developed worsening abdominal pain. Abdominal CT revealed free intra-peritoneal air. He underwent a subtotal colectomy with end ileostomy and debridement. The surgical specimen was notable for ischemia, necrosis with multiple perforations proximal to the sigmoid colon. His post-operative course was complicated by venous thrombosis, aspiration pneumonia, retroperitoneal hematoma and persistent peritonitis. He was transitioned to home hospice. While gastrointestinal side effects of ipilimumab has been reported in 28-30% of patients, severe enterocolitis rarely occurs. We report an unusual case of a fatality resulting from progressive enterocolitis complicated by colonic perforations occurring after a single dose of ipilimumab. The suggested mechanism for colitis is immune cell infiltration, autoreactive antibodies and inflammatory cytokines. Resolution of enterocolitis typically occurs after steroid administration. However, physicians must be aware of the potential progression of ipilimumab-induced enterocolitis, steroids masking symptoms and the possibility of colonic perforation and death.

[335C] Figure 3.

336 A ‘Tear’-ible Culprit Danielle Hoo-Fatt, MD1, Willie Moore, MD2, George John, MD3, Vivek Kumbhari, MD3, John Lin, MD4, Sandy Fang , MD3. 1. Johns Hopkins Bayview Medical Center, Perry Hall, MD; 2. Johns Hopkins, Baltimore, MD; 3. Johns Hopkins, Baltimore, MD; 4. John Muir Physician Network Member, Baltimore, MD. A 64 year old gentleman presented with hematuria, hematochezia, and melena. Nine years earlier he underwent radiotherapy for prostate cancer that was complicated by obstructive uropathy, and he sub-



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sequently underwent a transurethral resection of the prostate. Following this procedure, he became incontinent and had an artificial urinary sphincter placed; however, it was later removed due to urethral erosion. Seven years later, he developed urosepsis complicated by obstructive nephrolithiasis that required bilateral nephrostomy tube placement, and subsequent ureteral stenting. Upon removal of the urethral stents, his urethra was determined to be nearly completely strictured, so in November of 2014 a suprapubic catheter was placed. Upon presentation to Johns Hopkins, the patient was noted to have fecaluria, profuse melena and hematochezia, and was subsequently admitted for anemia with a hemoglobin of 4.6 requiring 4 units of blood. A CT scan of the abdomen and pelvis revealed a rectovesical fistula. An emergent colonoscopy was attempted in order to elucidate the source of a possible lower gastrointestinal bleed; however, the procedure was aborted upon visualization of a Foley catheter balloon within the sigmoid colon. Both colorectal surgery and urology were consulted. Repeat flexible sigmoidoscopy showed a very large rectovesical fistula with a narrow stricture of the anal canal adjacent to the bladder, which exhibited signs of radiation proctitis. A pelvic exenteration was performed. The patient tolerated the procedure well, and was discharged home with close follow-up. The most common source of a rectovesical fistula is adherence of abnormal bowel to the bladder. Typical fistulae causes include diverticulitis, inflammatory bowel disease, gastrointestinal malignancy, and trauma (including previous surgery). Factors that contribute to poor fistulae healing include the presence of a foreign body, radiation, infection/inflammation, epithelialization, neoplasm, and distal obstruction. In our case, the patient had multiple reasons for a non-healing fistula including a history of radiation, previous prostatectomy, epithelialization, and a distal obstruction.

[336C] Figure 3.

337 Chronic Recurrent Intestinal Pseudo-Obstruction (CIPO) Successfully Treated With Methylnaltrexone Presidential Poster Dustin Albert, MD1, Jeannette Collins, MD2, Manish B. Singla, MD2, Lawrence Goldkind, MD2. 1. Walter Reed National Military Medical Center, Silver Spring, MD; 2. Walter Reed National Military Medical Center, Bethesda , MD. We present a case of an acute exacerbation of chronic intestinal pseudo-obstruction (CIPO) successfully treated with methylnaltrexone. A 62 year-old man with systemic sclerosis and CIPO presented with 2 weeks of worsening abdominal pain, distension, nausea, vomiting, and no bowel movement in 24 hours. Medications were atorvastatin, losartan, bosentan, ranitidine, spironolactone, and monthly octreotide. He does not use opioids. He was bradycardic but afebrile and normotensive. Despite 72 hours of conservative management with NG suction and correction of volume and electrolytes, pain and distension worsened leading to mild respiratory compromise. Abdominal CT showed dilated loops of small and large bowel with no mechanical obstruction. Neostigmine was contraindicated due to bradycardia. In light of his deterioration an empiric challenge with methylnaltrexone 12 mg was given subcutaneously. Within 3 hours he had a liquid bowel movement with passage of a large volume of gas with dramatic symptomatic relief. He had an additional 5 bowel movements over the next 24 hours. By the next morning his abdomen was soft and nontender and he experienced substantial relief of pain, nausea, and distension. Within 48 hours after administration, he tolerated oral intake and was discharged. CIPO in systemic sclerosis is associated with a disturbance in the intrinsic cholinergic pathway of the bowel. Opioids inhibit peristalsis by binding receptors for endogenous opioid peptides, enkephalins, endorphins, and dynorphins. The μ-opioid receptor, the primary mediator of opioid-related effects in the enteric nervous system, inhibits release of excitatory neurotransmitters and stimulates release of inhibitory neurotransmitters. Endogenous opioids are known to inhibit peristalsis. Methylnaltrexone, a charged molecule due to an added methyl group with low lipid solubility, has restricted ability to cross the blood-brain barrier. It is a peripheral μ-opioid receptor antagonist used for opioid-induced constipation. This was the target of therapy in this patient. This is the first report of using methylnaltrexone for the treatment of intestinal pseudo-obstruction in an opioid naïve patient and should be considered in similar patients with contraindications to neostigmine. Given the brisk and prolonged response in this patient, a lower initial dose is advised if this therapy is to be considered.

[336A] Figure 1.

338 Intractable Rectal Pain Secondary to Colonic Stent Placement in Patient With Advanced Pelvic Cancer Successfully Treated With Hypogastric Nerve Plexus Neurolysis Turki Alkully, MD1, Umar Darr, MD2, Tariq Hammad, MD1, Joseph Atallah, MD1, Ali Nawras, MD, FACG1. 1. University of Toledo Medical Center, Toledo, OH; 2. University of Toledo Medical Center, Holland, OH. Introduction: Symptomatic treatment of advanced rectal cancer can prove sometimes difficult to manage. Untreated pain from cancerous origin can lead to decreased quality of life and increase in morbidity. Colonic stent placement is a tool to relieve bowel obstruction and improve quality of life. Complications with the hypogastric nerve with colonic stent placement is sometimes an unfortunate result. The technique of superior hypogastric nerve plexus neurolysis is a procedure that can be used to relieve pain from stent insertion in individuals suffering from cancers of pelvic origin. Case Report: A 59 year old Caucasian female presented to the pain clinic diagnosed with ovarian cancer stage IV status post debulking surgery, chemotherapy and radiotherapy. She was found to have recurrent cancer involving the rectum, liver and peritoneum. Uncovered self-expandable metallic colonic stent (25 mm x 120 mm) was placed at the rectosigmoid junction with distal end of the stent positional at 5 cm proximal to the anorectal junction to relieve bowel obstruction for better quality of life. The patient subsequently developed intractable rectal pain despite use of opioids. Diagnostic block of the superior hypogastric plexus followed by neurolysis was performed by pain management service under fluoroscopy to relieve this patient’s pain. The pain relief was achieved after neuolysis. Conclusion: Significant rectal pain is a potential complication of post endoluminal colonic stent placement. The condition could be alleviated by hypogastric nerve plexus neurolysis when medical therapy failed.

[336B Figure 2. The American Journal of GASTROENTEROLOGY


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Abstracts of ongoing diarrhea and fecal incontinence, 5 g BID serum-derived bovine immunoglobulin/protein isolate (SBI) was added to her therapy. SBI, a prescription medical food, has been shown to help manage chronic loose and frequent stools in patients with Irritable Bowel Syndrome with Diarrhea (IBS-D) and refractory Inflammatory Bowel Disease (IBD). As such, it was considered for this patient due to a lack of response to conventional therapies. A chart review was used to gather this patient level data. Approximately 3 weeks following initiation of SBI therapy, the patient was having 3-4 formed stools daily and no fecal incontinence. Her serum albumin levels had increased from 3.4g/dl to 4.0g/dl and she had discontinued use of the anhydrous morphine. This is yet another case report of a patient benefiting from the use of this prescription medical food for the management of refractory chronic loose and frequent stools. SBI has been used as a safe rescue therapy in this elderly patient to achieve normal bowel function. Several case series and case histories have shown SBI to be a useful nutritional management tool in severe and intractable cases of chronic loose and frequent stools.

340 An Interesting Case of Chest Pain After Colon Cancer Treatment Jason Rubinov, MD, Jonathan D. Weinberger, MD. Mount Sinai Beth Israel, New York, NY.

[338A] Figure 1.

A 64-year-old male with recently diagnosed Stage IIIA colonic adenocarcinoma presented with acute onset substernal chest pain. His past medical history was notable for hypertension, COPD, hyperlipidemia and a history of treated Hepatitis B. He was diagnosed with colonic adenocarcinoma three months ago and underwent surgical resection three weeks prior to presentation. The patient completed his first course of 5-flourouracil, folinic acid and oxaliplatin (FOLFOX) chemotherapy the day prior to presentation. On the morning of admission, he reported sudden-onset substernal, dull chest pressure with radiation to the left arm. Vital signs and physical examination were unremarkable. Laboratory testing was significant for an elevated troponin I to 0.039 ng/mL. ECG on presentation was notable for non-specific, diffuse 1-2 mm ST elevations in the inferolateral leads. Serial ECGs showed dynamic changes (Image 1) and the troponin I trended up to 0.260 ng/mL. The patient underwent urgent left heart catheterization. Coronary angiography showed normal coronaries but was significant for global hypokinesis with a severely reduced ejection fraction of 25%. The transthoracic echocardiogram (TTE) performed prior to starting chemotherapy showed no signs of a depressed ejection fraction. The new-onset cardiomyopathy was attributed to cardiotoxicity secondary to 5-flourouracil. He was started on a typical cardiomyopathy medication regimen. A TTE was performed the following day which showed some normalization of the previously observed global hypokinesis. The patient was discharged with intent to follow up cardiac function, with no plan on reattempting FOLFOX chemotherapy. 5 Fluorouracil (5-FU) is a core component of the treatment regimen of various gastrointestinal malignancies, including colorectal, pancreatic, and stomach malignancies. While it remains an effective treatment for malignancy it is not without potential adverse effects. 5-FU related cardiotoxicity is uncommon and is represented in literature mostly by way of case reports. It can manifest in various ways including acute coronary syndrome, coronary vasospasm, arrhythmia, cardiomyopathy, global systolic dysfunction, and sudden death. Whereas 5-FU related cardiotoxicity is in general uncommon, life-threatening cardiotoxicity is considered a rare occurrence. Toxic effects on the myocardium and endothelial cells are thought to play a role, though the exact etiology is still unknown. The majority of reported cases occur in patients without preceding cardiac history. Given the large number of patients receiving 5-FU treatment, keeping in mind the potential for cardiotoxicity remains of extreme importance, as cases such as this one illustrate. Careful risk stratification prior to treatment is recommended, as is monitoring for symptoms and prompt evaluation should symptoms arise.

[338B] Figure 2.

[340A] Figure 1.

339 Management of Severe Watery Stools With Fecal Incontinence in Ileorectal Anastomosis Patient With Serum-Derived Bovine Immunoglobulin Therapy Larry I. Good, MD, FACG1, Raymond M. Panas, PhD2. 1. South Nassau Communities Hospital, Lynbrook, NY; 2. Entera Health, Washington, DC. For patients with various colonic diseases, an ileorectal anastomosis is a connection of the terminal ileum to rectum and has been used for over 50 years as an alternative for a proctocolectomy and permanent ileostomy. The ileorectal anastomosis provides significant benefit and allows most patients an improved quality of life and a reasonable management of their condition. A 79 year old, Caucasian female arrived at an ER with severe abdominal pain, sepsis, and severe ischemic colitis. Despite aggressive therapy, she required surgery and had total colectomy and ileostomy. Following surgery, she was plagued by ileostomy dysfunction and frequent hospitalization for rehydration and electrolyte correction. After nearly 10 months, of recurrent relapses she had surgery to create an ileorectal anastomosis but experienced severe refractory diarrhea. This consisted of 13-14 watery stools per day and fecal incontinence despite treatment with loperamide, diphenoxylate/atropine and anhydrous morphine. After nearly 2 months


341 The Rare Presentation of Leptomeningeal Carcinomatosis in a Patient With Colorectal Signet Cell Adenocarcinoma Mehwish Mussarat Hussain , MBBS, Adnan Abdul Jabbar , MD, PhD. Aga Khan University Hospital, Karachi, Pakistan. Abstract: Colorectal carcinoma is the third most prevalent carcinoma in the world with almost equal distribution among men and women. Metastasis to the leptomeninges remains a rarely reported entity. Here we discuss the case of a young female with CRC, signet ring cell type, on systemic chemotherapy, who presented with progressive neurological complaints secondary to leptomeningeal carcinomatosis and with no evidence of systemic disease.


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[342B] Figure 2. [341A] Figure 1.

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acquired megacolon are neurologic, metabolic, systemic disorders, and medications. Treatments include colonic disimpaction, cathartics and laxatives, with surgery considered in refractory cases. This rare complication of a common problem underscores the importance of proactive treatment of chronic constipation before emergent and invasive intervention is required.

Extreme Fecaloma From Chronic Idiopathic Constipation Requiring Colectomy Drew Triplett, DO1, Nyla Hazratjee, MD2, Mustafa Musleh, MD3, Christopher Barde, MD2. 1. Wright State University Boonshoft School of Medicine, Dayton, OH; 2. Wright State University, Dayton, OH; 3. Wright State University, Miamisburg, OH.

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Constipation, defined as either hard or infrequent bowel movements, is a frequently encountered complaint in both clinic and hospitalized patients. Rarely severe constipation can lead to megacolon requiring urgent surgical intervention. We report an extreme case of rectosigmoid fecal impaction in a young female causing a large abdominal mass “fecaloma” secondary to severe idiopathic constipation requiring surgical resection. A 19 year old female who presented for constipation and increasing left sided abdominal pain admitted for constipation. She reported severe constipation for 2 months prior to admission, with alternating constipation and diarrhea with recurrent fecal impaction over her lifetime without formal diagnosis. On presentation, she was afebrile but tachycardic, with firm mass like abdominal distension. Initial labs showed normal chemistry panel, normal white blood cell count (6.1K/mm3), mild anemia (11.3g/dL) and normal platelets (212K/mm3). Abdominal x-ray showed immense stool burden with a severely dilated sigmoid colon (23 cm), with similar findings on Computerized Tomography (CT) scan of the abdomen and pelvis. Laxatives and enemas were administered with minimal stool passage. Endoscopic disimpaction was planned, however, on hospital day 2, she developed intense abdominal pain and tenderness, associated with leukocytosis (15.5K/mm3) and tachycardia. She underwent emergent subtotal colectomy for suspected intestinal perforation. Surgical specimen was a grossly distended colon with thinned walls containing impacted fecal matter throughout with proximal colon diameter measuring 15cm and sigmoid colon diameter measuring 30cm. Ganglion cells were identified both within the muscularis propria and in the submucosa throughout the length of the colon.Patient did well post-operatively and was subsequently discharged home. Chronic constipation is a frequently encountered problem affecting 2-27% of the population, which can lead to chronic megacolon, and in turn rarely result in colonic perforation. The most common causes of

Ischemic Colitis Managed by Serum-Derived Bovine Immunoglobulin/Protein Isolate

[342A] Figure 1.

[343A] Figure 1.


Satish Iduru, MD1, Bruce Burnett, PhD2. 1. GI Specialists of Houston, Houston, TX; 2. Entera Health, Cary, NC. There are numerous causes of ischemic colitis, including compromised vascular circulation due to disease or certain medications which can elicit a reflex mesenteric vasoconstriction and result in diarrhea. Reported are 2 cases which detail the outcomes of including serum-derived bovine immunoglobulin/ protein isolate (SBI) for the nutritional management of ischemic colitis with chronic loose and frequent stools. SBI has a unique mechanism which includes binding microbial components, maintaining normal GI immune balance, managing barrier function and improving nutrient utilization which may be useful in the management of ischemic colitis. Patient 1 was 82-year-old Caucasian female with a history of hypertension, diabetes mellitus and irritable bowel syndrome with diarrhea (IBS-D), with 4-5 bowel movements (BM)/day for 20 years. She was previously treated with dicyclomine and tricyclic antidepressants for 7 years. Her diarrhea worsened over the past 4 months to ~10 BM/day. Because of the change in patient’s chronic symptoms, a colonoscopy was performed, revealing mild to moderate colitis secondary to ischemia (Figure 1). Patient 2 was a 74-year-old African American male with ESRD/CAD/PVD admitted to hospital with an episode of rectal bleeding. Colonoscopy revealed ischemic colitis and the patient was discharged. He then developed diarrhea (5-6 BM/day). Clostridium difficile was negative by PCR so the patient was started on cholestyramine to help resolve the diarrhea but could not tolerate treatment. For both patients, SBI 5g QD was administered and the response reported here. Patient 1’s BM improved to 2-3/day within 4 weeks. A repeat colonoscopy was performed 2 months after initiating SBI therapy and there was no evidence of colonic inflammation or ulcers (Figure 1). Patient 2‘s symptoms improved dramatically within a couple weeks, with fully formed stools (1-2 BM/day). Both patients continue on


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Abstracts SBI 5g QD therapy for management of their condition and remain stable. Previously published reports of SBI in chronic mesenteric ischemia and other intestinal disorders support these patient observations. Although mesenteric ischemia can resolve on its own, the outcomes of these cases and the temporal nature of SBI administration suggest that these patients with ischemic colitis and associated chronic, loose stools may have benefited from this nutritional intervention. A well-controlled study in mesenteric ischemia patients is advised.

include loss of vascular pattern, aphthous ulcers, erosions and yellowish-white nodules. Yellowish-white nodules may be a characteristic finding of colonic lesions in strongyloidiasis. The clinical diagnosis of S. stercoralis is confirmed by detection of larvae in the stool. However, single stool microscopy has a sensitivity of only 30% when there is low parasite burden, underscoring the need for stool aspirate microscopy or endoscopic biopsy for diagnosis. Due to its non-specific presentation and the risk of hyperinfection, gastroenterologists must maintain a high index of suspicion for strongyloidiasis especially in the immunocompromised population presenting with non-specific GI symptoms and/or unexplained peripheral eosinophilia.

344 Elmiron-induced Colitis: A Rare Complication Ashraf Almashhrawi, MD1, Rubayat Rahman, MD, MPH1, Umair Sohail, MD1, Imran Ashraf, MD1, Jared Coberly1, Douglas Nguyen, MD2, Matthew Bechtold, MD, FACG1. 1. University of Missouri, Columbia, MO; 2. University of California Irvine, Anaheim Hills, CA. Introduction: Elmiron (Pentosan polysulfate sodium), approved in 1996, is primarily used for the treatment of interstitial cystitis. Gastrointestinal-related side effects have been reported in. Case: 32 year-old female with past medical history of interstitial cystitis presented for evaluation of chronic diarrhea for 7 months. She described loose bloody stools with approximately twenty bowel movements per 24 hours with nocturnal symptoms. This was associated with abdominal cramps that varied in severity over time. Apart from Elmiron and Mirabegron for her urinary problem and pregabalin for fibromyalgia, she took no other medications. Physical exam was unremarkable except for mild superficial diffuse abdominal tenderness. Stool studies including Clostridium difficile were negative. Initial colonoscopy showed an area in the sigmoid with loss of mucosal vascularity and scarring compatible with previous inflammation. Mucosal biopsies showed inactive chronic colitis. Over the following year, she was treated with several remedies including mesalamine, prednisone, rifaximin, dicyclomine, hycosamine, and amitriptyline with no significant improvement in symptoms. Elmiron was discontinued and her symptoms resolved over the subsequent few weeks. Repeat colonoscopy was performed with normal colonic biopsies. Discussion: Elmiron may rarely induce colitis and rectal bleeding. Providers should be aware of this potential side effect, especially at higher doses.

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[346A] Figure 1.

Colonic Obstruction by Ulcerating Lipoma: A Rare Case Ashraf Almashhrawi, MD1, Imran Ashraf, MD1, Rubayat Rahman, MD, MPH1, Umair Sohail, MD1, Jared Coberly, MD1, Douglas Nguyen, MD2, Matthew Bechtold, MD, FACG1. 1. University of Missouri, Columbia, MO; 2. University of California Irvine, Anaheim Hills, CA. Introduction: Lipomas are fatty tumors that can be found in any part of the GI tract. They are more in the right colon than the left with highest prevalence in the cecum, ascending colon, and sigmoid colon. Although lipomas are benign lesions and mostly asymptomatic, a few large lipomas, >4cm, may cause symptoms that can range from abdominal pain to bleeding, intussusception, or obstructive symptoms. This is a rare case of a large lipoma resulting in obstruction of the colon. Case: 51 year-old male presented with left lower abdominal cramps, constipation, intermittent hematochezia, and weight loss of 12.5 pounds over a month. Colonoscopy revealed a large mass nearly obstructing the sigmoid colon at 30cm from the anal verge. The mass had an ulcerated cap at the top. Multiple biopsies revealed normal colonic mucosa. MRI of the abdomen and pelvis showed a fat density lesion in the lumen/wall of the distal descending/proximal sigmoid colon measuring approximately 2.1 cm x 2.3 cm x 2.1 cm. Loop in loop appearance suggestive of intussusception is seen in the bowel proximal to the mass. The patient underwent robotic-assisted sigmoid colon resection. Histopathology revealed submucosal lipoma with overlying ulceration, granulation tissue and fibrosis. No evidence of malignancy. Margins were free of neoplastic changes. Discussion: Large lipomas should be considered in the differential diagnoses of colonic obstruction etiologies with other benign and malignant conditions. Although rare, large lipomas can ulcerate, bleed, and cause obstruction and mimic presentations of colon cancer.

[346B] Figure 2.

346 Asymptomatic Strongyliodes Found in a Colonic Polyp Daniel J. Waintraub, MD1, Dovid Moradi, MD2, Jason Rubinov, DO1, Andrew S. Korman, MD1, Emilio Madrigal, DO1, Songyang Yuan, MD1, Albert Min, MD1. 1. Mount Sinai Beth Israel Medical Center, New York, NY; 2. Mount Sinai Beth Israel, New York, NY. Strongyloidiasis, caused by Strongyloides stercoralis, is a worldwide parasitic disease endemic to tropic and sub-tropical regions. Typically the infection remains asymptomatic, however life-threatening hyperinfection may occur in immunocompromised hosts. We present a 73 year-old asymptomatic female with well-controlled HIV who was found to have strongyloides induced colitis on surveillance colonoscopy. A 73 year-old female with HIV on HAART (CD4 - 749) presented for surveillance colonoscopy. Lab work revealed chronic anemia with a hemoglobin between 10-11g/dL and an absolute eosinophil count greater than 10%. She denied any diarrhea or other gastrointestinal (GI) symptoms. History was notable for immigration from Puerto Rico many years ago. Colonoscopy five years prior showed two hyperplastic polyps. Repeat colonoscopy showed two 3-4 mm sessile polyps, which were removed with jumbo forceps. Pathology revealed eosinophilic rich mucosa and nematode (Figures 1,2) consistent with strongyloides induced colitis. The patient was treated with Ivermectin. Strongyloidiasis is a worldwide parasitic disease. The complex life cycle of the parasite promotes a prolonged auto-infection in hosts. Strongyloidiasis is asymptomatic in up to 30% of infected individuals, however GI symptoms including abdominal pain, watery diarrhea, weight loss, nausea and vomiting are common. The infection may occur in both healthy and immunocompromised hosts. However, in immunocompromised individuals, autoinfection may progress to disseminated infection with a mortality rate of approximately 60%. Many of the reported cases of colonic involvement in strongyloidiasis were associated with hyperinfection or disseminated strongyloidiasis. Colonoscopic features in strongyloidiasis


[346C] Figure 3. The American Journal of GASTROENTEROLOGY

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347 Fulminant Cytomegalovirus Colitis in a Renal Transplant Patient Daniel J. Waintraub, MD1, Michelle Tong, MD1, Andrew S. Korman, MD1, Emilio Madrigal, DO1, Lawrence Liu, MD2. 1. Mount Sinai Beth Israel Medical Center, New York, NY; 2. Mount Sinai Hospital, New York, NY. Cytomegalovirus (CMV) infection of the gastrointestinal (GI) tract affects 10-30% of transplant recipients and may present with non-specific GI symptoms such as abdominal pain, diarrhea, nausea and vomiting. The colon and esophagus are the most commonly affected GI sites. Colonoscopic findings of CMV colitis include diffuse inflammation, hemorrhage, frank ulceration, and potentially pneumatosis intestinalis. We present a case of fulminant CMV colitis in a renal transplant patient. A 39 year-old female with a past medical history of end stage renal disease secondary to hypertension on hemodialysis presented three months after a deceased donor renal transplant with one day of bloody diarrhea and generalized abdominal pain. The patient was taking immunosuppressive therapy including tacrolimus, prednisone, and mycophenolate mophetil. The patient was a CMV IgG positive transplant recipient and was taking valgancyclovir for prophylaxis. Physical exam was notable for generalized abdominal tenderness without rebound or guarding. Admission labs included blood urea nitrogen of 14 mg/dL, creatinine of 0.95 mg/dL, white blood cell count of 11,500 cells/uL and a hemoglobin of 15.6 g/dL. Colonoscopy showed a diffuse area of inflamed, ulcerated, exudative and friable mucosa from the mid-sigmoid to the proximal transverse colon (Figure 1). Biopsies taken from the ulcers were consistent with fulminant CMV colitis (Figures 2 and 3). CMV DNA PCR viral load was 14,546 IU/mL. The patient was treated with ganciclovir with complete resolution of symptoms. CMV is the most common viral cause of infection in transplant patients and typically appears 6-12 months after transplantation. More than 50% of transplant patients have laboratory or clinical evidence of CMV replication by the end of the first year post-transplant. When CMV colitis is suspected, colonoscopy earlier in the course of management is beneficial for early detection and treatment as examination of the GI tract and histopathologic examination of biopsies are required for diagnosis. Once the diagnosis is made, anti-viral medications such as ganciclovir and foscarnet should be rapidly initiated. CMV is a significant cause of morbidity and mortality in renal transplant recipients despite antiviral prophylaxis. Early diagnosis and anti-viral treatment are critical. Gastroenterologists must consider CMV colitis when immunosuppressed renal transplant patients present with non-specific GI symptoms.

[347C] Figure 3.

348 Colonoscopy Prep-Induced Ischemic Colitis Jennifer Behzadi, MD1, Reshi Kanuru, MD2, Sheryl Pfeil1. 1. The Ohio State University Wexner Medical Center, Columbus, OH; 2. The Ohio State University Wexner Medical Center, Dublin, OH. Introduction: Adequate bowel preparation is essential in order to achieve a successful screening colonoscopy. Suboptimal preparation can lead to missed adenomas. While practices vary, one commonly recommended preparation consists of bisacodyl tablets followed by polyethylene glycol (PEG) mixed in an electrolyte-containing beverage. Few case studies have reported ischemic colitis as a side effect of bisacodyl-containing colonoscopy preparations. Case Report: A 64 year old healthy female with a family history of colon adenocarcinoma presented for outpatient colorectal cancer screening. Her previous screening colonoscopy (4 liter PEG prep) was unremarkable. This time, she was provided with instructions for the low volume PEG/Gatorade split dose prep. She took 3 tablets of bisacodyl followed by 238g of PEG 3350 mixed with Gatorade. She began having frequent bowel movements within several hours, followed by significant abdominal cramping, nausea, and non-bloody emesis. She attempted to take the second dose of PEG 3350 three hours prior to her procedure but was unable to ingest much due to her symptoms. During the procedure she was found to have patchy moderate inflammation in the sigmoid colon, concerning for colitis, along with residual stool in the left colon. She was admitted to the hospital and given IV fluid hydration. A repeat colonoscopy was performed the following day and showed segmental patchy inflammation characterized by congestion, erythema, mucus and ulceration in the sigmoid colon. Biopsies showed acute inflammation, hemorrhage, and atrophic crypts surrounded by hyalinized lamina propria, consistent with ischemic injury. She was continued on IV hydration and treated with ciprofloxacin and metronidazole. Stool cultures and Clostridium difficile PCR assay were negative. She underwent an MRI angiography that showed patent celiac trunk, superior mesenteric, and inferior mesenteric arteries with patent distal branches of these vessels. Her symptoms improved over the next several days. Discussion: Bisacodyl is a frequent component of bowel preparations. In rare cases, patients have developed ischemic colitis. It is important to recognize the symptoms and treatment for bisacodyl induced ischemic colitis. Clinicians should be aware of this potential complication in patients with risk factors for ischemic colitis and should discuss the risks of the different bowel preps with them.

[347A] Figure 1.

[347B] Figure 2.


[348A] Figure 1.


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[348B] Figure 2.

[350A] Figure 1.

349 A Rare Case of Microscopic Colitis After Revascularization of Mesenteric Artery Stenosis Ellis Easterling, MD1, John Hunninghake, MD2, John Gancayco, MD3. 1. US Air Force, San Antonio, TX; 2. US Air Force, San Antonio Military Medical Center, San Antonio, TX; 3. US Air Force, JBSA Ft. Sam Houston, TX. A 71 year old female presented daily loose, non-bloody stools approximately three weeks after superior mesenteric artery stenting for chronic mesenteric ischemia. She was started on metronidazole and loperamide. She tested negative for C. Diff stool PCR and had no resolution of symptoms with therapy. She was hospitalized for worsening diarrhea and abdominal pain. Infectious workup, to include repeat C. Diff PCR, stool culture, ova and parasite evaluation, and cryptosporidium antigen were negative. She was treated with ceftriaxone empirically for infectious colitis without success. She underwent colonoscopy with no gross abnormalities except for thick, adherent mucus. Histology revealed mild epithelial damage and intraepithelial acute inflammatory cells without evidence of granulomas or architectural changes of chronic colitis. Diarrhea improved with loperamide, and she was discharged. Diarrhea returned shortly thereafter with seven or more loose, watery stools daily resulting in repeat admission for dehydration, electrolyte abnormalities, and acute renal failure. She was stabilized with supportive care and started on oral budesonide for lymphocytic colitis. She had resolution of diarrhea and was able to progress her diet over several weeks with improvement in post-prandial abdominal pain and loose stools. Discussion: To our knowledge, this is the first reported case of de novo microscopic colitis after revascularization of mesenteric artery stenosis. This patient experienced onset of symptoms three weeks after superior mesenteric artery revascularization requiring two hospitalizations for volume depletion and electrolyte abnormalities. After starting therapy with budesonide she experienced significant, sustained improvement and no return of mesenteric anginal symptoms.

[350B] Figure 2.

350 A Colonic-Pancreatic Fistulous Tract Masquerading as a Bleeding Diverticulum Michelle Vu, MD, Brian L. Huang, MD, Rome Jutabha, MD, Wendy Ho, MD. UCLA, Los Angeles, CA Background: Hematochezia is a commonly encountered symptom that often prompts endoscopic evaluation. Common culprits include hemorrhoids, polyps, inflammation, ulcers or malignancy, but more obscure causes may present a diagnostic dilemma. Case: We describe here a 55 year old man with stage IV pancreatic adenocarcinoma who presented with 4 days of painless hematochezia and fatigue. His abdominal exam was benign, but his hemoglobin had dropped to 7.5 g/dL (from baseline 14 g/dL). He initially declined endoscopy. Because his hematochezia persisted, colonoscopy was performed on hospital day (HD) 3 and revealed a single diverticulum in the splenic flexure with active oozing; this was tattooed and treated with 2 hemoclips. The remainder of the colon was normal, with no blood observed proximal to the splenic diverticulum. His hematochezia recurred and on HD 5, repeat colonoscopy showed a hemoclip and no bleeding. Endoscopic doppler ultrasound revealed a faint vascular signal, and the diverticulum was treated with epinephrine injection and 2 additional hemoclips. On HD 14, a third colonoscopy for recurrent hematochezia showed active oozing as well as intermittent bubbling from the splenic flexure diverticulum. Endoscopic doppler ultrasound revealed no vascular signal. A fistulogram confirmed that what was previously thought to be a diverticulum was actually a fistulous tract originating from the pancreatic tail mass. On HD 18, exploratory laparotomy revealed that the pancreatic tumor had eroded into the proximal descending colon. This was treated with partial colectomy and splenectomy, and he had no further bleeding. After a prolonged hospitalization, he was discharged home on HD 51 with antibiotics for Escherichia coli abscess. He was readmitted 7 days later with abdominal pain and found to have leukocytosis to 55, lactic acidosis to 19, and renal failure. On HD 8, he suffered a PEA arrest and expired. Conclusion: Atypical presentations of hematochezia provide a diagnostic dilemma for clinicians, and a broad differential diagnosis must be entertained. We report here a case of a fistulous tract originating from a pancreatic mass masquerading as a bleeding diverticulum.


[350C] Figure 3.

351 Schistosomiasis as a Mimicker of Inflammatory Bowel Disease Vadim Bul, MD1, Russell Brown, MD, FACG2. 1. University of Illinois College of Medicine at Chicago, Department of Internal Medicine, Chicago, IL; 2. North Shore University Health System, Division of Gastroenterology, Evanston, IL. A 36 year old Brazilian-born male without family history of colon cancer or significant travel history presented to the GI clinic for abdominal bloating and several years of chronic diarrhea which had recently become bloody. His physical exam was without abnormalities. Labs were notable for 7% eosinophils and elevated transaminases, AST 191 u/l and ALT 158 u/l. The patient underwent a colonos-


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copy which was notable for diffuse erythema of the rectum concerning for Inflammatory Bowel Disease. Biopsies of the right colon and rectum demonstrated “submucosal granulomas with structures suggestive of schistosomal eggs”. He later underwent a liver biopsy which showed “schistosomal organisms in granulomas with inflammation” and hypereosiniphilia as well as non-alcoholic steatohepatitis. The patient was given one day of Praziquantel and on outpatient follow-up had improvement in his diarrhea and normalization of his liver function tests. He was able to gain 20 pounds and did not require further medical care for his diarrhea. We can infer based on his Brazilian heritage that he was likely infected with Schistosoma Mansoni. Chronic schistosomiasis refers to colonization by one of the schistosoma trematodes. Patients with gastrointestinal manifestations can present with abdominal pain, tenesmus, diarrhea, rectal pain and hematochezia. Hepatic presence of the egg antigen induces a host-immune response leading to granuloma formation and neo-angiogenesis. This causes inflammation of the portal tracts which can lead to hepatomegaly and, if left untreated, irreversible hepatic fibrosis and portal hypertension. Patients with severe liver involvement manifest with complications of portal hypertension sooner than complications of hepatic dysfunction. With intestinal involvement, schistomsoma tend to reside in areas drained by the inferior mesenteric venous plexus and induce localized inflammation and fibrosis of the submucosa and hyperplasia of the mucosa. Endoscopic findings show edematous and congested mucosa with petechial hemorrages similar in appearance to inflammatory colitis. Left untreated, nodules and polyps with ulcerations can form. Nodules tend to have a gray-yellow appearance similar to those seen with pseudomembranous colitis. Although there is little to no risk of malignancy, polyps need to be endoscopically removed as they do not resolve with medical therapy alone. In non-endemic areas, post-treatment studies to confirm eradication are not necessary.

(IMHMV). There was no sign of inflammatory bowel disease. Prior to elective resection of the affected colon the patient developed a perforation of the sigmoid colon and underwent an emergent resection with a left end colostomy. Final pathology revealed muscular thickening of the intramural veins without changes in the accompanying arteries consistent with IMHMV. IMHMV is a rare disease entity typically affecting young, healthy males. It is often initially misdiagnosed as inflammatory bowel disease because of the similarity in patient demographics, clinical symptoms, and endoscopic findings. However, biopsies usually reveal non-specific ischemic changes. Interestingly, we were able to make a presumptive diagnosis prior to resection; usually the final diagnosis is made in histopathological analysis after surgical resection, which reveals non-thrombotic and non-inflammatory occlusion of the mesenteric veins secondary to myointimal hyperplasia. Recurrences have not been reported after surgical resection, raising the idea that it is likely curative, and our patient’s sigmoid perforation was likely related to IMHMV, suggesting that early treatment may be of benefit.

352 Clinical Management of Lymphocytic Colitis With Serum-Derived Bovine Immunoglobulin/ Protein Isolate (SBI) Christine Frissora, MD1, Ira Shafran, MD2, H. Steven Silver, MD3, Patricia Mitchell, PA-C4, Patricia Burguner, ARNP5, Bruce Burnett, PhD6. 1. Weill Cornell Medical College/Cornell University, New York, NY; 2. University of Central Florida Medical School, Winter Park, FL; 3. Knoxville Gastroenterology Consultants, Knoxville, TN; 4. San Antonio Gastroenterology Associates, San Antonio, TX; 5. Shafran Gastroenterology Associates, Winter Park, FL; 6. Entera Health, Cary, NC. The pathophysiology of lymphocytic colitis (LC) is not completely understood. Current hypotheses implicate abnormal mucosal immune response to luminal antigens in combination with genetic predisposition. Five cases detail the outcomes of adding serum-derived bovine immunoglobulin/protein isolate (SBI) for the nutritional management of these unresponsive LC patients. SBI’s unique mechanism includes binding microbial components and maintaining normal GI immune balance which makes it a candidate therapy in LC patients. Five patients were administered SBI for LC. All patients were female with an average age of 71±7.1 yrs. Patient 1 was admitted to the hospital with 20-24 bowel movements (BM) per day with cramps and urgency. Biopsies from a colonoscopy were consistent with LC. She was placed on mesalamine and methylprednisolone without any change. Patient 2 had tried and failed multiple tapering doses of budesonide for 2 yrs with continual multiple, loose stools per day. Patient 3 had been diagnosed with IBS-D for 15 yrs and failed all over-the-counter options. Recent biopsies, however, indicated LC. Patient 4 had a poor response to steroids and psyllium fiber for 2.5 yrs with a history of fecal incontinence (FI). Patient 5 had a diagnosis of LC for 1.5 yrs; she had a history of anal fistula repairs with multiple loose BM in the a.m. accompanied by intermittent episodes of FI. She had no response to mesalamine, loperamide or antibiotics. Incorporating SBI dramatically improved symptoms for all patients. Patient 1 was discharged from the hospital on SBI 5g QD and continued on 1.2g mesalamine having 4 formed BM without cramping, urgency or bleeding. However, if the patient missed more than two days of SBI, she quickly experienced 10-14 watery BM daily. Patient 2 first began SBI 5g BID with budesonide, but was able to discontinue the steroid while maintaining normal BM on SBi monotherapy. Patient 3 was placed on budesonide and SBI 5g QD normal BM within a week. Patient 4 began SBI 5g QD in addition to psyllium fiber and at follow-up reported formed stools with no episodes of FI. After initiating SBI 5g QD, Patient 5 reported 1-2 formed BM without FI. All patients are currently maintained on SBI in combination with the therapies indicated above for more than 6 months. No side effects have been experienced on SBI during that time. The exact manner in which SBI manages LC is not known. The outcomes of these cases, however, suggest that LC patients may benefit from the distinct nutritional proteins in SBI for management of their conditions. Larger, well-controlled studies in patients with LC and/or FI should be performed to corroborate these findings.

353 A Case of Idiopathic Myointimal Hyperplasia of the Mesenteric Veins Agam Patel, MD, Yecheskel Schneider, MD, Monica Saumoy, MD, Charles Maltz, MD, PhD, Heather Yeo, MD, MHS, Jose Jessurun, MD, David W. Wan, MD. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY. A 65 year old man with no significant past medical history was admitted to an outside hospital with 1.5 months of crampy lower abdominal pain associated with rectal urgency and tenesmus. Initial CT scan showed thickening of his rectosigmoid and mid to distal descending colon; follow-up colonoscopy revealed inflammation of the affected areas and biopsy showed focal lamina propria vascular congestion and sloughing epithelium in the rectosigmoid colon. A course of antibiotics followed by a course of oral steroids did not improve his symptoms. He was admitted to our institution with worsening pain. Initial laboratory studies were unremarkable except for a positive C. difficile PCR, though oral vancomycin did not lead to improvement. CT scan showed similar findings with pericolonic inflammation. Subsequent flexible sigmoidoscopy revealed cobblestoning and skip inflammation of the mucosa in the sigmoid colon with rectal ulcers concerning for Crohn’s Disease, but his symptoms worsened despite aggressive treatment with steroids and mesalamine. Biopsies returned revealing dilated mucosal capillaries without active colitis. His symptoms continued to worsen, so a repeat colonoscopy 9 days later demonstrated stricturing of the sigmoid colon and worsening of the mucosal ulceration. Repeat biopsies in the rectosigmoid colon showed severe ischemic injury with endothelial swelling, non-inflammatory fibrinoid necrosis, and capillary arterialization concerning for mesenteric venous occlusion from idiopathic myointimal hyperplasia of the mesenteric veins


[353A] Figure 1.

354 Clostridium septicum Bacteremia Warrants Exclusion of Colorectal Cancer Neetika Srivastava, MD1, Gregory Cooper, MD2. 1. Case Western Reserve University, University Hospitals, Cleveland, OH; 2. Division of Gastroenterology and Liver Disease, University Hospitals Case Medical Center, Cleveland, OH. Colorectal cancer (CRC) is the third leading cause of cancer death in the United States1 and is usually detected in patients with GI signs or symptoms. In addition, the finding of infection with certain bacteria should prompt workup for occult malignancy. Clostridium septicum is a rare organism also associated with CRC. It can vary in presentation from cellulitis to atraumatic gas gangrene.4 Recognizing the relationship between infections and malignancies is crucial as it can lead to prompt diagnosis and treatment of an otherwise occult malignancy. We report a case of a patient initially admitted for diabetic ketoacidosis; however, developed necrotizing fasciitis secondary to C. septicum and later discovered to have an occult colorectal cancer. A 79 year old female with diabetes and anemia presented with hyperglycemia and endorsed subjective fevers and low back pain. Initial vital signs were stable and physical exam revealed subcutaneous crepitus in her lumbar spine and multiple large bullae on her back. CT scan showed an extensive amount of free air in her lumbar spine, lower extremities, and abdomen. She was started on broad spectrum antibiotics and blood cultures grew C.septicum. Shortly after admission, she developed septic shock. Surgery was not recommended given her poor prognosis, and she expired within 14 hours of admission. Autopsy revealed a 3.5 cm cecal mass with biopsy confirming adenocarcinoma. Atraumatic gas gangrene is rare and almost exclusively caused by C. septicum, a gram positive, anaerobic, spore-forming organism that can live in aerotolerant environments and thus can infect healthy tissue.5,6 C.septicum is part of the normal GI flora; however, in immunosuppressed states it can lead to fatal sepsis. The proposed mechanism of infection in CRC is that there is increased anaerobic glycolysis and necrosis in tumors, which provides an optimal environment for spore germination5. Mucosal ulceration allows entry into the vascular system leading to distant seeding.7 Diabetes allows for colonization as persistent hyperglycemia leads to tissue hypoxia ideal for spore production.5 C. septicum releases toxins which causes muscle destruction and severe sepsis.5,6 This case is presented to create awareness about C. septicum’s subtle presentation and rapid progression, which can lead to death in less than 24 hours. Any patient who survives must undergo CRC screening as the infection may be the first sign of an otherwise occult malignancy.

355 Intramural Colonic Hematoma Brian T. Moy, DO1, Erik Olson, DO2, Michael S. Karasik, MD3. 1. Department of Medicine, University of Connecticut Health Center, Hartford, CT; 2. Division of Gastroenterology and Hepatology, University of Connecticut Health Center, Farmington, CT; 3. Connecticut GI, PC, Hartford , CT. Introduction: Intramural colonic hematomas are extremely rare, accounting for 5% of all intramural hematomas, and are usually found after acute trauma or in the setting of bleeding diatheses. Spontaneous intestinal intramural hematomas in patients on oral anticoagulant therapy occur in 1/2500 patients. We report here a rare and dramatic case of an intramural colonic hematoma in an 89-year-old male taking


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Abstracts anti-platelet agents with a colonic hematoma. Case Report: An 89-year-old male with history notable for ischemic cardiomyopathy (on aspirin and Clopidogrel) and chronic constipation presented to the hospital with urosepsis. His hospital course was complicated by 3 episodes of bright red blood per rectum and hypotension. He had no history of past gastrointestinal hemorrhage or abdominal trauma. He had a remote history of subtotal colectomy for colonic volvulus. He had never undergone any prior endoscopic evaluation. His physical exam was notable for moderate cachexia and a normal abdomen. There was bright red blood within the vault and external hemorrhoids, but no rectal mass. His hematocrit was 39.0% and INR was 1.1. Colonoscopy revealed a 19 cm intra-colonic hematoma extending to the recto-sigmoid junction (Fig. 1) with near complete obstruction. Computed tomography revealed the hematoma to be 8.0 cm x 8.8 cm in crosssection (Fig. 2). There was no intra-abdominal blood. The patient was successfully managed conservatively with a titrated bowel regimen and cessation of Clopidogrel. There was no evidence of colonic ischemia or recurrent bleeding. Discussion: We present here a rare case of an intramural colonic hematoma in the setting of anti-platelet agents. Although there was no obvious abdominal trauma, it is possible that increased intra-abdominal pressure due to constipation played an etiologic role. Intramural colonic hematomas should be considered in patients presenting with acute hypotension in setting of a bleeding diathesis, abdominal pain, and an acute drop in hematocrit, particularly when no gross GI bleeding is present. Our patient is unusual because he had no abdominal pain and exhibited rectal bleeding. The latter was a result of the hematoma tearing into the colonic lumen. Rare potential complications include obstruction and ischemia. Intracolonic hematomas are most often managed conservatively but may require surgical management in the setting of ischemia.

[355A] Figure 1.

[355B] Figure 2.


356 Intravenous Immunoglobulin in the Treatment of Severe Clostridium difficile Colitis and Toxic Megacolon Brian T. Moy, DO1, Sonia Dhillon, MD2, Booth Wainscoat, DO3. 1. Department of Medicine, University of Connecticut Health Center, Hartford, CT; 2. Department of Medicine, University of Connecticut Health Center, Farmington, CT; 3. Department of Infectious Disease, Hartford Hospital, Hartford, CT. Introduction: Intravenous immunoglobulin (IVIG) has been used in patients with recurrent or refractory Clostridium difficile colitis (CDC). Here we report a rare case of IVIG used in the treatment of severe CDC complicated by toxic megacolon. Case Report: A 48-year-old male with a past medical history of AIDS (CD4 count of 4) presented to the ER with severe and crampy right lower quadrant abdominal pain, nausea, and diarrhea. He was recently admitted to the hospital 3 weeks prior and was being treated for CDC (NAP1 +). Because he was lost to follow-up, he only received 8 days of oral vancomycin with his last dose being 10 days prior to arrival. In the ER he was normotensive, had a temperature of 102 F, heart rate of 121, and had multiple bloody bowel movements. On exam he had a distended abdomen, tenderness to palpation in the right lower quadrant, and hypoactive bowel sounds. His basic metabolic panel was normal. His white blood count was 2.6 thou/uL (absolute neutrophil count 1720), hematocrit was 24%, albumin was 2.1 g/dL, and his lactate was 3.1 mmol/L. Infectious workup for acute diarrhea was negative. Abdominal radiograph revealed a dilated transverse and descend-

[356A] Figure 1.

[356B] Figure 2.


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prior when the patient was diagnosed with mild acute sigmoid diverticulitis and was discharged on a 10 day course of oral ciprofloxacin and metronidazole. The second presentation was 4 weeks prior when the patient was again admitted for persistent diverticulitis and treated with IV antibiotics. Blood cultures on the day of that admission grew Clostridium septicum from 1 of 2 sets, with repeat cultures negative. He was discharged home on long term IV piperacillin/tazobactam, which he was still taking at the time of the current presentation. The patient was admitted for persistent diverticulitis and underwent a flexible sigmoidoscopy that revealed a sigmoid stricture with biopsy results consistent with poorly differentiated invasive adenocarcinoma. He was subsequently taken to the OR for colectomy; however, was found to have peritoneal, omental and liver metastases. The procedure was terminated and the patient was started on FOLFOX chemotherapy. Clostridium septicum is a gram positive, spore-forming anaerobe that is strongly associated with colonic and hematologic malignancies. Association with colonic malignancy alone ranges from 30-50% of all cases of C. septicum bacteremia. It is hypothesized that poorly vascularized tumors or areas of bowel provide a favorable anaerobic environment for the proliferation of C. septicum, which then translocates transmurally via areas of GI mucosal injury caused by the tumor. Despite its common assocation with colonic malignancies, C. septicum bacteremia is exceedingly rare accounting for C. septicum was not initially recognized during the patient’s second admission. Although the delay in diagnosis for this particular case did not likely play a significant role in his clinical outcome, this may not be the case for other patients. This case underscores the importance of considering colonic malignancy when patients present with rare infections like C. septicum. Furthermore, diagnostic evaluation should be expedited, as early diagnosis may lead to improved outcomes.

[356C] Figure 3. ing colon up to 7.5 cm consistent with toxic megacolon (Fig. 1). CT abdomen showed diffuse wall thickening throughout the entire colon, worst at the cecum, and no abnormally dilated small bowel loops (Fig. 2,3). He was started on oral vancomycin 500 mg every six hours and IV metronidazole 500 mg every 8 hours over the next three days, but had worsening serial abdominal exams. He was not a candidate for surgery given his comorbidities and the decision was made to treat his severe CDC and toxic megacolon with 1 dose of IVIG 500 mg/kg. The next day his KUB, lactate, abdominal pain, and diarrhea improved. Seven days later he had a benign abdominal exam, was tolerating oral intake, and was discharged from the hospital. Discussion: Patients with severe CDC have low levels of available serum IgG antitoxin that can bind to toxin A and B within the intestine to eliminate Clostridium difficile. The mechanism of IVIG in CDC is through the binding and neutralizing of toxin A by IgG anti-toxin A antibodies obtained from pools of healthy blood donors. IVIG has been used in patients with chronic relapsing CDC and is seldom reported in acute severe cases. In patients with acute severe CDC and toxic megacolon not responding to conventional medical therapy and not candidates for surgery, IVIG can be considered as an alternative treatment to prevent complications.

[358A] Figure 1.

359 Synchronous Multiple Lymphomatous Polyposis and Adenocarcinoma in the Colon: Case Report

357 The Association of Streptococcus gallolytics Subspecies Pasteurianus Bacteremia With the Detection of Premalignant Colonic Lesions Gaurav Chand, DO1, Leonid Shamban, DO2, Prabhat Sinha, DO1. 1. St. John Providence Hospital, Southfield, MI; 2. Genesys Regional Medical Center, Grand Blanc, MI. Streptococcus gallolyticus subspecies (subsp.) gallolyticus (formerly bovis bioptype I) bacteremia has been long associated with underlying colonic adenocarcinoma. The bovis species underwent taxonomic dissection in 2003 into five subtypes. Multiple reports showed different subtypes of gallolyticus are associated with colonic malignancy but are less frequent. As a result, the subtype strains are less recognized with colon cancer. A 71-year-old male with a history of hypertension was admitted with worsening lower back pain and fevers that had been ongoing for six weeks. Initial vital signs and laboratory data were within normal limits aside from leukocytosis of 11.2 K/mcL. MRI of the lumbosacral spine revealed enhancement of L3-L4 and L5-S1 disc spaces suspicious for osteomyelitis and broad-spectrum antibiotics were initiated. Initial blood cultures showed Streptococcus species, which prompted a transthoracic echocardiogram that revealed vegetations on the mitral and aortic valves later confirmed by a transesophageal echocardiogram (TEE). He was transferred to the intensive care unit, and the etiology for his endocarditis remained undetermined. A colonoscopy was suggested, but his clinical instability made such a procedure intolerable. Final blood cultures revealed Streptococcus gallolyticus subsp. pasteurianus (previously bovis biotype II). He was stabilized and discharged with intravenous Vancomycin. After completion of antibiotics and negative repeat blood cultures, he underwent successful aortic grafting with valve replacements. After undergoing months of rehabilitation and follow-up, he was readmitted for Streptococcus bacteremia and fever of 100.4° F. With a negative TEE, a colonoscopy was pursued, revealing a 2.5 x 3 cm cecal mass suspicious for his origin of infection. Months afterwards, he underwent a successful right hemicolectomy with pathology revealing a tubulovillous adenoma with high-grade dysplasia. Many clinicians understand the link between Streptococcus gallolyticus subsp. gallolyticus (bovis type I) and malignancy, but the new speciation may be unfamiliar to practitioners. S. gallolyticus subsp. gallolyticus has a much greater association than S. gallolyticus subsp. pasteurianus with colonic malignancies. As there are no guidelines for managing patients with S. gallolyticus subsp. pasteurianus bacteremia, a colonoscopy should be considered as a part of the evaluation when no definitive source is identifiable.

358 Colon Cancer Heralded by Clostridium septicum bacteremia Daniel Pievsky, DO, RD1, Patrick Mitchell, MD, PhD2, Renjit V. Thomas, MD3, Samit S. Desai, MD4. 1. Rutgers New Jersey Medical School, Jersey City, NJ; 2. Rutgers New Jersey Medical School, Newark, NJ; 3. Rutgers New Jersey Medical School, Union, NJ; 4. Hackensack University Medical Center, NJ. A 51 year old male with a history of diverticulitis presented with fever, chills and diarrhea for one day. He reported 8-10 bouts of watery, voluminous, non-bloody diarrhea along with one episode of non-bloody, non-bilious vomiting. He had two recent presentations with similar symptoms. The first was 6 weeks


Sun-Jin Boo. Department of Internal Medicine, Jeju National University School of Medicine, Jeju, South Korea. Introduction: Synchronous multiple lymphomatous polyposis and adenocarcinoma in the colon is very rare. We report a case in which a sporadic adenocarcinoma occurred on the lymphomatous polyp of colon was successfully resected using endoscopic submucosal dissection (ESD) technique. Case: A 69-year-old female presented with abdominal discomfort and intermittent anal bleeding for 3 months. Under the colonoscopy, there are numerous non-epithelial polyps with various size in the colon and a epithelial neoplasm larger than 4cm in the ascending colon. The biopsy of a non-epithelial polyp showed focal nodular lymphoid hyperplasia and the biopsy of the epithelial neoplasm revealed tubular adenoma with low grade dysplasia. A computed tomography demonstrated multiple tiny mural nodules in the colon and multiple homogeneous attenuated lymph node enlargement in Lt. gastric, paraaortic, aortocaval, ileocolic, mesenteric area. A about 4.5cm sized epithelial neoplasm in the ascending colon was completely resected using ESD technique. The ESD specimen showed intraepithelial well-differentiated adenocarcinoma and extranodal marginal zone B-cell lymphoma (MALT lymphoma). A about 0.5cm sized non-epithelial polyp was resected using endoscopic mucosal resection (EMR) technique. The EMR specimen revealed diffuse large B-cell lymphoma that may arise from MALT lymphoma. She received R-CHOP and salvage DHAP chemotherapy. However, she expired 15 month later due to disease progression. Conclusion: We report a rare case of synchronous multiple lymphomatous polyposis and adenocarcinoma in the colon.

360 A Challenging Case of Diarrhea After Fecal Microbiota Transplant Colleen R. Kelly, MD1, Sidney Olefson, MD, MBA2, Melissa Jackson, MD3. 1. Warren Alpert Medical School of Brown University/Women’s Medicine Collaborative, Providence, RI; 2. Warren Alpert School of Medicine of Brown University, Providence, RI; 3. Warren Alpert School of Medicine of Brown University, East Providence, RI. Tools for the diagnosis of Clostridium difficile infection (CDI) have recently increased in accuracy while decreasing in cost. However, clarifying the diagnosis remains a clinical challenge. We present the case of a 45 year old female with a history of systemic lupus erythematous on methotrexate and prednisone who presented to our center for evaluation of recurrent CDI. The initial episode occurred 18 months prior to presentation after she received an “antibiotic” around a dental procedure. She developed diarrhea, was found to have a positive C. difficile toxin PCR, and was treated with a 2 week course of oral vancomycin. Within a week of stopping therapy, urgency, foul odor, nocturnal bowel movements and fecal incontinence recurred. After 4 further CDI episodes, and repeated courses of oral vancomycin and probiotics, she underwent fecal microbiota transplantation (FMT). Her husband was the stool donor and the procedure was performed by colonoscopy, which was without any significant findings. Four weeks post-FMT, the patient reported irregular stools and mild constipation alternating with looser stool with associated right lower quadrant pain. Symptoms were attributed to post-infectious


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Abstracts irritable bowel syndrome (IBS) and a probiotic was recommended. Around 8 months post-FMT, she called to report 4 weeks of “on and off ” loose stools, which had recently become more watery and were associated with “ low grade fever.” C. difficile toxin PCR was positive, however, given intermittent and non-progressive symptoms, and that she was otherwise clinically well, vancomycin was not immediately initiated. Sigmoidoscopy performed the next day showed normal appearing mucosa in the rectum and sigmoid colon and random biopsies showed no evidence of colitis. This was determined to be colonization rather than active CDI and the patient was managed with a fiber supplement for IBS. This case highlights the diagnostic uncertainty that around CDI, despite increasingly sensitive assays. Enzyme immunoassay has largely been replaced with nucleic acid amplification testing, which is rapid and has high sensitivity. It tests for toxigenic strains but not toxins, so requires a clinical context. Risk factors for colonization include hospitalization, antimicrobial agents, anti-secretory drugs, and immunosuppressive agents. Post-infectious IBS is common after CDIand C. difficile PCR cannot distinguish colonization from symptomatic disease. We avoided unnecessary therapy with vancomycin in this patient who did not have evidence of colitis at the time of a positive C. difficile assay. Providers must consider colonization, especially in patients who have an atypical presentation, and should avoid inappropriate testing for cure.

361 Acute Tubular Necrosis as a Complication of Collagenous Colitis Marco Silva1, Hélder Cardoso1, Eduardo Rodrigues-Pinto2, João Magalhães3, Guilherme Macedo2. 1. Gastroenterology Department - Centro Hospitalar São João, Porto, Portugal; 2. Centro Hospitalar São João, Porto, Portugal; 3. Pathology Department - Centro Hospitalar São João, Porto, Portugal. Introduction: Microscopic colitis is a subdiagnosed cause of chronic diarrhea, especially among the elderly, although it can occur in patients of any age. This case evidences the potential seriousness of the pathology, in particular, the development of acute tubular necrosis which could be prevented by an early diagnosis. Case Report: An 80-year-old man, previously healthy, with a history of watery diarrhea, anorexia occasional abdominal cramps and weight loss (9 kg), in the last 5 months. He was submitted to a colonoscopy 1 month before, which did not showed endoscopic lesions, and treated with loperamide, but without improvement. There was no history of joint pains or swelling, fever or use of non-steroidal antiinflammatory drugs. He recurred to the emergency department due to worsening diarrhea, asthenia and dizziness. On the physical exam he was pale and dehydrated. Laboratory tests showed iron deficiency anemia, acute tubular necrosis (creatinine of 12.8mg/dL, eGFR of 4ml/min (1.73m2) and hypokalemia (K+ 2.4mEq/L). Urinary tract infection and obstruction were excluded and he was admitted on an intensive care unit. Stool cultures were negative, including specific tests forbacteria or parasites. The presence of celiac disease was excluded with normal duodenal biopsies and negative serologic testing. An ileocolonoscopy was performed, revealing a mucosa with normal appearance. Biopsies of the right and left colon were taken and the histopathological exam was consistent with the diagnosis of collagenous colitis. He presented progressive improvement of the renal impairment, with fluids and correction of the hydroelectrolytic disorders, without the need of haemodialysis. The patient was treated with oral budesonide with resolution of diarrhea. Budesonide was stopped after 1 year of treatment. Eighteen months after the diagnosis, he is currently being followed in outpatient clinic, asymptomatic, but complaining of occasional constipation.

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363 Resolution of Constipation, Anal Stricture, and Fe Deficiency Anemia After Iron Infusion: An Analogy With Plummer Vinson Syndrome Presidential Poster Vijaypal Arya, MD1, Shikha Singh, MD2, Shashank Agarwal, MD2, Arjun Ohri, MD2. 1. Wyckoff Heights Medical Center, Middle Village, NY; 2. Vijaypal Arya MD PC, Middle Village, NY. Introduction: Anal stricture is an uncommon and disabling condition which can be unresponsive to conservative management and the complications of dilatations and Anoplasty make it a formidable treatment challenge. Here we report the case of a patient with constipation, anal stricture and iron defi ciency anemia (IDA) where the triad resolved with IV iron treatment over 3 months. Case Report: A 69-year-old male presented to us with chronic constipation, rectal pain and easy fatigability. Physical examination revealed conjunctival pallor and laboratory findings were consistent with microcytic hypochromic anemia with iron deficiency (Ht- 31.6, Labs-Table 1). An upper endoscopy, CT Abdomen and Capsule endoscopy did not reveal any source of GI bleeding. Celiac panel was normal and there was no evidence suggestive of any other cause of anemia. Digital rectal examination (DRE) could not be completed because of severe rectal pain and markedly narrow anal canal. Under propofol sedation, Colonoscopy with GIF-Q 180 OLYMPUS scope, confirmed anal stricture with non-specific colitis. Conservative management with laxatives, high fiber diet and local anesthetics was initiated but the patient continued to have symptoms. Patient was referred to the hematologist for an evaluation of anemia and was started on IV Iron infusions. After 3 months of treatment, patient’s anemia and all of the symptoms resolved (Ht- 38.3, Table 1). A repeat DRE was painless and the anal stricture had resolved. Discussion: The triad of Constipation, Anal Stricture and IDA in this patient paints a similar picture as PVS which presents as Dysphagia, Esophageal webs and IDA. The patient’s symptoms of constipation and anal stricture resolved with iron treatment which has for long been known to resolve dysphagia and esophageal webs in PVS. Iron deficiency leading to loss of iron-dependant enzymes causes web formation and cancer development of the gastrointestinal tract. Tissue iron has been known to play an important role in the proliferation of epithelial cells. The epithelial layer of the alimentary tract is especially susceptible to iron deficiency because of its high cell turnover. Therefore, Iron replacement may provide a promising medical treatment benefit in high cell turnover GI tract and resolve rectal strictures along with the symptoms associated with them. The cause of PVS still remains a mystery. This analogy with PVS serves as a subject of further research and presents as an intriguing intellectual challenge in front of our medical fraternity.

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Table 1. Lab Values Pre and Post Iron Replacement Therapy Pre- Iron Replacement Therapy

Post- Iron Replacement Therapy

Hb

9.4 g/dl

12.1 g/dl

Ht

31.6 %

38.3 %

MCV

71.8 fl

84 fl

MCH

21.4 pg

26.5 pg

MCHC

29.9 g/dl

31.8 g/dl

RDW

19.1 %

13.2 %

Platelets

320 Thous/mcl

218 Thous/mcl 6.1 Thous/mcl

WBC

4.2 Thous/mcl

ALT

10 U/l

5 U/l

AST

30 U/l

21 U/l

Isolated Gastrointestinal Histoplasma Colitis Chitharanjan Duvoor, MBBS, MD, Samyuktha Ramavaram, MD, Daniel K. Brown. University of Arkansas for Medical Sciences, Little Rock, AR. Introduction: Histoplasmosis is the most common endemic mycosis in patients with AIDS. Gastrointestinal manifestations are infrequent and occur only in 3%–12% of patients. Antifungal therapy improves outcome for >80% of AIDS patients with histoplasmosis. Case Presentation: A 56 year old male with a past medical history of HIV on HAART, End-stage renal disease on dialysis presented with complaints of 2 week history of abdominal pain associated with intermittent bloody diarrhea. A CT abdomen was unremarkable. Stool studies were positive for Clostridium Difficle and treatment with oral Vancomycin was initiated. He returned within a week with abdominal pain and worsening bloody diarrhea. The patient stated that his symptoms improved but did not resolve completely. His most recent CD4 count was 43. A repeat CT of the abdomen revealed concentric bowel wall thickening involving the cecum and proximal ascending segment of the colon along with right lower quadrant lymphadenopathy. Colonoscopy revealed edematous cecum with inflamed, friable, ulcerated mucosa, multiple discrete punched out ulcers throughout the colon. Biopsies revealed abundant microorganisms with morphologic features consistent with histoplasma. Patient was successfully treated with a course of Amphotericin B. Discussion: The most common clinical setting for disseminated histoplasmosis is HIV infection, especially with CD4 counts less than 200/mm3. Gastrointestinal tract involvement with histoplasmosis can occur in patients with disseminated form of the disease. The lesions tend to occur in the ileocecal region due to abundance of lymphoid tissue. Patients present with fever, diarrhea, abdominal pain, GI bleed, or hepatosplenomegaly. Histoplasma colitis should be considered in residents of endemic areas or immunocompromised patients presenting with unexplained diarrhea. Pathologic examination and fungal cultures of GI tract tissue specimens are sensitive methods for diagnosing GI tract histoplasmosis. Grocott-Gomori methenamine silver nitrate staining of the tissue specimen may be used to aid in diagnosis. Endoscopy with biopsy is required for prompt and precise diagnosis. Current treatment modality includes amphotericin B for disseminated histoplasmosis for unstable patients with severe disease. In stable patients, treatment with itraconazole is recommended for 6 to 18 months. Our case is unique in that the disease was confined to the GI tract with negative serological and fungal blood cultures.


364 Colonic Mucosal Schwann Cell Hamartoma Incidentally Found on Screening Colonoscopy Ozdemir Kanar, MD1, Rahman Nakshabendi, MD1, Andrew C. Berry, DO2, Rommy Issa, MD1, Maryna Tarbunova, MD1, Matthew Clark, MD3, Amie Deutch, MD1. 1. University of Florida Health College of Medicine, Jacksonville, FL; 2. Department of Medicine, University of South Alabama, Muskego, WI; 3. University of Florida Health College of Medicine, Division of Gastroenterology, Jacksonville, FL. We present a 67 yo AAM with Pmhx significant for tubulo-villous adenoma s/p resection in 2010, with a repeat colonoscopy 1 year later showing 4 tubulovillous polyps. Family history was remarkable for colon cancer at age 65 on the mother’s side. He had no family history of colon cancer and no history of familial adenomatous polyposis, multiple endocrine neoplasia type IIb, neurofibromatosis type I, or Cowden syndrome. Pt had no specific complaints. He had normal bowel movements, denied melena, nausea, vomiting, or weight loss. On this repeat screening colonoscopy, two polyps were found with one polyp in the descending colon measuring 4mm and one in the sigmoid colon measuring 6 mm. Histopathology reveled tubular adenoma, and hamartoma respectively. Histologically, a polypoid fragment of colonic mucosa that had numerous spindle cells with elongated nuclei within the lamina propria was shown by hemotoxylin and eosin stains. The sigmoid colon biopsy showed proliferated cells that were strongly S-100 positive but CD117, α-smooth muscle actin and CD34 negative, histologically proving Schwann Cell phenotype. There was no dysplasia in the mucosa surrounding the biopsy site. Due to the benign findings, the patient was counseled to repeat a colonoscopy in 5 years with possible surveillance biopsies in light of prior polyp detections. Colonic hamartoma is a rare benign nerve sheath tumor disease. Clinically, this lesion has a benign natural history. There is no apparent association with any one of the inherited polyposis syndromes. A 2009 study by Gibson and Hornick analyzed 26 cases of colorectal polypoid lesions comprising pure Schwann


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cell proliferation, which were different from gastrointestinal tract schwannomas with no association with inherited syndromes. Colonic hamartomas usually present as any polyp in the GI tract: presenting with BPR, obstructive symptoms, or altered bowel movements, many times they may be incidentally found. It is important to differentiate this tumor from GIST tumor, as the latter may be malignant and warrants complete resection. The differential diagnosis of neural tumors is broad, and accurate diagnosis of a mucosal Schwann cell hamartoma is dependent on histologic demonstration of a lack of axons and immunohistochemically by strong staining for S-100 protein. As there is no evidence that this tumor has the potential to become malignant, there are no indications to repeat a colonoscopy sooner than expected. As with any polyp or masses found in the colon it is always important to follow pathology as to further guide diagnosis and management.

[364A] Figure 1.

365 Metastatic Renal Cell Carcinoma Presenting With Hematochezia and Chest Pain Janki R. Patel, MD1, Michael Chang, MD1, Denise Kalmaz, MD2. 1. University of California San Diego, San Diego, CA; 2. University of California San Diego, Division of Gastroenterology, San Diego, CA. Renal cell carcinoma (RCC) is known to have late recurrence even among patients with early stage disease and surgical resection.Typical sites for metastasis include lungs, bone, liver, and brain, whereas colonic metastasis is rare. A 54 year old man with past medical history significant for coronary artery disease, type II diabetes, hypertension, and stage 1 RCC status post right nephrectomy 3.5 years prior, presented with hematochezia, anemia, and chest pain. Initially, patient was admitted to an outside hospital with anemia, renal failure, and chest pain. He was diagnosed with non-ST elevation myocardial infarction and underwent a left heart catheterization significant for multi-vessel coronary artery disease. After starting dual anti-platelet therapy with aspirin and clopidogrel, he had frank hematochezia and worsening dyspnea, which prompted him to present to our emergency room. The vital signs were within normal limits and physical exam was significant for mild diffuse abdominal tenderness on palpation without rebound tenderness. Laboratory studies revealed hemoglobin of 9.2, mean corpuscular volume of 70.6 μm3, creatinine of 5.23mg/dL, iron 20mcg/dL, iron binding capacity 280mcg/dL, and ferritin 146ng/mL. Stool occult blood testing was negative. An abdominal computed tomography (CT) scan revealed a soft tissue mass in the right nephrectomy surgical bed measuring 3.2 cm x 3.7 cm, innumerable lesions within the left kidney, left adrenal mass, multiple pulmonary nodules and lymphadenopathy consistent with metastatic disease. The colon was noted to be unremarkable. The patient’s renal function improved with intravenous fluid hydration. No biopsy was performed given his dual antiplatelet therapy and he was discharged with referral for follow-up with oncology and gastroenterology. He was re-admitted 1 month later with chest pain and dyspnea where cardiac work up was negative for ischemia. A push enteroscopy and colonoscopy were performed for ongoing intermittent hematochezia. The enteroscope was advanced to approximately 40cm past the ligament of treitz and examination was entirely normal. The colonoscopy revealed an ulcerated 1.5cm pedunculated mass lesion 35cm from the anal verge (image 1) with biopsies consistent with clear cell RCC (image 2). Intestinal metastasis from renal cancers often present as hemorrhage, bowel intussusception, bowel obstruction due to luminal occlusion, or rarely as perforation. In our case, the patient presented with hematochezia secondary to RCC with metastatic spread to colon in the setting of recent initiation of antiplatelet therapy. Our case illustrates that although metastatic RCC is common, colonic metastases are rare and careful history and surveillance for recurrence should be performed for RCC patients presenting with abdominal symptoms.

[365A] Figure 1.

[364B] Figure 2.

[364C] Figure 3.


[365B] Figure 2.


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CMV Colitis Presenting as Intestinal Pseudo-Obstruction

Trichuris trichiura: A Rare Cause of Rectal Bleeding in Adults

Sajiv Chandradas, MD1, Walter Coyle, MD2. 1. Scripps Green Hospital, San Diego, CA; 2. Scripps Green Hospital, La Jolla, CA.

Amir Taefi, MD1, Suzan Ebrahimi2, Faryal Mirza, MD1, Vipin Verma1, Won Cho, MD1. 1. MedStar Washington Hospital Center, Washington, DC; 2. Washington Hospital Center, Chevy Chase, MD.

Intestinal pseudo-obstruction (Ogilvie Syndrome) represents a process where a patient presents with the signs and symptoms of a mechanical obstruction without any evidence of an actual mechanical cause. The most common causes include trauma, infection, medications, electrolytes disturbances, and cardiac disease. Little data exists for an association with CMV colitis. We present a 55 year old male with a history of HIV, who had stopped his HAART therapy for the last several months with a current CD4 count < 25, who was admitted for fevers and shortness of breath. The patient was found to have PCP pneumonia and was on appropriate treatment. Over the course of his hospitalization he developed abdominal distention with associated nausea, vomiting, and no stool output. A KUB revealed a dilated cecum to 8 cm leading to gastroenterology consultation. Based off of his clinical picture he was initially managed with conservative therapy – nasogastric tube decompression and bowel rest. Despite these measures the patient had persistent and worsening symptoms. He subsequently underwent a colonoscopy with plan for placement of a colonic decompression tube. During the colonoscopy, ulceration was noted on the ileocecal valve and was biopsied. Pathology from this biopsy revealed inclusion bodies consistent with CMV colitis. In addition, the patient’s serum CMV quantitative PCR came back positive at 1,410 IU/ mL. The patient was started on ganciclovir, and within 48 hours reported significant improvement in symptoms. This case highlights the importance of determining the underlying process behind intestinal pseudoobstruction as a means to guide therapy. CMV colitis represents a rare cause of Ogilvie syndrome, but this diagnosis should be considered in the immunocompromised patient.

Background: Trichuris trichiura is a type of roundworm that causes trichuriasis when it infects a human large intestine. It is commonly known as the whipworm, which refers to the shape of the worm. Most patients are not symptomatic, but most common symptoms are flatulence, weight loss, or diarrhea. Case: A 35-year-old Hispanic male with unremarkable medical history presented to the GI clinic with complaint of intermittent blood in the stool from 3 years ago. Episodes were painless, bright red blood, and mainly after defecation. He denied recent travel outside U.S. Patient denied nausea, vomiting, abdominal pain, fatigue, dysphagia, odynophagia, melena, poor appetite, weight loss or changes in bowel habits. On physical examination, vital signs were normal. Abdominal examination revealed a soft, nontender, nondistended abdomen with normal bowel sounds. There was no blood found on digital rectal exam. Fecal Occult Blood test was negative. Labs showed a normal CBC, basic metabolic panel. HIV tests were negative. Colonoscopy revealed a round parasite with inflammation around it. Several colon biopsies were obtained. Pathology report identified the parasite as Trichuris trichiura. Biopsy of the cecum revealed parasite with eggs, active colitis and eosinophilic infiltrates. The rest of the colon was found to be normal. Patient was prescribed Albenza with resolution of symptoms upon follow up. Conclusion: Although Trichuriasis is mostly seen in children residing in developing countries or in immunocompromised adults and is often asymptomatic, it should be considered as a rare cause of rectal bleeding in developed countries and immunocompetent adults as well.

[367A] Figure 1.

368 [366A] Figure 1.

The Stool Strikes Back: Fecal Transplantation for the Treatment of Clostridium difficile Infection Niket Sonpal, MD1, Samit Datta, MD2, Anish Mammen, MD3, Gregory Haber, MD3. 1. Lenox Hill Hospital, Happauge, NY; 2. North Shore-LIJ Lenox Hill Hospital, New York, NY; 3. Lenox Hill Hospital, New York, NY.

[366B] Figure 2.


Clostridium Difficile (CD) is a common hospital acquired infection that costs the healthcare system approximately 3 billion dollars per year. Approximately 10-25% of antibiotic-associated diarrhea is presumed to be secondary to CD. Treatment regimens have been well-defined for mild, moderate, and severe disease with Flagyl and oral Vancomycin as the mainstays of therapy. Following the initial recurrences, guidelines have not been well defined. The American College of Gastroenterology gives a conditional recommendation to consider the use of fecal microbiota transplant (FMT). FMT has been sporadically used in the United States since the early 1950s with recent FDA approval for the continued use in 2013. In this case, we present a patient who had resolution of her 4th recurrence and 3rd hospitalization of CDwith FMT. An 84-year-old female patient with presented with diarrhea that began one month prior to admission and was noted to be loose and watery stools with approximately 7-10 episodes per day. A recurrent positive C. Diff antigen on admission and was noted and the patient was started on a Vancomycin. This was the patient’s 4th episode of CD and therefore she was evaluated for FMT. She was tested for Ova and Parasites, stool culture, and Hepatitic/HIV, all of which were found to be negative.The patient then taken for an upper endoscopy to the level of the proximal jejunum for FMT. About 10cc sample of purified feces diluted to 60cc with sterile normal saline and was inserted into the proximal jejunum. The stool was obtained from our healthy system’s fully compliant stool donation for FMT system. She was then given one dose of loperamide following the procedure to allow microbiota growth. Following FMT, patient did not have any evidence of diarrhea for 48 hours following transplant and was safely discharged. CD s a severe hospital acquired infection that has a high cost burden to the United States healthcare system. Traditional therapeutic strategies have been shown to be very effective for initial infection however recurrence infections, especially those treatment failures should be considered for FMT.


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369 Isolated Sarcoidosis of the Gastrointestinal Tract Involving Multiple GI Sites Presenting as Chronic Diarrhea Lauren Stemboroski, DO1, Bilkisu Gaye, MPH, MD2, Emely Eid, MD3, Matthew Clark, MD3, Raafat F. Makary, MD, PhD2. 1. University of Florida Health College of Medicine, Division of Internal Medicine, Jacksonville, FL; 2. University of Florida Health College of Medicine, Jacksonville, FL; 3. University of Florida Health College of Medicine, Division of Gastroenterology, Jacksonville, FL. We present a 42 yo AAM with pmhx of recently diagnosed hereditary hemochromatosis and GERD, with complaints of abdominal pain and chronic diarrhea. He reported a 1.5 year history of loose, watery stools, which occur three times daily, denied rectal bleeding, fever or weight loss. Physical exam was unremarkable. Stool studies including ova and parasites, culture, fecal leukocytes and clostridium difficile were negative. Anti-transglutaminase and anti-endomysial antibodies, ESR, CRP and TSH were also negative. Colonoscopy revealed erythematous mucosa in the transverse colon and rectum; biopsies from the terminal ileum and each section of the colon revealed non-caseating microgranulomas that stained negative for acid-fast bacilli and fungi. EGD revealed diffuse erythema, erosions and duodenitis with non-caseating microgranulomas in the stomach and duodenum and H.pylori negative. CT of the abdomen and pelvis showed hepatosplenomegaly, however, recent liver biopsy did not show granulomas. CT enterography showed normal small bowel. CT Chest was unremarkable. Angiotensin converting enzyme was elevated. ANA, quantiferon gold, RPR, Tropheryma whippelii PCR, and Histoplasma antigen were negative. With a high suspicion for sarcoidosis, he was referred to rheumatology. He was lost to follow up, then returned two years later with abdominal pain and diarrhea, up to 15 episodes daily. The patient had a repeat EGD and colonoscopy, which again revealed non-caseating granulomas from the stomach to the left colon. Stains for Whipple’s disease and mycobacterium were negative. Prednisone 40 mg daily was started for likely GI sarcoidosis. Within three weeks, the patient reported his abdominal pain and diarrhea had resolved. Sarcoidosis is a granulomatous disorder that affects multiple organ systems and is characterized by noncaseating granulomas. GI sarcoidosis is an extremely rare entity of the disease and symptomatic involvement is even less frequent. When the GI tract is involved, the stomach is the most common site and the small intestine is the least common form of GI involvement. Colonic sarcoidosis has been reported in fewer than 20 cases. In addition to biopsies demonstrating non-caseating granulomas and no AFB or fungi, rapid improvement with corticosteroid therapy is supportive of the diagnosis. Diagnosing GI sarcoidosis is difficult, it is important to rule out other differential causes of granulomatous disease such as infection with mycobacterium, syphilis, Crohn’s disease, fungal infections, foreign body or idiopathic granulomatous reaction, prior to initiating therapy. The patient responded favorably to corticosteroid therapy, which highly supports the diagnosis of sarcoidosis. Our case is unique since the involvement of sarcoidosis was present throughout the GI tract (stomach, small intestine, and colon).

normal. Several epithelioid granulomas were noticed in the colonic biopsies and at least one granuloma was seen in the terminal ileum. The ileal mucosa was normal otherwise. Clinically, a diagnosis of microscopic form of inflammatory bowel disease was preferred over Crohn’s disease because of the lack of characteristic endoscopic findings. The patient was treated with budesonide starting at 9 mg/day for 30 days. At 1 month, his symptoms were almost completely resolved. He was then tapered to budesonide 6 mg/day for 4 weeks and then to 3 mg/day for 2 weeks and then stopped completely. At last follow-up, his diarrhea is completely resolved. Discussion: This case is unique because of the presence of granulomas in the setting of what otherwise appears to be microscopic colitis. Prior reports of granulomas in microscopic colitis have mostly described crypt rupture granulomas but granulomas seen in this case are well-formed, epithelioid granulomas. In retrospect, we think our case could be related to drug reaction because of the nature of the granulomas. Allopurinol could have been the culprit medication because of similar cases reported in literature. Our patient had been on allopurinol for several years prior to presentation. Since he responded well to a short course of budesonide, allopurinol was not stopped.

[370A] Figure 1.

[370B] Figure 2.

[369A] Figure 1.

370 Granulomatous Microscopic Colitis Due to Allopurinol Naveen Gara, MD1, Jose Crespo2, Thomas C. Smyrk, MD3, Darrell Pardi, MD, MS3. 1. Mayo Clinic College of Medicine, Mankato, MN; 2. Mayo Clinic Health System, Mankato, MN; 3. Mayo Clinic, Rochester, MN. Introduction: Microscopic colitis is a diarrheal Inflammatory Bowel Disease with essentially normal endoscopic findings in the colon but with significant chronic inflammation seen under the microscope in the form of Collagenous colitis or Lymphocytic colitis. We report a rare case of microscopic colitis with predominant granulomatous chronic inflammation. Case: A 77 year-old Caucasian male presented to the Gastroenterology clinic with explosive diarrhea and tenesmus for 10 months. He had Gout and Benign Prostatic Hypertrophy. His medications included allopurinol, tamsulosin, finasteride, aspirin 81 mg/day, fish oil, garlic, Viatmin D and atorvastatin. BMI was 39.1 kg/m2; abdominal exam was normal. Colonoscopy showed subtle loss of vascularity throughout the colon but no ulcers and normal appearing terminal ileum. Microscopic exam of the colonic biopsies showed diffuse mucosal inflammation with an abundance of lymphocytes in the crypt epithelium. Thickened collagen bands were seen focally in some biopsies from the right colon. The submucosa was


[370C] Figure 3.


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Abstracts

371 SURGIFLO to the Rescue: Endoscopy Assisted Human Thrombin Delivery for Hemostasis of Rectal Ulcers Niket Sonpal, MD1, Neal Mineyev, MD2, Lucy Martinek, MD2, Sonja Olsen, MD2. 1. Lenox Hill Hospital, Happauge, NY; 2. Lenox Hill Hospital, New York, NY. Lower gastrointestinal bleeding (LGIB) is a frequent cause of hospital admission and is a factor in hospital morbidity and mortality, and can result from bleeding diverticula, and even AV malformations. Ulcers can also occur, especially in immunocompromised patients, who are at risk for CMV or HSV induced ulcerations. We present a case of refractory rectal ulcer bleeding. A 66-year-old female with a history cryptogenic organizing pneumonia on steroids of recent metallic mitral valve replacement on heparin was noted to have continued rectal bleeding of several days, requiring 15 units of packed red blood cells to maintain perfusion. A full colonoscopy was performed that revealed 3 large crater-like ulcers with a “punched out” appearance with general mucosal friability and generalized oozing. No visible vessels were seen. Biopsies were performed which revealed viral inclusion bodies consistent with cytomegalovirus (CMV), and therapy was started. However the patient continued to bleed and require additional blood products to maintain her hematrocrit. Upper endoscopy was nonrevealing and so the decision was made to consider a repeat colonoscopy for hemostasis with topical hemostatic thrombin. A 22Fr Coude urinary catheter was used to safely access the sigmoid colon. The wide proximal end of the catheter was cut with scissors and the short tip luer lock applicator from the Floseal package was inserted into the end for a snug fit. Under direct visualization the modified Coude catheter was inserted along side the colonoscope, reaching the desired location of bleeding. 5cc of FloSeal and 5cc of SurgiFlo were prepared according to their included instructions. Once colonic bleeding was identified, the coude catheter was optimally positioned for sealant application into the bleeding ulcer beds. Both 5cc of SurgiFlo and 5cc of Floseal were attached to the luer lock and injected into the catheter. The stylet from the SurgiFlo endoscopic applicator was initially used to push the sealant contents through the catheter lumen with the small remaining amount being pushed through with air via syringe. No further bleeding was noted 48 hours after the procedure. We believe that the use of hemostatic matrices to topical bleeding lesions is a promising alterantive means of attaining hemostatis. We recommend further studies to validate the use of such compounds in the management of gastrointestinal bleeding.

[372B] Figure 2.

side effect of her chemotherapy regimen, the patient delivered a normal weight for gestational age child without complication. What is notable is that the patient’s prenatal course included office visits at 6, 12, 20, and 24 weeks with complaints of abdominal pain, constipation, and painful defecation recalcitrant to supportive therapy throughout the pregnancy. Therefore, it is important to recognize two lessons; 1) that a change in a gravid patient’s bowel habits and gastrointestinal complaints that are refractory to initial conservative therapy warrants further investigation for more serious secondary etiologies and are not be assumed to be physiologic nausea and emesis of pregnancy, and 2) chemotherapy for colon cancer in a 2nd trimester gravid patient has been used with little or no harm to the child in our patient as well as other case reports with short term follow-up (0-36 mos) and should be strongly considered.

372 Metastatic Colon Adenocarcinoma in a Gravid Patient Presenting as Persistent Constipation and Treated With Chemotherapy Vincent Petros, DO1, Matthew Maslonka, MD2, Nabiha Aziz, MD3, Michael Sedrak, MD3, Sreeram Parupudi, MD3. 1. University of Texas Medical Branch, Texas City, TX; 2. University of Texas Medical Branch, Galvetson, TX; 3. University of Texas Medical Branch, Galveston, TX. Case: A 26 year old Hispanic female at 26 weeks and 5 days gestation presented to the ER with constipation and right upper quadrant pain for two months. Ultrasound of the abdomen revealed enlarged liver with multiple masses. Laboratories were notable for Hgb 9.2, CA19-9 2836, CEA 694, AFP 200, AST/ALT 150/38. CT of the abdomen revealed an enlarged liver containing innumerable peripherally enhancing hypodense lesions as well as upper abdominal adenopathy that was consistent with metastatic disease. Colonoscopy found a 5 centimeter sigmoid colon mass, with histological examination of biopsy identifying moderately differentiated invasive adenocarcinoma. Liver biopsy confirmed metastasis from colorectal primary. In an attempt to get the patient to a point of safe fetal maturation for delivery, she underwent 5 cycles palliative chemotherapy with fluorouracil, oxaliplatin and leucovorin (FOLFOX) every two weeks from 27 weeks of gestation until 37 weeks when she delivered a healthy 6.4 pound baby girl without complications. Discussion: FOLFOX regimen typically used to treat Colon Adenocarcinoma has been reported to be used during pregnancy without harm to the child when followed from 2nd trimester prenatal until 3 years of age. We believe this is reassuring to treat colon cancer in pregnancy as early as 2nd trimester when organogenesis is complete and known published clinical vignettes reporting minimal or no harm to the child in short term follow up. Although intrauterine growth restriction was a possible

[372A] Figure 1.


373 Primary Adenosquamous Carcinoma of the Cecum: A Rare Entity Mihajlo Gjeorgjievski, MD1, Treta Purohit, MD2, Mitual Amin, MD2, Atulkumar Patel, MD, FACG2. 1. Department of Internal Medicine, Beaumont Health, Royal Oak, MI; 2. William Beaumont Hospital, Royal Oak, MI. A 65-years-old female with a 2 month history of fatigue and iron deficiency anemia was sent for a screening colonoscopy. Patient’s hemoglobin dropped to 8.9 g/dL from 11.4 g/dL in less than one year, despite patient being on iron supplementation. She denied any rectal bleeding, dark stools or change in bowel movements. There was no decrease in patient’s weight. Colonoscopy revealed a frond-like, villous, fungating, infiltrative mass in the cecum and infiltrative, polypoid mass at the hepatic flexure. Both of them were biopsied with the cecal mass revealing adenoma with areas of ulceration and stromal desmoplasia, which were suspicious for adenocarcinoma. A CT scan of the abdomen with contrast confirmed the large lobulated mass in the cecal lumen. It appeared to involve the proximal appendix as well as the terminal ileum. Patient underwent right colectomy with histology confirming an invasive colonic adenocarcinoma with squamous and mucinous differentiation. The squamous areas were stained positive for CK5/6 and accounted for approximately 25% of the tumor. The adenocarcinoma component was stained positive for CK20 and CDX2. There was also prominent mucinous component that accounted for 25% of the tumor.

[373A] Figure 1.


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375 An Unusual Case of Sigmoid Colon Gastrointestinal Stromal Tumor Miguel Lalama, MD, MPH1, Seth Lipka, MD2, Andrea C. Rodriguez, MD3, Reynaldo G. Geerken, MD, FACG4. 1. Digestive Diseases and Nutrition, Morsani College of Medicine, University of South Florida, Brandon , FL; 2. University of South Florida, Morsani College of Medicine, Division of Digestive Digestive Diseases and Nutrition, Tampa, FL; 3. University of South Florida, Morsani College of Medicine, Department of Internal Medicine, Tampa, FL; 4. James A. Haley Veterans Hospital, Tampa, FL.

[373B] Figure 2.

Adenosquamous carcinoma of the lower gastrointestinal tract is a rare malignancy representing only 0.06 percent of all colorectal and anal cancers. Mean age of appearance is 67 years with a female predominance, most commonly occurring in Caucasians. Hisitiogenesis is not fully understood with different theories including: malignant transformation of embryologic nests, presence of pluripotent stem cells with capability of multidirectional differentiation, squamous metaplasia of the intestinal mucosa as well as in situ transformation of squamous malignant neoplasm. Underlying condition is frequently involved into the process of squamous metaplasia and subsequent development of the tumor. Common conditions associated with adenosquamous carcinoma are: ulcerative colitis, human papilloma virus and radiation. There is no difference in clinical signs and symptoms of adenosquamous carcinoma when compared to adenocarcinoma. Both squamous and adenomatous components have a potential for metastasis, with squamous components metastasing more frequently. Paraneoplastic syndromes are common in this type of cancer, with hypercalcemia occurring very frequently. The prognosis of adenosquamous carcinoma is worse than the prognosis of colorectal adenocarcinoma with mean survival of 12 months. It is associated with higher overall morality and colorectal-specific mortality in comparison with adenocarcinoma. Surgical excision is the treatment of choice for adenosquamous carcinoma with adjuvant chemotherapy being part of every regimen.

Gastrointestinal stromal tumors (GIST), uncommon mesenchymal tumors, are driven by KIT or plateletderived growth factor receptor alpha (PDGFRA) mutations. They are most commonly diagnosed in older adults (median 62-63 years) presenting with GI bleeding or peptic ulcer-like symptoms, and most are found in the stomach (approximately 60%). GISTs are much more rarely diagnosed in the colon ( < 1%), with the sigmoid colon most commonly affected. We review the case of a 90-year-old white man who presented with one day of painless bright red blood per rectum. He denied abdominal pain, nausea, and vomiting. Past medical history included atrial fibrillation on warfarin, stroke, prostate cancer with retropubic radical prostatectomy, and hypertension. The patient was hemodynamically stable with a benign abdominal examination. Rectal examination revealed maroon blood but no hemorrhoids, fissures, or masses. Laboratory evaluation revealed hemoglobin 7.3 g/dL, WBC 7.6x10(9), INR 2.73, and creatinine 0.6 mg/dL. Electrolytes were unremarkable. A CT abdomen/pelvis revealed extensive bowel wall thickening focally, at the junction of the sigmoid and descending colon, with adjacent stranding (Figure 1). The patient underwent his index colonoscopy revealing a nearly-obstructing, necrotic, ulcerated mass with overlying clot 45 cm from the anal verge. (Figure 2). Several cold forceps biopsies were taken diagnosing a gastrointestinal stromal tumor, spindle cell subtype. Within the biopsy specimen there was no mucosal ulceration or mitoses and the ki-67 proliferative index was < 1%. By immunohistochemistry, the tumor cells expressed CD117 (c-kit), CD34, and SMA, and were negative for S100. Neither the c-KIT nor PDGFRA gene mutation was detected. Given the extent of disease and the patient’s comorbidities, surgical resection was not pursued and he was initiated on imatinib 400 mg daily. At six months the patient was tolerating therapy well aside from lower extremity edema, a common side effect of imatinib. An estimated 12-15% of adult GIST lack KIT and PDGFRA mutations, which are mutually exclusive, and are classified as wild type. This case highlights the importance of using several histopathology markers to aid in the diagnosis of GIST. Over 95% of GIST express CD117 and 70-90% also express CD34, as was seen in this case. Those with the mutations are more likely to respond to imatinib therapy, a tyrosine kinase inhibitor., which allows therapy to be individualized.

374 “I’ve Got What in My Colon?” Isolated Neuorfibroma on Screening Colonoscopy David DiCaprio, DO1, Angelica Nocerino, MD2, Robert Graham1, Ilan Weisberg1. 1. Lenox Hill North Shore-LIJ Hospital System, New York, NY; 2. North Shore-LIJ Lenox Hill Hospital, Bronx, NY. Neurofibromas are typically benign neoplasms of the peripheral nervous system that are commonly found in patients with neurofibromatosis type 1 and 2 (NF1 and NF2). Although rare, gastrointestinal neurofibromas can be found as an isolated entity without associated systemic findings. The case below is one of the few documented cases of isolated gastrointestinal neurofibromas in an asymptomatic patient. A 50 year old man was referred for an initial screening colonoscopy. The patient had no recent weight loss, abdominal pain, or change in bowel movements. On colonoscopy, he was found to have one sessile polyp in the rectum and another in the sigmoid, which were removed and sent for pathology. The rectal lesion was noted to be a hyperplastic polyp, and the sigmoid specimen showed to be a lamina propria neurofibroma, which was S100 positive on immunohistochemical staining. The patient denied any family or personal history of neurofibromatosis, and was referred to a neurofibromatosis specialist. An in depth exam was negative for cutaneous or mucocutaneous lesions and the conclusion was made that this was likely an isolated neurofibroma. NF1 and NF2 are autosomal dominant conditions that have 95% penetrance, so genetic testing is largely unnecessary and diagnosis is made clinically. They often involve systemic manifestations including the skin, nervous system, eyes, and GI tract. An intestinal neurofibroma, however, as a single pathological entity is very rare.The clinical presentation of GI neurofibromas often includes abdominal pain, constipation, or anemia. Serious complications including intussusception and perforation may result if left untreated. Only about 10 case reports of isolated neurofibromas have been described, and only two were noted to be asymptomatic, as in our patient. Biopsy followed by histologic analysis of these lesions is the gold standard for diagnosis. Histologically, tumor positivity for S100 suggests neurofibroma. Prompt local excision is the treatment of choice, as 2-16% of cases experience malignant transformation, which is concerning since colonic neurofibromas can be found in patients without a history of neurofibromatosis or gastrointestinal complaints. Because isolated lesions are so rare, there are no guidelines for surveillance. It is important for gastroenterologists to be aware that a neurofibroma may be an isolated finding, or the initial manifestation of a systemic disease, and that follow up is key.


[375A] Figure 1.

[375B] Figure 2.

376 Colonic Ischemia in a High-Performance Aircraft Pilot Adam Tritsch, MD1, Anthony Cochet, MD2, Craig Womeldorph, MD3. 1. Brooke Army Medical Center, Ft. Sam Houston, TX; 2. 47th Medical Group, Laughlin Air Force Base, Ft. Sam Houston, TX; 3. SAUSHEC Department of Gastroenterology, San Antonio, TX. Introduction: Those undergoing accelerated g-forces experience tissue ischemia due to pooling of blood within the extremities. While the most common side effect of accelerated g-forces is loss of consciousness, any part of the body at risk of decreased perfusion may be affected.


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Abstracts Case Description: A 23 year old Japanese male with no significant past medical history was sent to the United States for flight training at a local Air Force base. During a mission he reportedly experienced a gravitational force of 4.5 which was the highest yet in his training. Following the flight he immediately developed abdominal cramping with hematochezia that gradually improved over the following three days. Colonoscopy was performed and was significant for patchy, erythematous and edematous mucosa within the recto-sigmoid junction concerning for colonic ischemia and was otherwise normal. Biopsies of the affected areas were obtained and revealed non-specific lamina propria congestion which may be seen in healing colonic ischemia. The patient denied a personal or family history of thromboembolic disorders, tobacco use, recent travel, prescription or over the counter medication use. The patient was treated conservatively and was able to return to regular flight duty without any further incidents. Discussion: Colonic ischemia (CI) is not uncommon but is rarely reported in those who are healthy and younger than 50. The cause of CI is thought to be related to hypoperfusion followed by a reperfusion injury. Often times a specific cause for ischemia is not identified and the incident is attributed to non-occlusive ischemia. Risk factors for CI include hypoperfusion states such as heart failure, sepsis and physical activity, mechanical colonic obstruction, medications, and perioperative. A review of the literature reveals two case reports of adults who developed CI after transatlantic flights with no other risk factors identified. To our knowledge this is the first case report of CI following exposure to increased g-force.

377 Appearances Are Not Reality: A Rare Presentation of High-SAAG Malignancy-Associated Ascites

[377B] Figure 2.

Alan Urbina, MD1, Ena Mahapatra, MD1, Ferah Ciftci, MD1, John Erikson Yap, MD1, Benjamin Go, MD1, Bashar M. Attar, MD, PhD, FACG2. 1. John H. Stroger Jr. Hospital of Cook County, Chicago, IL; 2. John H. Stroger Jr. Hospital of Cook County/Rush University Medical Center, Chicago, IL. Malignancies that originate or metastasize to the abdomen can produce ascites by several mechanisms. As compared to cirrhosis, which is the most common cause of ascites in the US accounting to 85% of cases, malignancy-related ascites occurs only in 7% of cases. The serum-ascites albumin gradient (SAAG), which has 97% accuracy, is an excellent initial test to help differentiate the causes of ascites. 49-year old man with known alcohol abuse was admitted for abdominal pain, weight loss and intermittent non-bloody diarrhea for 4 months. His exam and laboratory analysis were unremarkable. Ultrasound showed mild liver enlargement and small amount of ascites, negative for hepatic/portal vein thrombosis. CT scan revealed evidence of colitis and abscess. Colonoscopy showed an erythematous lesion at the ileo-cecal valve, but pathology did not show any cryptitis, crypt abscesses or granulomas. Antibiotics were started and our patient was discharged with follow-up. He was re-hospitalized due to persistence of his symptoms. Examination was significant for cachexia, tense ascites, tender right lower quadrant and bilateral lower extremity edema. Patient underwent multiple large volume paracentesis and fluid analysis showed high-SAAG ascites and total protein < 2.5 g/ dL. However, there was no radiologic or biochemical evidence of cirrhosis. His presentation was concerning for malignancy. Multiple Esophagogastroduodenoscopies done were noncontributory, but repeat colonoscopy showed a partially obstructing circumferential narrowing with villous projections at 15 cm from anal verge. Peritoneal fluid analysis was positive for malignancy and exploratory laparotomy revealed diffuse peritoneal carcinomatosis. Omental biopsy demonstrated invasive poorly differentiated adenocarcinoma. Patient was deemed poor prognosis and expired 5 months afterwards. It has been seen in a study that 95% of patients with peritoneal carcinomatosis in absence of any liver metastasis or cirrhosis have a SAAG less than 1.1. The total protein in ascitic fluid with peritoneal carcinomatosis is usually higher than 2.5 and can be as high as 4.0. Using SAAG to narrow our differentials is a validated initial step, however it should always be interpreted in the context of the entire clinical scenario. It’s always reasonable to rely on alternative diagnostic tools when our clinical suspicion points towards a different direction as there is no perfect test. We present a patient with high SAAG ascites with no radiological or biochemical evidence of portal hypertension with a fluid total protein < 2.5g/dL.

The range of clinical severity with which Salmonella colitis presents may make differentiating it from inflammatory bowel disease challenging. A 32-year-old male who was otherwise healthy presented to the Emergency Department with 5 days of bloody diarrhea, tenesmus, cramping lower abdominal pain, and myalgias. The patient also described nocturnal bloody diarrhea and lack of appetite. Vital signs revealed a low grade fever, heart rate of 56 and a blood pressure of 101/65. Physical examination was notable for decreased skin turgor and tender abdomen with rectal examination revealing bright red blood. Laboratory examination revealed elevated CRP and ESR without leukocytosis or anemia. Stool cultures were sent for analysis. CT scan was performed and revealed left-sided contiguous inflammation with thickened folds, adjacent soft tissue stranding, and prominent vasa recta from the rectum to distal transverse colon. The distribution of disease on cross sectional imaging favored a diagnosis of ulcerative colitis. Because the patient was ill appearing with marked abdominal pain, hematochezia and signs of dehydration, he was admitted for further evaluation. Flexible sigmoidoscopy was performed to further evaluate the colitis seen on CT. This showed marked loss of vascular pattern, severe friability, multiple erosions and linear ulcerations from the rectum to distal transverse colon. Biopsies of the sigmoid and rectum exhibited diffuse acute inflammation with focal cryptitis, multiple foci of crypt abscess again raising concern for possible ulcerative colitis. The patient was treated with hydration and empiric antibiotics. On the third day of admission, stool culture results returned positive for nontyphoidal salmonella. The patient improved clinically and was discharged home. Follow up sigmoidoscopy was performed six weeks after discharge to evaluate for underlying ulcerative colitis. Endoscopic appearance was normal and biopsies revealed mild cryptitis without crypt abscesses or architectural distortion further validating there was no underlying inflammatory bowel disease present. The case illustrates how severe salmonella colitis may appear clinically and histologically similar to inflammatory bowel disease. It highlights the

[377A] Figure 1.

[378A] Figure 1.


378 A Severe Case of Salmonella Colitis Mimicking Ulcerative Colitis Marnonette Marallag, MD1, Amitkumar Patel, MD1, Stacie Vela, MD2. 1. Banner - University Medical Center, Phoenix, AZ; 2. Phoenix VA Health Care System, Phoenix, AZ.


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[379A] Figure 1.

pain to constant, watery rectal discharge. Treatment options also varied, but the majority of patients eventually needed a colostomy. It is imperative that the clinician always approach gastrointestinal complaints with a broad perspective, and keep metastatic cancer on the differential.

[378B] Figure 2.

380 Diminutive Polyps Indicating Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma on Biopsy in an Asymptomatic Patient Undergoing Colonoscopy Rohit Anand, MBBS1, Anita Sivaraman, MD2, Rakesh Vinayek, MD1, Roberto Martinez, MD1. 1. Sinai Hospital of Baltimore, Baltimore, MD; 2. Sinai Hospital of Baltimore, Hunt Valley, MD.

[378C] Figure 3.

importance of stool culture, histologic findings, and response to antibiotics in differentiating dysentery from inflammatory bowel disease.

Introduction: Chronic lymphocytic leukemia (CLL) is one of the most common leukemias in asymptomatic adults. Small lymphocytic lymphoma (SLL) is defined as CLL with predominant involvement of the lymph nodes. In some patients with primary colonic adenocarcinoma undergoing surgery with lymph node biopsy, pathology has revealed CLL/SLL. However, in asymptomatic patients undergoing screening colonoscopy, there are no reported cases of benign-appearing mucosal polyps found to be CLL/SLL. Case Presentation: A 61-year-old man underwent routine screening colonoscopy. His last colonoscopy in 2005 was unremarkable. He denied weight loss, rectal bleeding, abdominal pain, or systemic symptoms. Pre-procedure laboratory data showed a leukocytosis of 28,500 cells/mcL with 77% lymphocytes. On screening colonoscopy, the colonic mucosa had a nodular, cobblestone appearance with a few scattered polyps throughout the colon (Figure 1). A few small flat 2 mm polyps in the ascending colon and multiple diminutive flat polyps in the descending colon were removed by cold biopsy forceps and the pathology was consistent with SLL. He was referred to medical oncology for further evaluation. Flow cytometry showed monoclonal B-cells with an immunophenotype consistent with CLL/SLL, expressing CD5 and CD 23, with dim surface immunoglobulin and CD20 expression. Bone marrow biopsy showed multiple small lymphoid aggregates throughout, consistent with CLL/SLL. FISH was positive for 13q deletion. Contrast CT revealed diffuse abnormal lymphadenopathy in the neck, thorax, retroperitoneum, abdomen, and pelvis, without hepatosplenomegaly. He was diagnosed with CLL/SLL, RAI stage II with low risk cytogenic features. Discussion: Gastrointestinal (GI) involvement in CLL is uncommon ( < 5%). One case reported new CLL diagnosis with further workup identifying nodularity of colonic mucosa. Another patient reportedly had known CLL and presented with diarrhea, prompting endoscopic evaluation and identifying GI involvement. However, this case illustrates a unique GI manifestation of CLL/SLL in an asymptomatic patient. Some GI experts feel that obtaining biopsies of multiple diminutive < 2 mm polyps is unnecessary. The DISCARD study states that diagnosis during endoscopic visualization alone may be sufficient to assess polyp histopathology and surveillance intervals for polyps < 10 mm in size. Had our patient’s endoscopically benign-appearing polyps not been biopsied, CLL/SLL diagnosis may have been missed, thus supporting the need for continued analysis of all biopsies.

379 A Rare Case of Metastatic Urothelial Carcinoma Presenting With Rectal Obstruction Sheela Reddy, MD, Cuckoo Choudhary, MD. Thomas Jefferson University Hospital, Philadelphia, PA. Purpose: Urothelial carcinoma of the bladder is the fourth most common malignancy in men, and has metastatic potential, with the most common sites of metastasis being lymph nodes, bone, lungs, liver, and peritoneum. This is a rare case of metastatic urothelial carcinoma presenting with rectal obstruction. Methods: Case report and literature review. Results: We discuss here the case of a 59-year-old gentleman with a history of urothelial carcinoma of the kidney and bladder that was diagnosed 24 years ago and treated with BCG. Subsequently, he had involvement of both the ureters, and underwent resection as well as chemotherapy. The patient was referred to our institution for evaluation of new onset diarrhea. He had battled constipation for a few months, which responded to an aggressive bowel regimen. He had, however, noted that even after he stopped his bowel regimen, the diarrhea persisted and then started worsening. He reported having more than 10-20 liquid bowel movements daily, with some associated mild, crampy, lower abdominal pain. He also noted increased urgency, and decreased control over his bowel movements. Moreover, in the weeks preceding his appointment, the patient started wearing diapers, as he had developed almost continuous leakage of thin, yellowish, watery, stool. He was started on cholestyramine for symptomatic relief, and had an outpatient CT scan done showing gas and solid stool debris in ascending, transverse, and descending colon. The rectum and sigmoid colon were noted to have diffuse circumferential thickening, with extension into the anus. Subsequent colonoscopy demonstrated an area of annular constriction in the rectosigmoid, with biopsies consistent with metastatic urothelial carcinoma. Conclusion: It is unusual for metastatic urothelial cancer to present with rectal obstruction, and, to date, there are eight other case reports of patients with metastatic bladder cancer presenting with annular rectal constriction. Similar to our patient, the majority of these patients presented with symptoms of rectal obstruction, with symptoms varying from change in bowel habits with narrow caliber stools and rectal


[380A] Figure 1.


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381 A Case for Pathologic Blastocystis Hominis Mark Pence , DO1, Manish B. Singla, MD2, Steven P. Armbruster , MD3. 1. Walter Reed National Military Medical Center, Silver Spring , MD; 2. Walter Reed National Military Medical Center, Bethesda , MD; 3. Naval Hospital Jacksonville, Jacksonville, FL. Introduction: Blastocystis hominis is an anaerobic enteric protozoan parasite observed in humans and animals worldwide, with its highest prevalence in developing countries. It is thought to be spread via fecal-oral transmission. Since its discovery in the early 1900s, the clinical implications of Blastocystis have been debated as to whether or not it is pathologic and causes symptoms. We present a patient with abdominal discomfort, bloating, and diarrhea that argues for a pathogenic role of Blastocystis. Case: A 64-year-old male with a history of hereditary hemochromatosis presented with high frequency loose stools, nausea, and bloating for 2 months. The patient’s hemochromatosis was well controlled with no evidence of cirrhosis. Stool culture and Clostridium difficile toxin assay. Serum tissue transglutaminase IgA antibody was negative. Ova and parasite fecal testing was positive for Blastocystis hominis. The patient was treated with metronidazole 500mg three times daily for ten days with no improvement in symptoms. Repeat stool testing showed persistence of Blastocystis. The patient was then treated with a 7 day course of trimethoprim/sulfamethoxazole, and his symptoms improved for a period of time. Unfortunately, a few months later his symptoms of bloating and loose stools recurred. Testing for stool ova and parasites again showed persistence of Blastocystis. The patient was treated with one dose of 2g of tinidazole, and his symptoms resolved. Follow up stool testing showed eradication of Blastocystis. To date, the patient has had no further recurrence of bloating or loose stools. Discussion: The majority of individuals inoculated with Blastocystis are asymptomatic. This has led many to believe that the organism is not pathologic. A minority of patients with Blastocystis can develop symptoms of abdominal discomfort, bloating, and diarrhea; this may be secondary to co-infection with other pathogens, or may be related to the magnitude of parasite load. Our patient had persistence of symptoms with continued positive stools for Blastocystis until his third trial of therapy. Once his infection was eradicated, he had complete resolution of all symptoms. This case illustrates the potential for Blastocystis to be pathologic and how treatment should be approached for symptomatic patients. Author Disclosure: None.

[382B] Figure 2.

382 An Unusual Presentation of Peutz Jeghers (PJ) Rahul Nayani, MD, MPH1, Divyangkumar Gandhi, MD2, Getachew Mekasha, MD3. 1. Howard University Hospital, Falls Church, VA; 2. Howard University Hospital, Hyattsville, MD; 3. Howard University Hospital, Washington, DC. A clinical diagnosis of PJ syndrome is usually made when a patient has two or more characteristic PJ polyps or any number of PJ polyps detected in an individual with family history of PJS in close relatives or characteristic mucocutaneous pigmentation in an individual who has a family history of PJS in close relatives or any number of PJ polyps in an individual who also has characteristic mucocutaneous pigmentation. We report here an atypical presentation of PJ in an elderly 57 year old Black male who presented to the clinic with intermittent bright red blood mixed with stools for a few months associated with vague abdominal discomfort. Pt never had a screening colonoscopy before. He denied any weight loss or change in bowel habits. He had no past medical history and was not taking any medications. Family history was significant for paternal grandmother and great grandfather “having colostomy bags” for unknown reasons. Physical exam including rectal exam was unremarkable with normal oral mucosa. Labs revealed mild anemia with Hb 12.4. Colonoscopy showed multiple ulcerated polyps measuring 0.5 cm to 2.5 cm in mid and distal sigmoid colon and biopsies showed sessile serrated and tubular adenomas. Repeat colonoscopy was performed for polypectomy, but was complicated by bleeding. Biopsies showed inflammatory myoglandular polyps & serrated adenomas. Subsequently, patient underwent subtotal colectomy with ileorectal anastomosis. Histopathology of the colectomy specimen showed multiple hamartomatous polyps of Peutz-Jeghers type which was confirmed by a second independent pathology lab. Upper endoscopy was only remarkable for intestinal metaplasia on biopsy and CT abdomen/pelvis with contrast was negative for any small bowel polyposis. A few months later, the patient presented with hoarseness of voice and biopsy of a false vocal cord lesion showed high grade dysplasia necessitating

[382C] Figure 3.

subtotal resection of the vocal cord. This case highlights the possibility of late presentation of Peutz Jeghers without the characteristic mucocutaneous lesions and also the fact that inflammatory myoglandular polyps can mimic the appearance of Peutz Jeghers polyps by also having an arborizing pattern of radially arranged smooth muscle. The concurrent finding of multiple adenomatous polyps in this patient could be hypothesized to be supportive of the previously proposed hamartoma-adenoma-carcinoma pathway.

383 Ischemic Colitis Associated With a Male Enhancement Drug Kirbylee K. Nelson, MD1, Kimberly Kolkhorst, DO, MA2, Jennifer Reed, MD3, Reynaldo G. Geerken, MD, FACG3. 1. Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL; 2. University of South Florida, Department of Gastroenterology, Tampa, FL; 3. James A. Haley Veterans Hospital, Tampa, FL.


Ischemic colitis often poses a challenge to diagnose and treat in a timely manner. While intestinal injury is most frequently due to hypotension or hypovolemia, offending medications can also contribute. Currently, there are no studies or cases evaluating the role of phosphodiesterase type 5 inhibitors (PDE5 inhibitors) inducing ischemic colitis. We describe the first case of ischemic colitis associated with use of a PDE5 inhibitor analog, the male sexual enhancement drug Libigrow. A 35-year-old male with no significant past medical history presented with the sudden onset of nausea, abdominal cramping, tenesmus, and multiple episodes of bright red blood per rectum. Orthostatic vital signs were positive and exam was notable for epigastric and left lower quadrant tenderness. Rectal exam was unremarkable. Laboratory analysis was notable for mild leukocytosis (11.2 x 109/L), normal hemoglobin, and normal erythrocyte sedimentation rate and c-reactive protein. Abdominal radiograph was non-contributory. Colonoscopy showed diffusely erythematous, friable, and edematous mucosa with skip lesions and prominent lymphoid aggregates in the terminal ileum. Multiple random biopsies revealed benign colonic mucosa with lamina propria hyalinization, telangiectatic capillaries, acute inflammation, and reparative epithelial changes. Histologic changes were consistent with a resolving


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[383A] Figure 1.

[384A] Figure 1.

[383B] Figure 2. [384B] Figure 2. ischemic pattern of injury, likely drug induced. There were no features of inflammatory bowel disease identified. Based on pathology findings, the patient was further questioned about over the counter and illicit drug use, at which time he admitted to intermittent use of a male sexual enhancement drug, Libigrow. He was instructed to quit using the supplement, with repeat colonoscopy and biopsies three months later revealing normal colonic mucosa with resolution of drug-induced colitis. Medications, including over the counter supplements, can induce colonic ischemia. PDE5 inhibitors are known to lower blood pressure, thereby potentially compromising colonic blood flow. Pathologic findings seen in our patient correlated with both early and later lesions found in ischemic colitis, which is consistent with intermittent use of the offending agent. This case demonstrates the importance of adequate medication reconciliation, including herbal supplements, as well as patient education on potential side effects.

384 Angiotensin Converting Enzyme Inhibitor-Induced Angioedema Isolated to the Colon Mazen Shobassy, MD, MPH1, Salman Khan, MD2, Wendell Clarkston, MD1. 1. University of Missouri, Kansas City, MO; 2. University of Missouri School of Medicine, Kansas City , MO. Angioedema is self-limited, localized subcutaneous or submucosal swelling that can affect areas with loose connective tissue. Angiotensin converting enzyme inhibitor (ACEi) induced angioedema typically affects the face, lips, mouth and throat. ACEi induced angioedema isolated to the small bowel has been reported in previous case reports. To our knowledge, no prior reports have illustrated ACEi induced angioedema isolated to the colon. We present an atypical presentation of acquired angioedema in an 87 year old Caucasian female who presented with complaints of lower abdominal pain and bright red blood per rectum for one day. She had been having symptoms of diarrhea and lower abdominal pain intermittently for three months. Ischemic and infectious workups were negative. Sigmoidoscopy with biopsies showed a generalized edematous colon and internal hemorrhoids. Mucosal biopsies showed only generalized edema with no evidence of infiltration or malignancy. Hematochezia was attributed to internal hemorrhoids. When lisinopril and losartan were discontinued, her symptoms quickly resolved. After six months the patient continued to be symptom free. Although acquired angioedema of the small bowel is an established complication, it is under-diagnosed. ACEi-induced angioedema of the large bowel has been listed as a complication in the literature, but to our knowledge never formally reported. The diagnosis is primarily clinical as there is no test available to confirm the diagnosis. This case report serves to highlight this rare complication with hopes of limiting morbidity and mortality from complications due to unnecessary invasive procedures.



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385 Case Report: Tubulovillous Adenoma With Secretory Diarrhea Responding to NSAIDs Jeremy Louissaint, MD1, Yecheskel Schneider, MD2, David W. Wan, MD3. 1. Washington University Internal Medicine, St. Louis, MO; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, Brooklyn, NY; 3. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY. A 74-year-old male presented with diarrhea. He noted a >3 month history of intermittent (~4/day) loose stools (watery, small-volume, non-bloody) that recently increased in frequency (1/hour). He denied any unintentional weight loss. No recent travel, changes in diet, or antibiotic use. No nausea, vomiting, or rhinorrhea. The patient’s mother died of colon cancer at 86 years of age. Initial labs showed hyponatremia (129), hypokalemia (2.8), hypochloremia (83), WBC >20, BUN 148, Cr 4.5, and Hgb 17.4. An infectious workup (O&P, Stool Cultures, C. diff Toxin,) was sent and returned negative. CT imaging revealed an irregular, asymmetric circumferential thickening of the wall of the distal sigmoid colon and rectum concerning for a colonic mass. Colonoscopy revealed 3 medium-sized, semi-sessile, non-bleeding polyps in the sigmoid colon, the ascending colon, and the cecum. A large partially obstructing mass was seen in the anus. Small sessile polyps were seen throughout. Biopsy results indicated tubular adenoma with areas of villous features. Follow-up EUS confirmed a 20X35X17mm mass located 5cm from the anal verge and occupying 70% of the wall circumference. In the setting of possible secretory diarrhea secondary to a tubulovillous adenoma, indomethacin was started with a remarkable decrease in bowel movements. Along with fluid resuscitation, the use of indomethacin was associated with correction of the patient’s electrolyte disturbance and kidney injury. Most colonic polyps are asymptomatic, however tubulovillous adnenomas can cause a diarrhea with significant fluid and electrolyte losses. The diarrhea observed is rich in electrolytes (Na, K), and this secretory diarrhea is believed to be driven by the secretagogue, Prostaglandin E (PGE)2. The McKittrickWheelock Syndrome describes the clinical scenario of oversecretion of fluid/electrolytes in association with a villous adenoma. Hallmarks of the syndrome – secretory diarrhea with dehydration, hyponatremia, hypokalemia – can lead to renal (AKI, metabolic acidosis), CNS (seizures), cardiac (arrhythmias), and musculoskeletal complications, that require prompt fluid resuscitation3. Another treatment method uses the observed pathophysiology and seeks to counteract PGE2. Using Indomethacin, a PGE antagonist, reductions in fluid losses as high as 50% can be achieved4; thus preventing the massive fluid losses and organ dysfunction seen in McKittrick-Wheelock Syndrome.

partially obstructing rectosigmoid lesion which was biopsied, but pathology was non-diagnostic. CT abdomen and pelvis revealed a 3-cm intraluminal mass in the mid-sigmoid colon and a 4-cm well-circumscribed mass in the right adnexa. A pelvic ultrasound confirmed a complex right ovarian cyst, as well as a left hemorrhagic ovarian follicular cyst. Labs revealed normal CBC, CMP, CEA and CA-125 levels. The patient was referred to colorectal and gynecologic oncology surgery, and subsequently underwent robotic-assisted low anterior resection of the rectosigmoid colon with anastomosis, and total laparoscopic hysterectomy with bilateral salpingo-oophorectomy. Surgical pathology of the rectosigmoid colon ultimately revealed endometriosis involving the entire thickness of the bowel wall with focal extension into the mucosa. On follow up visits, the patient reported complete resolution of rectal bleeding and constipation. Discussion: Intestinal endometriosis rarely affect the entire thickness of the bowel wall, making endoscopic biopsies typically futile. In cases where mucosal endometriosis was confirmed with endoscopic biopsies, patients were post-menarche women with cyclic gastrointestinal symptoms and hematochezia, similar to our patient. Despite initial non-diagnostic endoscopic biopsies, our patient did prove to have mucosal involvement of the colon on surgical pathology. Symptomatology of cyclic rectal bleeding and severe constipation in post-menarche women may be an indication of transmural involvement of intestinal endometriosis and should be considered in the differential diagnosis. Moreover, these patients may benefit from more thorough endoscopic sampling which may improve the diagnostic yield of endoscopy.

386 Remote Recurrence of Colonic Adenocarcinoma Presenting as an Isolated Mass in the Pancreatic Head: A Case Study Michael Green, MD, Stephanie Pankow, MD, Najla Itani, MD, William Salyers, MD, MPH. University of Kansas School of Medicine, Wichita, KS. Pancreatic masses are usually primary tumors with metastasis representing only 1.8-7.6%. Colorectal cancer (CC) is the third most common cause of cancer death in the United States. The five year survival and recurrence rates are dependent upon the staging at the time of diagnosis but the incidence of recurrent CC is reported at 20-30% with 80% of recurrence occurring within the first two years of diagnosis and treatment. At the time of diagnosis, 20% of patients have distant metastasis, most commonly to regional lymph nodes, liver, lungs, and peritoneum. Metastasis of colonic adenocarcinoma (CA) to the pancreas is relatively rare and metastasis presenting 5 years from prior treatment is far more uncommon. We present a case of metastatic CA to the pancreas 5 years after initial diagnosis. An 80-year-old white female with a history of presumed stage II CA status post right-hemicolectomy five years ago, presented with cramping of the left lower quadrant. The patient reported 50 lb. weight loss over the prior three months but denied change in bowel habits. Computed tomography demonstrated uncomplicated left sided diverticulitis and a 3.2 x 2.9 cm soft tissue mass in the pancreatic head. Serum CEA was markedly elevated at 99.1 ng/mL with CA19-9 mildly elevated at 236 unit/mL. Endoscopic ultrasound revealed an irregular, hypoechoic mass measuring 30 x 30 mm in the pancreatic head and neck with poorly defined borders. There was evidence of invasion into the superior mesenteric vein and artery. Fine needle aspiration was positive for adenocarcinoma with immunohistochemical staining positive for CK20 and CDX diffusely and negative for CK7, chromogranin, and synaptophysin in a pattern consistent with CA of metastatic origin rather than primary pancreatic adenocarcinoma. Palliative chemotherapy was initiated but the patient opted to pursue hospice care after one cycle. Despite the fact that the identification of pancreatic lesions has become more feasible with the advent of EUS, the management of such lesions, particularly when metastatic in nature, remains unchanged. Depending on size and location, some metastatic lesions of CC can be surgically resected if detected early. In general, most professional societies differ with regards to post-treatment CC surveillance but all are in agreement that the minimum window should be five years. Although rare, metastasis should be suspected in any patient with a history of CC and newly detected pancreatic mass.

[387A] Figure 1.

[387B] Figure 2.

387 Transmural Rectosigmoid Endometriosis Causing Rectal Bleeding and Partial Colonic Obstruction Geoffrey You, MD1, Avik Sarkar, MD2, Aaron Bernard, MD2. 1. Rutgers Robert Wood Johnson Medical School, Newark, NJ; 2. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ. Introduction: Intestinal endometriosis occurs in 10% of endometriosis cases. Most patients are asymptomatic while some may experience non-specific gastrointestinal symptoms. Diagnosis is challenging due to lack of characteristic clinical, radiological, and endoscopic findings. Endoscopic biopsies are rarely helpful as intestinal endometriosis frequently involves deeper layers of the bowel wall. We report a rare occurrence of transmural rectosigmoid endometriosis and its unusual presentation as rectal bleeding and partial colonic obstruction. Case Presentation: A 46 year-old-woman presented with six months of severe constipation and hematochezia that worsened monthly, around the time of menstruation. Colonoscopy revealed a circumferential and


388 Noninvasive Colonic Phaeohyphomycosis Caused by Exophiala Oligosperma in a Patient With Crohn’s Disease Pratik Naik, MD, Michael Goldberg, DO, Rupal Mody, MD. William Beaumont Army Medical Center, El Paso, TX. Introduction: Exophiala oligosperma is an uncommon fungal pathogen which can cause infection in immunocompromised patients. The majority of these infections are cutaneous, but fatal systemic infections have been reported. There are no reported cases of E. oligosperma causing colonic infection in the literature. To the best of our knowledge, this is a first reported case of an E. oligosperma induced non-


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invasive colonic phaeohyphomycosis in an immunocompromised patient with Crohn’s disease treated successfully with voricanozole. Case Report: A 27 year old female with Crohn’s disease on adalimumab and prednisone presented with persistent fever for three weeks. Index Crohn’s symptoms were improving since initiation of adalimumab but diarrhea continued. The patient had no abdominal tenderness. Labs were remarkable for only mild anemia. After extensive work up, only colitis was noted on an abdominal computed tomography (CT) scan. A colonoscopy was done to attempt to further assess source of fever which showed worsened sigmoid colitis with pseudopolyps. Random biopsies showed infl ammation. Multiple tissue samples cultured grew black mold with speciation consistent with E. oligosperma. Tissue biopsies did not show invasive fungal elements. Adalimumab was discontinued and patient was started on voricanozole. Fever resolved and the patient reported improvement in diarrhea after starting antifungal therapy. Discussion: E. oligosperma is a fungal strain that was indentified in 2003 by de Hoog et al.There are only six reported cases of phaeohyphomycosis associated with E. oligosperma in the literature. Cutaneous infections are more common with this pathogen but invasive infections are reported, including prosthetic valve endocarditis, dialysis-associated peritonitis, and disseminated infections. We describe a case of noninvasive colonic phaeohyphomycosis associated with E. oligosperma manifested by fever and gastrointestinal symptoms. Gross appearance of colon mucosa can look inflamed or darkly pigmented. Tissue culture is often needed for diagnosis. Histological finding of granulation suggests invasive infection. Superficial colonic mucosal infection can be treated with voricanozole; however, invasive phaeohyphomycosis usually requires surgical resection.

[389C] Figure 3.

389 Non-familial Visceral Myopathy: An Atypical Presentation Mimicking Crohn’s Disease Celeste P. Pizza, MD, Kasra Adham, MD, Douglas J. Grider, MD, Alan Brijbassie, MD. Virginia Tech Carilion School of Medicine, Roanoke, VA. Introduction: Visceral myopathy is a very rare, poorly understood entity of the gastrointestinal tract mimicking various causes of acute abdomen. Case Presentation: A 40 year-old-female with a chronic history of recurrent partial small bowel obstruction deemed secondary to adhesions presents in extremis with cross sectional imaging defining high grade small bowel obstruction with concern for a transition point. Urgent exploratory laparotomy defines cecal volvulus with right hemicolectomy and ileo-colic anastomosis being per-

formed. Pathology reveals non-caseating granulomas in the ileum as well as within adenopathy in addition to evidence of marked enteritis (Figure 1). She was empirically treated as an acute flare of Crohn’s disease with systemic corticosteroids; however, her post-operative course was complicated by recurrent episodes of obstruction suspected at the anastomosis as defined on repeat cross sectional imaging. Ileoscopy fails to demonstrate an obstruction at the anastomosis. Her subsequent hospital course was complicated by pneumonia with acute respiratory failure requiring intubation, candida esophagitis, and fungemia in the setting of systemic corticosteroid use, and pulmonary embolism. Further pathological review demonstrates findings consistent with visceral myopathy (Figure 2) as the etiology of her acute presentation and prior episodes of intestinal pseudo-obstruction. Secondary autoimmune and mixed connective tissue etiologies were excluded during her comprehensive evaluation. Conclusion: Non-familial visceral myopathy is a rare clinical entity with scant available literature to define clinical outcomes. This case highlights an atypical mimicker of Crohn’s disease where early recognition may have proven critical to avoid associated morbidity. Visceral myopathy should be considered in any patient with recurrent episodes of intestinal pseudo-obstruction.

390 Strangulating Fallopian Tube Presenting as Isolated Right-Sided Colon Ischemia Elvin Hardy1, James Morris, MD2, Arthur Poch3, James Howell4. 1. LSU Health Shreveport, Department of Medicine, Section of Gastroenterology and Hepatology, Shreveport, LA; 2. Louisiana State University Health Sciences Center, Shreveport, LA; 3. Gastrointestinal Specialists, AMC, Shreveport , LA; 4. Bossier Surgical Associates, Bossier City, LA.

[389A] Figure 1.

A healthy 55 year old lady with a past medical history of a benign left ovarian tumor s/p resection 10 years ago presented to the emergency department with sudden onset of sharp right lower quadrant abdominal pain. A plain abdominal x-ray and CT scan of the abdomen and pelvis showed diffuse large dilated fluid filled loops of bowel involving the small bowel and colon raising concern for obstruction. Colonoscopy revealed ischemic and necrotic changes isolated to the cecum confirming suspicion of ischemic colitis. Colonoscopy was noted to have a tortuous right colon. Post-operative surgical diagnosis was a cecal volvulus arising from a strangulating right fallopian tube wrapping around the ascending colon causing ischemia and necrosis. The patient underwent a right hemicolectomy with right salpingectomyoophorectomy. This case demonstrates a rare occurrence, which has only been reported a limited number of times in our literature search. Ischemic colitis is the most common form of gastrointestinal ischemia, but isolated right sided ischemic colitis is a rare entity occurring in only 10 percent of cases. Patients usually present with abdominal discomfort and bloody diarrhea. Mucosal/nongangrenous ischemia requires only supportive measures and medical management, whereas transmural/gangrenous ischemia may require prompt surgical intervention. Patients with this pattern of colon involvement require surgical intervention twice as often as and have a mortality rate five times greater than patients with involvement of other areas of the colon. One must exercise a high index of clinical suspicion in order to ensure prompt surgical intervention.

391 Diverticular Disease in a Transposed Colon Gustavo Churrango, MD, Jose Churrango, MD, Sami Samiullah, MD, Zamir Brelvi, MD, PhD. Rutgers New Jersey Medical School, Newark, NJ.

[389B] Figure 2. The American Journal of GASTROENTEROLOGY

44 year-old man with a history of VACTERL with an esophagocoloplasty at age 8, presenting with acute dysphagia of both liquids and solids. This occurred after he swallowed a large piece of turkey. Urgent endoscopic evaluation revealed colonic type mucosa with folds and normal vascular pattern. Also noted, were multiple diverticulum, of various sizes. A food bolus was seen obstructing the lumen of the transposed colon and the impaction was relief with a Roth Net. VACTERL, described in 1972 by Quan and Smith, is an acronym that stands for bony spinal column (V), atresias in the gastrointestinal tract (A), congenital heart lesions (C), tracheoesophageal defects


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Abstracts (TE), renal and distal urinary tract anomalies (R) and limb lesions. The frequency has been estimated between 1/ 10,000 and 1/40,000 infants with large variations as there are multiple diagnostic criteria. Diverticular disease is one of the most common GI disorders. It is the thought that its pathogenesis is multifactorial. Anomalies in motility, environmental factors such as diet and heredity are the main categories implicated in the pathogenesis of diverticulosis. If in fact these factors are involve in the pathogenesis of diverticulosis in a colon in its normal habit, what is their role in the development of diverticular disease in the transposed colon of our patient. Since he had surgery early in life, it is assumed that he did not had diverticulosis at the time when the surgery occurred. In addition, studies has shown that peristaltic contractions are absent in the interposed colon. This negates the theory that colonic motility is involve in the development of diverticuli. It is even more difficult to consider environmental factors as a cause of diverticuli since this case demonstrates that divercular disease can occur even when the habit of the colon is different as in a transposed colon. Therefore, this case provides support that hereditable factors may be the most influential contributors to the pathogenesis of diverticulosis.

392 A Rare Presentation of Lymphangioma in a Patient With Hematochezia Sajiv Chandradas, MD1, Walter Coyle, MD2. 1. Scripps Green Hospital, San Diego, CA; 2. Scripps Green Hospital, La Jolla, CA.

[391A] Figure 1.

Lymphangiomas are rare benign cysts caused by congenital malformation of the lymphatic system. The incidence of lymphangiomas is between 1.2:1,000 to 4:10,000 births per year. Amongst lymphangiomas 80-90% originate from the head and neck. Intra-abdominal lymphangiomas make up about 5% of lymphangiomas. There is no specific data on the incidence of colonic lesions. We present a case of a 38

[391B] Figure 2.

[392A] Figure 1.




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year old female with no significant past medical history presenting with bright red blood per rectum. The patient had been having issues with chronic hematochezia since her teenage years, which had been attributed to hemorrhoids. The patient denied any early satiety, nausea, vomiting, unintentional weight loss, or black stools. Physical exam was unremarkable, except for a palpable mass on rectal exam. Laboratory evaluation revealed a microcytic anemia, but otherwise was within normal limits. She had never before undergone endoscopic evaluation. The patient subsequently underwent a full colonoscopy that revealed an extensive network of cyst like structures from just proximal to her dentate line to 15 cm. These lesions were examined radiographically, endoscopically, and via endoscopic ultrasound (EUS). EUS and MRI investigations demonstrated extent of disease down into the perirectal fat region, but with no invasion of adjacent structures. Biopsies of the lesion revealed multiple areas of dilated lymph vessels extending into the muscularis mucosae lined with endothelial cells, diagnostic of lymphangioma. The approach to treatment of lymphangiomas is varied, from conservative expectant course to sclerosant injections and aspiration, to surgical resection. There are reported cases of spontaneous regression, up to 15-20%. Recurrence rates of 50% are reported with surgery. Although very rare, there is a potential risk for malignant transformation. The patient ultimately elected for the expectant course. This case demonstrates a rare cause for hematochezia, which emphasizes the importance of a broad differential diagnosis, and the need to not discount patient’s symptoms regardless of prior evaluations.

393 Non-occlusive Mesenteric Ischemia Complicated by Intramural Hematomas: A Case Report

[393B] Figure 2.

Panida Piyachaturawat, MD, Satimai Aniwan, MD, Rungsun Rerknimitr, MD. Gastrointestinal Endoscopy Excellence Center, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok, Thailand. Introduction: Acute mesenteric ischemia (AMI) often mimics coagulopathy related intestinal intramural hematomas because their similar clinical settings and imaging features. However, their managements are difference. We report a case of non-occlusive mesenteric ischemia (NOMI) complicated by transmural hematoma. Case Presentation: A 49-year-old woman was admitted to the intensive care unit because of septic shock. She had an underlying diseases of undifferentiated connective tissue disease and severe pulmonary hypertension. She presented with fever, hypotension, respiratory failure and acute kidney injury. She received ventilator support, renal dialysis and a high dose intravenous of the combination of norepinephrine and adrenaline for maintaining her hemodynamic condition. Three days after admission, she developed abdominal distension and mucous bloody stool. Physical examination showed fever, marked abdominal distension, and absence bowel sound. Laboratory results showed platelet count 5,000/uL, prolong prothrombin time with INR at 1.58, and prolonged activated partial thromboplastin time 51.3 sec (control 26 sec). Stool examination demonstrated WBC 20-30 cell/mm3, RBC 10-20/mm3, negative C. difficile toxin test, and negative culture for bacterial pathogen. A computed tomography of abdomen demonstrated dilated and thickened bowel wall at the ileum and ascending colon with intramural hematomas. Pneumatosis intestinalis and ascites were demonstrated. (Figure 1) The vascular structures (SMA, SMV, IMA and IMV) were patent. Therefore, NOMI complicating bowel infarction with spontaneous intramural hematomas was diagnosed. She underwent an emergency surgery. The operation showed a gangrenous colon and distal ileum. The remaining bowel was non-gangrenous ischemia. Total colectomy with end ileostomy was successfully performed. Pathology revealed transmural hemorrhagic necrosis of the colon, appendix, and terminal ileum. (Figure 2) Unfortunately, she died from multiple organ failure a week later. Discussion: This patient initially presented with septic shock requiring inotropic drugs. With poor perfusion status, she was susceptible to AMI. While her condition had been worsening; she developed disseminated intravascular coagulation (DIC) on top of NOMI. As AMI progressed, an element of intramural hemorrhage could be seen. A combination of medical history, physical examination, and laboratory values are all important in establishing the correct diagnosis and activating the prompt treatment. AMI may necessitate emergency intervention to restore blood flow whereas coagulopathy related intramural hematoma requires medical management to correct coagulopathy.

394 Incidence of Ischemic Colitis in Patient Using Alosetron for IBS MHD Hussam Al Jandali, MD1, Maliha Naseer, MD2, Hussam Sabbagh, MD3, Eyoel Abebe, MD2, Alaeddin Maeza, MD2. 1. Wayne State University, Internal Medicine Department, Auburn hills, MI; 2. Wayne State University, Internal Medicine Department, Rochester , MI; 3. Wayne State University, Internal Medicine Department, Rochester, MI. Introduction: Ischemic colitis, a hypoperfusive injury to the bowel with numerous etiologies is a diagnosis to entertain in patients with sudden onset abdominal pain and hematochezia. The incidence of ischemic colitis is difficult to ascertain, as most cases are transient, not reported or misdiagnosed. Alosetron (Lotronex) is a medication prescribed for patients with severe diarrhea-predominant irritable bowel syndrome (IBS). The association of Alosetron and ischemic colitis is controversial in the current medical literature. We hereby present a case of acute ischemic colitis in a patient who was on Alosetron for IBS. Case: A 70-year-old Caucasian lady with a past medical history significant only for IBS on Alosetron presented to ED with generalized abdominal pain of 5-days duration which was followed by three episodes of bright red blood per rectum. Colonoscopy performed was evident for ischemic colitis. Stool culture, Clostridium difficile toxin, and Entamoeba histolytica adhesion antigens were negative as was her cardiac work up. Patient was managed conservatively with bowel rest, intravenous fluids and empirical antibiotics. Her pain resolved with conservative measures and was able to tolerate soft diet by the third day. She was eventually discharged on the 4th day in good condition. Discussion: Alosetron, a 5-HT3 receptor antagonist in the enteric nervous system has been used for the management of severe, diarrhea-predominant IBS. It was withdrawn from the market in 2000 owing to the occurrence of serious life-threatening gastrointestinal adverse effects but was reintroduced in 2002 with restricted use. The incidence of ischemic colitis and serious complications of constipation among patients using Alosetron is very low and is rarely reported. Ischemic colitis among patients using Alosetron should be considered as one of the serious life-threatening complications. Conclusion: Ischemic colitis should be regarded as one of the complications related to using of Alosetron in patients who have IBS, and it should be taken into account as one of the causes of ischemic colitis.

[393A] Figure 1.



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395 Appendiceal Adenocarcinoma Masquerading as an Ovarian Mass: A Case Report Kalpesh G. Patel, MD, PharmD1, Samik Shah2, Sowjanya Kanna3, Ravi Chokshi, MD4, Mark A. Galan, MD4, Michael F. Demyen, MD5. 1. Rutgers New Jersey Medical School, Caldwell, NJ; 2. Rutgers New Jersey Medical School, Pennington, NJ; 3. Rutgers New Jersey Medical School, Jersey city, NJ; 4. Rutgers New Jersey Medical School, Newark, NJ; 5. Rutgers New Jersey Medical School, Hoboken, NJ. Introduction: Primary appendiceal carcinomas are rare neoplasms of the gastrointestinal tract that have seen an increase in diagnosis over the past 10 years. The most common presentation is acute appendicitis or abdominal distension, although occasionally they may present as an adnexal mass due to their anatomical location. We present a case report of the diagnosis of an appendiceal adenocarcinoma found on colonoscopy that presented as a gynecological neoplasm. Case: A 77 year old female was referred to the office from gynecological oncology for evaluation an 8cm x 7cm right pelvic mass seen on CT scan. The CT was ordered due to complaints of several months of weakness, 30lb weight loss, and intermittent localized right lower quadrant abdominal pain. The mass was extensive and was causing deviation of her bladder and severe right-sided hydroureter. A colonoscopy done about 10 years ago was normal. History was significant for right-sided breast cancer status post right radical mastectomy, total abdominal hysterectomy, and 25 pack year history of smoking. Her family history was positive for esophageal cancer in her mother, but denied breast, ovarian, gastric, and colon cancers. Her vitals were within normal limits. Her abdominal exam was significant for tenderness to palpation in the right lower quadrant with fullness. On pelvic exam, there was a large, non-tender, fixed right-sided adnexal mass. Lab studies revealed CEA = 416.2; CA125 = 11; and CA 19-9 = 1. A colonoscopy was performed prior to her planned surgical resection. Initial observation was unremarkable, including examination of the distal terminal ileum. The markedly elevated CEA level and location of the lesion warranted more aggressive investigation, and the appendiceal orifice was gently probed with a closed cold forceps. This revealed a large friable, appendiceal mass which was biopsied. The biospies revealed adenocarcinoma, with markers suggesting colon over ovarian etiology. An attempt was made to resect the tumor, but due to the extent of the disease and co-morbidities, this was not done and a palliative bypass was performed. Discussion: In this case, based on the right lower quadrant/pelvic mass, ovarian and colonic tumors were considered. On colonoscopy, care was given to search for tumors, particularly inside the appendiceal orifice. With a known elevated CEA in a patient with a right lower quadrant mass, a diagnosis of appendiceal adenocarcinoma was able to be made preoperatively on colonoscopy. Diagnosis of appendiceal adenocarcinoma is rarely made on colonoscopy and is often found incidentally on appendectomy.

Case: A 40-year-old homosexual male with history of HIV on highly active antiretroviral therapy (HAART), presented with one week of intermittent rectal bleeding. The rectal bleeding began during anal intercourse and progressed over several days with accompanied malaise, chills, intermittent diaphoresis, and fever of 101 F. He also complained of left lower quadrant pain, rectal pain, and diarrhea. The physical exam was notable for tachycardia and tenderness in the left lower quadrant of his abdomen. Rectal exam revealed a perianal papular lesion, rectal tenderness, and no gross blood in the rectum. Laboratory tests are included in Table 1. CT abdomen and pelvis revealed descending colitis, proctitis, and enlarged perirectal and pelvic lymph nodes. Colonoscopy revealed proctitis with an ulceration. Endoscopic biopsy showed multifocal acute cryptitis, crypt microabscesses, and prominent lamina propria plasmacytosis. Histopathologic findings were suggestive of syphilitic proctosigmoiditis. Once the patient was diagnosed with syphilis, he received 2.4 million units of intramuscular penicillin G. There was no evidence that the patient acquired the infection within the last year; therefore, he was treated for late latent syphilis with intramuscular penicillin G, at weekly doses of 2.4 million units for a total of 3 weeks. Conclusion: As the incidence of syphilis is reported to be on the rise, it is essential for clinicians to be attentive to the signs and symptoms of syphilis. High suspicion should be maintained for patients such as MSM and HIV infected patients. It is crucial for clinicians to take a thorough sexual history to elucidate further risk factors and possible exposure sites. Thus, our case demonstrates that maintaining a low threshold for an infectious cause in the setting of a patient’s risk factors can lead to a timely diagnosis and appropriate treatment for patients.

[397] Table 1. Laboratory Values WBC count

13.6 K/ul, no left shift

Hemoglobin

14.7 g/dl

Rapid plasma reagin assay (RPR)

Positive

Treponema pallidum particle agglutination (TP-PA)

Positive

CMV PCR

Negative

Gonorrhea/Chlamydia RNA amplification Absolute CD4 count HIV 1 viral load

Negative 599 cell/ul 221 copies/ml

396 Skinning the Cat Twice: Refractory CDI in an Solid Organ Transplant Patient Requiring 2 Fecal Microbiota Transplants Sarah Ordway, MD1, Nieka Harris, MD2, Roy Wong, MD1. 1. Walter Reed National Military Medical Center, Bethesda, MD; 2. Walter Reed National Military Medical Center, Rockville , MD. Background: Recurrent clostridium difficile infection (CDI) remains a management challenge occurring in up to 20% of affected patients. Fecal microbiota transplantation (FMT) has been shown to be safe and efficacious in patients with recurrent CDI. There is a paucity of literature describing the efficacy and safety of FMT in solid organ transplant (SOT) patients. Case Presentation: A 64 year-old immunocompromised (IC) male with ESRD due to poorly controlled DMII and hypertension status-post living donor kidney transplant 8 years ago who presented with abdominal pain, 10 loose foul smelling stools daily and a positive C. difficile polymerase chain reaction (PCR) following antibiotic exposure for hospital acquired pneumonia. After failing a trial of metronidazole, transitioned to oral vancomycin (OV) with return to his baseline bowel movements (one formed stool per day). Two weeks later, he developed recurrent CDI (RCDI) with appropriate response to OV. He later developed pyelonephritis responsive to antibiotics but hospital course complicated by severe RCDI with endoscopic evidence of pseudomembranous colitis (PC). Declining FMT, he was transitioned to fidaxomicin 200mg BID for 20 days, followed by a 4-week vancomycin taper (VT) per Infectious Disease recommendations, with stools gradually returning to normal. Two weeks following VT he developed mild-moderate CDI with endoscopic evidence of PC, refractory to vancomycin. Patient underwent FMT via colonoscopy with baseline bowel moments the following day. Relapse within 72 hours prompting a second FMT was with return to baseline without evidence of recurrent infection for more than 6 months. Discussion: SOT recipients suffer a higher frequency of CDI, and tend to have more severe disease. RCDI proves clinically challenging in this population. Current transplant literature is notable for a case report with RCDI in a renal transplant patient 3 months post-transplant with response to FMT but nothing beyond that time frame. Additionally a retrospective case series of 66 immunocompromised patients was presented at the October 2013 American College of Gastroenterology meeting which include 20% SOT patients with 79% success rate with initial FMT. In this case report we present a renal transplant patient greater than 8 years out with refractory CDI responsive to sequential FMT without recurrence for 6 months post second FMT. This case suggests SOT recipients with RCDI who fail intial FMT may have more severe alterations in their intestinal microbiome and may benefit from sequential FMT.

[397A] Figure 1.

397 A Case of Syphilitic Proctocolitis in a Man With HIV Raman Bhalla1, Faisal Sheikh2. 1. North Shore-LIJ, NY; 2. North Shore-LIJ, Syosset , NY. Introduction: Primary and secondary syphilis are rare diseases in the current age, but there has been a rise in recent years. Notably, from a nadir of 2.1 cases per 100,000 in 2000-2001, there has been an increase in the overall rate from 2005-2013 with recent estimates of 5.3 cases per 100,000. Two major identified risk factors associated with exposure to syphilis include HIV infection and men who have sex with men (MSM).Though syphilis is a relatively uncommon cause of proctitis or colitis, we present a case of syphilitic proctocolitis in a male with a history of HIV and MSM.



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Colorectal Endometriosis Presenting as Proctalgia and Rectal Bleeding

Going All the Way: Endoscopic Full-thickness Resection (EFTR) of a Rectal Mass

Amaninder Jeet Singh. Dhaliwal, MD1, Taruna Bhatia, MD 2, Kinesh Changela, MD3, Garen Derhartunian, MD4, Yitzchak Moshenyat, MD1, Sury Anand, MD3. 1. NYU Lutheran Medical Center, Brooklyn, NY; 2. Mount Sinai/The Brooklyn Hospital Center, Brooklyn, NY; 3. The Brooklyn Hospital Center, Brooklyn, NY; 4. NYU Lutheran Medical Center, Glendale, CA.

Niket Sonpal, MD1, Anish Mammen, MD2, Gregory Haber, MD2. 1. Lenox Hill Hospital, Happauge, NY; 2. Lenox Hill Hospital, New York, NY.

Background: Endometriosis is defined as the seeding of endometrial glands and stroma at the extrauterine sites. These glands are mainly located in the pelvis but can also be found in the other parts of the body. Endometriosis is the one of the most common cause of chronic pelvic pain in women of reproductive age leading to debilitating symptoms. Here we report a case of 40 year old female with possible colorectal endometriosis. Case Report: A 40-year-old female with no co morbidities presented with multiple episodes of bloody stools for one day. As per patient, one day prior to admission, she reported proctalgia with menstrual periods. Few hours later, she had three episodes of bloody bowel moments (BM) which were bright red in color accompanied with blood clots which were similar to her menstruation. On arrival to ER at our facility her Hg was noted to be 11 gm/dl. She reports of having dysmenorrhea, dyspareunia, rectal and leg cramps since past year and was given a diagnosis of endometriosis by her gynecologist and was placed on medical therapy leuprolide depot monthly. She continued the treatment for 3 months with relief of her symptoms but self discontinued. On admission, vital signs were stable and physical exam was unremarkable. Rectal exam was grossly normal with no signs of active bleeding or hemorrhoids. Fecal occult blood testing was positive. Colonoscopy showed erythematous and beefy looking polypoid mass partially obstructing the lumen at 20 centimeters from the anal verge. Biopsy results were negative for any dysplasia or malignancy. Pt was discharged to follow up with gynecologist an outpatient for possible laparoscopy for the evaluation of endometriosis. Discussion: Endometriosis can present as debilitating symptoms in women of reproductive age. The pathogenesis of endometriosis is unclear and is thought to be due to retrograde menstruation. The most common sites for endometriosis are pelvis, sigmoid colon, abdominal cavity and rarely in thoracic and central nervous system. In majority of cases, laparoscopy is required but definitive diagnosis can be made only on histological evaluation of the specimen. The pre-operative diagnosis of colorectal endometriosis is difficult because of no definitive clinical and radiological findings that are suggestive or characteristic of this disease. Early recognition of symptoms suggestive of colorectal endometriosis should be made for more efficient therapeutic approach and better outcomes.

Endoscopic full-thickness resection (EFTR) is a minimally invasive method for en bloc resection of gastrointestinal lesions, such as early cancer or submucosal tumor. We present a case of young female with early rectal cancer treated successfully with EFTR of a rectal mass with clear margins on pathologic review. A 46-year-old female presents for initial screening colonoscopy. The patient had no GI complaints, and but her family history was significant for colorectal cancer in her father prior to the age of 50, but she had been delayed in obtaining a colonoscopy. An index screening colonoscopy was performed which a 3 cm semi-sessile mass was seen in the rectum about 1.5 cm from the anal verge. The mass was non circumferential and located at the posterior bowel wall. Biopsies of the rectal polyp revealed adenocarcinoma without lympho-vascular invasion. The large rectal mass was referred to our institution for resection, as the patient did not wish to undergo surgery. The periphery of the mass was injected submucosally with a solution of hyaluronic acid, hypertonic saline and methylene blue in order to raise the lesion and obtain an appropriate resection cushion. After a proper lift had been obtained, submucosal dissection was started. The dissection of the lesion began in the periphery moving towards the center. The 1.5 dual knife was used to create the initial mucosal incision and then dissect the submucosa with swift coagulation and endocut modes as deemed necessary. After the periphery of the lesion had been dissected, the center of the lesion was injected further with hyaluronic acid, hypertonic saline and methylene blue in order to raise the lesion. However, the center of the lesion did not raise well and it was difficult to separate the lesion from the muscularis. It was necessary to dissect through the muscularis to remove the lesion. The dissection was carried on until the whole lesion was resected completely. There was a 2 cm defect in the rectal wall afterwards. Apollo overstitch was used to close the defect using 4 running sutures. Pathology revealed moderately differentiated adenocarcinoma with clear mucosal margins. The patient did well after the procedure and has had no further complications. EFTR as a technique can achieve a full-thickness tumor resection with reliable closure of the bowel wall, but further refinements of the technique and device are necessary in order to reliably resect submucosal lesions, especially larger ones.

[398A] Figure 1.



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400 Acute Ischemic Colitis and Portal Vein Thrombosis in a Young Female Smoker on an Oral Contraceptive John Hunninghake, MD1, Brian Murray, DO2, Pedro A. Manibusan, Jr., DO, MBA3, Scott McNear, MD4, John Gancayco, MD5. 1. US Air Force, San Antonio Military Medical Center, San Antonio, TX; 2. San Antonio Military Medical Center, San Antonio, TX; 3. Brooke Army Medical Center, Ft. Sam Houston, TX; 4. San Antonio Military Medical Center, JBSA Ft. Sam Houston, TX; 5. US Air Force, JBSA Ft. Sam Houston, TX. Previous studies have shown an increased risk of arterial and venous thrombosis in the mesenteric vasculature in patients using an oral contraceptive pill (OCPs) that includes estrogen. While a few case series since the 1980s have detailed the severity of intestinal ischemia caused by this phenomenon, this case report highlights the important clinical features of a mesenteric thrombosis. Patient is a 23-year-old female who presented with a 1-day history of multiple syncopal events followed by acute onset abdominal pain and bloody diarrhea. Her PMH was significant for an H pylori infection treated three years prior. On admission, her only medication was an estrogen-including OCP. She reported smoking about one pack-per-day of cigarettes for the past year. Pertinent GI family history included colorectal cancer in a grandfather and two paternal uncles. Her stool studies were negative for an acute infection. CT imaging demonstrated wall thickening along the entire descending colon, nonspecific intrahepatic biliary duct dilation in the right hepatic lobe, and bilateral sacroiliitis. Follow-up MRCP visualized a portal vein thrombus without evidence of collateralization. Diffuse circumferential inflammation from the proximal sigmoid to the distal transverse colon was found on colonoscopy. Random biopsies demonstrated surface degeneration and withering of surface crypts, consistent with brisk acute inflammation. Due to the acute ischemia presumbly from a thrombus, the patient was started on coumadin with a weight-based lovenox bridge. Her abdominal pain improved without recurrence of bloody diarrhea. She was eventually discharged in stable condition. A laboratory workup for an inherited thrombophilia was ultimately negative. The etiology of the patient’s “reversible” acute ischemic colitis was attributed to a transient occlusion in the mesenteric vasculature, as suggested by the portal vein thrombosis and the patient’s clinical recovery. While the CT result was more consistent with an IMA distribution, the colonoscopy’s watershed findings suggested a vascular blockage at the SMA/IMA junction due to the spared sigmoid colon and rectum. The incidence of thromboembolic events in the mesenteric vasculature, which result in reversible ischemic colitis or progression to intestinal infarction, have been documented less as a complication of OCPs due to the decreasing estrogen dose. However, the combination of an estrogen-containing OCP with regular tobacco use caused an acquired hypercoagulable state placing this patient at higher risk for a mesenteric thrombosis. The combination of OCPs and smoking increase the risk for thromboembolism, which can result in transient reversible ischemic colitis if a thrombosis occurs in the mesenteric vasculature.

[401B] Figure 2.

cm in diameter (Fig. 2). The mass was highly suspicious for malignant mucocele. Multiple biopsies were obtained. The rest of the colon examination was not significant. Histopathology exam showed adenocarcinoma. The patient was referred for evaluation by multidisciplinary oncology team for further evaluation of the malignant esophageal and malignant appendiceal mucocele. Conclusion: The diagnosis of appendiceal mucocele can be suspected during colonoscopic exam of the appendiceal orifice. Mucosal ulceration favors the diagnosis of malignant rather than benign appendiceal mucocele.

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Endoscopic Appearance of Benign Versus Malignant Appendiceal Mucocele

Conservative Management of an Impacted Capsule Within the Appendiceal Orifice

Tariq Hammad, MD1, Yaseen Alastal, MD1, Turki Alkully, MD1, Basmah Khalil, MD2, Luis DeLasCasas, MD1, Mohammad Hammad, MBBS1, Ali Nawras, MD, FACG1. 1. University of Toledo Medical Center, Toledo, OH; 2. University of Toledo, Toledo, OH.

Ali Haider, MD, Sarosh Bukhari, DO, Kenneth O’Riordan, MD. Advocate Lutheran General Hospital, Park Ridge , IL.

Introduction: Appendiceal mucoceles are group of rare non-neoplastic or neoplastic cystic lesions characterized by an enlarged, mucus-filled appendix. Here we present two cases of incidentally found benign and malignant mucoceles. Case 1: A 62-year-old male underwent screening colonoscopy. He denied any gastrointestinal symptoms. Physical exam was unremarkable. The colonoscopy exam was normal except for a glossy, rounded, protruding mass arising from the appendiceal orifice that didn’t flatten with air insufflations (Fig. 1-A). Overlying mucosa was normal. Probing with the biopsy forceps revealed a hard lesion. The biopsy revealed normal mucosa. Abdominal computed tomography (CT) scan showed a low attenuation, wellencapsulated round cystic mass in the right lower quadrant adjacent to the cecum with no other abnormalities (Fig.1-B). The patient was diagnosed with appendiceal mucocele and underwent laparoscopic appendectomy. Intraoperative evaluation and surgical pathology confirmed the diagnosis of benign appendiceal mucocele (Fig. 1-C). Case 2: 70-year-old Caucasian male with history of Barrett’s esophagus was recently diagnosed with welldifferentiated adenocarcinoma of the esophagus. As a part of tumor staging, he had abdominal CT scan which incidentally revealed cystic mass in the right lower quadrant adjacent to the cecum. So the patient underwent colonoscopy which showed ulcerated mass involving the appendiceal orifice measuring 1.5

A fifty year old female with a history of anemia presented with acute worsening of chronic abdominal pain. She admitted to some nausea but no other associated complaints. She had a normal physical exam apart from mild right quadrant abdominal tenderness with palpation. Laboratory work was significant for a hemoglobin of 11.7 g/dl. Gallbladder ultrasound and Computed Tomography scan of the abdomen were normal. Upper endoscopy revealed mild gastropathy with duodenitis. Given her prior work up, a capsule endoscopy was done to exclude concerns for a small bowel etiology such as Crohns disease. The capsule report revealed a tortuous small bowel and the cecum was not visualized on the images. As the capsule was not retrieved, an abdominal X-ray confirmed a retained capsule in the right lower abdominal quadrant. Multiple attempts were made at flushing the capsule out with purgative agents and enemas. As serial abdominal X-rays confirmed the retained capsule even after several days, colonoscopy was performed to retrieve the capsule (Fig1). Upon endoscopic examination of the cecum, the capsule was noted to be lodged within the appendiceal orifice (Fig 2). We were able to dislodge the capsule using aggressive washing maneuvers and applying gentle pressure around the base of the capsule with the Roth net catheter. The Roth net was then used to remove the capsule from the colon. The patient did well subsequently and was discharged for outpatient follow up. Capsule endoscopy has become the accepted modality for evaluating small bowel pathology. Capsule retention is a complication with an overall incidence of 1-2%. Individuals with Crohn’s disease are at highest risk for capsule retention (13%) versus

[401A] Figure 1.



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x3.1 cm mass and moderate intra and extra hepatic biliary dilation with abrupt narrowing of the CBD in head of pancreas without any obvious peri-ampullary mass. Inspite of intussusception seen on CT scan, he did not have any symptoms of obstruction and was tolerating diet and having normal bowel movements. Colonoscopy was performed which showed near obstructing sigmoid colon mass. Colorectal surgery was involved and performed low anterior resection. Biopsy of the mass showed adenocarcinoma of colon, stage T2NOMO. Patient eventually underwent MRCP, brushings showed adenocarcinoma of CBD. Discussion: Based on the segments of intestine involved, intussusception is divided into enteric, ileocolic type, ileocecal and colocolonic types. A lead point such as tumor is present in 70-90% of adult intussusception in contrast to children where 90% cases are idiopathic. Tumors are the most common cause of intussusception in adults consisting of 60-75% of the cases, 75% of which are malignant-both primary and metastatic. Adenocarcinoma of colon is the most common cause of colocolonic intussusception. Unlike children, who present with acute abdomen, most adult patients present with subtle or chronic symptoms including nausea, vomiting, general malaise, poor feeding, diarrhea, abdominal pain, palpable abdominal mass and melena. Some present with partial or complete intestinal obstruction. Owing to the non-specific symptoms and signs, intussusception can be missed pre-operatively and often times are diagnosed during exploratory laparotomy. CT abdomen has 80-99% accuracy in detecting the site, level and cause of obstruction and also in detecting the viability of intestines. Management of adult intussusception requires consideration of the extent and anatomic location, underlying cause of intussusceptionbenign vs malignant. However, since most AI has underlying pathological lesions, many of the surgeons agree with laparotomy.

404 Buried Adenocarcinoma Masquerading as a Refractory Rectal Stricture Raghav Sood, MD, Ravi Prakash, MD, David Arboe, MD, Hemangi Kale, MD. MetroHealth Hospital, Cleveland, OH.

[402A] Figure 1.

45 year old African American female with a long standing history of Crohn’s colitis (involving the descending and sigmoid colon with perianal fistulas) and medication non-compliance presented with worsening constipation for months. Patient was not on medications at the time of presentation, but has a history of treatment with asacol, azathioprine and infliximab. Patient denied fevers, nausea, vomiting or rectal bleeding. Colonoscopy revealed a 5 cm long tight rectal stricture about 10 cm from the anal verge along with extensive pan colitis and normal small bowel. Biopsy of the stricture revealed inflammatory infiltrate. MR enterogram revealed a tight rectal stricture with enhancement indicating inflammation. Patient was treated with high doses of prednisone followed by infliximab infusions along with endoscopic dilations to which she had minimal response. This was followed by injection to infliximab directly into the rectal stricture with limited response. Patient was referred for surgery where she underwent abdominal perineal resection of rectum with end-colostomy. The stricture appeared benign on macroscopic examination but pathology reports revealed intra-strictural adenocarcinoma and normal overlying mucosa. She had to undergo repeat surgery for complete resection followed by radiation and chemotherapy. Discussion: The association between inflammatory bowel disease (IBD) and colorectal cancer (CRC) is well-known and has been widely described in literature. The risk of malgnancy is directly related to the severity of perianal involvement, extent of disease and its time course. In CD the risk is estimated to be around 30% after 25 years of diagnosis and noted to be higher in patients who receive the diagnosis before the age of 30. Our patient had long standing crohn’s colitis, which was uncontrolled due to medication non-compliance. In addition, she was a smoker which increases the risk of malignancy. The stricture was biopsied multiple times on endoscopy and imaged with MR enterogram, which failed to reveal malignancy. Even during surgery, the surgeon did not suspect malignancy on gross examination as the mucosa appeared normal. The pathology specimen (see figure) demonstrates buried glands with adenocarcinoma interspersed within the stricture. Overlying mucosa appears normal. This is the first report where we describe a case of adenocarcinoma buried within the stricture with normal overlying mucosa. It is important for clinicians to have a high suspicion of malignancy in strictures which fail to respond to intensive therapy.

[402B] Figure 2.

obscure GI bleeding patients with lowest risk. A thorough literature review revealed one other case report of an impacted capsule that was caused by appendicitis requiring an appendectomy. We demonstrate here in this case report the conservative management of an impacted capsule within the appendiceal orifice of a patient without any known bowel pathology, which, to the best of our knowledge, has not been previously described in the literature.

403 Colocolonic Intussusception: A Rare Entity in Adults Naga Saranya Addepally, Jagpal Singh Klair, MD, Mohit Girotra, Farshad Aduli. University of Arkansas for Medical Sciences, Little Rock, AR. Background: Intussusception is defined as telescoping of proximal segment of gastrointestinal tract into the lumen of subsequent segment. While it is a leading cause of intestinal obstruction in children, in adults it only accounts for 5% causes of intestinal obstruction and most of the times is asymptomatic. Case: A 66 year old white male who is a former smoker presented to ED with 10 day history of jaundice, pruritus, dark urine along with unintentional weight loss of 12-15 pounds over 4 months. In addition, he had one episode of bright red blood mixed with stools. His LFTs were consistent with obstructive pattern with TBil 4.2, ALP 1942, ALT 568, and AST 411. A CT abdomen showed distal colon thickening with telescoping appearance suspicious for colo-colonic intussusception in mid sigmoid region along with 2.8


[404A] Figure 1.


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[404B] Figure 2.

[405A] Figure 1.

[404C] Figure 3.

405 Colo-colonic Intussusception as the First Presentation of Diffuse Large B-Cell Lymphoma (DLBCL) in a Young Adult Anjali Mone, MD, Shannon Chang, MD, MBA, David Poppers, MD. New York University Langone Medical Center, New York, NY. Intussusception is a pathologic condition most commonly found in children, with only 5% of all cases occurring in adults. Primary gastrointestinal lymphoma is rare and is an extremely unusual etiology of intussusception with a limited number of cases reported in the literature. We present an interesting case of intussusception caused by a primary intestinal DLBCL in a man with a childhood history of hepatoblastoma. A 30-year-old man presented with 2 weeks of fevers, chills and night sweats, as well as several months of intermittent bloating, constipation, flank pain, and poor appetite. Examination revealed a mildly distended, soft abdomen. The rest of his exam was unremarkable. Laboratory tests revealed leukocytosis (21.6 K cells/μL), transaminitis, elevated lactate, and a positive urinalysis. He was initially diagnosed with pyelonephritis. CT scan of the abdomen and pelvis revealed a 5 cm colo-colonic intussusception at the level of the sigmoid colon. Flexible sigmoidoscopy revealed a 4-cm fungating mass obstructing the colonic lumen. Biopsy results diagnosed DLBCL, non GC-type (KI >95%). PET scan was notable for a sigmoid mass, increased attenuation in the axillary lymph nodes and the right kidney, and a small pulmonary nodule. Adult intestinal intussusception is a rare cause of intermittent chronic abdominal pain and is an unusual initial presentation of primary lymphoma. A limited number of published case reports suggest adult intussusception occurs more frequently in the small bowel. When this condition occurs in the colon, it is more likely to have a malignant etiology such as lymphoma, however few such cases have been reported. Our patient had none of the well-known risk factors for gastrointestinal lymphoma such as Helicobacter pylori infection, inflammatory bowel disease, autoimmune diseases, immunodeficiency syndromes, immunosuppression, transplantation, celiac disease, and nodular lymphoid hyperplasia. There has been no reported association between hepatoblastoma and DLBCL, although it would be intriguing to investigate the association of either hepatoblastoma or its treatment with subsequent development of lymphoma. This patient’s age at presentation is another unique aspect of this case, as intussusception secondary to lymphoma generally presents much later in life. In summary we present a rare and interesting case of DLBCL presenting as adult colo-colonic intussusception in a 30-year-old man with prior history of hepatoblastoma.


[405B] Figure 2.

[405C] Figure 3.


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Serrated Polyposis Syndrome: An Unusual Presentation Discovered After an Episode of Ischemic Colitis

Splenosis: A Benign Phenomenon Mimicking Metastatic Cancer

Geoffrey You, MD1, James R. Penn, MD2, Kevin Skole, MD3. 1. Rutgers Robert Wood Johnson Medical School, Newark, NJ; 2. Rutgers Robert Wood Johnson Medical School, Piscataway, NJ; 3. University Medical Center of Princeton at Plainsboro, Plainsboro, NJ. Introduction: Serrated polyposis syndrome is a disease characterized by numerous, large, proximal sessile polyps. The polyps are often flat and tend to develop within the haustral folds with adherent mucus, which makes them difficult to detect on colonoscopic evaluation. Case Presentation: A 64-year old female with a past medical history of Hypertension, Coronary Artery Disease, and no previous colorectal neoplasia screening presented with the acute onset of diffuse abdominal pain and hematochezia. There was no recent travel history or antibiotic use. CT scan of the abdomen revealed circumferential thickening of the colon from the splenic flexure to the rectum with associated soft tissue stranding. Flexible Sigmoidoscopy performed upon admission showed severe inflammation of the sigmoid colon consistent with ischemic colitis. The patient was treated supportively with improvement in her presenting symptoms. Several weeks after her hospitalization, she underwent a full colonoscopy, which revealed multiple sessile polyps proximal to the sigmoid colon. The majority of the polyps were located in the ascending colon, the largest of which measured approximately 20 mm. Most, but not all, were resected, and pathology was consistent with sessile serrated polyps. Several more sessile polyps were removed from the proximal colon during a follow-up exam performed three months later. Pathology was again consistent with sessile serrated adenomas. Discussion: Serrated Polyposis Syndrome remains both a diagnostic and therapeutic dilemma. It is relatively uncommon disease, representing approximately 1 case for every 2000 screening colonoscopies performed. Sessile serrated polyps are believed to be more aggressive than common tubular adenomas, therefore a high index of suspicion is required. However, the characteristics of sessile serrated polyps (flat with minimal discoloration) make detection difficult on routine colonoscopic evaluation. The flat nature of these polyps also makes for an increased risk of incomplete resection and possibly even colonic perforation. Surveillance intervals have also not been concretely defined, but current recommendations suggest repeat colonoscopy every one to two years as some studies suggest an increased future risk of colorectal cancer. Reference: [1]. East, J., Vieth, M., and Rex, D. “Serrated lesions in colorectal cancer screening: detection, resection, pathology, and surveillance.” Gut 2015;64:991-1000.

Rafael Tirado, MD, Walisbeth Class, MD, Doris Toro, MD, FACG, Eduardo Acosta, MD, Roberto Bordewyk, MD. VA Caribbean Healthcare System, San Juan, Puerto Rico. Splenosis is the benign heterotopic transplantation of splenic tissue that results from traumatic splenic rupture or splenectomy. Many clinicians are unfamiliar with this phenomenon, therefore it is often misdiagnosed and most patients undergo unnecessary invasive diagnostic procedures. We present a rare case of liver and splenic bed splenosis mimicking metastatic cancer. This is the case of a 58-year-old male with medical history of hypertension, migraine, bronchial asthma and nephrolithiasis who presented with diffuse abdominal pain, left flank pain and dark-colored urine for the past two days. He denied fever, chills, hesitancy, dribbling, or any other symptoms. Past medical history notable for splenectomy at age 5 secondary to a motor vehicle accident. Physical exam and laboratory tests were unremarkable except for hematuria on urine analysis. A non-contrast abdominopelvic CT identified a calculus at the ureterovesical junction with associated hydronephrosis. Also revealed evidence of prior splenectomy, a solid exophytic lesion at the right hepatorenal fossa measuring 1.8 cm x 2.3 cm, left upper quadrant lesion near the stomach measuring 1.8 cm x 1.5 cm, and small nodular lesion anterior to the rectum measuring 1.4 cm. Further evaluation included a colonoscopy which was essentially normal. A PET CT showed a bilobulated soft tissue density on the splenic bed and perihepatic soft tissue nodularities most likely representing splenosis. A Tc99m sulfur colloid liver-spleen scan demonstrated localized uptake by soft tissue densities localized on the splenic bed, left pelvic wall and right abdomen just below the right liver lobe compatible with active reticuloendothelial activity as it seen with post-traumatic migratory splenosis. We present a very interesting case of splenosis, which results from the auto-implantation of splenic pulp tissue usually due to trauma or following abdominal surgery. Frequency of splenosis varies according to type of injury, being more common after trauma that following elective surgical removal of the spleen. Spleen implants tend to be multiple as are seen in this patient who had spleen trauma at an early age. These are usually confined to the abdominal cavity; although there are reports of thoracic splenosis. On routine radiological studies, these lesions are usually indistinguishable from other benign or malignant lesions for which radioisotope studies are usually recommended to establish the diagnosis. Although most patients are asymptomatic, abdominal pain due to adhesion, torsion or spontaneous rupture can occur. Splenosis should be considered in all splenectomized patients; especially in presence of unexplained or asymptomatic abdominal mass. Whenever this entity is suspected, diagnosis is feasible through radioisotope scanning, avoiding the need of invasive procedures.

408 In the Knick of Time: A Case of Bowel Perforation in Granulomatosis With Polyangiitis and the Use of Rituximab Myung S. Ko, MD1, Cricket Fisher2, Lindsay Uribe, MD2, Matthew Cascino, MD3, Fernando Velayos2. 1. Department of Medicine, University of California at San Francisco, San Mateo, CA; 2. University of California San Francisco, San Francisco, CA; 3. Division of Rheumatology, Department of Medicine, University of California at San Francisco, San Francisco, California, San Francisco, CA. Granulomatosis with Polyangiitis (GPA), is an ANCA-positive vasculitis that affects the small and medium size vessels of various organs, including those of respiratory tract, lungs, and the kidneys. Gastrointestinal manifestation of GPA is rare, with an estimated prevalence of 5 to 11%. Furthermore, severe gastrointestinal involvement such as bowel perforation or hemorrhage, are even rarer manifestations of GPA. Although the use steroids and cyclophosphamide has become the standard of practice for treating GPA, there is insufficient evidence on the treatment of patients with severe gastrointestinal involvement. We report a case of a 50 year old previously healthy man who presented to our hospital with a 3 month history of migratory polyarthritis and new onset abdominal pain, bloody diarrhea, and oral ulcers after returning from a trip to French Polynesia. Based on laboratory, serologic, radiographic (Figure 1), and

[406A] Figure 1.

[406B] Figure 2.


[408A] Figure 1.


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[408B] Figure 2.

(Figure 1) which were removed. Biopsy showed ganglioneuromatous polyp. He did not have any clinical evidence of MEN syndrome. Fractionated free plasma metanephrines and 24 hour urine metanephrines were negative which ruled out Pheochromocytoma. There was no evidence of thyroid cancer on imaging. Ganglioneuromas are benign tumors composed of a clonal proliferation of neural crest cells to include nerve fibers, Schwann cells, and ganglion cells. They most commonly arise in the posterior mediastinum and retroperitoneum and less frequently in the intestinal tract. Intestinal ganglioneuromas can occur as part of three different processes including Solitary Polypoid Ganglioneuromas, Ganglioneuromatous Polyposis, and Diffuse Transmural Ganglioneuromatosis. Grossly they appear as small sessile polyps. They are indistinguishable from hyperplastic polyps and adenomas endoscopically. Most of them do not have clinical symptoms and found incidentally. On histologic examination the polyps will display a hypercellular and expanded stroma with cellular proliferation predominantly of spindle shaped Schwann cells with collections of ganglion cells interspersed. The Schwann cells will stain S-100 positive and the ganglion cells will stain with Neuron-Specific Enolase (NSE). If the ganglion cell component difficult to appreciate the diagnosis of neuroma may be considered. Ganglioneuromas have a strong association with Multiple Endocrine Neoplasia (MEN IIB)and to a lesser extent with NF1, Cowden’s disease, and Juvenile Polyposis. They have also been found to be associated adenomas and adenocarcinomas. However, in our patient, Ganglioneuroma was isolated. Pathology showed predominantly Schwann cells with ganglion cells (Figure 2) which were positive for S100 (Figure 3) and Neuron Specific Enolase (NSE). In the absence of Diffuse Polyposis Syndrome, diagnosis of Solitary Ganglioneuromatous polyp was rendered.

410 A Case of Intestinal T Cell Lymphoma Presenting With Gastrointestinal Bleeding

[408C] Figure 3.

endoscopic findings (Figure 2), he was diagnosed with GPA. Soon after the diagnosis, he suffered a colonic perforation, requiring an exploratory laparotomy (Figure 3). He was treated with Prednisone and Rituximab, which proved to be effective therapies in inducing and maintaining clinical remission. The patient currently remains 6 months out from his hospitalization, and has maintained clinical remission on rituximab and a steroid taper. He has continued to do well with no clinical evidence of disease activity, and normalization of his laboratory markers. Prompt diagnosis of GPA is important, as expeditious initiation of therapy is often necessary to reduce mortality and morbidity of multiorgan involvement. Gastrointestinal involvement is an uncommon presentation of GPA. Although local necrotizing arteriolitis of the intestine has been seen in 24% of GPA cases at autopsy, clinically apparent gastrointestinal manifestations of GPA have been reported only at a rate of 5-11%. Moreover, early intestinal perforation or rectal bleeding are even rarer manifestations of the disease, and have only been reported in a small number of cases. Given its rarity, there is limited data concerning the management of severe intestinal involvement in GPA. There have been series of reports that have shown successful use of Rituximab in patients with intestinal perforation secondary to GPA. In our patient’s case, early Rituximab therapy in combination with high dose steroids proved to be a safe and effective treatment of his severe gastrointestinal involvement. In conclusion, the presented case report illustrates that severe complications such as intestinal perforation and hemorrhage can be seen in early stage of GPA despite the rarity of intestinal involvement. In addition to high-dose steroids, anti-CD20 antibody Rituximab, was able to achieve successful induction and maintenance of remission.

Navkiran K. Brar, MBBS1, Roopjeet K. Bath, MBBS2, Lisa Rossi, MD3. 1. University of Connecticut Health Center, New Britain, CT; 2. University of Connecticut, Farmington, CT; 3. St. Francis Hospital and Medical Center, West Hartford, CT. Intestinal non-Hodgkin’s T-cell lymphoma (NHTCL) is a rare, extranodal manifestation of lymphoma. We report a case of a 67 year old man with a history of dyslipidemia, drug-induced neutropenia and low grade B-cell lymphoproliferative disorder (most consistent with B cell chronic lymphocytic leukemia) who presented with a two week history of melena and abdominal pain. An EGD was performed and did not reveal a bleeding source. The patient continued to have dark stool, hematochezia and progressive anemia, thus a colonoscopy was performed. Multiple 5mm ulcers were noted in the cecum, ascending and transverse colon on colonoscopy. Biopsies revealed an aggressive NHTCL. Cytology showed strong expression of CD2 and CD3 with absent expression of CD5, CD7, CD34 and TdT. An aggressive proliferation index of 75-80% was noted.

409 Rare Case of Isolated Colonic Ganglioneuroma and Review of Literature Prathab Devaraj1, Derrick Green1, Gorman Reynolds2. 1. West Virginia University School of Medicine, Morgantown, WV; 2. West Virginia University, Morgantown, WV. Isolated colonic Ganglioneuroma is extremely rare and only 16 cases have been reported so far 1 without MEN or colon polyposis syndrome. We are reporting one such case. 51 year old male with history of Hypertension, hyperlipidemia and GERD presented for screening colonoscopy. He denied abdominal pain, hematochezia or unintentional weight loss. He did not have family history of colon cancer. He underwent colonoscopy which revealed sessile polyps in the left colon


[410A] Figure 1.


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[410B] Figure 2.

On presentation he was tachycardic with pulse 110 bpm with positive orthostatics and afebrile. He had diminished visual acuity in both eyes and looked gaunt and frail. Labs were remarkable for normocytic anemia with Hgb 10 g/dl without leukocytosis. The most recent CD4 count was 103 with viral load 41700. Stool studies were negative for cryptosporidium, giardia and clostridium difficile as were routine stool cultures. Ophthalmology assessment revealed left eye optic nerve edema, bilateral anterior vitritis, and retinal whitening and the patient was commenced on empirical IV ganciclovir. Given the patients ongoing diarrheal symptoms a colonoscopy was performed which revealed mucosal edema with loss of vascular marking and micro abscess formation throughout the whole colon (figure 1). Subsequent biopsy with H&E stain did not show the spirochetes (figure 2) but it revealed spirochetes in ileocolonic mucosa when steiner silver stain was used (fi gure 3). VDRL was positive in serum with 128 dilutions on quantitative analysis. The patient was diagnosed with disseminated syphilis with neurosyphilis and bilateral syphilitic retinitis with colonic involvement and commenced on high dose parenteral Penicillin (Penicillin 4 million units IV q 4 hours) with good response to therapy. Syphilis is caused by the organism trepenoma pallidum and is thought to be an ancient disease recorded in many historical texts. Prevalence has fallen dramatically in the post antibiotic era, but the disease is now starting to increase in prevalence in the USA since 2001, due to HIV infection particularly in those with AIDS who are markedly immunosuppressed and those with high risk sexual behavior . GI tract involvement is rare in syphilis as compared to neurosyphilis which is a much more common manifestation of secondary syphilis. Case reports have described syphilis associated with proctitis, gastritis and gastroparesis which have usually responded to high dose penicillin therapy. HIV-positive persons are 17 times more likely to be co-infected with T pallidum than the general population, and as our case illustrates, needs to be in the differential for those high risk immunosuppressed patients with diarrheal illness. Early recognition is vital in ensuring appropriate treatment to prevent further morbidity and mortality as well as spread of infection.

[410C] Figure 3.

FDG-PET scan of the abdomen/pelvis revealed multiple foci of increased metabolic activity located in the abdomen, particularly associated with small bowel loops and mesenteric lymph nodes. A bone marrow biopsy was obtained and displayed kappa restricted CD5 coexpression consistent with history of small B-cell lymphoma. Bone marrow showed no immunohistochemical evidence of NHTCL, confirming the diagnosis of primary intestinal lymphoma in accordance with Dawson criteria.1 The patient was evaluated by oncology services at two separate centers, and it was agreed that the patient had primary NHTCL. He was placed on a clinical trial of CHOP-Belinostat. Three months after diagnosis, the patient developed severe, acute abdominal pain and was found to have bowel perforation. Laparotomy revealed extensive tumors in the small bowel, of which several had perforated. His clinical course was complicated and after a prolonged ICU stay, he was transitioned to comfort measures only and died shortly thereafter. Primary gastrointestinal (GI) lymphoma is rare, comprising 1-4% of all GI malignancies, of which less than 10% are of T-cell origin.1 We suspect this patient had Enteropathy Associated T Cell Lymphoma (EATL). Patients with EATL typically present at age 60 with lesions predominantly affecting the small bowel (especially jejunum), and less frequently the colon and stomach.1,2 There is a strong association with celiac disease, seen in at least one third of patients diagnosed with EATL.2 This patient had no known history of celiac disease and no villous atrophy was seen on EGD. EATL is aggressive and carries a poor prognosis, optimal treatment is not known.3

[411A] Figure 1.

411 An Uncommon GI Complication of AIDS Freeha Khan, MD, Tuyyab Hassan, MD, Sulieman Abdal Raheem, MD, Annette Kyprianou , MD. MetroHealth Medical Center/Case Western Reserve University, Cleveland, OH. A 43 year old male with a history significant for AIDS and spondylolisthesis presented with complaints of diarrhea for 5 weeks, with eye pain and vision loss, weight loss (30lbs), joint swelling and ulcerative skin changes. Prior to admission, he had been prescribed Stribild (fixed-dose combination tablet containing elvitegravir, cobicistat, emtricitabine, and tenofovir), and prophylactic doses of bactrim and azithromycin but was non compliant.


[411B] Figure 2.


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[411C] Figure 3.

412 [413A] Figure 1. The Spectrum of Pathology in Appendectomies: A Series of 5 Unusual Cases Niket Sonpal, MD1, Neal Mineyev, MD2, Brian Mitzman, MD2, Robert Andrews, MD2, Rebecca Kowalski, MD2. 1. Lenox Hill Hospital, Happauge, NY; 2. Lenox Hill Hospital, New York, NY. Right lower quadrant pain, tenderness, and an elevated WBC count remain the classic presentation of appendicitis. There has been recent data that has shown appendicitis can be treated effectively with antibiotics alone. The variety of pathology seen after appendectomy has been quite surprising at times. We present a spectrum case series of 6 patients with “appendicitis” who were managed operatively, whose pathologic findings were anything but routine. A 28 year old male who presented classic acute appendicitis, but had a non-classic finding of a perforated diverticulum with mucin in the appendiceal wall and mesoappendix. A 20 year old female presented with cyclical vague abdominal pain for 2 months and was found to have “tip appendicitis” on CT scan. Final pathology showed granulomatous appendicitis with a single acid fast positive bacillus in a small non-caseating granuloma. A 20 year old female presented with vague abdominal pain and was found to have both malrotation and a mucocele of the appendix on CT scan. She was found to have a low-grade appendiceal mucinous neoplasm. A 60 year old male with a history of widely metastatic gastric cancer presented with right flank pain and fevers, and was found to have a dilated appendix on CT. He was initially treated non-operatively but had a recurrence of his symptoms, so underwent appendectomy. He was found to have a low-grade appendiceal mucinous neoplasm on final pathology. A 51 year old female was noted to have an abnormal appendiceal orifice on screening colonoscopy, and a 2.2 cm appendix on CT scan. Frozen section of the appendix was consistent with adenocarcinoma, so a right hemicolectomy was performed. Two lymph nodes were taken with the appendix and were negative. There was no evidence of dysplasia or carcinoma in the colon specimen, and fifteen lymph nodes were negative for metastasis (0/15). This case series illustrates that the underlying mechanisms and etiology of inflammation causing “appendicitis” can actually be quite vast, and highlights the need to keep in mind the extensive possibilities of causes of appendicitis, as it will impact the management of appendicitis.

[413B] Figure 2.

413 McKittrick-Wheelock Syndrome: A Rare Cause of Diarrhea in a Young Woman Priya Kathpalia, MD, Lindsay Uribe, MD, Ryan A. McConnell, MD, Jeffrey K. Lee, MD, MAS, Jonathan Terdiman, MD, Aparajita Singh, MD, MPH. University of California San Francisco, San Francisco, CA. Tubulovillous adenomas account for 5% of all adenomas and have a higher incidence of becoming malignant than tubular adenomas. Larger lesions can also lead to obstruction and hypersecretory complications. McKittrick-Wheelock Syndrome is a rare cause of secretory diarrhea from a rectosigmoid villous adenoma generally >4 cm in size that can lead to severe electrolyte derangements, dehydration, renal failure, and even death. We present a rare case of McKittrick-Wheelock Syndrome in a young, pregnant woman. A 26 year old Hispanic woman in her first trimester of pregnancy presented to outside hospital with diarrhea and weight loss, initially treated conservatively. Over the next month she developed large volume mucoid diarrhea with hypotension and electrolyte abnormalities (Na 120 mmol/L, K 1.8 mmol/L) requiring IV hydration and up to 300 mEq/L of KCl supplementation per day. Sigmoidoscopy revealed a large obstructing rectal mass 8 cm from the anal verge. Cold forcep biopsies showed villous adenoma. Due to the obstructive nature of the mass, at week 19 of her pregnancy she underwent an open diverting transverse colostomy and was transferred to our institution for definitive management. MRI showed a large pedunculated mass extending from the anal verge, filling the lumen to 11 cm proximally with rectal thickening (figure 1, 2). Repeat colonoscopy showed a friable circumferential gelatinous mass from the anal verge to 15 cm (figure 3) with biopsies consistent with villous adenoma with low grade dysplasia; there were no synchronous lesions. She was diagnosed with McKittrick-Wheelock Syndrome with plan for definitive surgical resection post-partum. She remained hospitalized throughout her pregnancy and delivered successfully via C-section at 37 weeks. At 5 weeks post-partum she underwent


[413C] Figure 3.

low anterior resection of the rectal tumor which revealed a 13.2 cm secretory villous adenoma without high grade dysplasia. Within 1 week her mucoid rectal discharge ceased and her electrolytes stabilized. McKittrick-Wheelock Syndrome is a rare cause of secretory diarrhea. These lesions consist primarily of mucin-secreting goblet cells that secrete water and electrolytes; larger lesions entail a greater surface area that when in the distal-most portion of the colon limit the ability to absorb fluid. Hypersecretory rectosigmoid villous adenoma should be in the differential in patients with unexplained secretory diarrhea, and prompt diagnosis and early resection is prudent.


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414 Post-transplant Lymphoproliferative Disorder Presenting as Colonic Ulcers Uni Wong, MD1, Raymond Kim2. 1. University of Maryland Medical Center, Elkridge, MD; 2. University of Maryland Medical Center, Baltimore, MD. Introduction: Post-transplant lymphoproliferative disorder (PTLD) is a rare but potentially fatal complication of immune deficiency after solid organ or hematopoietic cell transplantation. PTLD are ususally of B-cell origin and are associated with uncontrolled Epstein-Barr virus (EBV) infection and proliferation, in the setting of compromised T cell immunity with immunosuppression. PTLD can be seen in up to 10% of all solid organ transplant recipients. We report a case of EBV-associated PTLD presenting as colonic ulcers diagnosed in a 66-year-old man six months after receiving lung transplant. Given wide array of presentation, a high clinical suspicion is warranted for early diagnosis and management. Case Report: A 66-year-old man with history of severe obstructive lung disease status post bilateral lung transplant six months prior presented with melena and diarrhea. Immunosuppression: Prograf, Mycophenolate, Valcyte. Clostridium difficile toxin was negative. Upper endoscopy was normal without a source for melena. Colonoscopy revealed large scattered non-bleeding deep ulcers throughout entire colon and in the terminal ileum. Biopsies on histology revealed showed diffuse infiltration of small and medium sized lymphocytes, immunoblasts and numerous plasma cells, and with cells with irregular nuclear contours. The lymphocytes are predominantly CD20 positive B cells; the immunoblasts also mark with CD20. Positive for CD79a. Increase in CD138 positive plasma cells that are lambda light chain restricted by in situ hybridization. Proliferative index by Ki67 is high (60%). Patient was EBV IgG negative prior to transplant. EBV-encoded RNA strongly positive. The overall morphologic immunophenotypic findings are consistent with polymorphic PTLD with plasmacytic differentiation. PET CT demonstrated metabolically active colon, mesenteric, retroperitoneal node, mediastinal lymphadenopathy as well as multifocal lung nodules consistent with lymphoproliferative disease. In addition to decreasing his immunosuppression, patient was initiated on rituximab. His repeat PET CT in 3-month and 6-month revealed resolution of lymphoproliferative disease. Discussion: PTLD is a rare but potentially fatal complication after solid organ or hematopoietic cell transplantation. While PTLD commonly present as lymphadenopathy or as a mass, clinical presentations can vary widely. In our patient, PTLD presented as colonic ulcers which is a rare presentation of the disorder. Therefore, a high index of suspicion is required to establish the diagnosis.

[415B] Figure 2.

416 415

Mesenteric Ischemia Following Orthotopic Heart Transplantation

An Unusual Case of Lower Gastrointestinal Bleeding

Manoj Thangam, MD, Kevin J. Dasher, MD. University of Texas Medical School, Houston, TX.

Anushka Baruah, MD, Gemy George, MD. John H. Stroger Jr. Hospital of Cook County, Chicago, IL.

Introduction: Gastrointestinal complications following orthotopic heart transplant (OHT) are well documented.1 Acute mesenteric ischemia (AMI) is not a reported complication of OHT. We report our experience of five patients with AMI following OHT. Methods: This case series is extracted from retrospective chart review of 107 consecutive OHT from October 2012 through May 2015. Results: Patient 1 underwent OHT for ischemic cardiomyopathy (ICM). On post-operative day 2 (POD), he developed a distended abdomen. He was found to have an ischemic colon requiring total colectomy. He died on POD11. Patient 2 underwent OHT for ICM. On POD2, he developed acute liver injury and a distended abdomen. At laparotomy, he was found to have extensive bowel ischemia. No intervention was performed and he died. Patient 3 underwent OHT for ICM. He experienced hypotension and cardiac arrest on POD1. On POD8, he developed pneumoperitoneum. He required a total colectomy for an ischemic colon. He died of multiorgan failure on POD25. Patient 4 underwent OHT for non-ischemic cardiomyopathy (NICM). On POD8, he developed pneumoperitoneum and underwent right hemicolectomy for an ischemic colon. He died on POD11. Patient 5 underwent OHT for NICM. Post-operatively, he developed multiorgan failure. On POD 32, he developed pseudoobstruction. Decompression colonoscopy resulted in perforation. He was found to have ischemic changes at time of right hemicolectomy. He died on POD34. Discussion: We report the incidence of five catastrophic cases of acute mesenteric ischemia in the early period following heart transplantation. Prior research has identified several parameters which increase the risk of mesenteric ischemia associated mortality in the cardiac surgery population, including age > 65, poor left ventricular function, hemodynamic instability, and a serum creatinine > 1.5. (3) The same risk factors have not been studied within the OHT population. In conclusion, mesenteric ischemia can be a lethal complication of OHT. Further study may elucidate specific risk factors for AMI in OHT recipients. This may influence future patient selection criteria and perioperative management strategies. [1]. Goldberg HJ. Colon and rectal complications after heart and lung transplantation. J Am Coll Surg. 2006 Jan 202 (1) 55-61. [2]. Hashemzadeh K. Predictors of outcome of gastrointestinal complications after cardiac surgery. Minerva Chir. 2012 Aug; 67(4): 327-35.

Harmful effects of non-steroidal anti-inflammatory drugs (NSAIDs) are well recognized in the stomach and duodenum. However, NSAID related damage to the colon is less common. We present the case of a 54-year-old female with a history of hypertension, chronic tension headaches, osteoarthritis of knees who presented to our hospital with complaint of painless bright red rectal bleeding for 2 days. Her medications included amlodipine 5 mg daily and ibuprofen 800 mg two times daily. On admission, her BP was 138/78, heart rate was 82/min, respiratory rate was 19/min and temperature was 98.4 F. Her physical exam was within normal limits. Laboratory investigations including complete blood count, basic metabolic panel and liver function test were within normal limits. ANA and ANCA were negative. CT abdomen did not reveal any acute intra-abdominal process. Colonoscopy was done which revealed erosions and 1-2 sharp circumferential ulcers in the ascending colon. Biopsy of these lesions revealed non-specific chronic inflammatory cell infiltrate with focal recent hemorrhage and superficial epithelial erosion. Patient was asked to discontinue ibuprofen and a repeat colonoscopy 8 weeks later revealed a normal colon. Based on presence of erosions and ulcers on the right side of the colon and normalization of the colon after discontinuation of ibuprofen, a diagnosis of NSAID colopathy was made. NSAID induced colopathy has been described as an important cause of lower GI bleeds. The use of enteric-coated NSAIDs has led to greater exposure of the colon to these medications predisposing the colonic mucosa to inflammatory damage and ulcer formation. Erosions, ulcers, diaphragms and strictures are typically present on the right side of the colon. Histopathological features are similar to ischemic colitis and it is important to correlate these with clinico-endoscopic findings. Withdrawal of NSAIDs leads to healing of ulcers and erosions. Long-term complications include colonic obstruction and perforation warranting endoscopic and surgical intervention. Therefore, it is pertinent to diagnose and treat this condition in a timely fashion.

417 Rectal Malakoplakia in a Healthy, Asymptomatic Female Sarah Flores, MD, Nimisha Parekh, MD, MPH, Subir Bhatia. University of California Irvine, Orange, CA.

[415A] Figure 1.


Introduction: Malakoplakia is a rare, chronic granulomatous disease that is thought to occur as an acquired phagocytic deficiency in macrophages leading to an inability to fully digest bacteria first described in 1902.1-3 The majority of cases involve the genitourinary tract, however 11% of cases occur in the GI tract.3-5 Malakoplakia is rare in healthy people and is typically associated with chronic illness or immunosuppression.6 Case Report: Our asymptomatic 62 year old female patient was referred to our practice for average risk colon cancer screening. She was not taking medications. She denied abdominal pain, altered bowel habits, weight loss, or blood in her stool. Screening colonoscopy was performed and was notable for four pink-tan sessile polyps measuring 1 mm in the rectum. Cold forceps polypectomy was performed and


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Abstracts cytohistochemistry was consistent with a diagnosis of malakoplakia. The patient confirmed no history of illness including autoimmune disease or chronic inflammatory conditions. Chemistry panel, CBC, hepatitis serologies, HIV, Immunoglobulin E, G, and M were all within normal limits. CT scan of chest, abdomen and pelvis showed no abnormalities. Endoscopic ultrasound of the rectum was normal. As patient was asymptomatic she received no further treatment. Discussion: Diagnosis of malakoplakia remains difficult given the variable clinical and endoscopic presentation.7 The endoscopic appearance of malakoplakia is heterogeneous.8-11 Accurate diagnosis requires histopathologic findings of histiocyte aggregates with eosinophilic cytoplasm, known as von Hansemann cells and the pathognomonic Michaelis-Gutmann bodies which are mineralized intracytoplasmic partially digested microorganisms within the lysosome that stain positive with periodic acid-Schiff, Von Kossa, and Prussian blue for their high glycogen, calcium, and iron content.6,12-17 The pathogenesis of malakoplakia is thought to involve infection followed by an inadequate host and inflammatory response.3,18-20 Previous studies have implicated bacteria as the source of infection with Escherichia coli being found in over 90% of cases21 but viruses, including HPV, have also been described.11 Roughly 40% of patients with malakoplakia have a primary or acquired immunodeficiency.22 Treatment includes cessation of immunosuppressive therapy, surgery, cholinergic agonists, or antibiotics.6,23-28 In asymptomatic cases such as ours, no treatment may be necessary.

418 Successful Endoscopic Management of Colonic Cavernous Vascular Malformation: A Rare Cause of Hematochezia Filipa A. Ligeiro, MD, Sandra Quezada, MD, MS. University of Maryland Medical Center, Baltimore, MD. Introduction: Vascular malformations of the gastrointestinal (GI) tract are rare entities that can present as overt or occult bleeding. We present a case of colonic vascular malformation presenting as rectal bleeding that was successfully resected endoscopically. Case Report: A 38 year old African-American male with HIV on antiretroviral therapy, prior Shigella infection, and irritable bowel syndrome presented for evaluation of 1-2 years of intermittent rectal bleeding associated with urgency and rectal pain. He denied abdominal pain or unintentional weight loss. He acknowledged anoreceptive intercourse and reported a remote family history of colon cancer in maternal grandmother. His vital signs were normal, and his physical exam was within normal limits. Laboratory studies revealed no anemia with hemoglobin 15.1 with a mean corpuscular volume of 93. Iron studies revealed iron level 70, iron saturation 19, total iron binding capacity 366, ferritin 22. Laboratory evaluation for Celiac disease and thyroid studies were normal. Clostridium Difficile PCR was negative. Colonoscopy was notable for large internal hemorrhoids and a 15 mm pedunculated polypoid lesion in the sigmoid colon. The polypoid lesion became progressively more erythematous toward the tip and contained a central umbilication which was ulcerated with overlying adherent blood and hematin at the umbilication. The polyp was completely removed with snare cautery polypectomy. There was no bleeding at end of the procedure. Histopathology revealed a submucosal vascular malformation with ulceration and reactive changes, and no evidence of Kaposi’s sarcoma. He remained stable on follow-up 24 hours and two weeks after resection, without recurrent rectal bleeding or pain. Discussion: Vascular malformations of the GI tract can occur anywhere along the GI tract and are exceedingly rare causes of hematochezia. They can be associated with syndromes such as the blue rubber nevus syndrome. Most patients present with bleeding which can be associated with iron-deficiency anemia. Physical exam is often unremarkable, although cutaneous lesions can be seen. Imaging and angiography can have a role in detecting lesions, although colonoscopy is crucial in the evaluation of these lesions. They can have pinpoint areas of bleeding, with overt ulceration rarely seen. They can also be associated with mucosal edema, nodularity and vascular congestion, which can be mistaken for inflammatory bowel disease. Misdiagnosis is common with confirmation of diagnosis on pathology. Endoscopic resection with cauterization can be successful, although biopsy is not recommended given the risk of bleeding. Surgery can provide definitive treatment. At this time there, is no clear association between colonic cavernous malformations and HIV or antiretroviral therapy.

[418B] Figure 2.

419 Spontaneous Rectal Expulsion of a Tubular Adenoma Mel A. Ona, MD, MS, MPH, MA1, Emmanuel Ofori, MD1, Jamil M. Shah, MD2, Sofia Nigar, MD3, Madhavi Reddy, MD4. 1. The Brooklyn Hospital Center, Brooklyn, NY; 2. The Brooklyn Hospital Center, Valley Stream, NY; 3. The Brooklyn Hospital Center, Yonkers , NY; 4. The Brooklyn Hospital Center, Forest Hills, NY. Colon polyps are estimated to be found in up to one-half of all adults. Endoscopic removal of polyps includes polypectomy with snare and excisional biopsy. We describe a rare case of spontaneous expulsion of a colon polyp during defecation. A 40-years-old woman with medical history of peptic ulcer disease, gallstones, severe persistent asthma, and renal calculi status/post lithotripsy, presented to the Emergency Department (ED) with lower abdominal pain and constipation for five days unrelieved by stool softeners and laxatives. She also reported defecating “pieces of flesh” after a bowel movement, which she brought to the ED. She denied nausea, vomiting, fevers, or chills. She reported no family history of gastrointestinal (GI) malignancy. Physical exam revealed mild distension, mild tenderness at the left lower quadrant, no rebound tenderness, and no organomegaly. Abdominal X-ray was normal. Her constipation was relieved with polyethylene glycol electrolyte lavage solution and she was subsequently discharged from the ED. Pathology of the specimen revealed a tubular adenoma. Follow-up colonoscopy revealed multiple polyps: 5mm cecal polyp, 6mm descending colon polyp, 6mm sigmoid colon polyp, and a semi-pedunculated 3.5cm rectal polyp. All polyps were removed by snare cautery polypectomy. While there are few reported cases of rectal expulsion of lipomas, spontaneous passage of tissue or colon polyps during defecation is exceedingly rare. We believe our report is the first case of spontaneous expulsion of a tubular adenoma. Conceivably, a hard, dry stool could shear a large pedunculated polyp causing it to be expelled from rectum. Such patients should undergo colonoscopy to evaluate for further polyps or other GI pathology.

420 Concurrent HPV Negative Squamous Cell Carcinoma of Anal Canal and Squamous Cell Carcinoma of Head and Neck Vivek Mehta1, Uzma Khan2, Nicholas Pozzessere, DO3. 1. Mercy Catholic Medical Center, Philadelphia, PA; 2. Mercy Catholic Medical Center, King of Prussia, PA; 3. Mercy Catholic Medical Center, Philadelphia, PA.

[418A] Figure 1.


Anal cancer is a relatively uncommon cancer of the GI tract which was initially thought to be associated with chronic perianal inflammation, but on further studies over the years, it has been discovered that it has a strong association with HPV infection and 90% of the anal cancers are associated with HPV 16 and 18. Squamous cell cancer is the most common tumor of anal/perianal region, the others being adenocarcinoma, basal cell carcinoma, melanoma, Bowen’s and Paget’s disease. Human Papilloma Virus has also recently emerged as an etiological agent in squamous cell cancers of the head and neck, particularly type 16, and has also been associated with the same high risk sexual behavior as anogenital cancers. HPV related head and neck cancers have also been shown to have better prognosis. A 58-year-old African American male with PMH of prostate cancer presented to the Emergency Department with complaints of right facial numbness, decreased hearing in his right ear, nasal obstruction and epistaxis on the right side. In addition to this, he also complained of dyschezia with a noticeable mass in the perianal region, which would bleed intermittently. On commencement of work-up, he was found to have a large soft tissue mass involving right tonsil, right nasal cavity, right maxillary sinus and ethmoid air cells and the right base of skull including parts of sphenoid bone and pterygoid plate with extension into adjacent masticator space and pterygopalatine fossa. A CT scan of the abdomen and pelvis was also done which showed a large perianal lesion on the left side measuring 7cm extending from the 12 o’ clock to 6 o’ clock position. He underwent biopsy of the right nasal mass and the perianal mass. Pathology demonstrated moderate to well differentiated squamous cell carcinoma from the perianal region and moderately differentiated squamous cell carcinoma of the nasal mass.


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The patient was tested for HPV and HIV and had a negative result. He underwent radiation therapy and chemotherapy with 5-FU and Cisplatin for both the anus and the sinuses. According to his latest scans he is in remission. This is an unusual case of concurrent carcinoma of head and neck and anal canal. Both of these cancers are associated with HPV but this patient was negative for HPV. Recent advances in the field of genetics have helped us better understand many genetic abnormalities and many more new genetic abnormalities are being identified as a cause of cancer. Report of similar cases can help us better understand etiology and pathophysiology of similar cancers.

Appendiceal neoplasms are commonly found incidentally during an appendectomy performed for an unrelated condition. LGIB from an appendiceal neoplasm as a presenting symptom is uncommon. In general, patients with LGIB originating from the appendix are treated with an appendectomy and for malignant lesions a right hemicolectomy is the current standard treatment. Our case highlights the importance of a close, repetitive and careful appendiceal examination in a patient with obscure or recurrent LGIB to rule out an appendiceal etiology.

422 Incarcerated Inguinal Hernia: A Rare Cause of Acute Large Bowel Obstruction

421 Playing Peekaboo: A Rare Case of Lower Gastrointestinal Hemorrhage Kunal Suryawala, MD, Elvin Hardy, MD, Ankur Sheth, MD, FACG. Louisiana State University Health Sciences Center, Shreveport, LA. Lower gastrointestinal bleeding (LGIB) can arise from many causes, with acute bleeding from the appendix being extremely rare and difficult to identify. Various etiologies of appendiceal hemorrhage have been reported in the English literature including appendiceal intussusception, diverticulitis, Crohn’s Disease, tumors, ulcers and erosions. We present a unique case of large volume LGIB secondary to an appendiceal tubulovillous adenoma. A 70 year white woman with a past medical history of polycythemia vera, dyslipidemia, and sigmoidectomy for recurrent diverticulitis presented to the hospital for evaluation of maroon colored blood in the stool for the past 10 days. Admission vital signs were stable, and physical exam was unremarkable other than maroon blood on rectal exam. Hemoglobin was 12.9 g/dL (baseline 16.4 g/dL), Hematocrit 37.6 %, and other labs were within normal limits. Colonoscopy revealed a normal terminal ileum with yellow bile and fresh blood pooling at the appendiceal orifice. On initial examination, the appendiceal orifice appeared normal (Image 1) other than active oozing. With careful examination and manipulation of the cecum and appendiceal orifice, a bleeding polypoid mass was seen slowly emerging through the orifice into the cecum (Image 2). The mass was not amenable to endoscopic resection and the bleeding continued despite attempting hemostasis using epinephrine injection. Due to persistent bleeding and suspected malignancy a right hemicolectomy was performed the same day. Surgical pathology showed a 1.3 cm by 1 cm polypoid mass protruding from the appendiceal orifice extending 1.7 cm into the appendix with the lumen containing blood clots. Histologically the mass was consistent with tubulovillous adenoma.

Joseph Schowalter, DO1, Brett Sleesman2. 1. University of Illinois Hospital and Health Sciences System, Chicago, IL; 2. University of Illinois, Chicago, IL. We report a 55 year old gentlemen with a prior history of seizure disorder who presented to the emergency department with a 7 day history of abdominal pain, distention and failure to pass stool or flatus. On examination the patient was febrile to 38.6 C, tachycardic to 113. The patient’s abdomen was significantly distended, tympanic to percussion with faint bowel sounds on auscultation. There was a large left inguinal hernia with audible bowel sounds in the scrotal sac. Multiple attempts failed to reduce the hernia at the bedside. His only significant lab was a troponin elevation to 0.29ng/ml without ECG changes consistent with ischemia. He initially underwent an obstructive series that showed massively dilated loops of colon up to 15cm with paucity of air at the right recto-sigmoid colon. A CT abdomen with PO contrast re-demonstrated diffuse colonic dilation, and verified the obstructing lesion as the terminal ileum tethering across the recto-sigmoid colon as it entered the inguinal canal. Colo-rectal surgery evaluated the

[422A] Figure 1.

[421A] Figure 1.

[421B] Figure 2.


[422B] Figure 2.


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Abstracts patient for surgical decompression, but felt he was a high risk surgical candidate secondary to his ongoing non-ST segment elevation myocardia infarction. Patient then underwent endoscopic decompression with rectal tube placement. Endoscopy was significant for a 2-3cm segment of externally compressed recto-sigmoid colon without endoscopic evidence of malignancy. After decompression, the patient’s inguinal hernia was easily reduced at the bedside. The rest of his hospital course was uncomplicated and he was discharged with outpatient surgical follow up. An inguinal hernia causing a large bowel obstruction without an underlying colon carcinoma is rare, with only a few cases being described in the English literature. The transition point in our case is displayed radiographically where the terminal ileum tethers across the recto-sigmoid colon. Other published case reports demonstrated resolution of the obstruction after the inguinal hernia was reduced. Our case was particularly challenging in that the hernia was unable to be reduced at the bedside and required urgent decompression. Decompression likely facilitated later inguinal hernia reduction by decreasing intra-abdominal pressure. Although evidence regarding management is lacking for large bowel obstructions secondary to an incarcerated inguinal hernia, endoscopic decompression with rectal tube placement may be considered in the acute setting especially if surgery is to be delayed.

423 Use of an Obstetric Vacuum Delivery System for Removal of a Large Rubber Ball From the Rectosigmoid Colon Vivek Kesar1, Neal Joseph, MD2, Delphine Tang1, Varun Kesar, MBBS3, Alex Chun, MD4. 1. Lenox Hill Hospital, New York, NY; 2. Lenox Hill Hospital, New York , NY; 3. Lenox Hill Hospital/ Mount Sinai Hospital, New York, NY; 4. Lenox Hill North Shore-LIJ Hospital System, New York, NY.

[423B] Figure 2. Introduction: Retained rectosigmoid foreign bodies are a common presentation in emergency departments. The retained objects may result from direct introduction through the anus or rarely from ingestion. While various methods for removal of a foreign body have been reported, the use of an obstetric vacuum delivery system has seldom been described. We illustrate a case of successful removal of a rectosigmoid foreign body using an obstetrics vacuum delivery system. Case: A 42-year-old man with HIV presented to our emergency department 12 hours after inserting a rubber ball in his rectum. Patient denied abdominal pain, nausea, and vomiting but did endorse constipation since insertion. Vital signs were stable. His abdomen was non-tender, mildly distended with normoactive bowel sounds, and no peritoneal signs. Rectal exam demonstrated normal tone, but no palpable foreign body. Lab work was unremarkable. His HIV viral load was undetectable a month before. Abdominal X-ray demonstrated an 8.5cm round rectosigmoid foreign body with moderate amount of air throughout small and large bowel. Both gastroenterology and colorectal surgery were consulted, and decision was made to attempt removal endoscopically with surgery on standby. Under sedation, multiple attempts to manually extract the foreign body were unsuccessful. A colonoscope was then advanced to the rectosigmoid junction and a red colored round ball was visualized. Attempts to remove the ball with conventional endoscopic instruments like rat tooth forceps were also ineffective. An obstetric “Kiwi” vacuum delivery system was then gently inserted into the rectum and the cup was applied to the ball. Before applying the vacuum, the cup was visualized with the colonoscope to ensure that no rectal mucosa was trapped between the cup and ball. Using a pressure of 600mmHg, the ball was gently suctioned and removed from rectum without complication. Repeat colonoscopy showed no trauma or mucosal damage at the site. Discussion: Rectosigmoid foreign bodies are commonly encountered in emergency departments. The approach to remove these objects depends on their shape and location. A patient with any peritoneal signs should have an emergent abdominal x-ray and surgical evaluation. As demonstrated in this case, the obstetric vacuum device can be a safe option for removal of objects in the rectosigmoid. Caution should be administered to not include rectal mucosa in the suction cup before applying the vacuum.

[423A] Figure 1.


424 A Rare Presentation of Cecal Plasmablastic Lymphoma in an HIV Positive Patient Jerard Z. Kneifati-Hayek, MD1, Kati Glockenberg, MD2, David W. Wan, MD3. 1. New York Presbyterian Hospital/Weill Cornell Medical Center, Brooklyn, NY; 2. Memorial Sloan Kettering Cancer Center, New York, NY; 3. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY. A 35 year old man with a history of HIV/AIDS (CD4: 39, Viral Load: 1.4 million) noncompliant with HAART and untreated hepatitis C presented with acute on chronic shortness of breath and abdominal pain associated with nausea and vomiting for one week. On admission, he was afebrile and hemodynamically stable. He appeared cachectic and tachypneic, with right upper quadrant tenderness, without rebound or guarding. Skin was notable for scattered non-pigmented nodules over his abdomen and groin. Labs were significant for a microcytic anemia (9.3 mg/dL) with a normal white blood cell count. Chest and abdominal CT showed right middle and lingual lobe collapse with calcified lymph nodes, as well as a heterogeneous mass in the cecum with peripheral air, but without obstruction or perforation. The patient was started on empiric antibiotics for pneumonia. He underwent an IR-guided biopsy of the mass, as well as a skin biopsy. Pathology was consistent with Epstein Barr Virus positive B-cell lymphoma with plasmacytoid features. PET-CT scan showed FDG avid lymph nodes in the head and neck with pulmonary nodules and skull based lesions. CSF was suspicious for lymphoma involvement. He received rituximab, etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin (R-EPOCH) with intrathecal methotrexate. He subsequently developed profuse diarrhea and E. coli septic shock in the setting of neutropenia. Given his overall poor prognosis, the patient’s family chose to pursue comfort measures and he expired shortly thereafter. Plasmablastic lymphoma (PBL) is a mature B-cell lymphoma. The majority of cases have occurred in patients who are immunocompromised, specifically HIV patients. Most cases are associated with EBV infection [1]. Pathogenesis of this relationship is still unclear, however. PBL is classically described as a lesion in the oral cavity in HIV positive patients but is rare to find in the GI tract, especially the cecum [2, 3]. It is an aggressive cancer without a definitive treatment protocol. Current literature suggests chemotherapy and radiotherapy, such as EPOCH [3, 4]. However, there have been improved regimens based on HAART therapy along with chemotherapy. [5]. Prognosis is poor in patients with PBL in the GI tract and literature reports an average survival time of 6 months [6]. This case highlights the importance of early diagnosis and treatment of this rare and aggressive form of cancer.

[424A] Figure 1.


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Cronkhite-Canada Syndrome: Complete Endoscopic Resolution of Polyposis With Immunosuppression

Infectious Proctitis: A Case of a Clandestine Cause for Proctitis

Krishna Gurram, MD1, Manav S. Sharma, MD2, Richa Bhardwaj3, Marcia Mitre, MD1. 1. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Allegheny Health Network, Pittsburgh, PA; 2. Department of Internal Medicine, Allegheny Health Network, PITTSBURGH, PA; 3. Allegheny Health Network, Pittsburgh, PA. Introduction: This is a case of a patient presenting with diarrhea, nausea, and abdominal pain who underwent endoscopies and was found to have numerous polyps. The diagnosis and treatment of polyposis syndromes is essential for good outcomes. Case Presentation: A 73 year old male initially presented in 2009 with nausea, watery diarrhea and 15 lb weight loss in one month duration. He was found to have moderate alopecia with hyperpigmentation of scalp, thinning of eyebrows and onychomycosis of toenails. Colonoscopy revealed a 5 cm irregular, hemorrhagic mass and 3 sessile polyps in the sigmoid colon. An EGD showed numerous polypoid lesions in the gastric body and antrum with thickened gastric folds. Biopsy from the colonic mass and gastric polyps revealed cystic glandular dilatation, lamina propria edema and chronic inflammation consistent with Cronkhite Canada Syndrome(CCS). Nutritional supplementation with zinc and multivitamin as well as high caloric diet were initiated. Symptoms of diarrhea and alopecia improved after 10 weeks. A few months later patient was diagnosed with un-differentiated autoimmune disease with lupus like features and treated with hydroxychloroquine 200 mg twice a day and prednisone 15 mg daily. Repeat EGDs and colonoscopies over the next 2 years revealed a slight reduction in the number of polyps. Follow up endoscopies in 2013 revealed complete resolution of gastric and colonic polyposis with near normal appearance of the mucosa. Patient continues to remain symptom free on follow up. Discussion: CCS is a rare and non-familial syndrome characterized by presence of diffuse GI polyposis, diarrhea, dystrophic nails, alopecia, cutaneous hyperpigmentation and weight loss. Approximately 400 cases have been reported in the literature thus far. Case reports have shown symptomatic relief with decrease in GI polyposis with various therapies such as nutritional supplements, corticosteroids, H2 blockers and antibiotics. Our case describes, previously undocumented, complete endoscopic resolution of GI polyposis and gastrointestinal symptom control with prednisone and hydoxychloroquine over treatment duration of 4 years. This correlates well with the proposed autoimmune etiology of the disease process and immune-suppressive mechanism of action of these medications. The polyps are typically benign histologically although cases of colonic and gastric malignancies have been reported. Colon cancer screening is complicated in these patients by the presence of multiple polyps and increased risk of bleeding. Therefore complete resolution of polyposis is beneficial in detecting colonic malignancies that could otherwise be missed. This highlights the need for further reseach regarding role of immunosuppressive medications in managing CCS.

Chioma Ihunnah, MD, MPH1, Fadlallah Habr, MD2. 1. Warren Alpert School of Medicine of Brown University, Bristol, CT; 2. Division of Gastroenterology, Warren Alpert Medical School at Brown University, Providence, RI. We present the case of a male patient who described four months of painful defecation, tenesmus, pruritus, hematochezia and mucous per rectum. Initial work-up by the primary care physician (PCP) included negative stool culture and ova and parasite studies. Family history was notable for a first-degree relative with ulcerative colitis. The patient’s medical history included adjustment disorder and acne. Social history was notable for sexual intercourse with men, including anal intercourse with inconsistent use of barrier protection. He had recent travel to the United Kingdom (UK) at which time he engaged in unprotected anal intercourse. He had no other systemic symptoms. Rectal exam was notable for visualization of bright red blood, without the presence of external hemorrhoids. Colonoscopy was performed for persistent symptoms, family history of inflammatory bowel disease (IBD), as well as risk for sexually transmitted infections (STIs). Multiple circumferential non-bleeding ulcers were found in the distal rectum and anal canal. Biopsies were negative for p16 protein, P63, CMV and HSV I and II. Pathology revealed ulceration and acute inflammation, with no viral inclusions. Recent rectal, throat and urine culture for gonorrhea and chlamydia were negative, however cultures were not obtained for these organisms via colonoscopy. Referral was made to colorectal surgery. Anoscopy revealed thick yellow drainage from anal crypt with associated ulcer. He was given a clinical diagnosis of infectious proctitis secondary to likely gonorrhea and empirically treated with ceftriaxone and doxycycline, with resolution of symptoms. Maintaining a wide differential is important when patients present with symptoms of proctitis. While IBD is a common etiology, social and clinical context provide information vital to making the correct diagnosis. Importantly, clinical suspicion should guide treatment, even when faced with negative test results. In the case of this patient, his initially negative rectal swabs for STIs likely delayed treatment. Finally, recognition of the current epidemiologic trends in specific patient populations, provides keys to diagnosis. Recent surges in infectious proctitis, including lymphogranuloma venereum (LGV) among men who have sex with men (MSM) in Europe have been documented. Consideration of this relevant data helps point to the correct diagnosis.

427 Closure of a Persistent Non-healing Gastrocutaneous Fistula (GCF) With a Porcine Biodegradable Fistula Plug (FP) and an Over-The-Scope Clipping Device John Dugan, MD1, Brian Weston, MD2, Boris Blechacz, MD, PhD2, Jeffrey H. Lee, MD, MPH, FACG3, Gottumukkala S. Raju, MD, FACG3. 1. University of Texas Medical School, Gastroenterology Department, Houston, TX; 2. University of Texas MD Anderson Cancer Center, Houston, TX; 3. MD Anderson Cancer Center, Houston, TX. Introduction: A 50yo M with a history of tonsillar cancer s/p chemoradiation and subsequent complications related to osteoradionecrosis of the left mandible required long-term placement of a PEG tube

[427A] Figure 1.



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Abstracts (24Fr). After removal the patient developed a persistent GCF. Attempts to close the site with endoclips were unsuccessful due to large size and difficulty opposing the edges of the internal defect. A large 14mm diameter over-the-scope clip was tried but could not be passed across a cervical esophageal radiation stricture. Due to extensive induration of the peristomal area, abdominal wall suture was not feasible. After disrupting the lining of the fistula tract with a cytology brush, a FP (7mm diameter) was placed in antegrade fashion percutaneously through the abdominal wall defect under direct endoscopic guidance. The distal tip of the trimmed fistula plug was secured internally with a 11mm over-the-scope clip. No sutures were required. Immediate closure of the GCF was achieved. Three weeks later, the fistula plug remains in place and is dissolving without leakage. Discussion: PEG tube tracts usually close spontaneously within a few days after removal. Infrequently, a GCF develops. Before attempts at endoscopic closure, disrupting the lining within the fistula tract with a brush or silver nitrate may be enough to facilitate closure if the tract is small. Potential endoscopic management options for refractory GCF usually include through-the-scope endoclips, over-the-scope clipping devices or endoscopic suturing devices. Percutaneous trans-abdominal suture placement or the use of tissue adhesives such as the fibrin sealant may also be considered when feasible. The use of a FP for GCF closure using a technique similar to PEG tube placement has been described in which the FP is pulled through the GCF by a percutaneously placed snare with base of plug located internally within stomach. This method requires sutures to be placed between either the internal and / or external buttons to secure the FP, which can be technically difficult. To our knowledge, this report is the first to describe this variation of technique in which a FP was used to close a large GCF secured internally with an over-the-scope clip. Conclusion: FP can be feasible alternative to consider for refractory GCF. They can be secured internally with an over-the-scope clipping device without the need for sutures.

428 A Diagnostic Journey: Ischemic Colitis Secondary to Mesenteric Small Vessel Vasculitis From Systemic Lupus Erythematosus Naveen Gnanabakthan, MD, MSc1, Joshua Harrison, MD2, Aditya Kalakonda2, Michael Kosters, MD2, Jivan Lamichhane, MD2. 1. SUNY Upstate Medical University, Liverpool, NY; 2. SUNY Upstate Medical University, Syracuse, NY. One of the differential diagnoses of acute abdominal pain in patients with underlying Systemic Lupus Erythematosus (SLE) is mesenteric vasculitis. While early diagnosis can prevent worsening of ischemic colitis and possible bowel infarction, lupus mesenteric vasculitis remains a difficult diagnosis to make unless one suspects it. Case: 64 year old female with a past medical history of SLE controlled on plaquenil, non-obstructive CAD, who presented to the emergency department with acute left lower quadrant abdominal pain and several episodes of bloody diarrhea for 1 day. Vitals were stable and physical exam was positive for left lower quadrant tenderness and blood in rectal vault without signs of hemorrhoids. Her labs were notable only for a mild leukocytosis, elevated CRP, while lactic acid was within normal limits. Autoimmune/ vasculitis panel, including complement levels and anti-phospholipid levels were negative. CT of the abdomen provided limited information due to poor contrast penetration. The patient persisted to have hematochezia, thus colonoscopy was done, which revealed significant diffuse ulcerated mucosa starting from the sigmoid to the transverse colon. Biopsies of affected regions demonstrated acute inflammation and histological changes consistent with ischemic colitis. A transthoracic echocardiogram ruled out embolic phenomenon. An arteriogram of colon revealed hypoperfusion at the descending sigmoid junction of the colon, without evidence of atherosclerosis or emboli, consistent with small vessel vasculitis. Taken together, her ischemic colitis was likely from a small-vessel vasculitis of the mesentary, within the spectrum of SLE. Patient was immediately started on high dose methylprednisolone and cyclophosphamide with resolution of her symptoms and needed no surgical interventions. The difficulties in diagnosing mesenteric vasculitis are evident here by our limited CT abdomen and negative vasculitis panel. This highlights the importance of being cognisant of mesenteric vasculitis in SLE population, as both CT scans and vasculitis panels, including complement levels can be normal. Colonoscopy and biopsies are important in diagnosing ischemic colitis, however, angiography is important in assessing the cause of ischemia, which could be embolic or from vasculitis in SLE patients. This distinction is important as management of either phenomenon is drastically different. In conclusion, one should maintain a high suspicion of ischemic colitis from mesenteric vasculitis in the SLE population complaining of abdominal pain.

429 Mantle Cell Lymphoma-Lymphomatous Intestinal Polyposis Ranje (RJ) Mohamadameen, DO, Bruce Le, DO, Dennis O’Leary, DO, Javier Sobrado, MD. Nova Southeastern University-Larkin Hospital, Miami, FL. Mantle Cell Lymphoma (MCL) is a rare and aggressive form of the mature B cell non-Hodgkin lymphomas (NHL) that commonly affects older individuals and has one of the worst outcomes of all the lymphomas. It comprises of about 7% of adult NHLs in the U.S. and Europe with an incidence of 4 to 8 cases per million persons per year. Most present with lymphadenopathy, extranodal disease is infrequent with GI tract involvement referred to as lymphomatous intestinal polyposis. Patients may have systemic B symptoms, such as fever, night sweats, and weight loss. Diagnosis often requires a combination of tissue biopsy, immunohistochemistry, karyotyping or fluorescence in situ hybridization (FISH). Prognosis is dismal especially with blastoid variant. It was first described and also reviewed by Cornes in 1961. Treatment may alter progression that consists of combination chemotherapy plus immunotherapy with or without autologous hematopoietic cell transplantation (HCT). Surgery and radiation is usually of no benefit except in cases of bowel obstruction or palliation. 76 y/o M with PMHx of Barrett’s esophagus, GERD, Anemia, and colon polyp presents for surveillance of his colon polyp and Barrett’s esophagus. He denies any dysphagia, abdominal pain, n/v/d, decrease appetite, GI bleed, fever, night sweats, or weight loss. Physical examination was normal. Labs were unremarkable except mild anemia. A scheduled surveillance EGD and colonoscopy showed negative Barrett’s


but revealed numerous polypoid lesions throughout left and right colon all pathologically confirming MCL. Immunochemistries were positive for CD5, Bcl-2, CD20, and PAX-5 with strong expression of Cyclin D-1. CD-3 was also positive. CD23 stain and PCR for t(11;14) were pending. Oncology referral was made for treatments of MCL. Mantle cell lymphoma with GI involvement i.e. lymphomatous intestinal polyposis is a rare phenomenon worth sharing for future research. The difficulty lies in differentiating disease burden because those with GI involvement are likely to have worse outcome. We conclude that we need a better predictor for highrisk population with diagnosis of MCL. We propose a retrospective study of all MCL cases to find a possible common factor for early recognition. Early treatment may improve survival, prevent recurrences, and potentially decrease resistance to treatment, especially in the blastoid variant of MCL.

430 Fecal Microbiota Transfer as Rescue Therapy: Is There a Role in Severe C. difficile Infection? Zaid Tafesh, MD, Sarah O’Neil, PA, Carl V. Crawford, Jr., MD. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY. Fecal Microbiota Transfer (FMT) has an important role in the treatment of recurrent Clostridium difficile infection (CDI). However, its use as rescue therapy in severe cases is less defined. We present three cases of severe CDI where FMT was used as salvage therapy for recalcitrant disease. Our first patient is an 87 year-old woman admitted for urosepsis and hypoxic respiratory failure. She developed severe CDI, WBC of 51K/uL, albumin of 2.0 g/dL, and pseudomembranous colitis. She was treated for 18 days with vancomycin and metronidazole with no improvement. She underwent FMT via a nasoduodenal tube and recovered with no relapses. She was discharged without recurrence of CDI to our knowledge. Our second patient is a 66 year-old woman with end-stage renal disease (ESRD), hepatitis C, autoimmune hemolytic anemia and diabetes who was admitted for hypoxic respiratory failure. She developed severe NAP-1 CDI with proctocolitis. Her albumin was 2.7 g/dL and developed abdominal distension and tenderness. Despite receiving metronidazole, vancomycin, and fidaxomicin, her diarrhea persisted for 28 days. She underwent FMT with resolution of her diarrhea but relapsed 2 weeks later. Our third patient is a 76 year-old woman with ESRD admitted to the ICU for septic shock in the setting of severe complicated NAP-1 C. difficile pseudomembranous colitis (WBC of 37K/uL, lactate of 2.0 mmol/L, and albumin of 1.6 g/dL). After no response to metronidazole and vancomycin she underwent a loop ileostomy with anterograde vancomycin irrigation. This was followed by FMT with no improvement. She continued to develop worsening multi-organ failure and expired during the admission. The use of FMT in severe cases of active CDI appear promising in a handful of case reports. However, the range of outcomes that we have described here may reflect variable patient and disease characteristics. Our first patient was elderly and relatively healthy which correlated well with her positive outcome. The one recurrence harbored the NAP-1 strain and ESRD, both markers for increased morbidity and mortality. The one death in the patient with NAP-1, ESRD and in multiorgan failure would suggest the limitations of FMT in very advanced stages of CDI, and suggest a point of no return. Therefore, when clinicians consider patients with severe CDI for FMT, timing, patient characteristics, comorbidities, burden of disease, and strain of Clostridium difficile should be taken into consideration.

431 Colon Metastasis From Gastric Adenocarcinoma Ashref Mohamed 1, Kenneth Nugent2. 1. Texas Tech University Health Sciences Center, Lubbock, TX; 2. Texas Tech University Health Science Center, Lubbock, TX. The colon is a common site of primary malignancy; however it is very rare metastatic localization. Here we describe a case of a signet ring cell carcinoma of the stomach metastasizing to the cecum and terminal ilium. Although colonoscopy finding was not very impressive, histopathology uncovers the diagnosis of clear cell adenocarcinoma of the colon and small intestine. 59 years- old male with history of Coronary artery disease who underwent percutaneous coronary intervention with stents in 2012. Few months later he developed hematemesis. EGD was performed which shows gastric ulcer. Biopsy revealed poorly differentiated clear cell adenocarcinoma Her 2 positive. Work up for metastasis was negative. It was staged as IIB. He underwent partial gastrectomy with Roux- en-Y Procedure. Subsequently, he received neo-adjuvant chemotherapy. Patient was then followed up with imaging and subsequent EGDs with no evidence of disease recurrence. In 2014 patient presented with melena. His CEA was elevated. Repeated EGD shows no evidence of recurrence. He also started to develop Melena. Colonoscopy was performed in Feb 2015 revealing hyper vascular area. Biopsy from the lesion showed poorly differentiated signet cell adenocarcima with similar histopathology and grading of previous gastric cancer. It was concluded that the malignancy is likely metastatic from gastric cancer. Patient underwent exploratory laparotomy with Right hemi colectomy. Two lesions were also noted in the terminal ilium that were resected. Histopathology confirms the diagnosis of signet cell adenocarcinoma in colon and small intestine. Patient underwent imaging for further staging which shown no evidence of other metastasis. He was then started on chemotherapy including Taxol and Herceptin. Metastases rarely involve the intestinal tract. As a matter of fact, gut metastases have been mostly described for specific tumors such as melanoma and contiguous Spreading of ovarian carcinoma. Gastric cancer spread to the colon is very rare, when it occur it carries a very poor prognosis and denotes likely poorly differentiated and aggressive type of cancer. Generally this unusual localization has been associated to Lauren’s diffuse type histology and peritoneal dissemination. In our patient gross colonoscopy finding was not impressive, however pathology revealed the diagnosis. Clinicians should be aware that because of infiltrative nature of the disease, grossly it can appear as only mucosal color changes and only lesion biopsy can reveal the diagnosis of such rare, though aggressive metastasis. Nonetheless, gastric adenocarcinoma, especially if it is poorly differentiated or the signet ring cell type, should be considered as one of the common tumors that have the propensity for rare intestinal metastases.


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432 A Case of Bleeding Rectal Ulcer Caused by Kaposi’s Sarcoma in AIDS Patient Annu Gupta, MD1, Kamran Sajid Zahid, MD2, Damodar Pandey, MD3, Hilary Hertan, MD, FACG3. 1. Montefiore Medical Center, SCARSDALE, NY; 2. Montefiore Medical Center, Bronx, NY; 3. Montefiore Medical Cente-Wakefield, Bronx, NY. Introduction: AIDS-related Kaposi’s sarcoma (KS) is a low-grade vascular tumor associated with human herpesvirus 8 (HHV-8) infection. We report the case of a 24 year old HIV male with rectal ulcer from disseminated KS with visceral involvement. Case: 24 year old male with AIDS/HIV (CD4 13) not on HAART, presented with rectal bleeding and weight loss. Examination revealed diffuse palpable lymphadenopathy and shiny papular, non-pruritic lesions in inguinal, scrotal and perirectal area. CT abdomen revealed lymphadenopathy and rectal inflammation. Initial infectious work up was negative for chlamydia, gonorrhea, HSV, CMV, stool for Cryptococcus, giardia, C.difficle, mycobacterium, pneumocystis smear. Colonoscopy showed large 3 cm necrotic, friable rectal ulcer and multiple focal erythematous lesions in rectum. Meanwhile, he developed epigastric pain with elevated liver tests, Ultrasound abdomen revealed new findings of splenomegaly, multiple nodules in liver concerning for abscesses vs. lymphoma. Based on findings, bone marrow and axillary lymph node biopsies were performed. Rectal ulcer and lymph node biopsies were positive for KS. The patient was diagnosed with disseminated KS involving the lung, GI tract, liver and spleen. He was started on HAART therapy. He was not a candidate for chemotherapy in view of multiorgan dysfunction. Patient eventually died. Discussion: AIDS related KS is the most common neoplasm in HIV patients, especially those with lower CD4 counts. Co-infection with HIV promotes the oncogenic capabilities of HHV-8, leading to the development of KS. KS is rare in the post HAART era. AIDS related KS preferentially affects homosexual or bisexual men. It frequently involves the skin, although extra cutaneous spread is common and may involve any organ. GI involvement is seen in 40% of untreated patients and portends a worse prognosis. Disease of the GI tract is typically asymptomatic but can present with abdominal pain, vomiting, diarrhea, weight loss, malabsorption and GI bleeding. Histopathology reveals a predominance of spindle cells. Immunohistochemical stains are positive for CD34 and CD31, which can confirm the diagnosis, although 10% of KS are CD34 negative. Treatment includes HAART therapy, chemotherapy is considered for more advanced disease using liposomal doxorubicin as the first line of treatment. KS should always be considered as a strong differential diagnosis in lesions of the gastrointestinal tract in HIV host.

doxycycline 100mg PO BID since his knee surgery two years prior due to an associated MRSA infection, but no new medications recently. He experienced a 25 pound weight loss over this time. The patient’s most recent colonoscopy was in 2008, at which time a tubular adenoma was identified. He denies a family history of inflammatory bowel disease, irritable bowel syndrome or gastrointestinal malignancy. The patient was admitted from clinic for dehydration and further work up. Physical examination revealed mild distension and normo-active bowel sounds. There was no hepatosplenomegaly. No rebound or guarding. Blood work revealed a potassium of 3.2 and a lipase of 211. Creatinine, other electrolytes, complete blood count, MCV and liver enzymes were within normal limits. Fecal occult blood testing was negative. An infectious work up consisting of a stool culture; stool leukocytes, ova and parasites exam, C. difficile nucleic acid, Giardia antigens and a Cryptosporidium smear were negative. Further studies including anti-gliadin IgA and IgG, anti–tissue transglutaminase IgA, fecal fat, pancreatic elastase, and TSH were also unrevealing. Stool electrolyte studies showed sodium 51, potassium 116, chloride 55, and osmolality 597. What is the cause of his diarrhea? The biopsy results of both sites demonstrated increased intra-epithelial lymphocytes, surface epithelial injury and an expansion of the lamina propria by lymphocytes and plasma cells as well as a focal increase in the sub-epithelial collagen layer. The increased intra-epithelial lymphocytes and sub-epithelial collagen suggests microscopic colitis but did not explain the visible findings on colonoscopy. Given the patient’s clinical course, the appearance of his colon on endoscopy, and otherwise negative testing, his presentation was felt to be most consistent with an atypical case of resolving infectious colitis superimposed on microscopic colitis.

433 A Case of Severe Ischemic Colitis in the Setting of a Type B Aortic Dissection Jeremy Louissaint, MD1, David W. Wan, MD2, Yecheskel Schneider, MD3. 1. Washington University Internal Medicine, St. Louis, MO; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 3. New York Presbyterian Hospital/Weill Cornell Medical Center, Brooklyn, NY. A 61-year-old male presents with a Type B aortic dissection involving the subclavian arteries, transverse aortic arch, and descending thoracic aorta. At the outside hospital, he was medically managed but represented with abdominal pain and paresthesias of the right leg. Imaging revealed new involvement of the bilateral common iliac arteries and flow studies illustrated low flow in the right renal artery. He was then transferred here for evaluation by CT surgery. Upon presentation, abdominal distension was noted, concerning for ileus secondary to acute ischemic colitis. Sigmoidoscopy displayed superficial sloughing in the splenic flexure, descending and sigmoid colon with areas of dusky-appearing mucosa, consistent with ischemia. Repairs to the descending aortic aneurysm and aortic arch as well as a right-toleft subclavian-aorto bypass were performed. The post-operative course was complicated by lactate>20, WBC>25, AST>10,000, and ALT>2000. Exploratory laparotomy revealed a perforated ischemic bowel and a subtotal colectomy, small bowel resection, and cholecystectomy were performed. Re-exploration with resection of necrotic bowel was later performed. His condition continued to deteriorate despite hemodynamic support and antibiotic therapy, and he expired 2 days later. Aortic dissections classified in the Stanford system are either Type A or Type B. The latter includes sites not involving the ascending aorta and is associated with 30-day mortality rates of 10%; rates much less than those seen in Type A.1 The initial formation involves a tear in the vascular intima that may eventually serve as an alternate, noncommunicating conduit for blood flow. Stable Type B dissections are treated medically with methods aimed at controlling factors such as hypertension. Surgical intervention is recommended in the setting of constant/worsening pain, dissection progression, rupture, or ischemia, as these are associated with increased mortality.2 These complications can arise from the progression of the false lumen to involve branches of the aorta (renal arteries, arteries supplying visceral organs, and arteries supplying the limbs), or from hypoperfusion related to the sequestration of cardiac output; manifestations include renal failure, mesenteric ischemia, and limb ischemia, respectively.3 Preoperative mesenteric ischemia portends an unfavorable prognosis with the risk ratio of mortality >35 and an overall mortality rate as high as 87%.4

[434A] Figure 1.

[434B] Figure 2.

434 A Curious Case of Chronic Bowel Symptoms Nikhil Seth, MD1, Franziska Jovin, MD2, James McGee, MD2. 1. University of Pittsburgh Medical Center, Pittsburgh, PA; 2. University of Pittsburgh Medical Center, Pittbsurgh, PA. Question: A 67 year-old Caucasian male with coronary artery disease, diabetes mellitus type II and morbid obesity presented to the General Internal Medicine Clinic with a chief complaint of diarrhea. The patient was in his usual state of health until 5 weeks prior to presentation, when he started to experience four to five bowel movements a day. The bowel movements were liquid in consistency with no reported gross blood or mucus, and not foul smelling. Most episodes were preceded by abdominal discomfort and bloating one hour prior to a bowel movement, and he did not experience any nocturnal episodes. There was no association with particular foods or recent consumption of undercooked foods or seafood. He denied any recent travel or other sick contacts in his household. Of note, the patient was on chronic


435 Breast Cancer Presenting as Inflammatory Bowel Disease Jose Mari Parungao, MD, Michael Piper, MD, FACG. Department of Gastroenterology, Providence Hospital, Southfield, MI. Our patient is a 72-year-old female with a past medical history of Stage 2 breast cancer treated with lumpectomy and adjuvant chemotherapy and radiotherapy in 2000 with recurrence and re-staging to Stage 4 in 2010 with re-treatment. She presented with chronic, non-bloody diarrhea and abdominal


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Abstracts pain. CT Scan of her abdomen and pelvis demonstrated ileitis and pancolitis, suggestive of inflammatory bowel disease. Laboratory work up was unremarkable at that time. She then underwent a sigmoidoscopy, with findings significant for a hard irregularity in her rectal exam, which on direct visualization appeared to be diffusely congested, highly irregular and nodular mucosa. In addition, a severe stenosis of unknown length with an inner diameter of approximately 6mm that could not be traversed even with a pediatric colonoscope was encountered at the sigmoid colon, approximately 25-30cm from the anal verge. Biopsies from these two suspect areas demonstrated marked edema and hemorrhage, most consistent with ischemic colitis. Her symptoms, in the meantime, persisted despite medical therapy so she was referred to colorectal surgery for evaluation. She underwent total proctocolectomy, and the specimen was found to be extensive metastatic carcinoma of breast primary, with 19 of 19 lymph nodes positive for cancer. Breast cancer remains the most common site of cancer in women, with metastatic disease commonly identified in the lungs, bone, liver, and brain. Although cancer metastasis to the GI tract is rare overall, breast cancer has been demonstrated to be one of the most common primary cancers to metastasize to the GI tract. The presentation of this disease may be non-specific and varied in nature. In patients with a known history of metastatic breast cancer, it is important to consider metastasis as an etiology when they present with non-specific GI symptoms. Endoscopic evaluation is critical, although in advanced cases biopsies may be non-diagnostic, especially if superficial. In these cases, prompt surgical evaluation should also be considered.

436 Hemophagocytic Lymphohistiocytosis in Ucelerative Colitis Ankur Varma, MD, MPH1, Medhavi Honhar, MBBS1, Modupe Idowu, MD2. 1. University of Texas, Houston, TX; 2. University of Texas at Houston, Houston , TX. Hemophagocytic lymphohistiocytosis (HLH) is a rare life threatening inflammation caused by pathologic immune activation causing phagocytosis of the bone marrow derived cells. It includes two varieties, the primary HLH that is sporadic and the secondary HLH that is due to triggers like infection occurring in the setting of immunosuppression. It is fatal if not treated promptly, making its diagnostic anticipation crucial for survival. We hereby present a rare case of HLH due to histoplasmosis in a patient of ulcerative colitis treated with infliximab. A 48 year old female with a history of hypothyroidism, migrane and ulcerative colitis presented to the emergency department with complains of fever, joint pain and generalized abdominal pain for 5 days duration. She had ulcerative colitis for many years and she had last received infliximab infusion a week before coming to the hospital. On presentation, vital signs were remarkable for a temperature of 101.7 F. Physical examination revealed ecchymosis on her forehead and upper and lower extremities. Laboratory data showed thrombocytopenia , mild anemia, elevated ALT, AST, ALP, INR, ferritin (>40,000ng/ml), low fibrinogen and a normal total bilirubin. Blood cultures were sent and she was started on broad spectrum antibiotics. She continued to spike fever and had now become pancytopenic. RUQ US was unremarkable. Contrast computed tomography (CT) of the abdomen and pelvis revealed mild thickening of the sigmoid colon, suggesting inflammatory colitis. Hematology was consulted for bone marrow biopsy and infectious disease was consulted for continued fever. BM biopsy was done and it was positive for budding yeast and increased hemophagocytes. Infectious panel came back positive for histoplasmosis. She met 5 out of the 8 criteria for diagnosis of HLH (fever, cytopenia, hypofibrinogenemia, ferritin>500, hemophagocytes in BM)was diagnosed as a case of HLH due to disseminated histoplasmosis. She was started on amphotericin and itraconazole and the fever resolved. HLH is a rare, often fatal disease if not promptly treated. Infliximab has been used in the past to treat refractory cases of HLH due to its anti TNF and cytokine activity. Here we present a case in which the patient had HLH due to the immunosuppression associated with infliximab use. Very few cases in literature have reported this indirect role of anti TNF therapy in predisposing a patient to HLH. Our case highlights the importance of considering HLH in patients with unexplained fever who receive anti TNF therapy.

437 The Bulbourethra Causing Colonic Obstruction? A Rare Case of a Patient Presenting With Small Bowel Obstruction Secondary to Extrinsic Compression by Adenoid Cystic Carcinoma of the Cowper’s Gland Sandeep Dayanand, MD1, Mohamad Kabach, MD2, Pradeep Dayanand, MBBS3. 1. University of Miami/ JFK Medical Center Palm Beach Regional GME Consortium, West Palm Beach, FL; 2. University of Miami/JFK Medical Center Palm Beach Regional GME Consortium, Atlantis, FL; 3. Mamata Medical College, Hyderabad, India. Introduction: Cancer of Cowper’s Gland is an extremely rare adenocarcinoma with a handful of cases reported in literature. Usual clinical presentation of patients with these tumors varies from lower urinary tract symptoms to acute urinary retention. Here in, we present a case of a patient who initially presented with a clinical presentation consistent with small bowel obstruction and subsequent workup revealed adenocystic carcinoma of the Cowper’s Gland. Case: The patient is a 68 year old male who presented with a 3 day history of vomiting, crampy diffuse abdominal pain and associated abdominal distension. Patient also reported several month history of fatigue, 40 pound loss of weight and symptoms of increase urinary frequency and urgency he attributed to his history of benign prostatic hyperplasia. Patient’s abdominal pain and vomiting worsened which prompted ER admission. Patient reported vomitus consisted of ingested food and bile. Patient was hypotensive and tachycardic on exam with significant volume depletion evident by dry mucous membranes. There was a high suspicion for advanced colon cancer causing obstruction based on patients history of weight loss and loss of appetite. Patient was appropriately hydrated with IV fluids and NG tube was inserted for decompression. CT of abdomen showed numerous bowel loops with no transition zone and evident pelvic mass. Pulmonary and Hepatic masses were also noted consistent with metastatic lesions. After detailed review of his abdominal CT the pelvic mass was thought to be the most likely primary and biopsy was performed. Biopsy revealed tubuloalveolar glands with positive stains for cytokeratin, actin and mucin all of which were consistent with adenocystic carcinoma of Cowper’s Gland. Surgical resection of primary tumor was performed subsequently, with the initiation of chemotherapy for adenocystic carcinoma. Symptoms of bowel obstruction resolved with conservative management and patient was discharged to receive chemotherapy outpatient. Discussion: Bowel obstruction can be caused by multiple etiologies including cancer. Carcinoma of other pelvic organs should be considered as part of differential during work up in this scenario. This patient had an extremely rare tumor of his bulbourethral glands causing bowel obstruction. The correct diagnosis requires a high degree of suspicion and knowledge of this entity.

438 Metastatic Breast Cancer to the Pelvis: Masquerading as Rectal Mass Elsa S. Tabrez1, Sana Nazir2, Arshia Akbar3, Shams Tabrez, MD4. 1. Saxon Medical Group, Windermere, FL; 2. Saxon Medical Group, PA, Lahore, Pakistan; 3. Saxon Medical Group, Attock City , Pakistan; 4. Saxon Medical Group, PA, Kissimmee, FL. Metastatic breast cancer to the pelvis: Masquerading as Rectal Mass. A 75 year old white female with a history of Breast Cancer s/p right mastectomy and radiation about 10 years ago, came in after her European tour with change in bowel habits, constipation, abdominal bloating, decrease in appetite, and some weight loss. She had a negative colonoscopy one year ago for Colon Cancer screening. She denies rectal bleeding. Her physical examination and laboratory test were within normal range. Colonoscopy revealed a mass like lesion in the mid rectum, seems like sub mucosal or extrinsic mass. Biopsy of this mass reported negative. Because of unavailability of the rectal ultrasound, barium enema was done, which raised the suspicion of extrinsic encasing of the rectum by a growth. Exploratory laparotomy was done, and on histopathology this mass was reported as Metastatic Lobular Breast Cancer. Breast Cancer is the second most common cause of death in The United States. According to National Cancer Institute, 1 in 8 women who live to be the age of 80 will develop Breast Cancer. Diagnosis of Metastatic Breast Cancer after the remission from the primary Breast Cancer can be challenging. Breast cancer can metastasize anywhere in the body but primarily to bones, lungs, regional lymph nodes, liver, and brain. In our case it had uniquely metastasized to the pelvic cavity and was causing extrinsic pressure on the rectum. The extra hepatic gastrointestinal metastases of the Breast Cancer ranges between 6% to 18% with the stomach most commonly affected organ, followed by the colon and rectum. In the patient with a history of Breast Cancer in the past and in remission, any change in the GI symptoms including new onset GERD, indigestion, change in bowel habits, bloating, weight loss, and rectal bleeding should be dealt aggressively with gastrointestinal investigations including endoscopy, colonoscopy, small bowel series, and CAT

CLINICAL VIGNETTES/CASE REPORTS COLORECTAL CANCER PREVENTION

439 [436A] Figure 1.

Rectal Small Cell Type Neuroendocrine Tumor: A Rare Mimicker of Internal Hemorrhoids Naga Saranya Addepally, Jagpal Singh Klair, MD, Mayank Pahwa, Mohit Girotra, Daniel K. Brown. University of Arkansas for Medical Sciences, Little Rock, AR Introduction: Neuroendocrine cells secrete hormones in response to neural or chemical stimuli and are present throughout the body. They contain secretory granules in the cytoplasm, which stain positive for chromongranin A (CgA), synaptophysin, neuron-specific enolase and CD-56. The presenting symptoms of neuroendocrine tumor (NET) are related to the hormone secreted.



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Case presentation: 81-year-old man presented with dizziness, constipation and intermittent hematochezia of 1.5 years duration. A colonoscopy only revealed sigmoid diverticulosis. A rectal exam was felt to demonstrate large internal hemorrhoids, which bled with light touch. A repeat colonoscopy showed active bleeding in rectum which was not amenable to endoscopic control. An urgent exam under anesthesia (EUA) revealed a 8x3x3cm friable bleeding mass in the rectum, which had benn previously mistaken for hemorrhoids. Biopsies revealed it to be a high-grade NET. CT, PET scan and bone scan did not show any evidence of metastasis. The patient initially declined surgery and received chemotherapy with cisplatin/etoposide. He subsequently developed a perineal abscess leading to a recto-cutaneous fistula necessitating debridement and diverting colostomy. He died 6 months later from infectious sequelae. Discussion: The World Health Organization in 2010, classified NETs into three grades depending on mitotic and Ki-67 indices: G1 = low grade (well differentiated with 2/hpf); intermediate grade (welldifferentiated with 2-20/hpf mitotic index and 3-20% Ki-67 index) and G3 = high grade (poorly differentiated with >20/hpf mitotic index and >20% Ki-67 index). The majority of GI tract NETs are G1 which are commonly referred to as carcinoid tumors. They have a low tendency for metastasis and an overall favorable prognosis. NET-G3 are very rare comprising only 0.1-3.9% of all colorectal malignancies and have a high potential for metastasis as well as a dismal prognosis. They present as a mass with constipation, pain, hematochezia or obstruction, but rarely have accompanying carcinoid syndrome symptoms. These patients may have elevated 24-hour urinary 5-HIAA and serum CgA. A biopsy is warranted for definitive diagnosis and tumor grading which then determines appropriate management strategy. G1/G2 tumors can be surgically resected but G3 tumors respond better to systemic chemotherapy. NETs must be considered in the differential diagnosis when evaluating patients with hematochezia.

440B] Figure 2.

440 A Preventable Case of Metastatic Colon Cancer Associated to Familial Adenomatous Polyposis in a Young-Adult Female Diana Otero, MD1, Emem Adolf, MD1, Aditya Gupta, MD1, Eduardo A. Rodriguez, MD2, Marcelo Larsen, MD3, Andrey Iliev, MD4. 1. Mount Sinai Bronx Program, Bronx, NY; 2. University of Miami Palm Beach Campus, West Palm Beach, FL; 3. University of Miami, Miami, FL; 4. North Central Bronx Hospital, Bronx, NY. In the United States, Colorectal Cancer (CRC) is the third most common cancer diagnosed in men and women and the second leading cause of death from cancer. A Family History (FH) of CRC is present in about 10% of adults and its increase in lifetime risk is about two- to six fold. Familial Adenomatous Polyposis (FAP) is responsible for less than 1% of the total CRC risk in the US. It occurs in 1 out of 20,000 live births and nearly 100% of people will develop CRC, usually before age 50. Physicians should be aware of this percentage for appropriate screening and surveillance so cases like the following can be prevented. 33 year old Female with History of Traumatic Brain Injury (TBI) and FAP, diagnosed 2 years ago with no histological evidence of CRC and then lost to follow-up, was admitted for abdominal pain, constipation and weight loss. FH positive for CRC in mother and sister at age 28 and 22, respectively. Physical exam was remarkable for pallor and LLQ abdominal tenderness. Laboratory findings significant for microcytic anemia, elevated alkaline phosphate, CA 19.9 and CEA. CT Abdomen showed multiple intraluminal masses and polyps within the sigmoid colon and rectum with several adjacent large lymph nodes and multiple lesions in the liver. Colonoscopy showed innumerable polyps in the colon, from the rectum up to 20 cm from the entry site, as well as an obstructing mass at 20 cm, biopsies were consistent with Adenomatous polyp and Invasive moderately differentiated adenocarcinoma. Liver biopsies were compatible with Metastatic adenocarcinoma consistent with colonic primary. Patient had diverting right transverse loop colostomy and was discharged with Oncology follow-up to received chemotherapy as outpatient. Current screening recommendations for FAP are to undergo APC mutation testing and flexible sigmoidoscopy or colonoscopy every 12 months starting at age 10 to 12 years and continuing until age 35 to 40 years if negative. Once colonic polyposis is established, a full colonoscopy should be performed to evaluate the extent of the colonic polyposis. Colectomy is recommended near the time of initial diagnosis in patients with profuse polyposis, multiple large (>1 cm) adenomas, or adenomas with villous histology and/or high-grade dysplasia. Cohort studies involving patients who have undergone colonoscopy and polypectomy, with apparent clearance of colonic neoplasia, have shown a 76 – 90% reduction in the

incidence of CRC on comparison with reference populations. CRC five-year survival is 90% if the disease is diagnosed while still localized, but only 10% if distant metastases are present. In our patient, she had TBI and physicians held the responsibility to make sure that patient underwent regularly surveillance colonoscopies. Perhaps with added vigilance metastatic disease may have been prevented in this patient.

441 Is There Need for New Screening Guidelines in Radiation-Treated Prostate Cancer Survivors? Fnu Sanna, MD1, Simranjit Singh, MD1, Vinod Kumar, MD1, Davendra Ramkumar, MD2. 1. University of Illinois at Urbana-Champaign, Internal Medicine Residency Program, Champaign, IL; 2. Christie Clinic, Champaign, IL. Introduction: Prostate cancer is the leading cause of cancer in men with radiation therapy being a highly effective treatment modality. Because prostate cancer is diagnosed increasingly at early stages, more patients are treated with radiotherapy resulting in more radiation induced rectal injuries. Radiation induced carcinoma may take anywhere from 5 to 15 years to develop, and possibly longer. This case series highlights the importance of early detection of rectal cancer in patients who received radiation therapy for prostate cancer. Case series: (1) A 64 year old male presented with rectal bleeding and was later diagnosed with poorly differentiated adenocarcinoma of rectum. 9 years prior he was diagnosed with prostate cancer and was treated with external beam radiation therapy (EBRT) with subsequent radiation proctitis. (2) A 69 year old male with history of prostate carcinoma treated with EBRT and subsequent radiation proctitis, presented 10 years later with diarrhea and stool incontinence. Colonoscopy and biopsies revealed radiation induced squamous cell carcinoma of the rectum. (3) A 91 year old male presented with with colovesical fistula. He had prostate cancer treated with radiation therapy 14 years ago. Flexible sigmoidoscopy revealed extensive circumferential ulceration of the rectum. Pathology showed invasive rectal adenocarcinoma. Discussion: The incidence of Radiation induced secondary colorectal cancer has been rising. Radiation treatment is a highly effective treatment modality for localized prostate cancer. Currently radiation therapy for prostate cancer is used in about 17% of patients and has been linked to many malignancies including colorectal cancer. As 10 year survival rate of prostate cancer is more than 80%, there is increased risk of radiation induced colorectal cancer. This secondary carcinoma has a latency period of more than 5 years with peak frequency between 5 and 10 years. Several studies have revealed that risk of colorectal cancer secondary to prostate irradiation is similar to patients with family history of colorectal cancer in first degree relatives. Based on this case series and literature review, we suggest the following screening guidelines: 1) Screening colonoscopy before starting radiation therapy for patients with prostate cancer if it wasn’t done in the last 3 years 2) Screening colonoscopy every 3-5 years beginning 5 years after prostate irradiation therapy, possibly with more frequent surveillance in patients who develop radiation proctitis.

CLINICAL VIGNETTES/CASE REPORTS ENDOSCOPY

442 Idiopathic Arythenoid Subluxation Eduardo A. Rodriguez, MD1, Tulisa LaRocca, MD2, Frederick Williams, MD2. 1. University of Miami Palm Beach Campus, West Palm Beach, FL; 2. University of Miami Palm Beach Campus, Atlantis, FL.

440A] Figure 1.


Arytenoid subluxation is a rare laryngeal injury that may follow instrumentation of the airway and refers to the partial displacement of the arytenoid within the cricoarytenoid joint. Knowledge of its clinical presentation helps in the correct diagnosis and early treatment. 80 year old male patient with no significant past history came complaining of dysphagia to solids for the last week. He reported only tolerating liquids and denied trauma, unintentional weight loss, hoarse-


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Abstracts ness, odynophagia, fever, chills, night sweats, hematemesis, hemoptysis, cough, shortness of breath, or abdominal pain. He did report undergoing a Nissen fundoplication 20 years ago, no other events of airway manipulation. On examination, vital signs were within normal limits. No hoarseness or muffled voice was appreciated. No neck erythema, masses, thyromegaly, JVD, or lymphadenopathy were present and respiratory and abdominal exam were also overall unremarkable. Basic metabolic panel revealed blood glucose within normal limits, a hemoglobin a1c of 6.2. ANA and rheumatoid factor came back negative. Barium swallow evaluation did not reveal strictures or mucosal irregularities. CT of the neck did not show signs of infections or abscess and subsequent upper endoscopy revealed a subluxated left arythenoid. Patient underwent speech therapy evaluation, and was recommended to start a soft mechanical diet. He tolerated this well, and was discharged from the hospital with a follow up appointment with ENT and speech therapy. He was advised to keep the head of his bed elevated at bedtime, and to avoid large meals before bedtime. Outpatient laryngoscopic evaluation showed the subluxated left arythenoid. The patient declined corrective surgery. He has noticed minor improvement since he was discharged from hospital. Arythenoid subluxation is found in less than 1 of every 100 direct laryngoscopic intubations. It differs from arythenoid dislocation by the fact it is a partial displacement of the arthenoid while the latter describes a complete separation. Recent airway instrumentation is by far the most described cause. The classic presenting symptom, hoarseness, is acute, and tends to occur in the recovery room. Less common presenting symptoms include odynophagia, dysphagia, and cough. Airway compromise is very rare. Chronic arythenoid subluxation has not been described before. Diabetes mellitus and connective tissue diseases are risk factors, and should be considered if no other explanation is found.

[443B] Figure 2.

443 Looks Like a Perforation.. Or Maybe Not? Post-Polypectomy Electrocoagulation Syndrome Abhishek Seth, MD1, Karandeep Maur, MD2, Kunal Suryawala, MD2, Kenneth Manas, MD2, James Morris, MD2. 1. LSU Health Sciences Center and Overton Brooks VA Medical Center, Shreveport, LA; 2. Louisiana State University Health Sciences Center, Shreveport, LA. Post polypectomy electrocoagulation syndrome is a rare complication that occurs in 0.003 to 0.1 percent of colonoscopies with polypectomy utilizing electrocautery. It ensues when an electrical current extends into the muscularis propria and serosa resulting in a transmural burn at the site of polypectomy, resulting in peritoneal inflammation in absence of frank perforation. A 56 year old black woman presented for a screening colonoscopy. She was noted to have multiple colon polyps, including a diminutive polyp in the cecum, ascending colon, and transverse colon. All polyps were excised with cold biopsy forceps. Additionally a 6 mm transverse colon polyp was removed with cold snare polypectomy. An 18-20 mm polyp on a short and broad base in the sigmoid colon was excised using hot snare polypectomy utilizing ERBE endocut current. Momentarily after initiating the electrocautery current, patient complained of moderate discomfort and tenderness in the right lumbar region of the abdomen. Polypectomy site showed no evidence of obvious wall defect. Due to concern for possible unexpected colonic wall injury, five hemostatic clips were placed to close the polypectomy defect. Postprocedural CT of the abdomen and pelvis without contrast was negative for pneumoperitoneum. Patient reported mild improvement of pain after a few hours, although the physical exam remained unchanged. Patient declined admission to the hospital, and was discharged with a course of oral Ciprofloxacin and Metronidazole. Due to worsening abdominal pain, the patient was admitted to the hospital the next day. Physical exam was unchanged from the day prior, and a repeat CT scan revealed mild wall thickening of mid-sigmoid colon in the vicinity of multiple surgical clips and mild inflammatory stranding within the adjacent mesentery without a pneumoperitoneum. Patient was treated with bowel rest, intravenous fluids, antibiotics and pain medication. She improved clinically over next 2 days and was discharged to complete the antibiotic course. Post polypectomy electrocoagulation syndrome is rare and can be mistaken for colonic perforation. The diagnosis should be suspected in patients presenting with abdominal pain, fever, tachycardia, or leukocytosis, who underwent polypectomy of large sessile polyps with electrocautery. Distinction from colonic perforation using CT scan is key, and early reorganization of this syndrome is paramount to prevent unnecessary invasive procedures.

[443A] Figure 1.


[443C] Figure 3.

444 A Case of Rectal Stricture Associated With the Use of a Fecal Management System Kshitij Chatterjee, MD, Jagpal Singh Klair, MD, Abhishek Agarwal, Aneet Kaur, Farshad Aduli. University of Arkansas for Medical Sciences, Little Rock, AR. Background: Diarrhea leading to fecal incontinence is a challenging problem in the acute and critical care setting. Fecal management systems (FMS) are widely used to prevent complications of fecal incontinence such as skin breakdown, pressure ulcers, wound infection & transmission of hospital acquired infections. We present a case of rectal stricture associated with the use of flexi-seal FMS resulting in intestinal obstruction. To the best of our knowledge, this is the first reported case of a high-grade stricture due to use of bowel management system that needed bowel resection surgery. Case: A 47-year-old male presented with progressive abdominal pain, distention over four weeks; nausea, vomiting and obstipation for two days. He had a 30-lb weight loss over the preceding 2 months. His medical history included hypertension and coronary artery disease. Three months ago, he had a prolonged hospitalization following orthopedic trauma due to a tornado. During this time, he developed clostridium difficile diarrhea and was treated with courses of metronidazole followed by vancomycin. The high volume diarrhea necessitated the placement of the Flexi-Seal FMS that remained in place for a week. Upon presentation, his vital signs were stable, abdomen appeared distended and tympanic. Plain x-rays showed dilated small bowel loops with multiple air fluid levels and paucity of air in the colon (Fig 1). A computed tomography abdomen showed narrowing at the rectosigmoid region with dilatation of proximal small and large bowel loops. A flexible sigmoidoscopy showed a severe stricture from a concentric ulcer at 15 cm from the anal verge (Fig 2). Even the smallest diameter (4.8 mm) endoscope could not be traversed past the stricture. The biopsy revealed inflammatory stricture with ulceration with no evidence of viral inclusions or malignancy. With failure of conservative management, patient underwent a laparoscopic converted to open rectosigmoid resection with end-colostomy. Discussion: FMSs have evolved as an efficient way to divert stool and reduce these complications; however they have been associated with complications such as mucosal tear, laceration, bleeding and pressure necrosis of rectal mucosa. In our case the inciting factor was thought to be pressure necrosis than sudden trauma. The duration of usage of the device has been recommended as 29 days in the study evaluating


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[444B] Figure 2.

[445B] Figure 2. its safety, The contraindications for using the device include previous anorectal surgeries or anorectal conditions such as stricture or stenosis, severe rectal hemorrhoids, rectal tumors or severe proctitis. The purpose of this case report is to familiarize the clinician about the benefits and possible complications of using an intra-rectal FMS in hospitalized patients with fecal incontinence.

445 Cylindrical Battery in the Stomach for Less Than 12 Hours: Should It Be Removed? Muhammad Bawany, MD1, Tariq Hammad, MD2, Yaseen Alastal, MD2, Ali Nawras, MD, FACG2, Osama Alaradi, MD3. 1. University of Toledo Medical Center, Ottawa Hills, OH; 2. University of Toledo Medical Center, Toledo, OH; 3. University of Toledo, Canton, MI. Introduction: Battery ingestion is a common form of foreign body ingestion. Compared to button batteries, cylindrical batteries ingestion is much less. Data on the outcomes of these ingestions are limited. Here we report a case of multiple cylindrical batteries ingestion as a mode of deliberate self-harm that resulted in severe gastric ulceration within 12 hours of ingestion, secondary to leakage of alkaline batteries content. Case: 31 years old African American female presented to the ED after she was witnessed intentionally ingesting 7 cylindrical batteries (5 AA & 2 AAA) 2 hours prior to presentation. She has had history of schizophrenia and multiple suicidal attempts. In ED, she denied any gastrointestinal symptoms. Patient was not in any acute distress and vitally stable. There were no signs of acute abdomen. Abdominal film revealed 7 cylindrical batteries in the upper abdomen (Fig 1). The patient underwent EGD. Large amount of food was seen in the fundus and body of stomach. Only 2 batteries were visualized in the stomach within the food and were successfully retrieved using Roth Net (Fig. 2). Rest of the batteries were presumed to be embedded within the food. Despite extensive irrigation and suctioning using a large bore NG tube; food could not be cleared and the other batteries were not visualized. No significant mucosal damage was visualized to the esophageal, gastric or duodenal mucosa down to the third part. Patient was kept nil per os and admitted for observation. Next morning, patient complained of mild abdominal pain with some tenderness in epigastric area. Repeat abdominal film showed 4 remaining batteries within gastric body and antrum and a fifth one probably in the small bowel (Fig. 3). Patient underwent repeat EGD 12 hours after ingestion. Stomach was clear from food and 3 AA batteries were seen in the body of the stomach with evidence of 3 deep ulcerations (2 in the antrum and 1 on the incisura) and multiple erosions (Fig. 4). Examination of the duodenum showed superficial mucosal erosions and another AA battery was visualized beyond the ligament of Treitz in the proximal jejunum. All the 4 batteries were retrieved successfully using Roth Net. Inspecting the batteries revealed erosions of the seal of the batteries with leakage of chemical contents on the poles (Fig. 5). Patient was started on proton pump inhibitor. She passed the seventh battery (AAA) per rectum 3 days later without any complications. She was discharged to an inpatient psychiatric center for further management.


[445C] Figure 3.

Conclusion: Current guidelines recommend removing cylindrical batteries if they remain in the stomach for longer than 48 hours. Our case clearly shows that serious and deep ulcerations can result from those batteries early after ingestion, which argues for our proposal of early removal of those batteries.

446 AIDS-related Visceral Kaposi Sarcoma (KS) Presenting With Protein-losing Enteropathy (PLE) Belen Tesfaye1, Rachel Dagne1, Kenneth Brown2, Stuart L. Horwitz, MD2. 1. Howard University Hospital, Washington , DC; 2. Providence Hospital, Washington , DC. Introduction: KS (Kaposi Sarcoma) is a low-grade vascular tumor associated with HHV-8 infection. The epidemic form, or “AIDS-related KS,” is an AIDS-defining illness and was the most common HIV-associated malignancy in the era before highly active antiretroviral therapy (HAART). Incidence has dropped post-HAART. Risk factors for KS include low CD4 count, high HIV viral load, and male-to-male sexual contact. Visceral KS can involve any organ but predominantly affects lymph nodes, lungs, and the GI tract.


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Abstracts Visceral involvement in the absence of skin findings is rare. GI-KS is often asymptomatic, but nonspecific complaints such as nausea, vomiting, abdominal pain, and dyspepsia do occur. Cases of hemorrhage, perforation, obstruction, diverticulitis, appendicitis, intussusception, and protein losing enteropathy (PLE) have been reported. Treatment is mainly with HAART but systemic chemotherapy with Daunorubicin, doxorubicin, and paclitaxel can be used in if lesions are extensive, rapidly progressive, or involve viscera. Case presentation: We report a case of a 19 year old homosexual male with recent diagnosis of HIV/AIDS who presented with bloody diarrhea, nausea, vomiting, dysphagia, odynophagia and anasarca. He had no skin lesion. His labs were notable for an albumin of 0.9mg/dl and a CD4 count of 35 cells / mm3. EGD and colonoscopy showed severe esophagitis and disseminated violaceous nodules in the stomach, duodenum and colon. Histopathologic examination of all lesions demonstrated extensive KS spindle cells, extravasated red blood cells, and inflammatory cells. Furthermore, immunohistochemical staining for human herpes virus 8 (HHV-8) revealed uptake in nuclei of the spindle cells consistent with a diagnosis of KS. Patient was

a poor candidate for chemotherapy due to poor performance status and could not tolerate HAART due to severe dysphagia, nausea and vomiting. Patient died with in 01 mo of initial diagnosis. Conclusion: PLE is a rare complication of KS and is due to a nonspecific loss of plasma proteins from the intestines due to mucosal injury or increased lymphatic pressure. Enteral protein loss can be demonstrated by measurement of the alpha-1 antitrypsin clearance preferably in the absence of diarrhea and GI bleeding as both falsely increase clearance. Low serum albumin is common in AIDS and may be partially explained by malnutrition, chronic disease, and other comorbidities; however, PLE is likely under diagnosed in this population. PLE should be considered in any AIDS patient with hypoalbuminemia, especially when GI symptoms are present and when loss of albumin is not attributable to cardiac, renal, or hepatic disease or to malnutrition.

447 Novel Endoscopic Placement of an Over-The-Scope Clip (OTSC) for Closure of a Recto-neobladder Fistula Paul Wetstein, MD1, James Wang, MD2, Gregory Thibault, MD, PharmD3, Ronald Gagliano, MD4, Benjamin Tabak, MD2. 1. Tripler Army Medical Center, Ewa Beach, HI; 2. Tripler Army Medical Center, Honolulu, HI; 3. Tripler Army Medical Center, Kailua, HI; 4. University of Arizona Cancer Center at DIgnity Health/St. Joseph’s Hospital and Medical Center, Phoenix, AZ. Case Report: A 69-year-old male with invasive bladder and prostate cancer underwent radical cystoprostatectomy and orthotopic ileal neobladder formation (Studer neobladder). A 60 cm segment of ileum was used for the neobladder. On postoperative day 8, he became tachycardic, with copious diarrhea, and large volume feculent drainage from his Foley catheter and suprapubic tube. A CT scan with rectal contrast identified a fistula from the anterior rectum to the neobladder, which appeared to involve the anastomosis between the neobladder and the urethra. He was managed with bowel rest, antibiotics and continued bladder drainage. However, the large volume fecal output from the rectum and bladder drains persisted. He was febrile to 101.6 F despite antibiotics. He was counseled that continued nonoperative management could require a prolonged bowel rest, total parenteral nutrition, and further hospitalization. In an effort to expedite his recovery and fistula closure, he was taken to the operating room for creation of an end sigmoid colostomy. Fistula output stopped following diversion and he resumed a regular diet four days after this procedure. The fistula was evaluated endoscopically nine days after diversion. Flexible sigmoidoscopy identified a 10 mm fistula in the rectum, approximately 5 cm from the anal verge (Figure 1). Ten days later a large bore therapeutic 2-channel gastroscope (Olympus GIF-2T-160) was used to reevaluate the fistulous opening which still appeared to be 10 mm wide. The

[446A] Figure 1.


[446C] Figure 3. © 2015 by the American College of Gastroenterology


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448 Bouveret’s Syndrome: An Unlikely Consequence of Cholelithiasis Ryan Busch, DO1, Nathaniel R. Krogel, DO2, Duane Moise, DO3. 1. Carolinas Health System - Blue Ridge, Morganton, NC; 2. Blue Ridge Digestive Health, Morganton, NC; 3. Carolinas Health System - Blue Ridge, Rutherford College, NC.

[447C] Figure 3.

scope was withdrawn and a 12/6T over-the-scope endoscopic clip (OTSC) was fitted. A double lumen endoscope was chosen to maintain the option of using both the anchor device and grasping forceps to get better opposition of the tissue. The anchor device was advanced through one of the working channels and used to pull healthy colonic tissue surrounding the fistula into the suction cap. Suction was applied and the OTSC was deployed. (Figure 2) The patient was discharged 5 days later. Two months later, resolution of the fistula was confirmed by repeat CT scan with rectal contrast and flexible sigmoidoscopy (Figure 3). His suprapubic and urethral catheters were then removed. Colonic continutity was restored one year after the index operation. Discussion: The OTSC system may be considered as an endoscopic alternative to surgical management of recto-neobladder and recto-urethral fistulas. Application appears to provide secure fistula closure and may help avoid extensive pelvic surgery. In this case, avoidance of pelvic surgery allowed the neobladder to be preserved. In the future, consideration may also be given to OTSC placement without proximal intestinal diversion.

Purpose: Bouveret’s syndrome is a rare form of gastric outlet obstruction caused by an impaction of a large gallstone in the pylorus or proximal duodenum following a cholecystoduodenal fistula. Case: A 53 year old Caucasian male with history of GERD, hypertension, and hypothyroidism presented to the emergency department with epigastric pain, nausea and vomiting for four days. Onset of symptoms were gradual, without any inciting factors. He reports to have an appetite, however he is unable to tolerate any food or liquid because of emesis. No prior history of abdominal surgeries. Initial labs demonstrated a normal CBC. Total bilirubin 1.5, alkaline phosphatase 107, ALT 28 and AST 52. CT of the abdomen and pelvis exhibited a fistula between the gallbladder and pylorus with a gallstone in the pylorus measuring approximately 3 cm in diameter. Mass like thickening of the gallbladder was noted and moderate pneumobilia in the central aspect of the liver. EGD was performed which showed grade A esophagitis and a 3 cm gallstone in the pyloric channel. Despite utilizing a snare, Roth net and 4-prong forceps the stone was unable to be removed. In the duodenal bulb a fistulous tract was visualized. Surgical attending was also present during the case and opted to proceed to surgical retrieval of the gallstone. The patient underwent a laparoscopic gastrostomy with removal of the impacted gallstone. After stone removal the procedure was terminated. The patient returned three months later for closure of fistula and gallbladder removal. On exploration the cholecystoenteric fistula had scarred closed, no communication between the gallbladder and the duodenum was seen. The gallbladder had scared down to the common bile duct the decision was made to leave the gallbladder because of high morbidity associated with this type of procedure. Discussion: Bouveret’s syndrome seems to be a relatively uncommon consequence of cholelithiasis, with formation of cholecystoduodenal fistulas. Cholecystoenteric fistula occurs when a gallstone erodes through the gallbladder wall, usually at the gallbladder neck and through adjacent mucosa; most commonly into the duodenum. Endoscopic management should be considered a first-line option despite the low success rate. Modalities such as endoscopic extraction, laser lithotripsy, extracorporeal shockwave lithotripsy, and intracorporeal electrohydraulic lithotripsy have been reported. If endoscopic approaches are unsuccessful then surgical management is the treatment of choice.

449 Gastrointestinal Primary Light Chain Amyloidosis (AL): Safety and Utility of Endoscopic Evaluation and Management of GI Bleeding John Dugan, MD1, Selvi Thirumurthi, MD2, William Ross, MD2, Manoop Bhutani, MD, FACG2, Gottumukkala S. Raju, MD, FACG3, Brian Weston, MD2. 1. University of Texas Medical School, Gastroenterology Department, Houston, TX; 2. University of Texas MD Anderson Cancer Center, Houston, TX; 3. MD Anderson Cancer Center, Houston, TX. Introduction: Multiple reports have cited the potential for GIB in patients with AL. We report 2 cases demonstrating the utility and risks of endoscopy in this setting.



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[449B] Figure 2.

Case 1: A 50yo F with multiple myeloma (MM) presented with recurrent hematemesis. Multiple gastric mucosal ulcers and submucosal hematomas (SMH) were found during initial EGD [1a]; biopsies confirmed AL. Repeat exam was performed prior to consideration of stem cell transplant (SCT) one year later. On scope insertion, patchy areas of scar with mottled mucosal discoloration were noted [1b]. On scope withdrawal, spontaneous development of multiple enlarging SMHs and mucosal tears were found in the gastric body related to scope +/- barotrauma not amenable to endotherapy [1c]. Clotting parameters were normal. Although no intervention was required, the patient was deemed not to be a candidate for SCT given high bleeding risk and was continued on lenalidomide. Case 2: A 69yo M with MM s/p SCT on therapy for relapse presented with recurrent hematochezia. During colonoscopy, multiple SMHs and ulcers were found with normal intervening mucosa [2]. Although negative on 3 prior occasions, repeat biopsies confirmed AL. Selective APC and endoclips had been tried without success. Bleeding continued and ultimately total colectomy was performed; unfortunately he passed soon after with complications from systemic amyloidosis. Discussion: AL results in abnormal extracellular protein deposition in various organs including the GI tract and is commonly associated with MM (>15%). Overt GIB may occur in ~40%. Amyloid infiltration of submucosal vessels induces ischemic change and increases vascular fragility as well as rigidity of the intestinal wall, which can lead to tearing with hemorrhage. Common endoscopic findings include diffuse mucosal erosions, ulcerations, and SMHs, which can be massive. SMHs are highly suggestive of AL in the proper clinical setting, although biopsy is still required to confirm diagnosis, which can be challenging. In most reported cases, SMHs were identified on endoscope insertion and were not thought to have resulted from scope-induced trauma or shear forces associated with scope manipulation. However our experience shows that endoscopy can be traumatic and should be considered high risk. Treatment is often difficult and of limited utility. Conclusion: Guidelines for endoscopy in the setting of GI amyloidosis and GIB are lacking and these patients should be approached with caution.

[450A] Figure 1.

[450B] Figure 2.

450 Endoscopic Ultrasound: Role in Diagnosis of Hepatic Sarcoidosis Andrew C. Berry, DO1, Rahman Nakshabendi, MD2, Cassandra Johnson, BS3, Hussein Abidali, DO4, Moustapha Abidali, DO5, Shirin Nafisi, MD5, Aaron Baltz, MD6, James Kwiatt, MD6. 1. Department of Medicine, University of South Alabama, Muskego, WI; 2. University of Florida Health College of Medicine, Jacksonville, FL; 3. Nova Southeastern University College of Osteopathic Medicine, Muskego, WI; 4. Department of Medicine, Banner-Good Samaritan Medical Center, Phoenix, AZ; 5. Department of Medicine, Banner-Good Samaritan Medical Center, Muskego, WI; 6. GI Associates, Muskego, WI. A 46-year-old female presented with shortness of breath, dry cough, and diffuse abdominal pain for one week. She denied issues with weight loss, pruritus, rectal bleeding, or hematemesis. Family history was notable for asthma; there was no family history of lung cancer or sarcoidosis. Physical exam was unremarkable with no cutaneous findings. Significant laboratory values included: aspartate aminotransferase (AST) 48, alanine aminotransferase (ALT) 64, alkaline phosphatase 375, erythrocyte sedimentation rate (ESR) 35, angiotensin-converting enzyme (ACE) 116. Tuberculosis testing, anti-mitochondrial and anti-smooth muscle antibody markers were negative. Due to her unknown etiology of abdominal pain, computed tomography (CT) abdomen and pelvis with contrast was performed showing mild dilatation of the pancreatic duct and a suggestion of a mass in the head of the pancreas (Fig. 1). Magnetic resonance imaging (MRI) of the abdomen confirmed abnormal-appearing confluent soft tissue within the porta hepatis and liver hilum, encircling the patient’s main portal


vein and extending into the periceliac and gastrohepatic regions. It appeared separate and of different signal intensity than adjacent pancreas and liver. An endoscopic ultrasound (EUS) was performed noting the mass (Fig. 2). Fine needle aspiration (FNA) followed with subsequent analysis. Cytology noted findings consistent with sarcoidosis. CT chest confirmed pulmonary involvement, including mediastinal and hilar lymphadenopathy. Roughly 50-65% of patients with sarcoidosis have hepatic granulomas on biopsy but only 5-15% of the patients present with symptoms. Unlike traditional cytologic diagnosis of hepatic sarcoidosis via invasive liver biopsy, our patient had an EUS-FNA of a suspicious mass located in the hilum of the liver. Traditionally, bronchoscopy with transbronchial lung biopsy is performed in suspected sarcoidosis patients. If unsuccessful, mediastinoscopy is often performed as the next diagnostic procedure. EUS-FNA provides a nonsurgical alternative by aspirating mediastinal lymph nodes from the esophagus. Our case is unique in that EUS-FNA did not sample mediastinal lymph nodes, but instead sampled the actual mass in the hilum of the liver. Hepatic granulomas may be due to other underlying causes, such as tuberculosis, primary biliary sclerosis, or drug-induced disease. Thus, in suspected cases of hepatic sarcoidosis, liver biopsy is recommended for moderate-severe liver function abnormalities to rule out other causes. EUS-FNA has superior predictive value and lower complication risk than traditional liver biopsy and should be considered as a modality for diagnosis of hepatic sarcoidosis.


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451 The Novel Use of a Uniquely Designed, Lumen-Apposing Stent in Benign Gastric Outlet Obstruction: A Case Series Ross Pinson, MD1, Induruwa Pathirana, MD2, John Magulick, MD2, Jeremy Domanski, MD2, Emuejevoke Okoh, MD2, Craig Womeldorph, MD2. 1. SAUSHEC Department of Internal Medicine, San Antonio, TX; 2. SAUSHEC Department of Gastroenterology, San Antonio, TX. Introduction: Benign gastric outlet obstruction (GOO) due to severe peptic ulcer disease or anastomotic strictures can cause significant morbidity. Conservative treatment with acid reduction therapy and sequential endoscopic dilations exposes the patient to the risks and costs associated with multiple procedures. Self-expanding metal stents have been used to alleviate obstruction in these patients; however, high rates of stent migration have limited their utility in this setting. We present two cases where a uniquely designed, fully covered, lumen-apposing, metal stent was used to alleviate benign GOO. Methods: In each case, the patient was admitted for symptomatic gastric outlet obstruction. Biopsies obtained during esophagogastroduodenoscopy (EGD) confirmed the obstruction to be benign. The first patient had severe peptic ulcer disease, and the second patient had an anastomotic stricture at the gastro-jejunal junction from prior bariatric surgery. Conservative therapy with high dose proton pump inhibitor (PPI) and balloon dilation were unable to provide relief, and the decision was made to proceed with placement of this novel stent. Results: Follow up EGD, at two weeks for the first patient and at three months for the second patient, showed appropriately placed, patent stents without migration. Both patients had symptomatic relief of their gastric outlet obstruction. One patient experienced a greater than 17% improvement in body mass index. Discussion: Covered metal stents have previously been used in benign GOO. However, they are complicated by a migration rate of up to 68% at 6-8 weeks post-placement. We have demonstrated two cases of successful placement of a uniquely designed, lumen-apposing, self-expanding, metal stent in benign gastric outlet obstruction. We postulate that its dumbbell-shaped design may significantly decrease the risk of migration in this clinical setting and provide a new option for the effective endoscopic management of benign GOO.

[451C] Figure 3.

452 Balloon Enteroscopy for Evaluation of a Lead Point in Small Bowel Intussusception Juan Reyes Genere, MD, Carol Semrad , MD, FACG. University of Chicago, Chicago, IL.

[451A] Figure 1.

A 34 year old male with intermittent episodes of abdominal pain presented to the emergency department with 2 days of abdominal pain associated with nausea and vomiting. The patient had several prior encounters for similar symptoms with a work-up that was unrevealing. On this presentation he had an oral contrast enhanced CT scan that demonstrated a jejunal intussusception. Additionally, there was an area of luminal hyper-density near the left paraumbilical area that was noted to be present on a non-contrast CT, 2 months prior. The next day he developed worsening abdominal pain, vomiting, and concern for ischemic bowel injury. The patient underwent emergent laparoscopy showing an area of intussuscepted jejunum that was reduced and marked with a suture. Anterograde double balloon enteroscopy through the marked bowel showed a food bezoar and these have been reported to cause intussusception. No intraluminal lesions were identified otherwise. The patient had resolution of symptoms post-op and was discharged home two days later. One month later in clinic he remained symptom free and repeat imaging did not show intussusception or lead point. Intussusceptions in adults are often an incidental radiographic finding and they are typically self-resolving. Pathologic intussusceptions with inflammation, ischemia, or involving a lead point are rare and require intervention. Identifying a pathologic adult intussusception requires clinical and radiographic correlation. Adult intussusceptions most commonly affect the small bowel (SB) and the majority of adult intussusceptions are associated with a lead point. Lead point lesions can be benign or malignant. When a lead point is suspected, a careful bowel exam is important to further characterize the lesion and to rule out malignancy. The advent of balloon enteroscopy has made it possible to examine the small bowel lumen through a natural orifice and avoid laparotomy. There are several applications for enteroscopy for managing adult intussusception in the non-emergent setting. In emergent cases, where laparoscopy fails to demonstrate ischemic bowel or lead point lesions, performing concurrent enteroscopy also provides useful diagnostic information. This case highlights a future application of a combined minimally invasive approach to manage emergent small bowel intussusception.

453 Spontaneous Pneumomediastinum After Upper Gastrointestinal Endoscopy: A Case Report Ze-Hao Zhuang1, Jing-Jing Wei2. 1. The First Affiliated Hospital of Fujian Medical University, Fuzhou, China; 2. The First Affiliated Hospital of Fujian Medical University, Fuzhou, China, Peoples Rep. A 60-year-old female presented with sore throat and CT confirmed pneumomediastinum after upper gastrointestinal endoscopy was admitted for suspected esophageal disruption or perforation. Physical examination revealed no abnormality, most of the standard laboratory tests were within normal ranges. Initial efforts were centred upon excluding iatrogenic esophageal perforation, however, there was no leakage of contrast medium in esophageal dynamic digital radiography, and no pneumothorax or esophageal injury signs were found. Spontaneous pneumomediastinum (SPM) was then diagnosed. The patient recovered completely with conservative treatment and was discharged on day 9. The most likely causes of SPM were alveolar rupture or esophageal rupture (termed as “Boerhaave’s syndrome”). SPM has been reported in association with many causes resulting in a sudden increase in intra-alveolar or esophageal intraluminal pressure, including severe cough, vomiting, childbirth, and Valsalva maneuver related activities. Except for the quality endoscopists should be improved to avoid the cervical esophageal rupture in the presence of Zenker diverticulum and pharyngeal cancer, great care should be paid to prevent the patient from vomiting, coughing and Valsalva maneuver during endoscopy. Even if it was inevitable, SPM shows a benign natural course with close observation and responds well to conservative treatment.

[451B] Figure 2.



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454 An Endoscopic Retrograde Cholangiopancreatography-Induced Subperiostal Orbital Hemorrhage Hugo Bernard, MD1, Annie Beaudoin, MD2. 1. Université de Sherbrooke, Sherbrooke, PQ, Canada; 2. Centre Hospitalier Universitaire de Sherbrooke and Centre de Recherche Clinique du Centre Hospitalier Uuniversitaire de Sherbrooke, Sherbrooke, PQ, Canada. Subperiostal orbital hemorrhage is not a complication reported in ERCP literature. We reviewed multiple cases reports or small retrospectives series of subperiostal hematoma but only one case of bilateral spontaneous orbital hemorrhage with symptoms onset immediately after ERCP; our case is then the second reporting this complication. A 38-years-old female was referred for symptomatic choledocholithiasis (painless jaundice, prurit, dark urine, acholic feces). Abdominal ultrasonography confirmed a 12 mm choledocholithiasis with 19 mm bile duct dilation. ERCP were performed for numerous lithiases difficult to extract with minimal tolerance by the patient. She had protracted valsalva on the fourth CPRE. She immediatly reported left ocular pain, diplopia and retroocular pressure as if her eye was going to pop out. Physical exam revealed left eye ptosis, tissue swelling, exophthalmia, diplopia with extremely painfull and partial eye movement. Urgent orbital contrast-enhanced computed tomography scanning was ordered. A left superior subperiosteal hemorrhage of 30 mm width by 32 mm anteroposterior by 10 mm vertical was shown, pushing inferiorly conal muscles, optical nerve and intraorbital fat resulting in grade II

[454C] Figure 3.

exophtalmia (fig 1-4). There were no nerve or vessel compromise and no active bleeding. Radiologist raised concern about an underlying orbital bone anomaly without obvious mass. Blood work the day of the ERPC were ; International normalized ratio 1.3, platelets 381, normal renal clairance. Thromboprophylactic heparin was suspended before the ERCP. She received 2 fresh frozen plasma to correct her minimaly increased INR after the hematoma was confirmed. The patient was treated with intraocular latanoprost (prostaglandin analog) 0.005% 1 drop hs and eye rest. She already did better the day after with partial pain resolution, minimal oblic diplopia and no other vision perturbation. Eleven days later an orbital magnetic resonance showed partial resorption of the hematoma, diminution of the mass effect with residual grade I exophthalmia and no underlying mass was shown. Patient was still jaundiced and magnetic resonance cholangiopancreatography confirmed persistence of choledocholithiasis. A subsequent ERCP was done under general anesthesia and stones were removed with mechanical lithotripsy. Six weeks later, the patient blood work was normal and she was asymptomatic. Subsequently, a 18 months follow-up orbital magnetic resonance was completely normal. In conclusion subperiostal orbital hemorrhage is an extremely rare complication of ERCP. ERCP endoscopits should all be aware of its nature because presentation can be less florid than our case and urgent surgical management may be needed to relieve vessel/vascular compromise.

[454A] Figure 1.

455 Isolated Duodenal Varices Without Cirrhosis Alexander Podboy1, James H. Tabibian, MD, PhD2, Stephanie Hansel, MD, MS3. 1. Mayo Clinic, Rochester, MN; 2. Division of Gastroenterology& Hepatology, Mayo Clinic, Rochester, MN; 3. Division of Gastroenterology, Mayo Clinic, Rochester, MN. A 61-year-old man with a remote history of idiopathic necrotizing pancreatitis complicated by need for multiple pancreatic necrosectomies and ultimately Roux-en-Y reconstruction presented with one day

[454B] Figure 2.


[455A] Figure 1.


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of epigastric pain radiating to the back and chills. He denied any recent trauma, alcohol ingestion, new medications, change in bowel habits, chest pain, palpitations, or dyspnea. On examination, vital signs were significant for a low-grade temperature of 37.6°C. He appeared in to be moderate distress secondary to acute abdominal pain which was worsened with palpitation. Physical exam revealed no stigmata of cirrhotic liver disease. Serum laboratory tests were notable for aspartate aminotransferase 99 U/L, alkaline phosphatase 570 U/L, bilirubin 0.5 mg/dL, and leukocyte count of 21.1x109/L; serum albumin and international normalized ratio were both normal. Computed tomography (CT) did not demonstrate any acute abdominal findings other than mild biliary ductal dilatation. Blood cultures revealed gram negative bacteremia, which in the context of the patient’s history of pancreatobiliary disease and his current presentation, prompted referral for endoscopic retrograde cholangiopancreatography. During ERCP, gross pyobilia and a distal common bile duct stricture were found, necessitating biliary balloon dilation, sweeping, and stent placement. In addition, and intriguingly, there was an incidental finding of extensive and nearly circumferential isolated duodenal varices (IDVs; see Figure 1). On review of the patient’s contrast-enhanced CT imaging, there was no evidence of cirrhosis or other varices (e.g. esophageal). In addition, abdominal ultrasound demonstrated normal hepatopedal flow in the portal vein. The patient was placed on a non-cardioselective beta blocker for variceal prophylaxis and was doing well at last follow-up six months later. Discussion: IDVs are a rare manifestation of portal hypertension whose precise incidence and prevalence remain uncertain. Representing approximately 15% of all ectopic varices, duodenal varices may be subclinical or can present with acute hemorrhage with hematemesis and/or hematochezia and mortality rates approaching 40% per episode. IDVs are typically secondary to cirrhosis-associated portal hypertension, whereas here we report a case of cryptogenic IDVs which were likely consequent to extensive intra-abdominal surgeries resulting in impaired superior mesenteric venous outflow and development of noncirrhotic portal hypertension.

457 Simultaneous Afferent and Efferent Stenting of Gastrojejunostomy After Whipple Operation Jamil M. Siddiqui, MD1, Dabo Xu, MD2, Steven Cunningham, MD3, Neeraj Sardana, MD4. 1. Department of Medicine, Saint Agnes Hospital, Catonsville, MD; 2. Department of Medicine, Saint Agnes Hospital, Baltimore, MD; 3. Saint Agnes Hospital and Cancer Institute, Catonsville, MD; 4. Department of Medicine, Saint Agnes Hospital, Fulton, MD. Introduction: Effective palliation of both afferent limb syndrome and gastric outlet obstruction after Whipple operation can be provided with simultaneous enteral stenting with self-expandable metallic stent (SEMS).

456 Heterotopic Salivary Gland Tissue in the Rectum of a Patient With Eosinophilic Colitis and Redundant Colon

[457A] Figure 1.

Shahzad Ahmed1, Micheal Lewis2, Robin Matuk3, Joseph Pisegna, MD2. 1. Cedars-Sinai Medical Center/VA Greater Los Angeles Healthcare System, Los Angeles, CA; 2. VA Greater Los Angeles Healthcare System, David Geffen School of Medicine at the University of California at Los Angeles, Los Angeles, CA; 3. VA Greater Los Angeles Healthcare System, Los Angeles, CA. Heterotopic tissue of the rectum is a rare and poorly defined clinical entity which can be found incidentally or be associated with hematochezia. Types of heterotopic tissue that have been described include gastric, pancreatic, salivary gland and respiratory mucosa tissues. Only 4 reports of heterotopic salivary gland rectal tissue have been previously reported in the literature. We report on a case of a 65 year old male referred for chronic diarrhea and fecal incontinence. The patient was taking Loperamide for chronic nonbloody diarrhea and on physical examination had a benign abdominal and rectal exam. Colonoscopy demonstrated redundant colon, a large rectal polyp measuring 2 cm which on gross examination was concerning for submucosal lipoma versus carcinoid lesion (Figure 1), two 5 to 6 mm diminutive colonic polys, moderate left colon diverticulosis and internal hemorrhoids. Histopathological evaluations of biopsies were significant for ectopic salivary gland tissue in the submucosa of the rectum with mixed serous and mucinous glands (Figure 2) as well as polypoid cecal and transverse colonic lesions with mild chronic colitis and tissue eosinophilia. Subsequent endoscopic ultrasound showed a normal 5-layer wall pattern of the rectal wall without perirectal lymphadenopathy or endosonographic abnormalities of the bladder, prostate and seminal vesicles. The association of heterotopic salivary gland tissue with redundant colon and chronic eosinophilic colitis has not been previously described suggesting a possible causal association.

[457B] Figure 2.

[456A] Figure 1.


[457C] Figure 3.


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Abstracts Case report: A 58-year-old male with a history of pancreatic head adenocarcinoma following neoadjuvant chemotherapy underwent the Whipple operation. He presented 6 months later with failure to thrive, weight loss, nausea, vomiting, abdominal discomfort and jaundice. EGD revealed partial gastric outlet obstruction due to marginal ulceration and edema at the gastrojejunostomy anastomosis, which failed medical therapy with pantoprazole and sucralfate. An elective percutaneous gastrojejunotosmy tube was placed and he was started on tube feeds with an initially good response. His symptoms soon recurred, however, leading to further evaluation. Laboratory findings included leukocytosis, direct hyperbilrubinemia and mild transaminitis. Computed tomography scan showed a massively dilated afferent limb (afferent limb syndrome [Image 1]) with hypodense lesions in the liver but no evidence of peritoneal recurrence. He underwent an exploratory laparotomy and with planned revision of gastrojejunostomy but unfortunately diffuse peritoneal implants were found, precluding anastomotic revision. Subsequently, he underwent simultaneous endoscopic stenting of afferent limb (colonic SEMS [Image 2]) and efferent limb (duodenal SEMS [Image 3]) of the gastrojejunostomy for afferent limb syndrome and gastric outlet obstruction, respectively. He fully recovered, was able to ambulate, visit with family, and tolerate full liquid diet without any nausea, vomiting or abdominal pain. He was discharged 10 days following placement of the stents to home hospice care, where he succumbed to his disease 1 month later. Discussion: Although peritoneal disease has been considered a relative contraindication to stent placement, recent experience suggests that gastrojejunostomy stents are safe and effective in this setting. Yet, very few cases of simultaneous afferent and efferent stenting are reported. SEMS can provide durable symptom relief without the morbidity associated with palliative surgery, and it may provide a better quality of life compared to alternatives. The prognosis after developing anastomotic strictures is usually poor and the median survival is 3.5 months after the procedure. The goals of stent placement are to provide relief from obstructive symptoms, to allow the patient to resume a normal diet, thereby improving quality of life.

458 Rare Case of Eroded Amplatzer Vascular Plug Found on EGD Nabeel Chaudhary, MD1, Isabel Zacharias, MD2. 1. UMass Memorial Medical Center, Boston, MA; 2. UMass Memorial Medical Center, Worcester, MA. Introduction: Amplatzer vascular plugs are embolic devices used as alternatives to coils or detachable balloons to embolize medium to large vessels. Complications due to migration or erosion into the gastrointestinal tract are exceedingly rare but do exist. To date, there are few cases reporting this complication. This case demonstrates the complications of migration and erosions. Case Report: We report a case of a 41 year old male with a past medical history of chronic hepatitis C and Laennec ‘s cirrhosis. He had a TIPS placed 2 years prior to this presentation. He presented to an outside hospital with 2-3 days of hematemesis and hematochezia. He underwent upper endoscopy and was noted to have a foreign material in the gastric fundus. He was transferred to our hospital for further assessment. He had a CT scan of the abdomen showing three Amplatzer devices noted likely placed during TIPS procedure. Two were normally positioned within gastric varices. The remaining one appeared intraluminal within the posterior gastric fundus. He had a repeat EGD showing the foreign body was the Amplatzer

vascular plug eroding into the gastric lumen. The plug was pulled in completely into the gastric lumen during the endoscopy. There was minor mucosa injury. There was no evidence of full thickness perforation. Endoclips were used for hemostasis. He was monitored for a few days. He remained hemodynamically stable without any further episodes of hematemesis or hematochezia and was discharged. Discussion: This case describes a rare complication of vascular plug erosion. This is a rare complication. In the few reported cases these were described as delayed complications. The earliest reported case of coil erosion was 3 months after initial placement and the latest was reported 10 years after initial placement of the plug. This case adds to current literature by informing others of the potential for erosion and migration of vascular plugs and coils.

459 Endoscopic Visualization of Endometrioma Serving as a Nidus for Ileocecal Intussusception David DiCaprio, DO, Prashant Muddireddy, MD, Alex Chun, MD, David Robbins, MD. Lenox Hill North Shore-LIJ Hospital System, New York, NY. Intussusception is uncommon in adults, with an incidence of only 0.15%, and when it does occur it is often due to organic cause such as malignancy or polyp. Endometriosis can involve the bowel, however it most commonly affects the sigmoid colon or rectum, and does not usually cause intussusception. Interestingly, very few cases of intussusception have been diagnosed preoperatively by endoscopy and even fewer cases with the lead point being endometriosis. We present a case of endometriosis causing ileocecal intussusception that was visualized by endoscopy prior to surgery. A 30 year old female presents to the ED with 1 month intermittent, inferior abdominal pain that is accompanied by bloating. She is passing gas and stool and has no fevers, chills, nausea or vomiting. She had hematochezia 6 months ago, but no blood in stool since that time and her LMP was 5 days prior. The patient’s vitals are stable. Abdominal exam reveals moderate distention, normal bowel sounds, the abdomen is soft with mild tenderness in the right lower quadrant without rebound or guarding. Urine pregnancy test is negative; other labs were unremarkable. Pelvic US is negative. CT reveals concentric hyperdense rings (target sign) at the ileocecal junction with crescentic mesenteric fat (Figure 1). Endoscopy is performed revealing an erythematous, centrally opaque and ulcerated mass telescoping into the cecum at the ileocecal junction (Figure 2). The patient goes to the OR for a right hemicolectomy including terminal ileum, appendix and cecum, and an end-to-end anastomosis. On gross examination a 5.3x4.4x3.1cm white, rubbery transmural mass is found from the resected bowel involving the ileocecal wall and occluding the appendiceal orifice. Microscopic analysis reveals cecal endometriosis associated with focal transmural acute and chronic inflammation, edema and fibropurulent serositis. Two of eighteen lymph nodes have endometriosis. The patient recovers from the procedure and is discharged free of pain. There have been few cases of intussusception due to endometriosis, and in our literature review we were unable to find a case where the lesion was visualized on endoscopy. While imaging identified the sole lesion in our case, small lesions with can be missed. In adults, the cause for intussusception is often neoplastic and colonoscopy is a useful tool prior to surgery to examine if there are further less obvious lesions that may require the surgical plan to be modified.

[459A] Figure 1.

[459B] Figure 2.



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Don’t Count Out EUS: Insulinoma Diagnosed by Endoscopic Ultrasound in a Gastric Bypass Patient

Management of Symptomatic Internal Hemorrhoids With HET System Using a Modified Technique: A Single-Center Experience

Jessica McKee, DO1, Waseem Butt, MD2, Mustafa Huseini3, Harshit S. Khara, MD2, Michael Komar, MD, FACG4, Amitpal S. Johal , MD2. 1. Geisinger Medical Center, Selinsgrove, PA; 2. Geisinger Medical Center, Danville, PA; 3. Geisinger Medical Center, Danville, PA; 4. Geisinger Health System, Danville, PA. Insulinomas are rare pancreatic neuroendocrine tumors that present with hypoglycemia. Timely diagnosis and localization of the tumor is critical. We present a rare case of an insulinoma in a gastric bypass patient able to be localized with endoscopic ultrasound (EUS) when CT and MRI were negative. A 63-year-old female with a history of obesity status post gastric bypass presented with a 6-month prodrome of increased frequency and severity of hypoglycemia which became refractory to administration of IV dextrose. Endogenous hyperinsulinemia was evident with a normal C –peptide (3.9 ng/mL), hypoglycemia with elevated insulin levels (36 uU/mL), elevated pro insulin level of 89.2 pmol/L and a negative hypoglycemic medication panel. Diazoxide was initiated for treatment. Octreotide scan showed no radiotracer activity in the abdomen. MRI and CT of the abdomen showed no mass in the pancreas. EUS was subsequently performed showing a round 7x8mm hypoechoic mass in the pancreatic neck adjacent to the portal confluence. Endoscopic borders were well defined with an intact interface between the mass and the portal vein suggesting lack of invasion. FNA was performed through a transgastric pouch approach with a 22-gauge needle. Cells were small with round nuclei, smooth nuclear borders, coarse chromatin and minimal cytoplasm. The background contained numerous fragments of normal pancreatic acini. Immunocytochemical assays demonstrated strong positivity for synaptophysin and focal positivity for chromogranin. Cytology was suggestive of a pancreatic neuroendocrine neoplasm. Resection of the mass was performed. A1.5x1.3x1.0 cm well-circumscribed tan-white, mildly indurated nodule with focal areas of necrosis was identified consistent with a well–differentiated pancreatic neuroendocrine tumor, low grade, WHO Grade 1. Postoperative glucose ranged from 92 – 235 mg/dL without glucagon or diazoxide. Timely diagnosis and localization of an insulinoma is critical. There are many noninvasive modalities including CT, MRI and Somatostatin receptor scintigraphy, however, a significant proportion of insulinomas are not detected and require invasive modalities for tumor localization preoperatively. EUS is safe, highly effective and has been demonstrated to detect tumors as small as 2-3 mm. In the setting of surgically altered anatomy, particularly gastric bypass surgery, EUS should still be considered as a diagnostic modality.

Truptesh Kothari, MD, MS1, Tom Jose, MD2, Guobao Wang, MD3, Shivangi Kothari, MD1, Vivek Kaul, MD, FACG1. 1. University of Rochester Medical Center, Rochester, NY; 2. Western Reserve Health Education/ Northeast Ohio Medical University, Youngstown, OH; 3. Sun Yat-Sen University Cancer Center, Rochester, NY. Symptomatic internal hemorrhoids are a common problem, with an estimated prevalence of 4.4% in the US, based on a large epidemiologic study. In both genders peak incidence occurs between the age of 45-65 years. Methods: We conducted a retrospective chart review of patients with symptomatic internal hemorrhoids who received treatment with the modified HET (Hemorrhoidal Energy Treatment) technique from March – June 2015 at our center. The modified HET technique utilizes simultaneous insertion of an endoscope (typically a gastroscope) to improve vision/accuracy and a pediatric forceps to grasp the supra-hemorrhoidal rectal tissue, to enhance suction of the tissue into the HET device, which in turn leads to better delivery of heat energy to the targeted area. All procedures were carried out using enema prep, unsedated or using moderate sedation, depending on patient preference/ clinical setting. Results: A total of 13 patients received modified HET therapy during the study period. Demographics of the patients are detailed in the table below. All patients had actively bleeding hemorrhoids and had not previously responded to conservative therapy. All 13 patients had either grade 1 or grade II internal hemorrhoids. Two patients underwent HET without sedation as requested by the patient. All patients denied any pain or discomfort after the procedure. Out of 13 patients, 11 received HET under moderate sedation immediately following a diagnostic colonoscopy. Three columns of internal hemorrhoids were targeted with HET in each patient, for the initial session. A single therapeutic HET session achieved treatment success in 11/13 patients. All patients were followed up with telephone calls at 1 and 6 weeks post procedure. 2 patients required an additional treatment session for recurrent bleeding. In these 2 patients, 5 columns were targeted at the 2nd session. Both remain asymptomatic 4 weeks status-post second session. Discussion: Several treatments options exist for non-surgical management of symptomatic internal hemorrhoids: band ligation, bipolar diathermy and infrared photocoagulation. HET is a promising new therapy which is effective and minimally invasive. We have modified the HET technique by adding an endoscope and pediatric forceps, for enhancing vision, accuracy and delivery of thermal energy to an adequate amount of tissue. Our single institution experience confirms that HET bipolar system is an effective technique in addition to being quick, safe, and painless. Targeting 5 columns of internal hemorrhoids may help avoid recurrent bleeding in refractory cases.

[460A] Figure 1.

[460B] Figure 2.


[461A] Figure 1.


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Abstracts

462 Painful Purple Papules: An Interesting Case of Visceral Kaposi Sarcoma Jason D. Jones, MD1, Ashley M. Lane, MD2. 1. Wake Forest School of Medicine, Department of Internal Medicine, Winston-Salem, NC; 2. Wake Forest School of Medicine, Department of Internal Medicine (Gastroenterology), Winston-Salem, NC. Introduction: AIDS-related Kaposi sarcoma (KS) is the most common tumor arising in HIV-infected persons. However, visceral involvement as the initial manifestation of KS is relatively uncommon. Case Report: A 24 year old African American male with recently diagnosed AIDS (CD4 count 50) presented with three weeks of progressive, non-radiating, cramping, peri-umbilical abdominal pain. The pain was associated with nausea, non-bloody emesis and weight loss. On physical exam, he had tenderness in his right upper quadrant and peri-umbilical region. He was also noted to have several cutaneous violaceous nodules on the nasal tip, chest wall, abdominal wall, and left lower extremity. His laboratory evaluation was notable for WBC 4.1, Hgb 8.7, platelets 458, iron 10, and ferritin 3. A contrasted computed tomography scan of the abdomen and pelvis was notable for extensive peritoneal necrotic lymphadenopathy. Esophagogastroduodenoscopy and endoscopic ultrasound revealed multiple raised isolated violaceous or hemorrhagic nodules in the oropharynx, esophagus, stomach and duodenum. Biopsies of the lesions were consistent with KS. Given his symptomatic visceral disease, he was started on chemotherapy with doxorubicin in addition to anti-retroviral therapy. Discussion:Of the four epidemiologic forms of KS, AIDS-related KS is most commonly associated with visceral disease. KS has been observed in almost all visceral sites, but the most frequent sites of non-cutaneous disease are the oral cavity, gastrointestinal tract, and respiratory system. Visceral involvement as the initial manifestation of the disease is uncommon and portends a poor prognosis. Gastrointestinal involvement can occur even in the absence of cutaneous disease; lesions may be silent or may cause abdominal pain, upper or lower gastrointestinal bleeding, nausea and vomiting, malabsorption, weight loss and/or intestinal obstruction. Gastrointestinal lesions can occur anywhere along the gastrointestinal tract, and can be easily recognized by an endoscopist as isolated or confluent hemorrhagic lesions. The diagnosis of KS should be confirmed by biopsy, although lesions tend to be submucosal, which can make histologic diagnosis difficult. Therapy is dictated by the extent of disease, as well as the presence or absence of symptoms. Severe and symptomatic disease is usually managed with anti-retroviral therapy and systemic chemotherapy.

[462C] Figure 3.

463 Intestinal Ganglioneuroma: Endoscopic Findings of Cowden Syndrome Sridivya Parvataneni, Dhara Chaudhari, James Swenson, Mark Young, MD. East Tennessee State University, Johnson City, TN. Introduction: Intestinal ganglioneuromas are rare tumors composed of ganglion cells, nerve fibers, and supporting cells that occur in isolation or as a part of syndrome. Here in we report a young male with endoscopic findings of cowden syndrome.

[462A] Figure 1.

[462B] Figure 2.


[463A] Figure 1.

[463B] Figure 2.


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Case: 38 year old male presented to the emergency department with 3 day history of abdominal pain and intermittent episodes of hematochezia. Past history is significant for dysplastic nevi, family history: colon cancer in father, and breast cancer and benign thyroid nodules in sister. On physical examination, his vitals are stable, has macrocephaly with head circumference of 65.5 cm and lipoma on back. He was hemodynamically stable and was sent home to be followed up with gastroenterology for consideration of endoscopy. On colonoscopy, multiple colonic polyps were found, which were ganglioneuromas by biopsy (Figure 1). Surveillance esophagogastroduodenoscopy revealed esophageal glycogenic acanthosis (Figure 2) and hyperplastic gastric polyps raising a suspicion of Cowden syndrome. Thyroid ultrasound was done which showed multiple thyroid nodules. He met the international Cowden consortium criteria for diagnosis of Cowden’s syndrome with one major (macrocephaly) and 3 minor (thyroid lesions, intestinal ganglioneuromas and lipoma) and was referred to genetic counselor. Discussion: Cowden’s syndrome is autosomal dominant disorder with incomplete penetrance and variable expressivity. It is associated with mutations in the PTEN gene and carries an increased risk for both benign and malignant tumors. Thyroid, colorectal and renal cancer surveillance should be done in these patients. In addition, women with Cowden’s syndrome need screening for breast and endometrial cancers.

464 Bouveret’s Syndrome: A Challenging Cause of Gastric Outlet Obstruction Ahsan Khan, MD1, Hafiz M. Khan2, Liliane Deeb , MD3, Moiz Ahmed, MD4, George G. Abdelsayed5, Sherif Andrawes, MD2. 1. Staten Island University Hospital, Bellerose, NY; 2. Staten Island University Hospital, Staten Island, NY; 3. Staten Island University Hospital/NorthShore LIJ Health System, Staten Island, NY; 4. Siuh, Staten Island, NY; 5. North Shore-LIJ/Staten Island University Hospital, Union City, NJ.

[464B] Figure 2.

Bouveret’s syndrome is a clinically distinct form of gallstone ileus caused by the formation of a fistula between the gallbladder and duodenum, where typically a large gallstone is impacted in the pylorus or proximal duodenum. This rare condition could be associated with high morbidity and mortality rates, hence increased awareness is waranted. We report a case of Bouveret’s syndrome in a patient with gastric outlet obstruction due to a 7 cm gallstone chronically impacted in proximal duodenum. 78-year-old male with history of atrial fibrillation and COPD presented with epigastric pain and bilious vomiting of 1 week duration. Physical exam revealed abdominal distension. Laboratory tests revealed elevated WBCs, liver enzymes and lipase. CT scan of abdomen showed a 7 x 4.4 cm gallstone in proximal duodenum, a cholecystoduodenal fistula and pneumobilia (Figure1). EGD revealed a complete obstruction secondary to a stone impacted beyond the duodenal bulb (Figure2). Endoscopic removal was attempted initially, aiming to fragment the stone via mechanical and electrohydraulic (EHL) lithotripsy. The large size was a limitation to the mechanical approach. EHL was partially effective in fragmenting the stone despite using the highest available energy level and multiple catheters. Other tools were attempted thereafter in order to pull the stone in the stomach for further fragmentation, including fluoroscopy assisted wire-guided biliary balloon, assisted TTS dilation balloon extraction, snare assisted and loop assisted removal. The stone was adherent to the wall of the duodenum. The patient underwent successful surgical removal of the stone through duodenotomy (Figure 3) followed by cholecystectomy and cholecystoduodenal fistula repair. Patient did well postoperatively. Bouveret’s syndrome is an uncommon cause of gastric outlet obstruction and an important diagnosis worth considering especially in patients with history of biliary colics, large gallstones or chronic cholecystitis. Abdominal imaging and endoscopy are the mainstay of diagnosis. Treatment options include endoscopic and surgical management. Endoscopic removal should always be attempted first, despite the reported limited success rate of 10%. The addition of mechanical and/or electrohydraulic lithotripsy has been used with some success. Surgery is required in over 90% of cases, with mortality rates ranging from 19% to 24%. Surgical options include enterotomy and removal of stone with or without cholecystectomy and repair of fistula, or gastric bypass surgery. In this case we present a unique case of chronic Bouveret’s syndrome where the size (7 cm) and adherence of the impacted stone to the duodenal wall was a major limitation hindering the success of the endoscopic approach. Increased clinical awareness is of utmost importance for the timely management of this rare syndrome.

[464C] Figure 3.

465 Esophageal Hyperkeratosis: An Extreme Case and Its Clinical Impact Abdelhai Abdelqader, MD1, Joel Hammer, MD2, Albert Fleisher, MD2. 1. MedStar Franklin Square Medical Center, Rosedale , MD; 2. MedStar Franklin Square Medical Center, Baltimore, MD.


Esophageal hyperkeratosis (EH) is a benign histologic finding, but given its association with mucosal malignancy it should not be ignored. We present an extreme case of EH presenting as an arachnoid-like esophageal mass. We discuss the manifestation of extensive EH and explore clinicopathologic associations. 69-year-old male with ongoing alcohol use presented with recurrent dysphagia and 50lbs weight loss over 4 months. Physical exam was normal. Initial esophagogastroduodenoscopy (EGD) showed strictures and plaque (Fig. 1) with high-grade squamous dysplasia. Repeat EGD showed EH, esophageal parakeratosis (EP) and Candida. Six months later, EGD showed a fixed mass causing critical narrowing at the distal esophagus (Fig. 2). Biopsies revealed similar findings, but with actinomycosis. This was treated with intravenous antibiotics for six months. However, resolution of the esophageal findings did not occur suggesting that actimomycosis was not the underlying cause, rather a secondary phenomenon. Repeat EGDs showed same endoscopic and histologic changes (Fig. 3), noting heavy growth of a mixed bacterial flora and yeast that colonized a keratotic


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Abstracts

466 Think Twice With That Tuna Tartare Donald Tsynman, MD1, Lan S. Wang, MD2, Li Zhang, R-PAC3, Poline Yiu, R-PAC3, Anthony J. Ng, MD1. 1. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 2. Mount Sinai Beth Israel, New York, NY; 3. Ng Medical, New York, NY.

[465A] Figure 1.

Case: A 67 year-old Chinese male presented to our practice in downtown Manhattan with epigastric pain. He had a history of a gastric ulcer at age 17. He reported no prior EGDs or testing for H. pylori. He consumed a diet typical for Chinese individuals living in NYC and did note a prior history of ingesting raw tuna and shrimp. EGD was performed for suspected H. pylori-associated peptic ulcer disease. Linear erythema and diffuse pangastritis was found. Additionally, a 5mm clean based shallow ulcer was found. Immediately adjacent, was a white string-like foreign body which was superficially embedded into the mucosa. This was removed with biopsy forceps. Pathology revealed active chronic H. pylori gastritis and intestinal metaplasia. The foreign body was sent to the Department of Health and identified as an Anisakis larva. The patient was treated for H. pylori and after starting a PPI, his symptoms improved. Discussion: Symptoms from acute Anisakiasis can be categorized into symptoms caused by the direct interaction of the larva with the GI tract and IgE-mediated reactions. Non-invasive Anisakiasis is asymptomatic. Occasionally, a “tickling throat syndrome” may occur as the worm migrates up the esophagus. Conversely, the larva can burrow directly into mucosa of the stomach, small intestine, and colon. Gastric invasion causes sharp epigastric pain, vomiting, and diarrhea. Ulcers and abscess formation is common. Intestinal invasion takes several days and manifests with diffuse lower abdominal pain, small bowel or colonic obstruction, and perforation. Extraintestinal involvement includes lymph nodes, pancreas, and the mesentery which can cause small bowel strangulation via granulomatous inflammation. Both type III and IV reactions to Anisakis allergens occur. When the intestinal epithelium is breached, intestinal permeability can become altered. Chronic Anisakiasis is rare. Symptoms include vomiting, diarrhea, abdominal pain, and chronic urticaria. Serology is important in these cases as larva typically dies within 8 weeks and becomes difficult to identify radiographically or endoscopically. Diagnosis can be made by IgG and IgA to Anisakis, which can last up to 12 months. Removal of the parasite by regurgitation or endoscopy is definitive. Albendazole and steroids have also been used in small series with success. From a public health perspective, prevention of Anisakiasis is easily achieved by cooking seafood to 70ºC or freezing to -20ºC for at least 72 hours. In our case, given the patient’s simultaneous infection with H. pylori and Anisakiasis, it is difficult to tell which of his abdominal symptoms can be attributed solely to the latter. As the worm was found intact, the infection was likely acute. The endoscopic removal constitutes successful treatment of the infection.

467 Diagnosis of Rare Pseudomyxoma Peritonei via Endoscopic Ultrasound-Guided Fine Needle Aspiration: A Case Report Umar Darr, MD1, Turki Alkully, MD1, Calvin Feng1, Basmah Khalil, MD2, Ali Nawras, MD, FACG1. 1. University of Toledo Medical Center, Toledo, OH; 2. University of Toledo, Toledo, OH.

[465B] Figure 2.

Introduction: Pseudomyxoma peritonei is a rare condition caused by mucinous adenocarcinoma cancerous cells that produce abundance of mucin or gelantinous ascites. This cancer can cause tissue fibrosis and can impair normal organ function. Diagnosis can utlize multiple imaging modalities including CT scan. There have been few cases of endoscopic ultrasound diagnosed via guided fine needle aspiration for this condition. Here we present a rare case of pseudomyxoma peritonei in a post-appendectomy patient via endoscopic ultrasound guided fine needle aspiration as the primary means of diagnosis. Case Study: Our patient is a 66 year old male with history of appendectomy presenting with intermittent abdominal pain for two years and weight loss of forty pounds over two months. Esophagogastroduodenoscopy and colonoscopy performed at outside hospital was unremarkable. CT abdomen revealed perigastric ascities and liver lesions. ESR was elevated at 75. At our facility, Endoscopic Ultrasound was performed revealing a peri-gastric and omental mass measuring 36.6mm x 25.5mm. Fine needle aspiration of the mass and ascetic fluid revealed bland-appearing mucinous epithelial clusters embedded in dense mucin material consistent with low grade mucinous adenocarcinoma with mucinous deposits in

[465C] Figure 3.

mass with continued failure to thrive. Ultimately, due to continued alcohol use and poor surgical candidacy for esophagectomy, a gastrostomy tube was placed for nutritional therapy. EH has been endoscopically described as patchy or confluent plaques and/or mucosal thickening with prominent furrows or rings1,2, and even as flat, elevated lesions mimicking neoplasia3. In our case, EH presented as an arachnoid-like mass with critical narrowing of the distal esophagus exacerbating severe malnutrition. Given the abnormal endoscopic findings, we were obligated to investigate for an underlying neoplastic process due to evidence associating EH and EP with malignancy. A prospective study found that EH in the setting of non-BE was commonly associated with esophageal and head and neck squamous dysplasia or carcinoma4. In a postmortem series of esophageal cancer, parakeratosis was histologically identified in the non-cancerous portions in 90%5. In this case, we have documented the unusual finding of extensive EH initially presenting with leukoplakia then later a mass in a patient with alcohol and tobacco abuse, esophageal manipulations, and super-infections. Despite the unclear malignant potential, EH can serve as a histologic marker for squamous dysplasia and invasive squamous cell carcinoma of head and neck and hence warrants close endoscopic surveillance. This case highlights the challenge of managing a male with risk factors for esophageal neoplasia and failure to thrive in the setting of extensive EH progressing to an obstructive mass.



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11 months. After octreotide he had no further GIBs and no transfusions for 12 months. Overall, these patients required a median of 2 endoscopic procedures (range 0-3) and a median of 8 units pRBCs (0-16) after octreotide LAR was started. In the two patients with GIBs despite octreotide, dosing was increased to twice monthly with no further bleeding. There were no thrombotic events after starting octreotide. Discussion: In post-LVAD patients, octreotide appears to markedly decrease the frequency of GIB with a reduction in transfusion requirements and endoscopic procedures. Octreotide reduces mesenteric blood flow and portal venous pressure, and has been used for treatment of small bowel AVMs with an excellent safety profile. Octreotide may be an effective therapy for secondary prevention of GIB in patients with an LVAD and warrants further prospective investigation.

Table 43. Summary of Findings Episodes of GIBPrior to Octreotide

Episodes of GIBAfter Octreotide

# of pRBCs TransfusedBefore Octreotide

# of pRBCs TransfusedAfter Octreotide

#1

7

3

36 Units

16 Units

#2

4

2

32 Units

8 Units

#3

2

0

33 Units

0 Units

Patient

[467B] Figure 2.

469 Novel Treatment of Malignant Gastric Outlet Obstruction With a Stent-Within-Stent Approach Secured With Apollo OverStitch™ Shawn Kaye1, Katherine Kim1, Neha Chaurasia2, Jason B. Samarasena, MD3. 1. University of California Irvine School of Medicine, Irvine, CA; 2. Carnegie Mellon University, Pittsburgh, PA; 3. University of California Irvine, Orange, CA.

[467C] Figure 3.

the peritoneum. On cell block, tumor cells were focally positive for cytokeratin 7 and cytokeratin 20consistent with diagnosis of pseudomxyoma peritonei. Conclusion: Endoscopic ultrasound guided fine needle aspiration can be a reliable and safe technique in diagnosis of pseudomyxoma peritonei

468 Management of Left Ventricular Assist Device (LVAD)-Related Gastrointestinal Bleeding (GIB): A Retrospective Case Series Presidential Poster Konstantin Peysin, DO1, Jonathan Buscaglia, MD2, Satish Nagula, MD2, Michelle Weisfelner Bloom, MD3, Allison McLarty, MD3, Hal Skopicki, MD3, Juan Carlos Bucobo, MD4. 1. Stony Brook University Hospital, Coram, NY; 2. Stony Brook University Hospital, Department of Medicine, Division of Gastroenterology, Stony Brook, NY; 3. Stony Brook Hospital, Stony Brook, NY; 4. Stony Brook University Hospital, Department of Medicine, Division of Gastroenterology, Stony Brook, NY. Introduction: GIB complicates 17-30% of postoperative LVAD placements. Despite attempts to modulate anticoagulation and prescreening to prevent bleeding, there is no consensus on treatment for these patients. Our objective is to evaluate the potential role of octreotide LAR in patients with an LVAD for secondary prevention of GIB. Methods: Forty patients underwent LVAD implantation at our institution between 12/2012 and 12/2014. Ten developed GIB during their postoperative course (25%). Eight had bleeding secondary to arteriovenous malformations (AVMs) in the small bowel and two secondary to ulcers. Four patients suffered a recurrent GIB which was not controlled by endoscopy and were placed on octreotide. Three of the four were placed on octreotide LAR. We evaluated the clinical scenarios of these patients. Results: Three patients (2 men and 1 woman; ages 60-72) received octreotide LAR. None had a GIB prior to LVAD implantation. Post implantation, patients had a median of 5 endoscopic procedures for GIB prior to starting octreotide(range 2-9). AVMs were the cause of GIB in all 3 cases. The first patient had 7 GIBs with 36 units of packed red blood cells (pRBCs) transfused over the course of 12 months. After octreotide was started, she had 3 GIBs with 16 units of pRBCs transfused over the following 16 months. One GIB was after a missed octreotide dose and required 8 of the 16 units of pRBC. The second patient had 4 GIBs with 32 units of pRBCs transfused over 2 months. After octreotide he had 2 GIBs requiring 8 units of pRBCs over 6 months. The third patient had 2 GIBs with 33 units of pRBC transfused over


Uncovered self-expandable metal stents (UCSEMS) are commonly used for palliative treatment of malignant tumors resulting in gastric outlet obstruction (GOO). Tumor ingrowth is a frequent complication leading to stent restenosis and treatment failure requiring the need for additional intervention. Placement of a fully covered self expandable metal stent (FCSEMS) within an UCSEMS has been reported with successful alleviation of re-obstruction caused by stent ingrowth. While this technique can provide relief, it can be further complicated by stent migration of the fully covered stent. Placement of clips at the proximal ends of secondary stents has been shown to decrease stent migration rates. To our knowledge, no other stent-in-stent securing methods have been evaluated. We describe the successful treatment of recurrent GOO with a duodenal stent-within-stent secured in place with Apollo OverStitch (Apollo Endosurgery, Texas). A 56-year-old male with metastatic cholangiocarcinoma presented with worsening nausea and vomiting. Prior to presentation, the patient underwent placement of an UCSEMS through the pylorus and duodenum for GOO from tumor burden. The patient subsequently developed a repeat duodenal obstruction from tissue ingrowth and had a second UCSEMS deployed within the first stent 6 months after the original stent placement. At our evaluation, 4 months after the 2nd stent placement, it was noted that there was yet another stricture from further tissue ingrowth. Gastrojejunostomy tube placement was offered to the patient, but he declined. The decision was made to place a 3rd stent for symptom palliation. On endoscopy, a tight stricture was noted within the existing stents. Under endoscopic and fluoroscopic guidance, a wire was placed distally into the duodenum and a 100mm x 18mm FCSEMS was placed within the previous stents. Using Apollo OverStitch, the proximal edge of the stent was sutured into the antral gastric mucosa, and the lateral side of the stent was sutured into the proximal edge of the original stents. The patient tolerated the procedure well. The patient’s symptoms of nausea and reflux resolved and follow-up at 6 months revealed continued resolution of obstructive symptoms. The Apollo OverStitch has shown a high technical success rate of securing stents in benign gastrointestinal conditions. Novel use of the OverStitch for stent fixation, particularly stent-within-stent fixation, is promising.

470 Endoscopic Submucosal Dissection for the Complete Resection of the Rectal Remnant Mucosa in a Patient With Familial Adenomatous Polyposis Presidential Poster Naoki Ishii, MD, Yoshiyuki Fujita, MD, Mai Ego, Kaoru Nakano. St. Luke’s International Hospital, Tokyo, Japan. Ileorectal anastomosis (IRA) is sometimes performed for patients with familial adenomatous polyposis (FAP) instead of ileal pouch-anal anastomosis (IPAA) because it produces better functional outcomes and decreased infertility rate after surgery. However, neoplasms that occur in the rectal remnant after IRA require additional surgical procedures, including secondary proctectomy]. Endoscopic submucosal dissection (ESD) has recently been performed for the treatment of superficial digestive neoplasms. Herein, we applied circumferential ESD to the management of the rectal remnant polyps in a patient with FAP and completely resected the rectal remnant mucosa using ESD technique. A 47-year-old female who underwent prophylactic colectomy and IRA for FAP 18 years ago and 5 separate transanal endoscopic microsurgeries for the removal of subsequent rectal remnant polyps. She was referred to our gastroenterology center for the treatment of recurrent rectal polyps. Proctoscopy revealed


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Abstracts decreased vomiting. He was then referred for surgical intervention and a laparoscopic assisted G-POEM was performed. Laparoscopy revealed a distended stomach. An upper endoscope with an Olympus tapered cap was introduced into the stomach. Approximately 5cm proximal to the pylorus a 10cc anterior submucosal injection was made with Indigo Carmine, saline, and epinephrine. Using an Olympus triangle knife a mucosotomy was performed and the endoscope was introduced into the submucosal space. A submucosal tunnel was created using injection and spray cautery to a point 2cm distal to the pylorus. This position was confirmed by laparoscopy. The stomach muscle fibers were divided 3cm proximal and 1cm distal to the pylorus using the triangle knife. The mucosotomy was closed with endoclips. A gastrograffin contrast study was negative for leaks at the mucosotomy site. Clear liquid diet was started on POD #4. The patient was discharged on POD #6 on normal diet. Two weeks following the procedure the patient reported minimal nausea and vomiting. Discussion: Following the advent of POEM for achalasia, endoscopic pyloromytomy was entertained using a similar submucosal tunneling technique. While the first endoscopic pyloromyotomy was performed in 2011, there have been few procedures performed. The limited published data in 10 cases reported technical success, safety, and short term efficacy. We report a successful laparoscopic assisted G-POEM for a patient with diabetic gastroparesis who had transiently responded to botulinum toxin injection to the pylorus. Although early in its evolution, G-POEM appears to be a safe and effective alternative to surgical pyloroplasty for gastroparesis with the theoretical advantage of shorter postoperative recovery. More investigation is needed to determine long term efficacy of the procedure and the optimal patient selection criteria for G-POEM.

472 [470A] Figure 1.

Endoscopic Repair of Gastrogastric Fistulas After Roux-en-Y Gastric Bypass Jason D. Jones, MD1, Rishi Pawa, MBBS2, John A. Evans, MD2. 1. Wake Forest School of Medicine, Department of Internal Medicine, Winston-Salem, NC; 2. Wake Forest School of Medicine, Department of Gastroenterology, Winston-Salem, NC.

[470B] Figure 2.

Introduction: Gastrogastric fistulas are a rare complication of Roux en Y gastric bypass. Several options exist for repair. Our goal was to present our experience with the use of an over the scope clip system for endoscopic intervention. This is a retrospective review from a university hospital where three patients have undergone endoscopic repair of gastrogastric (GG) fistulas using an over the scope clip (OTSC) system developed by OVESCO™. Case Presentations: Patient 1, a 58 yo female, presented with increased food intake. She was found to have a GG fistula 2 months post Roux en Y bypass (RNY). Her postoperative course was complicated by a left subphrenic abscess and left empyema which necessitated a VATS procedure. Two fistulas were found at EGD, one of which measured 14 mm and the other 5 mm in diameter. Two hemoclips and one OTSC (12/6 GC) were applied to the larger defect and one hemoclip was applied to the smaller defect. Repeat upper GI series one month post EGD showed failure of fistula closure. Patient 2, a 69 yo female, presented with epigastric abdominal pain and was found to have a 4 mm GG fistula 34 months post RNY. She had lost ~118lbs since bypass. On initial repair attempt the fistulous tract appeared to have closed after APC and hemoclip placement x 2, however the fistula was again noted on repeat upper GI series 4 months later. A follow up EGD was performed with successful OTSC deployment (12/6 GC). Patient 3, a 44 yo female, presented with epigastric abdominal pain, nausea, emesis, and weight gain and was found to have a 5 mm GG fistula 66 months post RNY. She had lost ~ 435 lbs since bypass. Successful OTSC deployment was performed (12/6 GC). The patient experienced symptom relief on follow up. Discussion: The success of gastrogastric fistula repair using an OTSC system appeared to be influenced by several factors including size, acuity, and post operative complications. Smaller fistulas were closed with greater success. The time interval between bypass and fistula development seems to have influenced success as well with fistula closure achieved in patients with a mean development interval of 50 months. Small superficial mucosal tears, with no evidence of bleeding or perforation, were noted in the proximal esophagus in both successful cases. The use of an OTSC system represents a safe, minimally invasive strategy for endoscopic closure of gastrogastric fistulas ≤5 mm.

multiple polypoid lesions in the rectal remnant (Figure 1A). Polypoid lesion biopsy specimens showed high grade adenomas. Because the polyps circumferentially extended throughout the rectal remnant and the oral portion of the lesions spread onto the anastomotic site, ESD was planned for the complete resection of the rectal remnant mucosa. Although the dissection of the submucosa at the anastomotic site was difficult because of severe fibrosis, the rectal remnant mucosa was completely resected in two pieces without perforation using a hook knife (KD-620LR; Olympus Medical Systems) (Figures 1B-D). The pathological examination of the resected specimens demonstrated high grade adenoma. Post-ESD stricture was prevented using betamethasone suppositoryand finger bougie. The follow-up proctoscopy performed 9 months after ESD did not reveal any recurrence in the rectal remnant (Figure 2). We consider circumferential ESD to be a safe and effective treatment for the complete resection of the rectal remnant mucosa after IRA in patients with FAP.

471 Successful Laparoscopic-Assisted Gastric Per Oral Endoscopic Myotomy (G-POEM) in Refractory Diabetic Gastroparesis Marie L. Borum, MD, EdD, MPH, FACG1, Steven Zeddun, MD2, Najeff Waseem, MSIV2, Frederick Brody, MD2. 1. George Washington University, Washington , DC; 2. George Washington University, Washington, DC. Introduction: Current medical options are not always effective in treating gastroparesis. Data suggests that surgical pyloroplasty can improve symptoms in selected patients. More recently endoscopic myotomy has been considered as a therapeutic option. However, few cases have been performed. We report a successful laparoscopic assisted G-POEM in a patient with refractory diabetic gastroparesis. Case: A 30 year-old man with diabetes presented with 10 months of refractory gastroparesis requiring TPN. Prokinetic agents resulted in minimal response. Botulinum injection of the pylorus resulted in


[472A] Figure 1.


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474 Safety and Efficacy of Dynamic Submucosal Injection Technique for the Mucosal Resection of Large Colorectal Neoplasia Ashraf Almashhrawi, MD1, Fazia Mir, MD1, Hazem Hammad, MD1, Tonya Kaltenbach2, Roy Soetikno3. 1. University of Missouri, Columbia, MO; 2. Veterans Affairs, Palo Alto, CA; 3. Singapore General Hospital, University of Singapore, Singapore, Singapore.

[472B] Figure 2.

Introduction: Endoscopic mucosal resection (EMR) of large colorectal polyps is efficacious and safe with the selection of the appropriate polyp and resection technique. Several studies have demonstrated the short and long term efficacy of EMR. Several techniques have been used to improve the efficacy and to minimize complications. Submucosal injection has been conventionally used to create a submucosal bleb that facilitates snaring the lesion off. Dynamic submucosal injection (DSI) technique employs several steps including adjusting the angle of the injecting needle, moving the needle while injecting in a path that is envisioned by the endoscopist, applying suction, and rapidly injecting the solution. We present our experience with the use of DSI technique in resecting large colorectal polyps. Results: We have performed 101 EMRs on 82 patients with a mean age of 65 years (60% males) between August 2013 and November 2014. The mean polyp size was 29mm (range 15-60mm). The mean procedure time was 57 minutes. 64% of the lesions were in the right colon. Histopathology showed tubular adenoma with low grade dysplasia (TA-LGD) (n=50), sessile serrated adenoma (n=26), tubulovillous adenoma (n=9), tubulovillous adenoma with focal high-grade dysplasia (n=6), tubular adenoma with focal high-grade dysplasia (n=4), intramucosal adenocarcinoma (n=2), invasive submucosal adenocarcinoma (n=3), and Maltoma (n=1). Complete removal was achieved in all cases and lesions were removed en bloc 30% of the time. A mean of 38ml of normal saline (with indigo carmine) was injected. Argon plasma coagulation was used in 73% of the resections with mucosal defect closure with endoclips performed in all. Complications included bleeding (n=1), postpolypectomy syndrome (n=1), and postprocedure emesis (n=1). In the twenty five patients that have undergone follow up colonoscopies so far, we have found 2-3mm residual polyp tissue (TA-LGD), only in 3 patients (10%). One of the intramucosal adenocarcinoma lesions underwent surgical resection as margins were involved. The other intramucosal lesion was removed en bloc with unremarkable computed tomography scan and rectal ultrasound and no recurrence on follow up. Of the three patients with invasive submucosal adenocarcinoma, two had subsequent colectomy with no residual cancer and negative lymph nodes. Discussion: DSI technique for endoscopic mucosal resection of large colorectal lesions is efficacious and safe.

475 Successful Endoscopic Treatment of Jejunal Perforation Caused by a Migrated Plastic Pancreatic Stent Parit Mekaroonkamol, MD, George Philips, MD, Field Willingham, MD, MPH, Qiang Cai, MD, PhD, FACG. Emory University, Atlanta, GA.

[472C] Figure 3.

473 Endoscopic Band Ligation of Symptomatic Inflammatory Rectal Polyps Imran Ashraf, MD, Umair Sohail, MD, Fazia Mir, MD, Matthew Bechtold, MD, FACG, Hazem Hammad, MD. University of Missouri, Columbia, MO. Introduction: Non-neoplastic colonic polyps are usually classified as mucosal, submucosal, hyperplastic and inflammatory types. Inflammatory polyps, also referred sometimes to as pseudopolyps, form because of healing of mucosal ulceration with regeneration and are typically seen in the setting of infl ammatory bowel disease (IBD). Histologically, they are characterized by abundance of stroma with inflammatory cells, spindle cells and eosinophils. Although typically seen in IBD patients, these polyps can also be found in patients without any underlying colonic disease. We report a case of a young female patient with symptomatic inflammatory rectal polyps without any prior history of IBD which were successfully treated with band ligation. Case: A 33 year-old female patient presented to the gastroenterology clinic for intermittent hematochezia and rectal discomfort for the last few months. She had a history of a 5 cm inflammatory anorectal polyp for which she underwent a transanal surgical excision 6 years ago. She underwent a diagnostic colonoscopy which showed three large 1-1.4 cm sessile polyps and two 8 mm sessile polyps, all arising just above the dentate line. Biopsies confirmed inflammatory nature. Options for treatment included surgical resection, endoscopic mucosal resection, or band ligation. After discussion with the patient, we proceeded with a flexible sigmoidoscopy with band ligation of these polyps in two stages. In the first stage, we banded the three large polyps using the multi-band mucosectomy device, placing a total of three bands. She tolerated the procedure well and was treated with analgesics and stool softeners for few days postprocedure. Two months later, we performed a repeat flexible sigmoidoscopy and found healed scars from previous band ligation just above the dentate line. We also performed band ligation of the remaining two small 8 mm polyps in a similar fashion. She tolerated the procedure well. She was evaluated in the clinic four weeks later and reported complete resolution of her symptoms. Discussion: We propose that symptomatic inflammatory rectal polyps can be treated with endoscopic band ligation, such treatment option appears to be effective and seems to be relatively safe compared to other options such as endoscopic mucosal resection or surgical resection.


Intestinal perforation from stent migration is rare with an incidence of less than 1%. Most perforations occur in the duodenum by biliary stents. There have been only two reports of jejunal perforation from migrated pancreatic stents . Both cases were treated surgically. We report here, a case of jejunal perforation caused by a migrated pancreatic stent that was treated endoscopically. A 65-year-old female with systemic lupus erythematous, a history of sigmoidectomy for perforated diverticulitis, and distal pancreatectomy for a benign pancreatic mass that was complicated by pseudocyst from pancreatic ductal leak underwent a papillotomy with a 7 Fr, 11 cm straight plastic stent placement in the pancreatic duct. A 4–week follow-up CT scan showed improvement of pseudocyst but with a migrated stent to distal duodenum. The stent was not retrieved due to lupus flare and lack of any obstructive symptoms. She returned 4 months later with severe acute abdominal pain without peritoneal signs. CT abdomen found small free air and the migrated pancreatic stent eroding through jejunal walls with its tip embedded in the mesentery. An urgent small bowel enteroscopy revealed the migrated stent lodging in the proximal jejunum with both ends projecting outside the lumen. After tattooing the sites, a rat-tooth forceps was used to grasp one end of the stent and pulled it back into the lumen. Mucosal evaluation revealed three small full thickness defects. Three endoclips were deployed to

[475A] Figure 1.


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Abstracts A 59-year-old male with a history of Alcohol abuse presents with maroon bloody bowel movements and generalized weakness that started on the day of the admission. The patient was found to have severe normocytic anemia, Hemoglobin 5.5g/dl, thrombocytopenia with mildly elevated aspartate aminotransferase and low albumin level suspicious for advanced alcoholic liver disease. Proton pump inhibitor and octreotide drips were both started along with blood transfusion. Shortly after, the patient underwent EGD which revealed a small tortuous varix in the second portion of the duodenum. A minimal oozing of blood from the varix was noted with a moderate amount of fresh blood in the surrounding area. The decision was made to perform band ligation which successfully controlled the bleed. The next day, the patient had a melena and slight drop in the hemoglobin level. The patient was taken back to the endoscopy suite. The repeat EGD confirmed the previously placed band still in place without a stigmata of recent bleed. The patient was stable during the rest of the hospital course and was discharge on Non-Selective Beta Blocker (NSBB) to follow with us in the outpatient clinic. The duodenal varices are usually found in the setting of portal hypertension that lead to an increased pressure in the cystic branch of the superior mesenteric vein, the pancreaticoduodenal veins, the gastroduodenl vein, and the pyloric vein. In general, bleeding from ectopic varices is rare and represents 1% to 5% of all variceal bleeding. The bleeding of the duodenal varices make a significant challenge since the literature is rare and consists of case reports and few case series. The reported therapeutic approaches include endoscopic sclerotherapy, endoscopic detachable nylon loops, Endoscopic Band Ligation (EBL), surgical intervention, and radiologic interventions including Transjugular Intrahepatic Porto-systemic Shunt (TIPS) and Balloon-Occluded Retrograde Transvenous Obliteration (BRTO). The previously mentioned approaches have had variable success rate with occasional significant adverse events. EBL approach is an attractive initial approach due to the ease of use, minimal invasiveness and adverse events, availability, and the low cost. The variceal size, the acuity of the presentation and the local expertise may dictate the proper approach but the ultimate therapeutic approach is yet to be identified with larger and better design studies in the future.

[475B] Figure 2.

[476A] Figure 1. [475C] Figure 3.

approximate the perforation sites. The stent was retrieved uneventfully. The patient recovered well with complete resolution of abdominal pain 4 days afterward. Small bowel follow-through with gastrigrafin showed no extravasation of the contrast. Certolizumab was resumed at 6-weeks post-procedure with good resolution of her lupus flare. This case underscores the rare complication of migrated pancreatic stent and the role of endoscopic closure for intestinal perforations without peritonitis. Previous reports suggest that diverticulosis, history of abdominal surgery, altered intestinal anatomy, peritoneal carcinomatosis, and straight stents are risk factors for intestinal perforation. We believe that intraabdominal adhesion and lupus flare predisposed the perforation in our case. Close clinical monitoring should be endorsed when pancreatic stent migrates. Should perforation occur, early endoscopic closure is a viable option when there is no frank peritonitis.

476 Endoscopic Variceal Banding as an Initial Approach to a Bleeding Duodenal Varix Youssef Botros, MD1, Fady Asslo, MD2, Joseph Shami, MD3, Walid Baddoura, MD1. 1. St. Joseph’s Regional Medical Center, Paterson, NJ; 2. St. Joseph’s Regional Medical Center, Woodland Park, NJ; 3. St. Joseph’s Regional Medical Center, Paterson, NJ. Duodenal varices are usually found in the setting of portal hypertension and most commonly due to liver cirrhosis. The duodenal varices may rupture and cause severe upper GI bleed which poses a challenge due to the significant morbidity and mortality rates in the absence of clearly effective therapeutic approach. Endoscopic band ligation is an attractive option and may help control the bleed in the acute setting.


[476B] Figure 2.


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478 Endoscopic Removal of Bravo® pH Probe: Report of Two Cases Rubayat Rahman, MD, MPH1, Umair Sohail, MD1, Ashraf Almashhrawi, MD1, Imran Ashraf, MD1, Douglas Nguyen, MD2, Matthew Bechtold, MD, FACG1. 1. University of Missouri, Columbia, MO; 2. University of California Irvine, Anaheim Hills, CA. Introduction: The Bravo pH monitoring system is widely used to further investigate the patients with refractory or atypical GERD. The pH probe is attached by deploying a locking pin that is passed through the esophageal mucosa and pulled by appropriate suction into a small cup in the side of the probe. Subsequently, the probe sloughs spontaneously from the mucosa within 1-2 weeks and passes uneventfully through the GI tract. Most patients have no or mild symptoms while the probe is attached, but more severe chest pain, odynophagia, or dysphagia occurs in about 10% of patients. We report two rare cases of patients requiring endoscopic removal of Bravo pH probe. Case 1: 34 year-old female who presented with persistent heartburn despite maximal acid-suppressive therapy underwent endoscopic placement of Bravo pH probe at 6 cm proximal to GEJ. One hour after the procedure, the patient complained of significant chest pain at the site of Bravo pH monitoring probe and after 3 hours, the pain was persistent with no change in severity. Repeat endoscopy was performed. The Bravo pH probe was identified. A cold snare was placed around Bravo pH probe but was unsuccessful at removal. A hot snare was used and Bravo capsule probe was dislodged and advanced to stomach. Probe was snared and removed with endoscope via mouth. Patient’s pain resolved immediately. Case 2: 37 year-old male who had persistent chronic mild-to-moderate heartburn even after treatment with maximal proton-pump inhibitor for appropriate duration underwent endoscopic placement of Bravo pH probe at 6 cm proximal to GEJ. However, due to technical difficulties, the probe did not register with the monitor. Subsequently, another EGD was performed and the Bravo pH probe was removed via hot snare, after cold snare was again unsuccessful, and removed via mouth. A second Bravo pH probe was placed successfully and was working properly. Discussion: Bravo pH probes may require removal in certain situations. These cases show that both cold and hot snare techniques are safe and simple endoscopic procedures for the removal of the Bravo pH probe. We recommend the cold snare method as a first option with the hot snare method in cases the former fails.

[476C] Figure 3.

477 Gastric Antral Vascular Ectasia: Can Radiofrequency Ablation Be the Answer? Saurabh Chandan, MD1, Akriti Deewanwala, MD2, Jad Bou-Abdallah, MD2, Jacquelyn Ritchie, PA2. 1. Department of Medicine, University at Buffalo, The State University of New York, Omaha, NE; 2. Division of Gastroenterology, Western New York VA Hospital, Buffalo, NY. Background: Gastric antral vascular ectasia (GAVE) was first reported in 1953. The pathophysiology remains unknown. Conditions characteristically associated with GAVE are cirrhosis, autoimmune disorders e.g. scleroderma, chronic kidney disease, bone marrow transplantation. Surgical treatment options like gastric antrectomy have significant associated morbidity and mortality (Jensen et al, 2004). And while Argon plasma coagulation (APC) is an effective treatment, it requires frequent sessions and is rarely curative. (Tuveri et al, 2007). Case Report: A 62 year old white male was referred to our GI clinic for chronic iron deficiency anemia. His medical history included CAD s/p PCI, Cryptogenic cirrhosis s/p TIPS and he presented with multiple GI bleeds in the past. He underwent several endoscopies revealing portal hypertensive gastropathy, grade II esophageal varices and bleeding GAVE lesions. APC was performed twice at outside facilities for GAVE and symptomatic anemia. On evaluation, patient denied overt bleeding. Examination revealed anicteric sclera with pale conjunctivae. Abdomen was soft and distended with hepatosplenomegaly and 1+ pitting leg edema. Laboratory data revealed iron deficiency with Hb 10gm/dl. Despite undergoing 8 APC sessions at our facility, he remained iron deficient and symptomatic from anemia, requiring repeated transfusions. As he was refractory to APC therapy, decision was made to proceed with Radio Frequency Ablation (RFA) with Halo 90. A total of 5 sessions over 1 year led to resolution of anemia and transfusion requirements (Details in Table 1). Discussion: GAVE is an uncommon etiology of upper GI bleeding. These patients usually present with iron deficiency anemia. Medical, surgical and endoscopic therapies have been proposed with varying results and APC is considered a good first line treatment (Sebastian et al, 2004). Data regarding the utility of RFA for GAVE is limited to a handful of cases refractory to APC (Gross et al, 2007). Our patient showed significant improvement in symptoms, anemia and transfusion needs. Prior to RFA, he required 80 units of blood transfusions over 2 years. Post RFA session 1, he required 2 units and has since been transfusion free for the last 2 years, with a significantly improved quality of life. Whether the improvement in anemia has a linear relationship with the number of RFA sessions remains unknown. Challenges remain in treating GAVE patients due to the rarity of this condition and the lack of available literature. We propose that RFA be considered a treatment option for patients who fail APC therapy.

479 Mediastinal Histoplasmosis Diagnosed by Endoscopic Ultrasound-Guided Core Needle Biopsy Alan Putrus, MD1, Francis Edeani, MD1, Ashirf AlGhanoudi, MD, MPH1, Mohd Amer Alsamman, MD2, Joshua Max, MD1. 1. Trihealth-Good Samaritan Hospital, Cincinnati, OH; 2. Good Samaritan Hospital, Cincinnati , OH. Introduction: Histoplasmosis and its causative agent, H. capsulatum, are most prevalent along the Ohio and Mississippi River valleys. Fewer than 5 percent of exposed individuals develop symptomatic disease. Pulmonary histoplasmosis is rarely complicated by enlarging, caseating mediastinal lymph nodes, a syndrome known as mediastinal granuloma. Case presentation: A 36-year-old male presented with dry cough, dyspnea, and mild chest discomfort for 2 months. He noted a 50-pound weight loss during his illness. He was treated initially with azithromycin, montelukast inhaler and beclomethasone inhaler. However, his symptoms persisted and he developed intermittent fever, occasional chills and drenching sweats. An abnormal chest X-ray was followed by a CT scan showing a 12 mm right lower lobe lung nodule and enlarged subcarinal, precarinal and periaortic nodes. He was referred for endoscopic ultrasound (EUS), which revealed mediastinal lymphadenopathy, predominantly in the subcarinal region. A 3.7 cm necrotic-appearing subcarinal

Table 44. RFA Session Date & No.

Pre Treatment Hemoglobin (g/dl)

Post Treatment Hemoglobin (g/dl)

PRBC Transfusion post RFA

May 15th 2013

8.4

9.5 (July 2nd 2013)

Yes, 2 Units

July 17th 2013

9.1

11.2 (September 19th 2013)

No

August 29th 2013

10.7

15.1 (December 11th 2013)

No

November 14th 2013

12.3

13.9 (August 28th 2014)

No

May 15th 2014

13.3

14.6 (January 15th 2015)

No


[479A] Figure 1.


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Abstracts to choledocholithiasis and was treated via ERCP and cholecystectomy. One month after cholecystectomy he developed nausea, vomiting, and epigastric pain. Computer Tomography (CT) abdomen/pelvis with contrast demonstrated an 8 cm pseudocyst in the pancreatic body. Medical management was determined to be the best course of action secondary to resolution of symptoms. His symptoms returned after two months and CT imaging demonstrated enlarging pseudocyst to 23 cm with impingement on the stomach (Figure 1). Pseudocyst drainage via endoscopic approach was the best approach because of overlying bowel making a percutaneous approach difficult. Endoscopic ultrasound (EUS) demonstrated a clear window for transmural cyst-gastrostomy and an insertion of a 10 x 40 mm FCSEMS produced copious amounts of “dishwater” type fluid into the stomach. He continued to have epigastric pain with no resolution of the pseudocyst per CT imaging and open gastrocystostomy was performed. His symptoms resolved shortly after surgery. Over the next 5 years he did well with only intermittent epigastric pain associated with eating fatty foods. Current presentation demonstrated vitals within normal limits, abdomen was non distended, soft, nontender, and no palpable mass. Two melenic stools were noted. CBC and CMP were unremarkable. EGD and colonoscopy performed didn’t identify a bleeding source. A FCSEMS was noted in the gastric antrum and colonoscopy demonstrated FCSEMS protruding into the splenic flexure (Figures 2 &3). Attempts were made to remove the FCSEMS but were not successful due to tissue ingrowth. He is currently awaiting further treatment with argon plasma coagulation to remove ingrown tissue and attempt to remove the stent. Discussion: Cyst-gastrostomy are not without complications and without close follow up can cause complications, as demonstrated by our patient developing a gastrocolonic fistula secondary to long term placement of a FCSEMS.

[479B] Figure 2.

[480A] Figure 1.

[479C] Figure 3.

lymph node was sampled via transesophageal core biopsy (figure 1). Pathology showed granulomatous inflammation in the lymph node (figure 2). GMS (silver) stain was positive for fungal yeast forms, consistent with histoplasmosis (figure 3). Histoplasma antibody titer by complement fixation was elevated at 1:32. He was treated with itraconazole with resolution of his constitutional symptoms. Follow up imaging has not yet been obtained. Discussion: Our patient was a generally healthy 36-year-old male who developed debilitating symptoms secondary to mediastinal involvement of histoplasmosis. EUS-guided core biopsy enabled a pathologic diagnosis and should be considered an accurate and minimally invasive diagnostic modality in these cases.

480 Gastric Colonic Fistula Formation After Fully Covered Self-Expanding Stent Utilized for CystGastrostomy of a Pancreatic Pseudocyst Justin Cochrane, DO1, Greg Schlepp, MD2, Witchit Srikureja, MD3. 1. Providence Sacred Heart Internal Medicine Residency, Spokane, WA; 2. Spokane Digestive Disease Center, Spokane, WA; 3. Providence Gastroenterology, Spokane, WA. Introduction: Endoscopic cyst-gastrostomy demonstrates equality to surgical drainage of pancreatic pseudocyst but is not without complications, infection and bleeding. We present a case of 34 year old male who developed a gastric colonic fistula secondary to erosion of fully covered self-expanding metal stent (FCSEMS) into the splenic flexure. Case: Mr. L is a 34 year old male with multiple episodes of acute pancreatitis who presented with abdominal pain, diarrhea and bright red blood per rectum. Six years prior he developed pancreatitis secondary


[480B] Figure 2.


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[480C] Figure 3.

481 The Use of “Through-the-Scope” Fully Covered Self-expanding Metal Stent to Stop Refractory Variceal Bleeding in a Patient With Hemorrhagic Shock Justin Cochrane, DO1, Greg Schlepp, MD2. 1. Providence Sacred Heart Internal Medicine Residency, Spokane, WA; 2. Spokane Digestive Disease Center, Spokane, WA. Introduction: A Sengstaken-Blakemore tube is often utilized in cases of severe variceal bleeding. Limitations for this treatment included a high rate of bleeding recurrence upon removal, and increased rate of esophageal perforation with placement. Esophageal fully covered self-expanding metal stents (FCSEMS) have been proposed as a possible treatment option for severe variceal bleeding in place of a SengstakenBlakemore tube. Case: Mr. S a 49 year old male with history of cirrhosis from alcohol and hepatitis C who presented with bright red blood per rectum. Two weeks prior, anesophagogastroduodenoscopy (EGD) demon-

[481A] Figure 1.


[481B] Figure 2.

[481C] Figure 3.


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Abstracts strated grade 2 esophageal varices for which he underwent banding. Hematemesis resolved and Hgb stabilized and he was discharged home. Vital signs including orthostatic vitals were unremarkable. His mucous membranes were moist without pallor and abdomen was soft/nontender with minimal fluid wave. Laboratory data demonstrated Hgb 10.8 mg/dL, platelets 98 u/L, INR 1.9 and total bilirubin 1.9 mg/dL. Liver enzymes were within normal limits. Proton pump inhibitor and octreotide drips were initiated for treatment. EGD identified a new varix closely associated with an ulceration from previous banding. An attempt was made to band this new varix, but with reinsertion of the endoscope the varix ruptured. Exsanguination ensued and banding nor sclerotherapy could be performed secondary to inability to visualize the bleeding vessel. He progressed to hemorrhagic shock and then pulseless electrical activity. Cardiac resuscitation was performed. A Sengstaken-Blakemore tube was unsuccessful secondary to inability to pass the tube. An 18mm x 120 mm “through the scope” (TTS) FCSEMS (Taewoong Medical Co.) was advanced into the gastric lumen under direct endoscopy and withdrawn into the esophagus. Exsanguination ceased after stent deployment. A 3 cm laceration was noted in the anterior esophagus from the Sengstaken-Blakemore tube placement attempt and a second FCSEMS was placed. His pulse returned after cessation of bleeding and rapid transfusion of red blood cells. However, he sustained severe anoxic brain injury and after several days care was withdrawn. Discussion: Patients with exsanguination from ruptured varices may benefit from placement of TTS esophageal FCSEMS instead of a Sengstaken-Blakemore tube. TTS esophageal FCSEMS allow for direct endoscopic placement, limited risk of perforation, and longer treatment time to stabilize patients for a more definitive treatment, such as TIPS.

482 Pneumomediastinum a Rare Complication of Colonoscopy Polypectomy Successfully Treated With Conservative Management Charles Rives, MD1, Mohsen Pourmorteza, MD2, Eric Carter, DO1, Mark Young1. 1. East Tennessee State University, Johnson City , TN; 2. Department of Internal Medicine, East Tennessee State University, Johnson City, TN. Colonoscopies are a relatively safe and are associated with few complications. We present a rare case of post-colonoscopy polypectomy resulting in a pneumomediastinum and subcutaneous emphysema. Case Report:An 84 year old male with a history of colonoscopy with polypectomy the day prior was admitted due to a syncopal episode. The only complaint was a small amount of dark red blood per rectum. On examination vital signs were stable, the patient appeared pale with dry membrane mucosa, abdominal and pulmonary exam were benign, labs were concerning for a Hgb 6.9 g/dl. Chest x-ray depicted free air beneath the right hemidiaphragm, computed tomography (CT) demonstrated pneumoretroperitoneum, pneumomediastinum and subcutaneous emphysema. Visceral angiogram failed to demonstrate any source of active bleeding. Due to the overall stable condition of the patient conservative management with prophylactic zosyn and transfusion of 2 units of packed red blood cells was initiated. Patient was discharged 5 days after admission with stable respiratory and hemodynamic signs. Discussion:Diagnostic colonoscopies are relatively safe procedures with the most common complications being bleeding and perforations, with an incidence of less than .2%. Though perforations are rare they are associated with a high mortality and morbidity. Causes of perforation can be due to excessive insufflations and instrumental trauma and usually present with intra-abdominal free air but rarely with a pneumomediastinum. A pneumomediastinum is the presence of free air within the mediastinum and in our case was due to a micro-perforation from a colonic polypectomy. The colonic wall defect allowed free air into the retroperitoneum, which spread along the fascial planes and entered the mediastinum and subcutaneous tissues. The most sensitive test for pneumomediastinum is computed tomography and extra-pulmonary causes of pneumomediastinum can be successfully treated conservatively with rest and antibiotics. Though complications from polypectomies are rare, they can be associated with a high morbidity and mortality but rarely associated with pneumomediastinum and in certain stable patients can be treated with conservative management.

[482B Figure 2.

483 Creating a New Path: EUS-Guided Gastrojejunostomy With Lumen-Apposing Stent Niket Sonpal, MD1, Anish Mammen, MD2, Gregory Haber, MD2. 1. Lenox Hill Hospital, Happauge, NY; 2. Lenox Hill Hospital, New York, NY. Malignant small bowel obstruction is a frequent complication in advanced cancer patients, especially in those with abdominal tumors. A small bowel obstruction occurs when there is blockage of the forward flow of gastric and intestinal contents through the gastrointestinal tract. This results in a delay or inability of gas and fluid to move through the tract. Surgery should be considered for patients in with a single level of occlusion. Less invasive approaches such as duodenal or colonic stenting should be considered when the patient is a poor surgical candidate, or if there are multiple levels of obstruction. However small bowel decompression through lumen opposing stent technology is rare and has yet to be fully described. We present a case of an elderly male with a small bowel obstruction secondary to metastatic colon cancer that was relived with a lumen-apposing stent (Axxios). An 84-year-old male with a metastatic colon cancer, with deposits to the proximal small bowel presented with nausea, vomiting and abdominal distension. The patient noted not having bowel movements or passing gas for several days prior to presentation. The vomit was non-bloody and non-bilious and at times was dry heaving. He stated the nausea was not relieved by anti-emetics including high dose ondansetron. The gastroscope was inserted into the esophagus, which was unremarkable. The gastroscope was exchanged for a linear scope, which was advanced to the gastric antrum. A dilated loop of small intestine was seen adjacent the gastric wall. A cystotome was used to puncture the gastric and small intestinal walls to gain access to the dilate loop of bowel. A guide-wire was advanced into the loop of bowel. The Axxios stent was deployed over the wire, securing the tract between the stomach and dilated loop of bowel. About 2 liters of fluid drained into the stomach from the dilated loop of bowel and was suctioned. Contrast injected into the Axxios stent was seen entering loops of bowel on fluoroscopy. The patient subsequently felt better after the procedure. Treatment options for malignant bowel obstruction must be carefully explored with the patient and family. This diagnosis is often an indication of disease progression, further highlighting the noncurable nature of the underlying disease. EUS Guided gastrojejunostomy with an Axxios stent for a malignant proximal small bowel obstruction should be considered in patients who require decompression. The system allows for a bypass of the small bowel in patients who are poor surgical candidates due to multiple comorbidities or for palliative purposes.

484 Navigating a Tight Spot: Anastamotic Stenosis in Crohn’s Disease During Pregnancy Eric J. Mao, MD1, Sidney Olefson, MD, MBA2, Melissa Jackson, MD3, Samir A. Shah, MD4. 1. The Warren Alpert Medical School of Brown University, Providence, RI; 2. Warren Alpert School of Medicine of Brown University, Providence, RI; 3. Warren Alpert School of Medicine of Brown University, East Providence, RI; 4. Warren Alpert Medical School/Gastroenterology Associates, Providence, RI.

[482A] Figure 1.


A 33-year-old woman with ileal Crohn’s disease diagnosed at age 18, with a history of ileocecal resection in 2007 and previously on infliximab from 2004 to 2010, presented at 12 weeks gestation with abdominal pain and vomiting. Magnetic resonance enterography without contrast demonstrated multiple fluidfilled loops of bowel to the level of the anastomosis suggestive of partial small bowel obstruction and inflammatory markers were mildly elevated. A colonoscopy 6 months earlier showed narrowing at the anastomosis estimated to be 9 mm and no active disease. She was managed non-operatively with IV glucocorticoids, bowel rest, nasogastric tube decompression and parenteral nutrition. She had difficulty with a pureed/liquid diet and after reviewing options, outpatient colonoscopy with propofol sedation was


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done at 16 weeks gestation showing a 3 mm opening at the anastomosis that was treated with sequential colonic balloon dilatation to 15 mm. Immediately after the procedure, she was able to tolerate a low residue diet. The remainder of the pregnancy was uneventful and she delivered a healthy, term infant. The management of the pregnant inflammatory bowel disease (IBD) patient is complex. Even without active disease, inflammatory markers can rise in pregnancy and imaging modalities are limited. Our patient had persistent debilitating symptoms from an anastomotic stricture impacting her nutrition and pregnancy. Her intervention in the second trimester is the optimal time for endoscopy that cannot wait until after delivery. This approach was less risky than surgery and perhaps less risky than parenteral nutrition. The patient was tried on a pureed/liquid diet but remained symptomatic. No fetal monitoring was done or is recommended in the second trimester for endoscopic procedures. Limited data exists on safety and long term outcomes after endoscopic procedures in pregnant IBD patients. Colonoscopy does not induce labor nor increase risk of congenital malformations. Risks include fetal risk from endoscopic medications, post-procedural hypotension, electrolyte disturbances related to bowel preparation. If a compelling indication exists and the benefits outweigh the risks, endoscopy can be safely performed as in our case with a happy outcome for the mother and baby.

485 Novel Treatment Approach for Rectal Dieulafoy Lesion With Over-The-Scope Clip (OTSC) Kasra Adham, MD, Marrieth Rubio, MD, Merritt J. Bern, MD, Robert Moylan, MD, Paul Yeaton, MD, Alan Brijbassie, MD. Virginia Tech Carilion School of Medicine, Roanoke, VA.

[484A] Figure 1.

Rectal Dieulafoy lesion is a rare cause of lower gastrointestinal bleeding. Though such lesions can be present anywhere in the gastrointestinal tract, they are often present in the stomach or small bowel. A 35-year-old man was admitted with a one day history of large volume bright red blood per rectum. Urgent upper endoscopy performed on the day of admission was unremarkable. Following his upper endoscopy, urgent flexible sigmoidoscopy demonstrated a rectal Dieulafoy lesion (Figure 1) which was treated with traditional hemoclips (through-the-scope clips). The patient had recurrent bleeding the following day. Repeat flexible sigmoidoscopy demonstrated recurrent bleeding from the rectal Dieulafoy lesion. The area was injected with epinephrine. Hemoclips were removed with rat-tooth forceps. Next, an over-the-scope clip (OTSC) was applied to the lesion (12/6 gc Ovesco clip, Ovesco Endoscopy, Tübingen, Germany). Hemostasis was achieved (Figure 2). Over-the-scope clip is an effective treatment modality for bleeding rectal Dieulafoy lesions. Using Boolean logic, we searched PubMed and Google Scholar regarding the treatment of such lesions. To our knowledge, there is no other literature demonstrating the utility of OTSCs to achieve hemostasis of specifically rectal Dieulafoy lesions.

[484B] Figure 2.

[485A] Figure 1.

[484C] Figure 3.


[485B] Figure 2.


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486

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Mediastinal Malignant Peripheral Nerve Sheath Tumor (Epithelioid Variant) Diagnosed by EUS-Guided Fine Needle Aspiration

Hematemesis in a Post-Whipple Patient

Tariq Hammad, MD, Yaseen Alastal, MD, Umar Darr, MD, Abdallah Kobeissy, Mohammad Hammad, MBBS, Ali Nawras, MD, FACG. University of Toledo Medical Center, Toledo, OH. Bacground: Neurogenic tumors are the most common cause of posterior mediastinal masses. The majority of these tumors are benign. Malignant peripheral nerve sheath tumor (MPNST) of the mediastinum is a rare tumor. It is usually associated with neurofibromatosis type I. Tissue examination is the mainstay of diagnosis. Here, we present a rare case of posterior mediastinal MPNST diagnosed by endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) in a patient presenting for evaluation of mediastinal mass. Case presentation: A 72 year old male patient with past medical history of neurofibromatosis type I presented with worsening dysphagia and weigh loss over 3 months. Esophagiogram showed displacement and compression of the midesophagus by a possible mediastinal mass. Chest computed topography showed a large posterior mediastinal mass compressing on the esophageal wall and causing moderate grade stricture. The patient was referred for endosonographic (EUS) evaluation. Endoscopic exam of the esophagus revealed moderate grade stricture caused by external compression on the wall of the midesophagus measuring 5 cm in length and extending from 25 cm to 30 cm from the incisors. EUS exam of the mediastinum revealed a large hypoechoic heterogeneous well-demarcated mass abutting the esophageal wall and measuring 76.3 mm x 73.9 mm (Fig. 1). EUS guided fine needle aspiration (FNA) was performed using a 25-gauge needle (Fig. 2). Rapid on-site evaluation by the cytopathologist confirmed the adequacy of the sample. Histopathology examination was suggestive of MPNST with epithelioid differentiation. A battery of immunostains was performed on cell block material revealed immunoreactivity of tumor cells with S100 protein (nuclear and cytoplasmic) and CD99. Neoplastic cells were negative for desmin, myogenin, CD56, pancytokeratin, CD34, CD117, synaptophysin, and Mart 1. Considering the clinical settings (neurofibromatosis type 1), imaging studies, cytomorphology and immunoprofile, the diagnosis of MPNST epithelioid variant was made. The patient was referred for oncology clinic for further management. Conclusion: This case shows that EUS-FNA is an effective and minimally invasive technique for the precise tissue sampling to diagnose mediastinal malignant peripheral nerve sheath tumor, epithelioid variant.

Sajiv Chandradas, MD1, Andrew Cummins, MD2, Walter Coyle, MD3. 1. Scripps Green Hospital, San Diego, CA; 2. Scripps Mercy Hospital, San Diego, CA; 3. Scripps Green Hospital, La Jolla, CA. Pancreaticoduodenectomy is a complex surgery that lends itself to a wide array of complications. The most common post-operative complications include post-operative hemorrhage, anastomotic leak, bile leak, pancreatic fistula, delayed gastric emptying, and intra-abdominal abscess. Post-pancreaticoduodenectomy hemorrhage occurs about 2-4% of the time with a mortality ranging from 11 to 54%. It is most often associated with the presence of a pancreatic fistula. We present a case of a 80 year old male with recent diagnosis of a pancreatic head adenocarcinoma who was taken for a Whipple with a pancreaticogastrostomy anastomosis, (as opposed to the traditional pancreaticojejunostomy) 2 weeks prior to admission. Two weeks after surgery the patient presented with overt hematemesis. He was noted to be pale, diaphoretic, and hypotensive. He was emergently taken for upper endoscopy. We encountered a significant amount of fresh blood, but after aggressive washing and suctioning we were able to identify an active arterial hemorrhage from the exposed surface of the pancreas within the stomach. In order to achieve hemostasis we employed 3 clips and 4 1 cc epinephrine injections directly into the pancreas. Hemostasis was obtained successfully after these interventions and the patient was subsequently transferred to the ICU, where he had a remaining uneventful hospital course. This case demonstrates a relatively common complication in the post-operative period that presents in a somewhat unique location – the transected surface of the pancreas. The majority of post-pancreaticoduodenectomy bleeds occur near the anastomosis site, rather than the actual surface of the pancreas. The endoscopist must be aware of all the potential sources of a bleed, especially in the emergent setting.

[487A] Figure 1.

488 Erosive Iron Pill Gastritis

[486A] Figure 1.

[486B] Figure 2.


Tatiana Teslova, MD, Aaron Tokayer, MD, Swathi Gopalakrishnan, MD. Montefiore Medical Center, Bronx, NY. Introduction: Oral iron therapy is a usual treatment for iron deficiency anemia. Common adverse effects include nausea, constipation and dark stool. Iron pill gastritis, a rare complication of oral iron therapy, is being increasingly recognized; ingested iron causes corrosive damage to gastric mucosa. We present a case of iron pill gastritis in a woman on oral iron therapy. Case report: 70 year-old-woman with medical history of recurrent GI bleeding attributable to multiple ectasias and duodenal neoplasm had many hospitalizations for recurrent symptomatic anemia. She had iron deficiency anemia and was on iron therapy (ferrous sulfate) for several years. She presented with two days of dizziness, fatigue and melena. Hemoglobin was 10g/dl from baseline 15.2g/ dl. EGD showed multiple linear ulcerations and exudative mucosa in the gastric body and fundus (image 1). Biopsies revealed mild chronic inflammation, focal erosion and gastric epithelium with brown pigment, compatible with iron (image 2). Findings suggested iron pill induced gastritis. The patient was switched from oral to IV iron. A month later she was re-hospitalized for melena. Repeat EGD showed active bleeding from a duodenal ectasia, which was ablated with APC. Notably, gastric mucosa appeared normal. Discussion: Oral iron causes mucosal injury in any organ in the upper GI tract. Mechanism of injury is the direct corrosive effect of ferrous and ferric ions that catalyze the production of free radicals resulting in tissue necrosis. Endoscopic findings include esophagitis, gastritis, ulcers, erosions or dark mucosal plaques. Ulcerations and erosions are commonly found in the esophagus and less frequently in the stomach. Specific findings of iron deposition, such as linear brown streaks and pigmented mucosa, are rarely seen. Alternative options for patients with iron pill induced gastritis include liquid or intravenous iron. Our case illustrated that oral iron causes erosive gastritis that is reversible with discontinuation of oral iron therapy. Gastroenterologists should be suspicious of iron pill induced mucosal injury in any patient on oral iron with otherwise unexplained dysphagia, anemia, or melena.


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[489A] Figure 1.

[488A] Figure 1.

490 Dental Injuries From EGD: Report of Three Cases and Literature Review Estela Mogrovejo, MD1, Mihajlo Gjeorgjievski, MD2, Mitchell S. Cappell, MD, PhD1. 1. William Beaumont Hospital, Royal Oak, MI; 2. Department of Internal Medicine, Beaumont Health, Royal Oak, MI.

[488B] Figure 2.

489 Coronary Artery Stenting May Predispose to von Willebrand Factor (vWF) Deficiency and Bleeding Gastrointestinal Angiodysplasia

Introduction:Although dental injuries are well described complications of laryngotracheal intubation for general anesthesia for surgery, scant data exist regarding dental injury from esophagogastroduodenoscopy (EGD). Three cases of dental injury during EGD are reported. Case 1: A 65-year-old female with a history of diabetes and CAD referred for EGD for dysphagia and pyrosis. The patient had intact teeth with very poor dentition. An anesthesiologist evaluated the patient, administered sedation (propofol, etomidate), and monitored the patient. An Olympus GIF-Q160 endoscope was introduced under direct vision revealing a hiatal hernia, chronic esophagitis, and a Schatzki’s ring which was dilated using a Rigiflex Microvasive hydrostatic balloon at 6 ATMs. EGD was accomplished without difficulty. After EGD, the patient’s family noted that a left incisor was very loose and had to be removed. Case 2: A 72-year-old male with a history of cirrhosis referred for EGD for coffee-ground emesis. The patient had extremely poor dentition. An anesthesiologist evaluated the patient, administered moderate sedation (etomidate), and monitored the patient. An Olympus GIF-Q180 endoscope was introduced under direct vision revealing erosions in the distal esophagus. EGD was accomplished without difficulty. After EGD, anesthesiologist noted that lower right frontal bottom tooth was barely attached, tooth removed for patient safety. Case 3: A 46-year-old male with a history of HIV referred for EGD for iron deficiency anemia, vomiting, and weight loss. The patient had documented caps and intact bonding. An anesthesiologist evaluated the patient, administered moderate sedation (propofol), and monitored the patient. An Olympus GIF-Q180 endoscope was introduced under direct vision revealing a hiatal hernia and ulcerative esophagitis. EGD was accomplished without difficulty. After EGD patient stated bonding of his two top front teeth were missing, patient found part of the lying bond on stretcher. Discussion: The incidence of dental injury during general anesthesia is approximately 1:1000 endotracheal intubations. Data on the incidence associated with EGD are limited, with a literature review revealing only one report of 2 cases of dental injury in a study of 5,000 EGDs. In this prior report the two patients had partial dentures that replaced most of their teeth and were removed for EGD, a practice that the authors discouraged. These three cases alert endoscopists of the dangers of dental injury during EGD.

Ana Petrova, MD1, Yetian Zhang, PhD2, Cherif El Younis, MD, FACG2. 1. SUNY Downstate Medical Center, New York, NY; 2. Brookdale University Hospital, Brooklyn, NY. Introduction: Angiodysplasia (AD) is a common cause of GI bleeding, GI AD has been linked to several medical conditions including renal failure, cirrhosis, aortic stenosis, and certain medications. In many cases, no clear etiology is evident. We present a series of cases of bleeding GI AD in the setting of coronary stenting. Patients and Methods: Over 6-months period, 29 cases (age 45-78), of AD were diagnosed at endoscopy (figure). 2 cases were associated with aortic stenosis, 4 cases with renal failure and hemodialysis, 3 cases with cirrhosis. In the remaining 20 cases, no obvious etiology was identified. Of these, 15 cases were documented in patient with history of coronary stenting. In this subset, all patients were either on aspirin (14), or aspirin and Plavix (10) at the time of presentation. In 3 patients from stenting group, a low level of factor VW factor was documented. Discussion: AD is a common cause of GI bleeding. The cause of these lesions is unclear, as is what precipitates bleeding, although certain associations have long been established. In this series, a large number of patients with AD have undergone coronary stenting. The extent of AD was greater among those with multiple stents. In 3 cases, von Willebrand factor (vWF) was also lower than control. It is known that vWF is proteolysed due to high shear stress in the setting of highly turbulent blood flow ( e.g. aortic stenosis). The deficiency of vWF is most active in vascular beds with high shear stress, and increases the bleeding risk from such lesions. We theorize that stenting generates shear stress around the involved vessels and degrades VW factor and pave the way to bleeding vasculopathy. Conclusion: The findings suggest that coronary stenting may be associated with increased risk of bleeding GI AD. Acquired deficiency of VWF may play a role. Given the potential therapeutic implications, a large prospective study would be necessary.


491 Use of AXIOS Stent in a 5-Year-Old for Management of a Pancreatic Fluid Collection Alexander H. Kim1, David L. Diehl, MD2. 1. Geisinger Medical Center, Danville, PA; 2. Division of Gastroenterology and Hepatology, Geisinger Medical Center, Danville, PA. Transluminal pancreatic pseudocyst drainage may be technically challenging. Endoscopic ultrasound (EUS) guided drainage of pancreatic fluid collections is preferred to surgery due to less morbidity associated with this procedure. Recently a lumen apposing stent (AXIOS, XLumena, Mountain View, CA) was introduced which has simplified the creation of the cystgastrostomy. Several case series have reported efficacy and safety of AXIOS stent in the adult population. However, there are few previous reports on the use of an AXIOS stent in the pediatric population. Herein, we report a case of successfully treated pancreatic fluid collection with an EUS-guided AXIOS stent placement in a 5 year old patient. A 5-year old male was diagnosed with nasopharyngeal and retroperitoneal/pancreatic Burkitt’s lymphoma in December 2014. The body and the tail of the pancreas were involved with a large retroperitoneal mass. He was treated with chemotherapy which resulted in replacement of the mass by a cystic structure measuring 3 x 2cm. He was admitted for evaluation of neutropenic fever while receiving chemotherapy, 3 months after initial diagnosis; contrast CT of abdomen showed an increase in the size of the cystic lesion, which was now 6 x 5 cm. MRI confirmed the cystic lesion in the tail of the pancreas; it did not contain debris, and did not clearly communicate with the pancreatic duct. Because of ongoing chemotherapy, neutropenia, and thrombocytopenia, the pediatric surgical service requested endoscopic cystgastrostomy. Prior to introduction of the linear therapeutic echoendoscope, predilation of the esophagus was done up to 15mm with Savary dilators. Following this, the EUS scope


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492 Problematic PEG: A Case of Enteral Feeding Tube Seeding Malignancy to the Abdominal Wall Jilian R. Sansbury, MD1, Elvira Umyarova, MD2, Keisuke Shirai, MD2, Brad Keith, MD2. 1. Medical University of South Carolina, Myrtle Beach, SC; 2. Medical University of South Carolina, Charleston, SC.

[491A] Figure 1.

The patient is a 57yo African American male with a history of tonsillar squamous cell carcinoma who presented with abdominal pain, distention and leakage from his enteral feeding tube site. He underwent uncomplicated percutaneous gastrostomy and tracheostomy placement following cancer resection surgery 3 years prior. The tracheostomy was removed shortly afterward, but gastrostomy tube was retained for medications and nutrition. Over the next several months, the patient developed worsening pain and drainage at the gastrostomy tube site. He then developed an exophytic mass that grew rapidly to surround the gastrostomy tube and tract. A CT scan of the abdomen described a 5.5 x 4.0cm solid, left anterior abdominal wall mass along the percutaneous gastrostomy tube tract. The patient underwent biopsy of the mass, which showed metastatic invasive tonsillar squamous cell carcinoma. Upon identification of metastatic cancer, the patient was tried on several systemic chemotherapeutic treatments without improvement. The treatment regimen was supplemented with palliative local radiation to the abdominal wall metastasis. For over 6 months following the addition of palliative radiation, the metastatic mass remained quiescent and the patient was symptom free. He was able to use the enteral feeding tube for nutrition and medications without complication. Despite thorough treatment, the mass enlarged and gastrostomy leakage returned. A gastrostomy-jejunostomy tube was placed, which temporarily helped control the leakage and improved delivery of medications and nutrition. During the last two months of the patient’s life, he was transitioned to parenteral nutrition supplementation. He was eventually started on a patientcontrolled anesthesia regimen for pain control and discharged to inpatient hospice. Following surgical intervention for many head and neck cancers, patients typically require tracheostomy and enteral feeding tube placement to allow for adequate healing. Seeding of an enteral feeding tube site with oral, head and neck cancers is a rare occurrence. Two theories for seeding currently exist: hematogenous spread versus direct tumor transplantation during endoscopic placement usually seen with traumatic PEG placement or multiple passes of the endoscope during placement of the enteral feeding device. In the setting of development of metastasis to the abdominal wall, local chemoradiation can be used to improve quality at the end of life. This case highlights the importance of utilizing local chemoradiation as a palliative measure for certain patients. Palliative care in this situation should be personalized to the patient, and should include discussion of enteral or parenteral feeding options if indicated in the end of life.

[491B] Figure 2.

[492A] Figure 1.

[491C] Figure 3.

passed easily. Cystgastrostomy was done under EUS and fluoroscopic guidance, and a 10 mm diameter AXIOS stent was placed. Cyst fluid had elevated amylase of 2747. The patient did well after AXIOS placement. The stent was endoscopically removed 2 months later. Our patient never had pancreatitis, and we believe that his large retroperitoneal mass became cystic after a robust response to chemotherapy. EUS-guided pancreatic cyst drainage is generally preferred to surgery, but the use of an AXIOS stent has been rarely reported in children. This case gives further evidence that the AXIOS stent can be used safely and successfully in children.


[492B] Figure 2.


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Discussion/Conclusions: The OTSC device is an excellent tool for treating GI tract hemorrhage, small perforations, and post-op fistulae. While evidence in management of various conditions mentioned above is accumulating, large-scale head-to-head studies are lacking. Further studies are necessary, but the OTSC device represents a valuable tool for high-risk patients that are poor surgical candidates. We describe a case series of patients in which the OTSC device was used for a variety of challenging indications in endoscopic practice.

494 Successful Endoscopic Closure of an Iatrogenic Duodenal Perforation From a Biliary Stent Eric J. Mao, MD1, David Anjelly, MD1, Jonathan Movson, MD1, Samir A. Shah, MD2. 1. The Warren Alpert Medical School of Brown University, Providence, RI; 2. Warren Alpert Medical School/ Gastroenterology Associates, Providence, RI.

[492C] Figure 3.

A 92-year-old man with chronic kidney disease presented with 2 weeks of epigastric, post-prandial pain, weight loss, and jaundice. Laboratories revealed alkaline phosphatase of 357 and total bilirubin of 19. CT of abdomen revealed marked intrahepatic biliary ductal dilatation and a mass consistent with a Klatskin tumor. ERCP revealed severe stricture at the bifurcation and dilation of both left and right hepatic ducts. A metal uncovered stent was placed into the right hepatic duct. A plastic stent was placed into the left hepatic duct with difficulty inserting it with 3 cm extending into the duodenal lumen. Dark bile flowed through both stents. Cytology brushings revealed adenocarcinoma consistent with cholangiocarcinoma. Bilirubin downtrended and pain resolved. Two days after ERCP, patient developed new, constant epigastric pain with leukocytosis of 18. Repeat CT of abdomen revealed focal contained perforation at the 2ndportion of the duodenum at the enteric end of the plastic stent with surrounding phlegmon; intra-

493 The Over-The-Scope-Clip Device: An Indispensable Tool in Interventional Endoscopy: A Case Series Shivangi Kothari, MD1, Christine M. Granato, MD1, Saloni Sharma, MD1, Truptesh Kothari, MD, MS1, Noelle Fagan1, Margaret Adamcewicz, DO1, Guobao Wang, MD2, Asad Ullah, MD1, Vivek Kaul, MD, FACG1. 1. University of Rochester Medical Center, Rochester, NY; 2. Sun Yat-Sen University Cancer Center, Rochester, NY. The Over-The-Scope Clip (OTSC) is a novel endoscopic clipping device designed for tissue approximation. It offers an effective endoscopic approach for fistula closure, luminal perforation, GI bleeding, and resection of intra-diverticular colon polyps. We report successful use of this device in a variety of challenging endoscopic scenarios (Figure 1). Cases: 1) 53M with history of (h/o) prior feeding tube, presented with (p/w) a non-healing gastro-cutaneous fistula that was successfully closed using one OTSC. 2) 64M with h/o of PUD s/p Billroth II and chronic pancreatitis underwent ERCP with stent placement for CBD stricture. He presented 6 weeks later with perforation of the lateral duodenal wall by the stent. The stent was removed and the perforation was successfully closed using one OTSC device. 3) 67M with h/o cirrhosis p/w a massive GI bleed. Evaluation with EGD and angiogram x2 failed to reveal a source. Push enteroscopy showed an actively bleeding duodenal varix. Ethanolamine injection and band ligation were ineffective. Deployment of the OTSC over the varix resulted in complete and immediate hemostasis. 4) 49M p/w hematemesis. EGD revealed a 2cm duodenal bulb ulcer with a large (>2mm) vessel. Attempts to treat the vessel using standard hemostasis techniques were unsuccessful. One OTSC was deployed over the bleeding vessel with successful hemostasis. 5) 63F with colo-vaginal fistula secondary to Crohn’s disease was referred for endoscopic closure. One OTSC device successfully closed the fistula.

[494A] Figure 1.



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Abstracts He also reported associated nausea without vomiting. His vital signs were within normal limits. Physical examination elicited tenderness in the right upper quadrant and epigastric regions with mild guarding. Peritoneal signs were absent. Laboratory tests revealed iron deficiency anemia (IDA) with hemoglobin of 4.0g/ dl. Computed tomography scan of the chest, abdomen and pelvis with contrast revealed a large paraesophageal hernia with organoaxial volvulus. There was no obstruction or strangulation. Double contrast barium cine esophagram and upper GI study showed complete herniation of stomach above the hemi diaphragms with organoaxial volvulus. EGD revealed a shortened esophagus. The greater curvature of the stomach was displaced rostrally. Minimal resistance to the passage of the endoscope into the stomach and moderate resistance into the duodenum were encountered. This resolved after devolvulation using the alpha loop maneuver. EGD also revealed Cameron’s lesions and mild submucosal hemorrhage. The patient underwent non-urgent laparoscopic paraesophageal hernia repair and Nissen fundoplication. The herniated stomach was reduced from the mediastinum. The patient had an uneventful recovery and was discharged after 3 days of hospitalization. On his 3 week follow up visit, he was doing well tolerating a regular diet. Discussion: Gastric volvulus is rare. It involves the abnormal rotation of the stomach along the long axis (organoaxial) or along the short axis (mesenteroaxial). This leads to obstruction, strangulation and eventually necrosis. The condition requires high clinical suspicion in patients with unexplained abdominal pain as mortality associated with strangulation is as high as 50%. In cases of complete volvulus, it is impossible to pass a nasogastric tube into the stomach. The combination of pain, unproductive retching, and inability to pass a nasogastric tube is called Borchardt’s triad. If gastric infarction is absent, endoscopic detorsion can be attempted with consideration for endoscopic gastropexy by placement of percutaneous gastrostomy. Surgical treatment includes reducing the stomach, resecting infarcted tissue and repairing the anatomic defects. In this case the patient presented with acute gastric volvulus associated with paraesophageal hernia. Endoscopic intervention was successful in devolvulation in the technique described by Tsang et al. Given the stable vital signs and in the absence of overt GI bleeding it was concluded that the submucosal hemorrhage was likely acute, secondary to the volvulus while the Cameron lesions were thought to be the cause of the IDA.

[494B] Figure 2.

496 Rare Duodenal Pyloric Gland Adenoma David J. Bromberg, MD1, Jeffrey A. Gill, MD2. 1. University of South Florida, Tampa, FL; 2. Department of Gastroenterology, Division of Digestive Diseases and Nutrition, James A. Haley VA Hospital, University of South Florida, Tampa, FL.

[494C] Figure 3.

Pyloric gland adenomas (PGAs) are rare neoplastic polyps of the gastrointestinal tract that exhibit pyloric gland differentiation. They arise predominantly in the gastric corpus, however extragastric sites have been even less frequently identified in the esophagus, duodenum, gallbladder, and bile ducts1. PGAs are a rarely documented entity, but remain clinically significant due to malignant potential. We present a unique case of a patient found to have a pyloric gland adenoma of the duodenum. An 86 year old male with a past medical history of Clostridium difficile colitis and anemia presented to the outpatient gastroenterology clinic due to melena. Abdominal exam was unremarkable, vital signs stable, and hemoglobin of 12.6 was not significantly changed from baseline. An esophagogastroduodenoscopy (EGD) and colonoscopy were performed. Interestingly, the EGD showed a subcentimeter raised oval area with a cerebriform surface and normal surrounding rim of tissue distal to the major papilla in the duodenum (Figures 1, 2). The lesion was biopsied for pathology and the remainder of the EGD was only evident for a small, non-bleeding angioectasia in the duodenum. Subsequent colonoscopy found three small polyps that were managed with snare polypectomy. Pathology of the duodenal polyp showed evidence of pyloric-type glands with eccentrically placed round-to-flattened nuclei pushed toward the basement membrane, and cells containing clear to foamy cytoplasm that were slightly eosinophilic and glass-like in appearance. These findings were characteristic of a pyloric gland adenoma (PGA) of the duodenum. A repeat EGD was done two months later for resection via endoscopic mucosal resection. Post-operative pathology again confirmed a PGA. PGAs are a rarely documented finding, particularly in extragastric sites such as the duodenum, gallbladder, and bile ducts. The differential diagnosis of PGA should include folveolar-type dysplasia and conventional tubular adenomas. In this case, the lack of a foveolar mucin cap precluded the diagnosis of folveolar-type dysplasia. Although the nuclei in this case were elongated, they were not stratified and crowded as classically seen in conventional tubular adenomas2. To date, the two largest studies evaluating PGAs have found a 12-30% risk of malignant progression despite their bland cytologic appearance, and it is therefore recom-

venous ciprofloxacin and metronidazole were started. Upper gastrointestinal series confirmed the focal contained leak of extraluminal contrast. EGD revealed a plastic stent perforating the duodenal wall. Stent was pulled back from the wall with forceps and removed completely with snare. There was a small round hole in the duodenal wall. Three metallic clips were successfully placed to close the hole. Repeat upper gastrointestinal series revealed successful endoscopic repair of duodenal leak. Abdominal pain resolved. He tolerated oral diet and was discharged to nursing home. This case represents a successful endoscopic closure of an iatrogenic perforation with metallic clips in a patient who was not a surgical candidate. Perforation likely resulted from malposition of the stent with a long segment within the duodenal lumen. This case highlights the importance of monitoring patients after complicated therapeutic procedure such as biliary stenting. In retrospect, the plastic stent should have been removed when not optimally placed. New abdominal pain, fever, worsened exam, and leukocytosis were signs of perforation. Critical to the success of endoscopic closure in this case was early recognition of complication and imaging to guide removal of stent and perforation closure prior to the procedure. The patient recovered from the complication and returned 6 months later with stent obstruction requiring placement of a second metal stent.

495 A Case of Gastric Volvus Associated With Paraesophageal Hernia Rami El Abiad, MD1, Kalyani Meduri, MD2. 1. University of Iowa Hospitals and Clinics, Iowa City, IA; 2. University of Iowa, Iowa City, IA. A 48 year old Hispanic male with history of chronic gastroesophageal reflux disease presented to the emergency department with sudden onset severe post prandial abdominal pain radiating to mid scapular area.


[496A] Figure 1.


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The linear echoendoscope was advanced into the stomach. A large bulge was seen in the gastric body. A large fluid collection was visualized on ultrasound. An Expect 19 gauge needle was inserted into the cyst under ultrasound guidance. A guidewire was advanced into the cyst. A hurricane balloon was advanced over the wire and used to dilate the opening to 6mm. An AXIOS 15x10mm was deployed through the opening to create the cyst gastrostomy, bridging the stomach and the pancreatic pseudocyst. Approximately 2 liters of brown liquid was drained from the cyst and was suctioned. The patient’s symptoms improved and eventually he was able to be discharged home. On follow up the patient was able to eat, had gained weight and appeared well. In conclusion, the FC-SEMS utilizes a single-step stent deployment system to effectively drain peripancreatic fluid collections. Larger trials are required to determine the final role of AXIOS stent.

499 Retroflexion for Right Colon Angioectasia: A U-Turn for Obscure Overt GI Bleeding Jigar Bhagatwala, MBBS, MPH1, Siegfried Yu, MD2, Abdul Rehman, MD1, Sherman Chamberlain, MD1. 1. Georgia Regents University, Augusta, GA; 2. Georgia Regents University, Evans, GA.

[496B] Figure 2. mended that PGAs be completely resected by polypectomy3. The origin of PGAs arising in the duodenum and their role in the pathogenesis of adenocarcinoma still requires further investigation.

497 Duodenal Perforation Secondary to Endoscopic Choledochoduodenostomy: Successful Closure With Over-The-Scope Clip Tarun Kukkadapu, MD1, Muhammed Sherid, MD1, Sidhartha Tulachan, MD, PhD2, Sumanth Daram, MD1. 1. Georgia Regents University, Augusta, GA; 2. Geogia Regents University, Augusta, GA. Introduction: Duodenal perforation during upper endoscopic procedures is a rare complication associated with significant morbidity and mortality. With the advent of newer endoscopic procedures like sub-mucosal dissection, endoscopic myotomy and EUS-guided pancreato-biliary drainage, iatrogenic gastrointestinal perforations are more frequently seen than before. We are reporting a first case of EUSguided choledochoduodenostomy induced duodenal perforation, which was successfully treated with endoscopic placement of an over-the-scope clip. Case description: A 82 year old female was referred to our institution for further evaluation of painless jaundice with total bilirubin of 6.3, ALP 481 U/L, CA 19-9 451 U/ml, AST 122 U/L and ALT 121 U/L; CT scan demonstrated a pancreatic head mass with dilatation of common bile duct and pancreatic duct. On EUS evaluation, a 5.7x4.1cm cystic mass was visualized in the pancreatic head/uncinate process, with associated severe extra-hepatic and moderate intra hepatic biliary ductal dilatation and moderate pancreatic ductal dilatation. ERCP was performed and biliary cannulation with stent placement was attempted, which, however was unsuccessful due to a severe distal biliary stricture and distorted duodenum. EUS-assisted choledochoduodenostomy with placement of a fully-covered self-expandable metallic stent (SEMS) was performed to decompress the biliary system. The procedure was technically successful. However, significant abdominal distension was noted during immediate post procedure period; which resolved with naso-gastric suction. She was admitted for observation and IV antibiotics were administered in addition to maintaining nothing per oral status. Jaundice did not improve the next day, prompting a CT abdomen to evaluate for stent migration. The biliary end of the stent was displaced external and posterior to the bile duct and there was evidence of free intraperitoneal air and fluid collection in the porta hepatis. Percutaneous biliary decompression was performed, followed by endoscopic removal of the SEMS from the duodenal bulb; an over-the-scope clip (OVESCO™) was used endoscopically to close the 1cm perforation. Follow-up imaging using oral contrast confirmed absence of contrast extravasation. Conclusion: EUS-assisted biliary drainage is now an established modality for biliary decompression. Our case is perhaps the first to report the use of an over-the-scope clip to close an acute duodenal perforation secondary to EUS-assisted biliary drainage. Highlighting the risk of bowel perforation, our case also stresses the need to be familiar with the use of new endoscopic accessories such as over-the-scope clips and endoscopic suturing devices to effectively manage perforations that may arise during high-risk endoscopic procedures.

Introduction: The retroflexion maneuver during right colonic evaluation has been used for detecting adenomas, however its role in improving the diagnostic yield for gastrointestinal bleeding (GIB) is unclear. We present a case of recurrent obscure overt GI bleeding (OOGB) due to right colon angioectasia (AE) detected by cecal retroflexion. Case: A 57 year-old female with a medical history of hypertension and hypothyroidism presented with anemia and recurrent hematochezia, resulting in multiple hospitalizations over a two month time period, and required a total of 10 units of blood transfusion. The patient had no underlying coagulopathy, nor NSAID, antiplatelet, or anticoagulant medication use. During this period, her diagnostic work-up included an upper endoscopy, 2 colonoscopies, an enteroscopy, a video capsule endoscopy (VCE), and a tagged RBC scan. The upper and lower endoscopic procedures showed no evidence of bleeding, but the tagged RBC scan indicated a suspected GIB site in the right colon. VCE revealed the presence of blood in the cecum but no small bowel source. A colonoscopy was repeated due to ongoing active lower GIB, and the entire colon appeared normal, however, when retroflexion was performed in the cecum, a 5-mm AE was seen in the ascending colon adjacent to the cecum. The lesion was treated with Argon Plasma Coagulation (APC) and endoclip placement. The patient had no further symptoms of GIB at 6 month follow up. Discussion: Distribution of bleeding GI AEs are most commonly found in the jejunum (80%) followed by the duodenum (51%), stomach (22.8%), and right colon (11.4%).The current literature on retroflexion views during colonoscopy shows that right-sided retroflexion may obtain a small but statistically significant increase in lesion detection, but may not differ significantly from a second look forward-view. This has not been studied in the evaluation of GIB. Due to the flat nature of AEs, retroflexion views may offer a considerably improved yield in patients with OOGB. Conclusion: Because bleeding GI AEs involve primarily the right colon, a targeted retroflexion maneuver in the right colon should be considered during the evaluation of patients with OOGB.

500 Ingestion of Multiple Batteries: A Case Report Juan Tejada, MD1, Lyna Campo2, Andrea Culliford, MD3, Jay P. Babich, MD4. 1. The Brooklyn Hospital Center, Brooklyn, NY; 2. St. Barnabas Hospital, Bronx, NY; 3. St. Barnabas Hospital, SBH Health System, New York, NY; 4. St. Barnabas Hospital, SBH Health System, Teaneck, NJ. Introduction: Single foreign body ingestion is a scenario that gastroenterologists commonly see. However, multiple foreign body ingestion provides the endoscopist with significant challenges in management. We describe a case of ingestion of sixteen AA batteries that successfully passed the gastrointestinal track with conservative management after endoscopic attempt at removal.

498 Getting to the Center of the Matter: Pancreatic Pseudocyst Drainage Through a Novel, Double-Flanged, Lumen-Apposing, Fully-Covered, Self-Expandable Metal Stent Niket Sonpal, MD1, Anish Mammen, MD2, Gregory Haber, MD2. 1. Lenox Hill Hospital, Happauge, NY; 2. Lenox Hill Hospital, New York, NY. Pancreatic fluid collections represent a complication of acute pancreatitis. Endoscopic management of PFCs is an alternative to surgery. Plastic stents can be placed via endoscopy to drain pancreatic fluid collections. Covered metal stents are larger in diameter and can be inserted easily, but can migrate and lead to further morbidity. However using a novel lumen-apposing, covered, self-expanding metal stent the issues with migration repeat access are mitigated. We report a case of a 56 year old male who developed severe post ERCP pancreatitis, and a subsequent pseudocyst drained endoscopically via lumen apposing FC-SEMS - AXIOS (Xlumena Inc., Mountain View, California, USA). A 56 year old male with a history of Wilson’s disease, underwent an ERCP for the evaluation of chronic persistent right upper quadrant abdominal pain. At that time, the ERCP was successful, but the patient then developed severe pancreatitis requiring a lengthy hospital stay. He then began to complain of epigastric fullness, decreased appetite and weight loss of greater than 25 pounds. Repeat CT scan revealed a large pseudocyst measuring 17.7 x 16.0 x 27.3 cm. Given the patient’s symptoms the patient was taken for a cyst gastrostomy.


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Abstracts Discussion: Ingestion and/or insertion of foreign objects is seen in young, alcoholic or psychiatric patients. The incidence has not been established, but in a study between 2000 and 2006, in a urban hospital among 262 cases, 92% were intentional ingestion, 85% involved psychiatric patients, and 84% had history of prior ingestion. The dilemma is whether to allow the foreign body to pass spontaneous or to remove either endoscopically or surgically. Endoscopic approaches are recommended, especially for objects wider than 2.5 cm because they are less likely to pass the pylorus, although limited data exists to support this recommendation. Objects that fail to pass beyond the stomach by 3 to 4 weeks should be removed endoscopically to prevent obstruction. In this case evidence of progression throughout the gastrointestinal track was proved by daily abdominal x-ray without clinical deterioration. Successfully expulsion of the objects without further endoscopic intervention was possible.

501 Stop for the Stop Light Sign in Colonic Pseudo-Obstruction! Samip J. Parikh, MD, MPH1, Siegfried Yu, MD2, Abdul Rehman, MD1, Subbaramiah Sridhar, MBBS, MPH, FACG1. 1. Georgia Regents University, Augusta, GA; 2. Georgia Regents University, Evans, GA.

[500B] Figure 2.

Introduction: Acute large-bowel obstruction (ALBO) is an emergency and carries high morbidity and mortality if left untreated. Ogilivie syndrome/Acute colonic pseudo-obstruction (ACPO), can resemble ALBO, and can occur with pelvic surgery/fractures, post-partum state, trauma, systemic infection, cardiac events, transplantation, opiate therapy, and in ICU settings. ACPO is a common source of gastroenterology consultation, however, ALBO must be appropriately excluded to make this diagnosis. We present a patient with incarcerated inguinal hernia (IH) presenting as massive colonic distention, initially thought to be ACPO. Case: A 70 year-old male with a medical history of coronary bypass surgery, cardiomyopathy and prior left inguinal hernia repair was admitted for the treatment of cardiac failure. He developed a cardiac arrest and required invasive ventilation and vasopressor support. Serial abdominal x-rays (AXRs) obtained to investigate worsening abdominal distention with lack of bowel movements (BMs) showed prominent air-filled loops of large bowel measuring up to 10 cm, associated with hypokalemia and leukocytosis. Because of the typical AXRs, cross-sectional imaging was not obtained, and decompression was requested. A presumptive diagnosis of ACPO was made and a rectal tube was placed. Urgent colonoscopy was attempted and the scope was passed with difficulty to 40 cm, revealing an initial spastic segment suspicious for volvulus, with ulcerative changes suspicious for ischemia, and could not be advanced further. The scope tip was palpable in the left inguinal area, with positive skin transillumination, suggesting a strangulated IH. CT showed an ALBO due to proximal sigmoid colon trapped in the left IH and inflammatory changes. An emergent surgical repair of the incarcerated IH with orchiectomy was performed, which resulted in complete resolution of the abdominal distension and prompt return of BMs. Discussion: Both ACPO & ALBO may present with similar clinical features, including abdominal pain & distention, nausea, vomiting & constipation. ACPO is dominated by marked gaseous abdominal dilatation, which is paradoxically well tolerated clinically. Altered/depressed mental status may limit an appropriate history or clinical findings, especially in the ICU setting, and AXRs alone are not sufficient for the diagnosis. CT is the imaging method of choice as it can establish the diagnosis and cause of ALBO. Conclusion: An abrupt stop during colonoscope insertion associated with transillumination in the inguinal region can establish the diagnosis of incarcerated IH, the Stop Light Sign. Before a diagnosis of ACPO is made, CT imaging should be obtained to exclude mechanical ALBO.

502 Diagnostic Utility of Endoscopic Ultrasound Guided Fine Needle Aspiration for a Rare Presentation of Abdominal Burkitt’s Lymphoma Jigar M. Patel , MD1, Lauren Halvorson, MD2, Dennis Nguyen, MD3, Mitesh Patel, MD, FACG4. 1. MedStar Washington Hospital Center, Hyattsville, MD; 2. MedStar Georgetown University Hospital/ Washington Hospital Center, Silver Spring, MD; 3. MedStar Georgetown University Hospital, Arlington, VA; 4. MedStar Washington Hospital Center, Washington, DC. A 61 year old obese Caucasian male presented with constant epigastric pain, nausea, and vomiting for 5 days along with early satiety and significant weight loss over the past year. On examination a firm right upper quadrant mass was palpable and succusion splash was present. Initial blood chemistries were significant for elevated lipase, bilirubin, transaminases, and CA-19-9. MRI of the abdomen

[500C] Figure 3.

Case: 32-year-old female with history of schizoaffective disorder, presented with epigastric pain after ingested sixteen AA batteries in a suicide attempt. Patient underwent upper endoscopy with successful retrieval of 2 batteries. The other fourteen batteries had already passed beyond the ligament of Treitz. Surgical management was not indicated. Patient was kept NPO during the first two days, with intravenous fluid, proton-pump inhibitors and stool softener. Since abdominal pain improved, diet was advanced to clear liquids. During the hospital course, electrolytes, white blood cell count and kidney function remained stable. Daily abdominal x-rays were performed to monitor progression. After multiple failed oral therapy attempts, a nasogastric tube was placed to guarantee compliance with laxatives. After therapy with rapid colonoscopy preparation protocol, the patient successfully passed the remaining 14 batteries without complications at day 8.



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[502B] Figure 2.

at an outside hospital showed a soft tissue mass measuring 11x12x13 cms involving the pancreatic head, and colon (transverse, ascending and hepatic flexure). CT angiogram of the abdomen revealed the presence of a large soft tissue mass 12x11x13 cms in the right upper quadrant which circumferentially surrounded the duodenum and was indistinguishable from the head of the pancreas and hepatic flexure of the colon. No retroperitoneal lymphadenopathy was identified. EGD showed extrinsic compression of the mid-to-distal stomach on the lesser curvature and gastric antrum. The endoscope was unable to reach the duodenum. EUS from the gastric body showed an irregular round heterogeneous mass in the RUQ perigastric peritoneal space. The pancreatic duct was dilated and measured 5 mm. FNA was performed with histomorphological and immunohistochemical staining features showing Burkitt-like subtype of B-cell lymphoma. The patient was started on chemotherapy with Hyper-CVAD regimen which resulted in symptomatic improvement of his gastric outlet obstruction within 5 days. A repeat CT scan after 2 months showed complete resolution of the abdominal mass. This case is a unique presentation of a solitary intra-abdominal mass of sporadic Burkitts lymphoma without lymphadenopathy in an adult. Despite the use of MRI and CT abdomen, it was not possible to determine the origin of the right upper quadrant mass causing gastric outlet obstruction in this patient. Inability to introduce the scope into the duodenum limited further characterization by ultrasound. Therefore obtaining a tissue sample was the only means of accurately knowing the origin of the mass, vital information to guide treatment options. This case illustrates the benefit of EUS with FNA in the prompt tissue diagnosis and treatment resulting in complete resolution of the mass. It further demonstrates that more invasive procedures such as CT guided biopsy and laparoscopy can be avoided in such patients.

503 Successful Esophago-Pleural Fistula Closure via Esophageal Stent-in-Stent Anchored With Endoscopic Suturing Thomas R. McCarty, MD1, Tarun Rustagi, MD2, Mena Bakhit, MD3, Harry R. Aslanian, MD2. 1. Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, Yemen; 2. Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT; 3. Department of Internal Medicine, Yale University School of Medicine, New Haven, CT.

ago-pleural fistula, and right-sided empyema with chest tube placement presented with an increase in purulent chest tube drainage. The patient was previously treated with a 23mm x 155mm esophageal fully covered self-expanding metallic stent (FCSEMS) for dysphagia secondary to stricture with no evidence of fistula or leak on esophagogram prior to discharge. Esophagogram during his most recent admission showed distal stent migration and a fistulous communication between the esophagus above the proximal end of the distally migrated stent (black arrow-head) and pleural cavity (esophago-pleural fistula; black arrows) [Image A]. The existing stent was pulled up proximally using a rattoothed forceps and repositioned to cover the esophageal fistulous opening. A second 23 mm x 120 mm FCSEMS was placed overlapping into the prior stent (stent-in-stent). The proximal end of this stent was anchored with endoscopic suturing. Follow-up esophagogram showed overlapping SEMS with no contrast leakage [Image B]. Discussion: Gastrointestinal leaks and fistula have classically been managed surgically; however, endoscopic techniques have emerged providing a viable and less invasive approach. Intrathoracic leaks, as illustrated on this patient’s esophagogram, have a higher mortality rate compared to cervical leaks. Endoscopic approaches may involve a variety of closure devices including endoscopic clip placement (through-the-scope clips and over-the-scope clips), endoscopic suturing, endoscopic glue application, as well as luminal stenting as was chosen for this patient. SEMS, despite a known failure rate of up to 15%, remain a useful option. Most complications arise as a result of stent migration with recent studies demonstrating FCSEMS migration rates between 30-60%. Stent-anchoring methods, including endoscopic clipping and suturing, have been used to reduce the risk of migration. Endoscopic suturing has been shown to be more effective in preventing stent migration compared to endoscopic clipping. Here we present a case of successful esophago-pleural fistula closure via stent-in-stent placement, with stentanchoring using endoscopic suturing.

504 Invasive Esophageal Adenocarcinoma Masquerading as Buried Bumper Syndrome Sarina Kapoor, MD1, Swapna Gayam2. 1. West Virginia University Hospital / Ruby Memorial Hospital, Morgantown, WV; 2. West Virginia University School of Medicine, Morgantown, WV. Advanced esophageal and gastric cancers are often complicated by the development of dysphagia, which can lead to malnutrition and weight loss. Percutaneous endoscopic gastrostomy (PEG) placement is controversial and can be used for nutritional support in patients who are not amenable to esophageal stenting or surgical resection. Buried bumper syndrome is a well described complication of PEG tubes, which can lead to tube impaction in the gastric wall and gastric perforation. This report describes a 75 year old male with recently diagnosed esophageal adenocarcinoma complicated by distal esophageal stricture not amenable to esophageal stenting, resulting in dysphagia, malnutrition, and weight loss. He underwent PEG tube placement one month prior to presentation. At the time of PEG tube placement, his disease confined to the gastro-esophageal junction and did not involve the gastric body. He developed profuse hematemesis with three gram decrease in hemoglobin. On endoscopy, he was found to have a large ulceration with edema and active oozing of blood surrounding the PEG tube site concerning for buried bumper syndrome. Biopsies of the area revealed invasive, poorly differentiated adenocarcinoma. Computed topography of the abdomen and pelvis demonstrated malpositioning of the PEG tube with the bulb outside the gastric lumen (Figure 1) and within the anterior peritoneal cavity. The clinical and pathological assessment was consistent with invasion of the underlying carcinoma into the area surrounding the PEG site, causing a buried bumper syndrome. Percutaneous endoscopic gastrostomy (PEG) placement is generally considered a safe adjunct for nutritional support in patients with advanced gastric and esophageal cancers complicated by malnutrition and weight loss who are not amenable to esophageal stenting. Buried bumper syndrome is generally attributed to excessive tightening of the bumper against the gastric wall resulting in ischemic necrosis. Our case is unique its presentation of a buried bumper syndrome because it occurred secondary to adenocarcinoma invasion of the surrounding gastric wall. Endoscopic evaluation should be performed in these patients for early recognition and prevention of this well described PEG tube complication in patients with invasive adenocarcinoma.

Clinical Vignette: A 70-year-old male with a past medical history of metastatic distal esophageal squamous cell cancer status-post chemoradiation complicated by distal esophageal stricture, esoph-



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[504B] Figure 2.

[505A] Figure 1.

506 Successful Removal of a Fully Covered Metal Biliary Stent in the Setting of Severe Sepsis Jason Sloane, Aamir Dam, MD, Michael Tadros, MD, MPH. Albany Medical Center, Albany, NY.

[504C] Figure 3.

505 Cross-sectional GI Imaging Should Precede Capsule Endoscopy in Evaluation of Overt-Obscure GI Bleeding With Negative Endoscopic Work-up

Self-expandable metal stents (SEMS) and plastic stents are commonly used to achieve biliary decompression in patients with benign and malignant strictures. The choice between different types of stents depends on clinical factors, cost, and local expertise. Other important considerations are stent related factors including rates of stent patency, migration and need for surgery. Our patient presented four years after insertion of a covered metal stent with severe sepsis and cholangitis. The case illustrates the technical difficulties in urgent removal of a covered metal stent years after it has been placed. We present a 60-year-old male who was transferred to us from an outside hospital with severe sepsis and epigastric abdominal pain. He has a history of chronic pancreatitis and several years ago developed obstructive jaundice and a fully covered metal stent was placed for a suspected malignant biliary stricture. Patient had declined surgical intervention and was lost to follow up for over 4 years. Upon arrival to our institution, patient had severe sepsis with acute kidney injury, coagulopathy with INR >9, and florid disseminated intravascular coagulation. Labs were notable for a significant leukocytosis and liver function tests revealed total bilirubin of 2.5, AST 104, ALT 52, alkaline phosphatase 267, and lipase 23. Imaging a complex fluid collection measuring 10 x 8 cm in the pancreatic tail, distended gallbladder and a biliary stent noted in the common bile duct. CT-guided aspiration of the collection was consistent with a polymicrobial infection. Patient underwent an emergent ERCP, which revealed an occluded metal biliary stent (Figure 1), and 10 Fr by 10 cm plastic stent was successfully placed into metal stent. No attempt was made to remove the stent at that time because of the coagulopathy and high risk. Patient underwent repeat ERCP once stable and the covered metal stent was removed with ease from the biliary tree using a

Eric J. Mao, MD1, David Anjelly, MD1, Kenneth Friedman, MD1, Jonathan Movson, MD1, Jamsheed B. Vakharia, MD1, Samir A. Shah, MD2. 1. The Warren Alpert Medical School of Brown University, Providence, RI; 2. Warren Alpert Medical School/Gastroenterology Associates, Providence, RI. A 54 year old female with GERD on daily omeprazole presented with 2 days of maroon stools which progressed to melena. She denied abdominal pain, hematemesis, or NSAID use. Physical exam was notable for stable vital signs, benign abdomen, and rectal exam with black stool positive for occult blood. Her hemoglobin was 8.2g/dL, decreased from 12 a week earlier, and BUN was 21mg/dL. She was started on IV pantoprazole and EGD revealed a few small fundic gland polyps, but no blood or ulcers. Colonoscopy revealed hematin scattered throughout the entire colon and distal terminal ileum. The patient continued to have melena and was referred for CT enterography (CTE). A 4.1 x 4.8 x 4.7 cm hypervascular mass was seen arising from the wall of the terminal ileum with large feeding vessels from the superior mesenteric artery. She underwent exploratory laparotomy with excision of an isolated mass and resection of 14cm small bowel. Pathology demonstrated a submucosal lesion without hemorrhage or necrosis with normal overlying mucosa; high-power exam showed bland spindle shaped cells with varying degrees of eosinophilic cytoplasm arranged in fascicles. Mitoses numbered < 2 per 50 high power fields. A c-kit (CD117) stain was positive, confirming the diagnosis of low-grade GIST. This case illustrates an example of active, overt-obscure GI bleeding (OGIB) diagnosed by CTE following negative colonoscopy and EGD. In this setting, guidelines favor proceeding to capsule endoscopy (CE) as a first-line diagnostic tool for evaluation of the small bowel. The few prospective studies directly comparing diagnostic yield of CTE vs CE for OGIB are conflicting, as sensitivity is influenced by lesioncharacteristics and timing of exam, among other factors. In this patient who was unable to receive a CE in the hospital, CTE presented a safe, noninvasive initial step towards an expedient diagnosis. Most guidelines incorporate both CE and CTE after negative colonoscopy and endoscopy. With overt-obscure bleeding, we believe CTE may be superior given its widespread availability and ability to detect masses and bleeding lesions. Further prospective studies are needed to elucidate the optimal approach. In the meantime, we as endoscopists evaluating GI bleeding should think beyond just endoscopic approaches and consider CTE in the appropriate setting.


[506A] Figure 1.


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rat-toothed forceps (Figure 2). Pus and sludge were drained from the common bile duct and two plastic stents were placed to maintain patency. Cultures grew multi-drug resistant E Coli. Patient recovered and has been doing remarkably well since discharge. Early covered SEMS were designed primarily for the palliation of biliary malignancies, although are increasingly being used for benign disease. If left in place for prolonged periods, the feasibility of removal decreases as the stent can migrate proximally and become embedded due to hyperplastic-tissue ingrowth of the distal uncovered end. Our case is unique in that we were able to successfully remove an occluded covered metal stent more than four years after placement.

507 Endoscopic Ultrasound (EUS) Guided Fiducial Placement for Stereotactic Body Radiotherapy: A New, 22-gauge, “Pre-loaded” EUS Fiducial Needle Reduces Procedure Time Compared to the Traditional Needle “Re-loading” Technique Truptesh Kothari, MD, MS1, Shivangi Kothari, MD1, Alan Katz, MD1, Noelle Fagan1, Guobao Wang, MD2, Dushyant Damania, MD3, Vivek Kaul, MD, FACG1. 1. University of Rochester Medical Center, Rochester, NY; 2. Sun Yat-Sen University Cancer Center, Rochester, NY; 3. University of Rochester Medical Center, Webster, NY.

[506B] Figure 2.

Fiducial guided SBRT has been approved for the treatment of various malignancies. Stereotactic radiosurgery system delivers radiation with high precision using real-time image guidance, using radiographic markers (gold fiducials) implanted in the tumor as reference points. EUS guided fiducials have been traditionally placed using the “re-loading” technique of the EUS fine needle aspiration (FNA) needle. We compared the efficiency of a new dedicated, “pre-loaded” EUS fiducial needle with the traditional needle “re-loading” technique. Objective: To assess the efficiency of a new preloaded (with 4 gold fiducials) EUS fiducial needle compared to the traditional FNA needle which requires “re-loading” with placement of each new fiducial. Methods: Patients were initially selected for SBRT based on clinical presentation and after multidisciplinary tumor board review. These patients were then referred for EUS guided fiducial placement. 14 consecutive, eligible patients underwent EUS guided fiducial placement between 4/2014 and 11/2014 at our center. The first 8 patients (GrpA) underwent fiducial placement with the traditional “re-loading” technique using a EUS FNA needle (19 or 22 gauge); the next 6 (Grp B) underwent the procedure with a new 22-gauge “pre-loaded” EUS fiducial needle (see Table 1 for details). All patients received intra-procedural antibiotics. Data was retrospectively reviewed per medical records.

[507A] Figure 1.



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Abstracts Results: Patient & procedure details are listed in Table 1. Mean patient age was 65.6 yrs; 11 (78.8%) were males. EUS-guided fiducial placement was successful in all 14 patients. All patients underwent successful SBRT. Average fiducial placement time (time from first fiducial placed to last fiducial placed) was 12.38 minutes in Grp A and 7.17 minutes in Grp B (p=0.0236). There were no infections, complications or deaths related to the procedure. All procedures were performed on an outpatient basis and patients were discharged home after an uneventful procedure & recovery. Conclusion: This series represents the first report that compares the fiducial placement time between the 2 currently available EUS based fiducial placement platforms. EUS-guided fiducial placement using a new 22-gauge “pre-loaded” needle is safe, effective and very efficient. Average procedure time was reduced by 58.1 % using this needle, compared to the traditional approach of re-loading a EUS FNA needle for multiple fiducial placements in the same session. Successful deployment was achieved in all 14 patients. The pre-loaded nature of the needle simplifies the procedure, reduces overall procedure time and eliminates potential needle-stick exposure for ancillary staff. Further experience with this needle will clarify its role and impact in interventional EUS.

508 ERCP for Cystic Duct Stones After Cholecystectomy Katherine M. Wang, MD1, Aamir Dam, MD1, Pushpak Taunk, MD2, Michael Tadros, MD, MPH1. 1. Albany Medical Center, Albany, NY; 2. Thomas Jefferson University Hospital, Philadelphia, PA. This is a case of a 67 year old male who was referred for recurrent cholangitis. The patient had undergone a laparoscopic cholecystectomy for symptomatic gallstones five years earlier. Since the surgery, the patient has been hospitalized multiple times for cholangitis. ERCP with sphincterotomy was performed on two separate admissions without definitive identification of common bile duct (CBD) stones. After being asymptomatic for six months, the patient again presented with fever, jaundice and right upper abdominal quadrant pain and was referred to us for ERCP. His labs were significant for AST 154, ALT 355, alkaline phosphatase 116, and total bilirubin 9.0. MRCP was suggestive of distal CBD stone and filling defects in the cystic duct remnant. ERCP confirmed a long, dilated cystic stump containing multiple filling defects and one stone in the lower third of the CBD. The cystic duct stump was accessed with an angled tip wire and a retrieval basket was used to extract sludge and small calculi. One 10 Fr by 7 cm plastic stent was placed in the CBD. He underwent repeat ERCP two months later for stent removal. During this ERCP, the cholangiogram was notable for a persistently dilated cystic and common bile duct without any residual fi lling defects. Clinically, the patient was doing well and remained asymptomatic. Surgical options will need to be explored if he has recurrence of symptoms. The incidence of calculi in the cystic duct remnant is less than 2.5%; however, this diagnosis should be entertained in a patient with recurrent right upper quadrant abdominal pain post-cholecystectomy. A long cystic duct remnant (> 1cm) is more commonly seen in those who undergo a laparoscopic cholecystectomy versus an open procedure. The long remnant duct can predispose to inadequate stone removal and biliary stasis leading to new calculi formation. In our case, given the patient’s recurrent symptoms, the cystic duct was targeted and stones were extracted using a retrieval basket. Other reports have used the addition of extracorporeal shock wave lithotripsy to aid in the removal of stones. In refractory cases, surgical extraction of the stone with excision of the cystic duct remnant may be necessary. Cystic duct remnant stones are difficult to diagnose and while their removal can be technically challenging, ERCP should be considered as first line therapy.

510 Metastatic Melanoma to the Small Intestine Causing Obscure Occult Gastrointestinal Bleeding Kirbylee K. Nelson, MD1, Jonathan Keshishian, MD2, M. Thure Caire, MD3, Jeffrey A. Gill, MD4. 1. Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL; 2. University of South Florida, Tampa, FL; 3. University of South Florida, Morsani College of Medicine, Brandon, FL; 4. Department of Gastroenterology, Division of Digestive Diseases and Nutrition, James A. Haley VA Hospital, University of South Florida, Tampa, FL. Malignant melanoma is the most common tumor to metastasize to the gastrointestinal tract. While small bowel involvement is found at postmortem in 50-60% of melanoma patients, diagnosis is only made during life in less than 10% of cases. Capsule endoscopy (CE) is an easy, noninvasive, and effective diagnostic modality to investigate small bowel involvement. A 64-year-old male presented to our facility with worsening anemia, fatigue, and dyspnea. Two years prior, he was found to have malignant melanoma status post wide local excision with sentinel node resection (2/2 positive for melanoma) and subsequent lymph node dissection (1/32 nodes positive). Final pathology was consistent with Stage IIIc (pT4bN2bMx) disease. Subsequent imaging over the past two years had shown no evidence of disease. He denied changes in bowel habits, melena, hematochezia, or bright red blood per rectum. Complete blood count showed a microcytic anemia (hemoglobin 7.6 g/dL, mean corpuscular value 65.8) with a 5 g drop compared to baseline three months prior. In the previous five months, he had undergone esophagogastroduodenoscopy and colonoscopy, both of which were unrevealing for etiology of anemia. Due to prior workup, we proceeded with CE. CE was notable for a single, polypoid intraluminal lesion 10 minutes into the small intestine without active bleeding. Subsequent anterograde push enteroscopy revealed a 3-4 cm ulcerated, friable, mass in the proximal jejunum that was actively oozing blood. Tattoos were placed proximal and distal to the lesion. Biopsies were consistent with metastatic melanoma, BRAF negative. Unfortunately, restaging PET/CT showed several hyperavid regions in the small bowel and left chest highly concerning for malignancy. Surgical consultation was obtained who elected to not perform metastectomy due to oligometastatic disease. He is planned to initiate systemic immunotherapy with Ipilimubab. The prognosis for patients with metastatic small bowel melanoma is poor with a median survival of 12.5 months. Survival is increased considerably with early detection and curative resection. Currently, there is no gold standard for the detection of small bowel metastasis. CE has been shown to detect the presence and extent of small bowel metastasis in melanoma patients more accurately than conventional imaging modalities. CE should therefore be considered in the workup of melanoma patients with suspected small bowel disease, as early detection may impact management and outcome.

509 Rare Case of Sigmoid Volvulus Following Single Balloon Enteroscopy Katherine J. Hahn, MD1, Philip Sarges, MD1, Kathy P. Bull-Henry, MD2. 1. MedStar Georgetown University Hospital, Washington, DC; 2. Georgetown University, Washington, DC. Introduction: Single balloon enteroscopy (SBE) has revolutionized visualization of the small bowel. Common complications include perforation, abdominal pain, and mucosal tears. In this case report, we describe sigmoid volvulus (SV) presenting 48 hours after SBE. Clinical Case: A 69 year-old man received an outpatient SBE for evaluation of small bowel polyps. The procedure lasted 29 minutes and 71 liters of CO2 were used. No therapeutic intervention was performed. Forty-eight hours after discharge, the patient noted severe left lower quadrant pain. His past history was significant for irritable bowel syndrome - diarrhea predominant, appendicitis s/p appendectomy, and inguinal hernia repair. Physical exam showed a soft, distended abdomen with hyperactive bowel sounds and no peritoneal signs. Rectal exam had normal anal sphincter tone without masses. A CT scan revealed a dilated sigmoid colon to 12 cm due to SV. Laboratory values revealed white count of 8.0, creatinine of 0.71, and lactate of 2.7. Flexible sigmoidoscopy for decompression was attempted, but unsuccessful. On hospital day 2, a segmental resection of the sigmoid colon with end colostomy was performed. Intraoperatively, the sigmoid colon was found to be significantly dilated; however, no redundant bowel, long mesentery, or adhesions were noted. The patient was discharged home 5 days after surgery. Discussion: SBE has been shown to be a safe and effective procedure for evaluation of the small bowel. Complication rates in SBE are reported to be similar to double balloon enteroscopy (DBE). Generally, complications are reported in 1% of SBE cases. Of those, the most serious are perforation (1.3-2.7%) and mucosal tears. In this case report, we describe sigmoid volvulus presenting after SBE. Sigmoid volvulus is responsible for 8% of all intestinal obstruction in Western countries, and is particularly common in the elderly. Other predisposing factors include male gender, chronic constipation, redundant bowel/ mesentery, and adhesions. Sigmoid volvulus after SBE has not been reported. As this patient’s only risk factors were his gender and age, it is unclear if his sigmoid volvulus was a direct complication of the SBE or simply a coincidental occurrence. As balloon assisted enteroscopy becomes a more common method of evaluating the small bowel, physicians should be aware that sigmoid volvulus may be an unexpected but potentially life threatening complication of this procedure.


[510A] Figure 1.

511 A Tubo-ovarian Abscess Identified via Colonoscopy Jeannette Collins, MD1, Dustin Albert, MD2, Manish B. Singla, MD1, Lawrence Goldkind, MD1. 1. Walter Reed National Military Medical Center, Bethesda , MD; 2. Walter Reed National Military Medical Center, Silver Spring, MD. A tubo-ovarian abscess (TOA) is an inflammatory mass involving the fallopian tube and ovary and may extend to the surrounding structures. We present a case of a TOA manifesting as a mucosal defect with intraluminal drainage seen on colonoscopy. A 44-year-old female presented with one month of fevers, chills, left lower quadrant abdominal pain, and 10-20 daily episodes of small volume diarrhea with passage of mucous. She had been admitted to the psychiatry unit for a month due to depression and anxiety secondary to the recent suicide of her daughter. Diarrhea had persisted since her admission. However, upon discharge, she began to have fevers and chills. She had no history of sexually transmitted infections but had an intrauterine device removed at the onset of her symptoms. A CT scan showed a large, complex left ovarian mass involving the rectum and sigmoid with thickening of the colon from the rectum to the transverse colon suggestive of colitis. Due to concern for malignancy, she underwent a colonoscopy, which revealed extrinsic compression of normal sigmoid mucosa and two 2 mm punctate mucosal defects in the sigmoid colon. During careful examination with insufflation, the defects excreted opaque, exudative material. She underwent explor-


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atory laparotomy, modified radical hysterectomy, bilateral salpingo-oophorectomy, and rectosigmoid resection with end-to-end anastomosis. A left-sided fixed mass from ovary to rectosigmoid expressing purulent material was seen with normal appearing bowel. Colon histology showed acute and chronic inflammation and fibrosis of the serosa, muscularis propria, and submucosa with unremarkable mucosa. Ovarian pathology showed acute and chronic inflammation and granulation tissue consistent with a ruptured TOA. Cytology was negative for malignant cells. She was treated with parental antibiotics and made an unremarkable recovery. A TOA is a severe complication of pelvic inflammatory disease (PID). Mortality is low prior to rupture and historical data suggests that mortality from a ruptured TOA may be from 1.7-3.7%. PID may be associated with insertion of an IUD, but rarely with removal. 60-80% of TOA may resolve with antibiotics, but surgery is indicated for ruptured abscesses. Anatomic proximity to the sigmoid colon allows direct involvement with the potential for colonic perforation, fistula formation, or diverticulitis.

512 Mediastinal Schwannoma Masquerading as a Cystic Lesion: A Case Report and Review of the Literature Neelam Gidwaney, MD, Amy Tilara, MD, Swati Pawa, MD. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ. Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) is a safe and minimally invasive diagnostic technique for the analysis of mediastinal lesions. This approach, however, may result in life-threatening mediastinitis. Here we report a rare case of mediastinal schwannoma presenting as a cystic lesion and pose an important question of risk versus benefit of aspiration of cystic lesions. A 39-year-old man developed persistent non-productive cough and dysphasia to solids for several months. A computed tomography (CT) of the chest revealed a large posterior upper mediastinal mass measuring 6.3 x 4.5 x 8.0 cm displacing the esophagus to the right and the trachea anteriorly, with a standardized uptake value (SUV) of 2.8. The patient then had a bronchoscopy, which showed marked extrinsic compression of the mid trachea without endobronchial disease. An esophagoduodenoscopy (EGD) and EUS were performed and were notable for an 8 cm oval, well-demarcated anechoic lesion with both solid and cystic components adjacent to the esophagus. FNA was intentionally not performed due to the risk of mediastinitis. The patient had a subsequent magnetic resonance imaging (MRI) of the chest showing the 9.3 x 4.1 x 6.0 cm midline retrotracheal superior mediastinal mass. He ultimately underwent posterolateral thoracotomy with excision of the lesion. A frozen section was consistent with a neurogenic tumor. Final pathology revealed a schwannoma. Diagnosis of mediastinal masses poses a significant challenge. The differential diagnosis for a posterior mediastinal mass alone includes neurogenic tumor, neuroblastic tumor, non-neurogenic tumor, paraspinal abscess, hernia, lymphadenopathy or lymphoma, foreget duplication cysts, and thoracic meningocele. EUS-FNA is a minimally invasive and a safe procedure with a complication rate (i.e. infection, bleeding, acute pancreatitis) of approximately 1%. This rate, however, increases when the lesion contains a cystic component rather than a purely solid lesion. Several case reports have described cystic infection and mediastinitis despite accepted techniques including prophylactic antibiotics. Schwannomas generally appear as solid lesions when imaged by either CT or MRI. In 23-30% of cases, this subtype of neurofibromas may be cystic and performing a FNA may result in serious consequences. More data are needed to accurately provide the risks and benefits of EUS-FNA of mediastinal cystic lesions and to validate the use of prophylactic antibiotics for aspiration of cystic lesions.

[511A] Figure 1.

513 Removal of Gastric and Jejunal Polyps With Single Balloon Enteroscopy in a Patient With Peutz Jeghers Syndrome Jacqueline Young1, Seth Lipka, MD2, Patrick Brady, MD, FACG3. 1. University of South Florida, Orlando, FL; 2. University of South Florida, Division of Digestive Diseases and Nutrition, Tampa, FL; 3. University of South Florida, Morsani College of Medicine, Tampa, FL.

[511B] Figure 2.

Introduction: Peutz-Jeghers syndrome (PJS) is an autosomal dominant disease characterized by multiple hamartomatous polyps anywhere along the gastrointestinal tract. It is also recognized by pigmentation on lips and oral mucosa. PJS is associated with an increased risk of gastrointestinal and nongastrointestinal cancer. We describe a patient managed with surveillance single balloon enteroscopy in a patient with PJS with small bowel polyps. Case Description: A 64 year old woman with a past medical history of Peutz-Jeghers Syndrome diagnosed at birth presented with routine surveillance CT abdomen showing possible mass in the small bowel in the RUQ of the abdomen. She had prior surgery for pancreatic carcinoma (s/p Whipple) and small bowel resection for intussusception (in 1995). The patient was asymptomatic and denied nausea, vomiting, constipation or diarrhea. She did not notice any blood in the stool and stated that her stool was of normal consistency. A single balloon enteroscopy was performed to better visualize and remove the mass in the small bowel. Innumerable small polypoid polyps were found throughout the body of the stomach and cardia. Two large gastric polyps were removed. Multiple polyps were also found in the jejunum. Four polyps measuring between 5 to 8 mm were removed. All six polyps showed hamartomatous polyp, consistent with Peutz-Jeghers syndrome and no dysplasia or malignancy were identified. The plan going forward is to continue to use single balloon enteroscopy every two years to monitor because of the malignant potential of hamartomatous polyps. Discussion: This case illustrates the unique use of single balloon enteroscopy for removal of gastrointestinal polyps. In Peutz Jeghers Syndrome (PJS), polyps most commonly occur in the small bowel (60 to 90 percent) and more specifically in the jejunum. Complications of not removing polyps in a timely manner include gastrointestinal bleeding, obstruction, intussusception, and the malignant potential of hamartomatous polyps. Single balloon enteroscopy with resection of significant small bowel polyps are useful in asymptomatic patient to avoid aforementioned complications. Surveillance programs are being used to follow up with patients affected by PJS. Prophylactic polypectomy of small bowel polyps are being evaluated as a possible first line treatment for the conservative approach in the management of PJS patients.

514 Esophageal Perforation 2 Years After Cervical Hardware Implantation Aaron Goodwin, MD1, Kristi Moore, MD1, Rebecca Rawl, MD2. 1. Carolinas Medical Center, Department of Internal Medicine, Charlotte, NC; 2. Carolinas Medical Center, Department of Internal Medicine, Division of Gastroenterology, Charlotte, NC.

[511C] Figure 3.


A 44 year-old man presented to the emergency department with an 8-12 month history of progressive dysphagia to solids and liquids, 80 pound weight loss, odynophagia, and significant dyspepsia. Medical history included type 2 diabetes mellitus and a cerebral vascular accident 3 years prior with residual leftsided extremity motor weakness but no speech or swallowing dysfunction. Surgical history was significant for traumatic right arm amputation and multiple cervical spine surgeries, with most recent anterior fixation of C3-C7 two years prior.


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Abstracts Initial plain films and computed tomography (CT) imaging of head and neck showed surgical fixation of C3-C7 with anterior displacement of C6/C7 hardware and screws into the prevertebral soft tissue without frank intrusion in the esophagus. Barium esophagram and flexible laryngoscopy the following day showed no focal abnormalities to the esophagus, nasopharynx, hypopharynx, and larynx. Endoscopy found surgical hardware visualized at the level of the cricopharyngeus. Six days after presentation, the patient underwent removal of cervical hardware and repair of esophageal perforation with placement of percutaneous endoscopic gastrostomy (PEG), tracheostomy, and salivary bypass. Purulent fluid was found surrounding the cervical hardware, and cultures isolated viridans streptococci, Candida albicans and Methicillin-resistant Staphylococcus aureus. He was treated with a total course of four weeks with IV vancomycin and oral fluconazole. Post-operative course was unremarkable and he reported no dysphagia by follow-up. Anterior cervical spinal fixation has become a common management modality for multiple spinal pathologies. While esophageal perforation most often occurring in the early post-operative phase, lateonset cases have been reported occurring more than 10 years after the initial surgery. Common symptoms include neck and throat pain, odynophagia, dysphagia, hoarseness, and aspiration. Less-common presenting symptoms include recurrent pneumonia, fever, cough, and subcutaneous emphysema. Prompt detection and intervention is crucial as mortality and complication rates rise significantly with delayed detection and intervention. Multiple modalities including CT imaging, endoscopy, and even surgical exploration may be required for diagnosis. Negative imaging should not be used as the sole means to rule out esophageal erosion or perforation. Esophageal perforation is most common at the C5/C6 or C6/C7 level. Essential components of therapy include surgical removal of hardware, abscess drainage with culture-directed parental antibiotics, and salivary fluid diversion. Swallowing function has been reported within 10-14 days after the surgical repair.

515 Successful Treatment of Gastric Sleeve Leaks With Insertion of Removable Self Expanding Metal Stents: A Case Series

[514A] Figure 1.

Vinod Kumar, MD1, Shobha Shahani, MD2, Simranjit Singh, MD1, Fnu Sanna, MD1, Wael Youssef, MD3. 1. University of Illinois at Urbana-Champaign, Internal Medicine Residency Program, Champaign, IL; 2. University of Illinois at Urbana-Champaign, Champaign, IL; 3. Carle Clinic, Urbana, IL. Background: Laparoscopic sleeve gastrectomy, a standard procedure for the surgical treatment of patients with obesity is associated with post operative gastric sleeve leak and cause significant morbidity and mortality. Case presentation: We describe four cases of patients with leak after gastric sleeve surgery for morbid obesity. Post operatively the patients were noted to have gastric sleeve leak. All four patients underwent placement of the self expandable metal stent in the leaking gastric sleeve. The stents were left in place for four to eight weeks for the leaks to heal and then removed. All four patients showed healing of the leak after the stent was removed and no further leaks were observed. In one patient the stent was noted to migrate and functionally obstruct at the distal end due to narrowing and mucosal swelling at the gastric sleeve. The stent was fully recovered and replaced with another stent. The leak later healed well and the stent was subsequently removed after six weeks. Discussion: Gastric sleeve surgery is usually done for morbid obesity. Although the surgery helps in reducing morbidity, it also has its known complications including gastric sleeve leak, staple line bleeding, strictures and enterocutaneous fistulas. Out of all the complications gastric sleeve leak causes highest morbidity. Removable stent placement is fairly new treatment option for gastric sleeve leaks and is gaining popularity. The stent placement helps in recovery in most patients. Gastric leaks at proximal and mid aspect can be treated with endoscopic stent placement. The complications related to stent placement include stent blockage, migration or kinking. Conclusion: Gastric sleeve leaks can be treated successfully with removable self expandable metal stents placed endoscopically and is associated with fewer complications.

[514B] Figure 2.

516 Endoscopic Introduction of an Over-The-Scope Clip Through an Overtube to Close Gastrocutaneous Fistula in a Patient With a Complex Upper Esophageal Stenosis Paul Kröner, MD1, Marco D’Assunção, MD2, Sandhya Mudumbi, MD2, Klaus Mönkemüller, MD, PhD2. 1. Mount Sinai St. Luke’s Roosevelt Hospital Center, New York, NY; 2. University of Alabama at Birmingham, Birmingham, AL.

[514C] Figure 3.


A 51-year-old male with history of laryngeal cancer requiring total laryngectomy and forearm skin graft into the hypopharynx (Figure A) developed a non-healing gastrocutaneous fistula after gastrostomy tube removal. Injection of Indigo-carmine through the skin allowed for perfect localization of the 3-4mm diameter gastrocutaneous fistula, which was located within thickened gastric folds (Figure B). Although the gastroscope could be passed into the stomach after dilating the stenosis sequentially using 9, 10 and 12mm Savary bougies, passing the over-the-scope clip (OTSC) system (Ovesco Endoscopy, Tübingen, Germany) through the hypopharynx was still not possible. Contrast esophagogram performed after dilation did not show any endoluminal esophageal damage. Therefore, an overtube (Guardus® overtube-esophageal, inner diameter 16.7mm, outer diameter 19.9mm, US Endoscopy, Ohio, USA) was inserted into the esophagus. The large diameter overtube served as a “giant working channel”, thus permitting the passage of the endoscope loaded with the 11/6t OTSC device (Figure C). The overtube was primarily used to open the space and allow for better passage of the scope loaded with the device, especially in the presence of endotracheal intubation, which was performed under general anesthesia. The fistula was successfully closed (Figure D). This was further documented by using water-soluble contrast administered through the endoscope. The overtube and endoscope were removed and additional contrast administration at the hypopharynx and upper esophagus did not reveal any damage, leak or extravasation. This case demonstrates a case of “extreme endoscopy”. First, the complex fistula could be found using interventional chromoendoscopy. The esophageal stricture was dilated and an overtube was inserted into the stomach. The overtube served as a bridge of the upper esophageal stenosis, allowing for the smooth passage of the scope with a large fistula closing device, such as the OTSC system.


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[517B] Figure 2.

[516A] Figure 1.

A seemingly-impossible situation turned into a therapeutic solution by combing elements widely available in the endoscopy suite such as fluoroscopy, overtubes, dilation balloons, clipping devices and chromoendoscopy.

clinically stable, surgery was not performed. She was discharged home on day 10. A third upper GI series was completed 6 days later at which time the duodenal leak was not present. Early diagnosis of endoscopic perforation of the duodenal wall allows early surgical intervention, and primary repair of the perforation may be all that is necessary. Mortality rate increases with late surgical management. However, despite meeting criteria for surgical management indicated by the presence of intraperitoneal free air on CT imaging and active extravasation of contrast on upper GI series, conservative management proved to be successful in this case. In conclusion, nonperiampullary duodenal wall perforation with active leak may be conservatively managed in certain cases where the leak is small and contained around the perforation site and as long as the patient displays stable clinical status.

518 Endoscopic Stricturotomy and Stent Placement for Refractory Gastrojejunal Anastomotic Stricture in a Patient With Roux-en-Y Gastric Bypass Surgery: A Case Report Bhupinder Romana, MD, Sameer Siddique, Imran Ashraf, MD, Roger De La Torre, MD, Ghassan Hammoud, MD, MPH. University of Missouri, Columbia, MO.

517 Conservative Management of an Endoscopic Duodenal Wall Perforation With Active Leak Clark Gunnerson, DO1, Sobia N. Khan, DO2, M. Joshua. Shellenberger1. 1. Geisinger Medical Center, Danville, PA; 2. Geisinger Medical Center, Danville , PA. Acute iatrogenic perforation during endoscopy is defined as the presence of gas or luminal contents outside the gastrointestinal tract. Nonperiampullary duodenal perforation is usually caused by direct trauma from the endoscope or therapeutic interventions, requiring surgical management. The indications for surgery include extravasation of contrast medium, presence of a fluid collection, severe peritonitis or severe sepsis. We present a rare case of endoscopic lateral duodenal wall perforation with active leak which was managed conservatively despite meeting criteria for surgery. A 62 year old female with cirrhosis secondary to non-alcoholic steatohepatitis underwent liver biopsy of both hepatic lobes via endoscopic ultrasound. The procedure was completed successfully without apparent complication. Soon after the procedure she developed severe abdominal pain in the right upper quadrant with referred pain to the right shoulder. Abdominal computed tomography (CT) without oral contrast showed inflammatory changes surrounding the first and second portions of the duodenum, scattered foci of free intraperitoneal air,and a tiny focus of air adjacent to the duodenal bulb. She was admitted to the hospital and antibiotics were started. She refused endoscopic closure attempt. On day 3, upper gastrointestinal (GI) Gastrografin imaging study showed evidence of perforation of the duodenum distal to the duodenal bulb with a leak localized around the duodenum and small pockets of intraperitoneal air. On day 7, upper GI study again showed persistent leak from the duodenum. As she remained

Introduction: Gastro-jejunal (G-J) anastomotic strictures are a common complication after Roux-enY gastric bypass. We present a case of symptomatic refractory post RYGB G-J stricture treated with endoscopic stricturotomy using an ERCP sphincterotome. Case: A 62-year-old female with prior gastroplasty and RYGB conversion developed an intractable stricture. She underwent open revision of her gastrojejunostomy, complicated by an anastomotic leak. She remained well for nearly 5 years and re-presented again with nausea and vomiting. Endoscopy confirmed a tight G-J anastomosis restricting passage of the adult upper endoscope. The stricture underwent serial dilations using hydrostatic balloon every 4 weeks. After 3 CRE balloon dilations to 10mm, the stricture remained stenosed. Following her 3rd visit, hydrostatic dilation with fully covered metal stent placement was discussed with the patient and surgical team. Balloon dilation was performed initially to 14mm, allowing passage of the radial echoendoscope to evaluate thickness of the stricture and muscularis propria. Using a 4.4 Fr sphincterotome, mucosal incisions were made at 3 O’clock and 9 O’clock positions followed by placement of a TTS duodenal stent. The patient’s symptoms improved dramatically following the procedure. On repeat endoscopy 4 weeks later, the G-J anastomosis remained patent. Consequently, the stent was removed. The patient remained asymptomatic on follow up. Discussion: Gastro-jejunal (G-J) anastomotic strictures are a common complication after RYGB occurring in 5-10% of post-operative patients. While endoscopic balloon dilations are effective, they are associated with recurrence, restenosis and rarely may need surgical revision of the anastomosis. Our patient had intractable symptoms of nausea and vomiting due to a G-J anastomotic stricture. Prior surgeries with complicated post-operative periods meant that she was not deemed an appropriate surgical candidate. Endoscopic balloon dilation is a safe and effective option in the management of anastomotic stricture following RYGB with a low incidence of perforation rates. However, in our patient, balloon dilation every 4 weeks did not result in any significant improvement in the luminal diameter of her stricture or her symptoms. Eventually, she successfully underwent a stricturotomy with stent placement as described above. Following her stricturotomy, her symptoms improved and she tolerated an oral diet. To our knowledge, this is the first described case of endoscopic stricturotomy using a biliary sphincterotome for refractory G-J anastomotic stricture. Conclusion: In RYGB patients who are not surgical candidates, endoscopic stricturotomy and stent placement may have a role in management of intractable symptomatic G-J strictures.

519 Endoscopic Resection of a Bleeding Brunner’s Glands Hamartoma Hugo Bernard, MD1, George Rateb, MD2, Dusanka Grbic, MD1. 1. Université de Sherbrooke, Sherbrooke, PQ, Canada; 2. Université de Sherbrooke, Sherbrooke, PQ, Canada.

[517A] Figure 1.


Brunner’s glands hamartoma is a rare and benign lesion arising from the brunner’s glands of the duodenum. This proliferation can be symptomatic with bleeding or obstruction, rarely with chronic pancreatitis. Around 200 cases have been reported and tumors are rarely more than 5 cm. A 81 years-old lady known for gastroeosophageal reflux on proton pump inhibitor and a 28x18 mm pedunculated submucosal lesion (hyper echoic with small hypo echoic foci) of the duodenum which was stable in appearance and size in 2009 presented with a 5 days history of melena with abdominal discomfort. Her blood work was remarkable for haemoglobin of 64 g/L (127 g/L previously).


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The upper endoscopy showed a more than 5 cm duodenal polyp with multiples ulcerations and friability without active bleeding. Placement of a ligating device to prevent the rebleeding, polyloop 30mm (Olympus: HX-400U-30), was impossible due to the size and position of the lesion. A CT-scan confirmed a polypoïd lesion anchored in the duodenal bulb without extra digestive extension of suspicious ganglion. An endoscopic ultrasonography showed a more than 4x3 cm lesion of the duodenal bulb with a relatively short and thick peduncle originating from the mucosa with complete sub mucosa infiltration. This lesion was diffusely homogenous with a hyper echoic pattern. There was no muscular layer infiltration. Considering the advanced age of the patient an endoscopic resection was considered acceptable. A second endoscopy was performed. An « en bloc » resection with a 3x6 cm Acusnare polypectomy snare (Cook Medical: ASJ-1-S : G22630) at the base of the peduncle. The polyp was displaced in the stomach with some resistance and an arterial bleeding from the base of the polypectomy was control with a Resolution Clip (Boston Scientific: 2261). Two other clips were installed and a polyloop 30 mm surrounding the clips closed the mucosal defect. The polyp was then grabbed with the snare but was too big to pass the gastro oesophageal junction. We unsuccessfully tried to cut the polyp in two pieces. A 16.7 mm inner diameter 50 cm length Guardus gastric overtube (USEndoscopy: BX00711149) was placed in the stomach. The polyp was grabbed again with the snare and impacted 50% of its length in the distal portion of the overtube. All items (polyp, scope, overtube) were removed « en bloc » without much resistance. Pathology showed a 5.5x4x2.2 cm lesion with a 1.2x2 cm insertion site considered a brunner’s glands hamartoma without dysplasia with multiple superficial ulcers. The resection was incomplete with lesion at the insertion site. The patient had no complication or further bleeding and was discharged home. A six months follow-up upper endoscopy is pending.

520 Parasitic Egg Consistent With Schistosoma on Rectosigmoid Biopsy Tyrrell Jenkins, MD, MPH1, Belen Tesfaye, MD2, Momodu Jack, MD3. 1. Howard University College of Medicine, Washington, DC; 2. Howard University Hospital, Washington, DC; 3. Howard University Hospital, Washington, DC. A 39 years-old Ethiopian male presented with complaints of changes in bowel habits, diarrhea, and rectal pain of less than one month. He denied any previous episodes and does not have any past medical his-

[520C] Figure 3.

tory. He states that he does not take any medications, and has not changed his diet in the past month. His history is significant for recent immigration to the United States. The patient was referred to a gastroenterologist for an elective outpatient colonscopy and esophagogastroduodenoscopy. The patient’s initial complete blood count demonstrated mildly elevated eosinophil percentage (7.2%) and a slightly elevated mean corpuscular hemoglobin (33.1 pg). His basic metabolic panel was within normal limits. The coagulation profile demonstrated a decreased international normalized ratio (0.93). Findings on colonscopy demonstrated a normal appearing terminal ileum; however, mild colitis in the rectosigmoid junction [Figure 1] and rectum. The mucosa was erythematous and edematous. Three cold forcep biopsies were taken [Figures 2, 3]. There were also three polyps measuring less than 5mm in size found in the rectosigmoid junction. Furthermore, there were two polyps measuring 5 and 3 mm found in the rectum. Both were completely removed by cold snare polypectomy. Internal hemorrhoids were also noted. Then the patient had an esophagogastroduodenoscopy. There were moderately erythematous mucosa found in the antrum, body, and fundus of stomach. Four biopsies were taken. There were also evidence of duodenitis in the duodenal bulb and the second portion of the duodendum. The patient was instructed to follow-up in two weeks for biopsy results, start a high fiber diet, and avoid non-steroidal anti-inflammatory drugs. Biopsy results from the rectosigmoid showed a parasitic egg consistent with Schistosoma species [figure 3], patchy acute and chronic inflammation with mucosal eosinophilia. The polyps biopsied in both the rectosigmoid junction and rectum were consistent with hyperplasia. While biopsy results from the gastric biopsies were consistent with chronic active gastritis, with immunostain for H. pylori being positive. Slides from specimens were reviewed for quality assurance and consensus regarding diagnosis of parasitic egg consistent with Schistosoma species. The patient was treated with praziquantel. He will follow up in 6 months for antigen testing of stool and urine for excreting eggs and direct assays for eggs in stool and urine via microscopy. He instructed to return sooner if symptoms recur.

521 Superglue to the Rescue: Use of Cyanoacrylate Spray to Stop Bleeding From Large Peptic Ulcer Siddharth B. Javia, MD1, Asha Kuruvilla, MD1, Sushovan Guha, MD, PhD2, Nirav Thosani, MD1. 1. University of Texas, Houston, TX; 2. University of Texas Health Science Center, Houston, TX.

[520A] Figure 1.


Introduction: Standard endoscopic therapy of peptic ulcer disease (PUD) related bleeding involves epinephrine injection, clip application and thermal therapy. Cyanoacrylate is a class of synthetic glue that rapidly solidifies on contact with weak bases, such as water and blood. It is used off-label for endoscopic interventions especially for gastric variceal bleeding. We report a case of cyanoacrylate spray use to control bleeding from large PUD, which was refractory to standard endoscopic therapy.


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Clip closure was attempted but unsuccessful due to large size of the ulcer. Subsequently, bipolar electrocoagulation was used selectively but complete treatment was not possible due to risk of perforation. Due to lack of any other means to control bleeding, we proceeded with cyanoacrylate glue spray over the ulcer bed as a salvage therapy. A total of 10 ml cyanoacrylate glue was sprayed topically over the ulcer bed. No active oozing was noted after the therapy. Patient was followed clinically for 9 days without any evidence of bleeding. Learning points: Initial endoscopic treatment of active bleeding from PUD involves use of thermal therapy, epinephrine injection, clip application. Repeat endoscopy with hemostatic therapy should be performed in patients with clinical evidence of recurrent bleeding and high-risk lesions. Use of cyanoacrylate glue spray should be considered for management of bleeding from large, deep ulcers not amenable to thermal therapy or clip application.

522 Refractory Gastrointestinal Bleeding From Portal Hypertensive Gastropathy Hao Chi Zhang, MD, Ashish Sharma, MD, Milena Gould. Suarez, MD. Baylor College of Medicine, Houston, TX.

[521A] Figure 1.

[521B] Figure 2.

Introduction: Portal hypertensive gastropathy (PHG) may cause acute bleeding with incidence ranging from 0.8% to 12%. However, refractory bleeding from PHG is very rare. We present a case of refractory GI bleeding from PHG with review of current treatment modalities. Case presentation: A 54-year-old woman with a history of decompensated hepatitis C cirrhosis and CKD stage 4, resulting from MPGN secondary to hepatitis C infection, presented with symptomatic anemia and melena. She denied hematochezia, hematemesis, and abdominal pain. Her exam was mostly unremarkable with stable vital signs. Pertinent labs revealed: hemoglobin 7.4, platelets 101,000, BUN 29, creatinine 3.2, and albumin 2.6. Abdominal ultrasound with Doppler revealed cirrhotic liver, splenomegaly, small ascites, and no evidence of portal vein thrombosis. EGD showed hemorrhagic PHG without evidence of esophageal or gastric varices. The patient was initiated on octreotide and propranolol. She received multiple blood transfusions due to recurrent declines in her hemoglobin to below 7.0. She soon underwent placement of TIPS for refractory upper GI bleed; HVPG was 13 mmHg. Despite this measurement, she continued to remain transfusion-dependent for upper GI bleed with melena over the next few days. The TIPS was confirmed to be patent and her repeat HVPG was 8 mmHg. She underwent two additional EGDs for persistent melena, with application of APC to a few dominant lesions in the cardia and incisura, with achievement of hemostasis. Despite these interventions, melena persisted with decrease in hemoglobin to below 7.0. She continued to require transfusions every 1-2 days. She required 84 units of blood transfusions over the course of 4 months. The patient succumbed to her illness after unsuccessful resuscitation efforts. Discussion: Refractory bleeding from PHG is rare. The first-line therapy for acute bleeding is octreotide or terlipressin. If this is successful, patients can be transitioned to a non-selective beta-blocker. However, if this fails, other treatment modalities include shunt procedures or endoscopic therapy. Shunt procedures include TIPS or surgical shunt; endoscopic therapies include APC or hemospray application. Our patient continued to have GI bleeding despite successful TIPS and significant reduction in HVPG, highlighting findings of a published study which found no association between HVPG and bleeding from PHG, suggesting a role of local mucosal factors in the development of PHG.

523 A Case of Plummer-Vinson Syndrome in an Afro-Caribbean Female Eugene M. Cooper, MD, MHA1, Anjali Chandra, MD2. 1. GastroCare Bahamas, Nassau, Bahamas; 2. Centerville Medical Center, Nassau, Bahamas. Plummer-Vinson is defined by the classic triad of dysphagia, iron deficiency anemia and upper esophageal web(s). Although quite rare, and predominantly found in white, middle aged women, we report a

[521C] Figure 3.

Case: A 67-year-old Caucasian male with medical history of hypertension and hyperlipidemia, who presented with multiple orthopedic injuries after a motor vehicle accident. He was on mechanical ventilation since admission. Patient was on aspirin for suspected carotid artery dissection, enoxaparin for DVT prophylaxis and celecoxib for pain control. Patient was not on any stress ulcer prophylaxis. On day 11 of hospital course, patient developed melena and acute blood loss anemia. Laboratory values showed platelets counts of 337000 per microliter and rapid-thromboelastography k-value of 0.8 (normal 0.6-2.3). Endoscopic evaluation: EGD showed a large ulcer with adherent clot in pyloric channel encircling ¾ circumference, extending into the duodenal bulb and invading muscularis propria. This was treated with epinephrine injection, mechanical clot removal followed by bipolar electrocoagulation. Bipolar electrocoagulation was used only superficially due to the risk of perforation. No further bleeding was noted at the end of the procedure. Recurrence of bleeding: Repeat EGD was performed three days later due to recurrent bleeding. Active bleeding was noted from the pyloric channel ulcer. Bleeding continued despite epinephrine injection.


[523A] Figure 1.


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Abstracts and antrum and the revealed chronic active gastritis associated with intestinal metaplasia, H. pylori organisms were not identified. Multiple biopsies taken from the proximal duodenum showed no evidence of celiac disease. A Continuous Radial Expansion balloon was used to dilate the stricture to 15mm. On the first post operative day the patient had significant improvement in her symptoms and was able to tolerate a regular diet. She was discharged on Ferrous Sulphate 325mg and Vitamin C 1000mg daily. Repeat iron studies performed 8 weeks later showed a serum iron of 17 ug/dl and a serum ferritin of 6ng/ml.

524 Successful Aortoesophageal Fistulous Tract Closurse Using Endoscopic Clips and ENDOLOOP® After Previously Failed Endoscopic Therapy Andrea Rodriguez, MD1, Seth Lipka, MD2, Ashok Shiani, MD3, Jeffrey A. Gill, MD4. 1. Department of Medicine, University of South Florida, Morsani College of Medicine, Tampa, FL; 2. University of South Florida, Morsani College of Medicine, Division of Digestive Digestive Diseases and Nutrition, Tampa, FL; 3. University of South Florida, Morsani College of Medicine, Tampa, FL; 4. Department of Gastroenterology, Division of Digestive Diseases and Nutrition, James A. Haley VA Hospital, University of South Florida, Tampa, FL.

[523B] Figure 2.

case of PV in a middle-aged Afro-Caribbean female managed with mechanical dilation and iron supplementation. A 43 year old female presented with progressive dysphagia to liquids and solids for a duration of 2 years. Several weeks prior to presentation she reported several episodes of regurgitating undigested food. A review of systems was significant for a 50-lb weight loss, headaches and fatigue. She was given a diagnosis of anemia by her General Practitioner approximately 12 years prior to presentatiion but no additional work up was done. She denied menorrhagia, hematuria, hematochezia, and any gastrointestinal symptoms. She denied taking any NSAIDS. On examination, her blood pressure was 164/99 mmHg and her pulse rate was 67 beats per minute and regular. She was afebrile. Mucus membranes were pale but moist. Evaluation of the mouth revealed atrophic glossitis and there was pallor of the nail beds but no koilonychia. Systemic examination revealed an ejection systolic murmur over the precordium but no other abnormalities. Laboratory investigations showed a hemoglobin of 5.6 g/dl with a mean corpuscular volume of 54.9 fl. White blood cell count was 4.51 K/ul and platelets were 311,000 K/μl. The serum iron was 13 μg/dl, iron saturation 3%, and serum ferritin 3ng/mL. Alanine transaminase, serum creatinine and Thyroid Stimulating Hormone were within normal limits. A modified barium swallow revealed a short smooth segment of stenosis immediately inferior to the pharynx and anterior to the 4thcervical vertebrae. An upper endoscopy confirmed a smooth mucosal narrowing 24cm from the incisors, consistent with a mucosal web. The gastroscope was advanced with gentle pressure into the stomach and proximal duodenum; both were normal. Biopsies were taken from the gastric body

Introduction: Aortoesophageal fistulas(AEF) are a rare but catastrophic cause of upper gastrointestinal bleeding. AEF are usually diagnosed at autopsy as patients massively hemorrhage prior to diagnosis. We present a case of a 65 year old with an actively bleeding aortoesophageal fistula closed using an endoloop cinched around two endoscopic clips. Case: A 65 year old male with a complex history of an aortic dissection requiring previous emergent thoracic endovascular aortic repair(TEVAR) presented to the ED with active hematemesis. The patient previously underwent the repair 3 years prior, but was complicated by the development of an AEF which were unable to be repaired. On last admission a covered esophageal stent was placed to tamponade the bleeding from the AEF. On the current admission his hemoglobin was down to 8.7 from a baseline of 10. Emergent CT angiography was performed revealing an aortoesophageal fistula in the proximal esophagus in addition to a distal enhancement suspicious for endoleak. Emergent EGD was performed revealing the esophageal stent; however, it was not large enough in diameter to provide tamponade and the fistula was still oozing blood. The esophageal stent was removed. Initial attempts to close the fistula with clipping, banding, and fibrin glue application were all unsuccessful as the tissue was depressed and scarred down. EGD was aborted, hemoglobin was closely monitored and the patient was transfused. A second EGD was performed showing ongoing bleeding from the site. The inner opening of the AEF was coagulated to irritate the tissue and help enable closure over time. An endoscopic clip was placed just proximal and distal to the AEF and these were cinched together with an endoloop. The hole was monitored for several minutes and appeared to be closed successfully. The patient was discharged home in stable condition a few days later without complications. Discussion: Aortoesophageal fistulas are estimated to occur in 1.7%–5% of TEVAR patients. Several etiologies are thought to cause fistula formation. These include erosion of the aortic stent into the esophagus, and disruption of the arterial supply inducing ischemic esophageal necrosis. AEF should be suspected in patients with a history of an aortic aneurysm or dissection, along with hemodynamically significant hematemesis. The mainstay of treatment is emergent surgery. However, surgery entails arterial and alimentary tract reconstruction which may not be feasible for critically ill patients or those with multiple comorbidities.Recently less invasive modalities like esophageal and aortic stents have been used to stop bleeding from an AEF. We present a unique case here using an innovative endoscopic closure technique using hemoclips and an endoloop.

525 A Rare Cause of Obscure Gastrointestinal Bleeding Andrea C. Rodriguez, MD1, Steven B. Clayton, MD2, Patrick Brady, MD, FACG3, Jay Mamel, MD2. 1. University of South Florida, Morsani College of Medicine, Department of Internal Medicine, Tampa, FL; 2. University of South Florida, Tampa, FL; 3. University of South Florida, Morsani College of Medicine, Tampa, FL.

[524A] Figure 1.

Introduction: Amyloidosis results from the extracellular deposition of abnormal immunoglobulin light chains. Dysfunction of normal organ function occurs when these proteins accumulate leading to destruction of normal tissue architecture. Rarely, amyloid deposition can lead to obscure GI bleeding without systemic symptoms. Case: A 63 year old female with a history of multiple myeloma, chronic obstructive pulmonary disease, and cryptogenic cirrhosis presented to the ED with melena. EGD and colonoscopy both did not identify an active bleeding source. Hemoglobin dropped from 13.1 to 9.2 mg/dl. Repeat EGD/Colonoscopy

[524B] Figure 2.



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[525A] Figure 1.

Case: Our patient was an 86 year old male patient with a past medical history significant for coronary artery disease and stage 3 colorectal cancer status post resection and chemo –radiation, presented from an outlying facility for intractable sharp abdominal worse postprandially, one week in duration, associated with early satiety, anorexia and 5lbs weight loss in one week. A CT at the outlying facility showed possible choledochoenteric fistula, and a distended stomach. An esophagogastroduodenoscopy (EGD) was performed revealing a large 2.5 – 3 cm stone lodged in the duodenal bulb. The stone was extracted in 2 pieces after mechanical lithotripsy was performed. The duodenum was then reexamined and a posterior wall duodenal bulb ulcer and fistula tract orifice was noted. Examination of the CBD using endoscopic ultrasound pneumobilia. Conclusion: Endoscopic management of Bouveret syndrome is can immediately help in alleviating the gastrointestinal symptoms suffered by patients. Mechanical lithotripsy is one of a number of endoscopic options that can be utilized, especially in stones that are otherwise too large for extraction.

[525B] Figure 2.

did not reveal active bleeding. She had persistent melena. Capsule endoscopy revealed congestive enteropathy and active bleeding in the proximal small bowel. Anterograde enteroscopy was performed which revealed severe jejunitis with ulceration and active bleeding involving the proximal jejunum. Hemostasis was achieved using several endoclips (Figure 1). Biopsies were stained with congo red histochemical stain and results demonstrated apple green birefringence consistent with amyloid deposition (Figure 2). Patient stabilized and was discharged home. Discussion: Primary amyloidosis (AL) is a rare condition occurs after the deposition of aberrant β-pleated sheets onto the surface of organs and is commonly seen in patients with multiple myeloma (MM). Amyloidosis may affect the entire GI tract and could present with a wide array of symptoms including macroglossia, abdominal pain, malabsorption, bleeding, pseudo-obstructions, and motility disorders just to mention a few. Localized gastrointestinal amyloidosis presenting as overt obscure gastrointestinal bleeding is uncommon with few cases reported in the literature. The exact mechanism of the bleeding is unknown but multiple theories have been proposed factors. For instance, it is hypothesized that amyloid deposition may lead to vessel fragility resulting in bleeding. Light chain deposition has also been associated with necrotic ulceration leading to bleeding. Unfortunately, there are no specific therapies available to treat GI related symptoms secondary to amyloidosis. Although, small bowel amyloidosis is rare, this should remain in the differential for patients with history of multiple myeloma presenting with obscure GI bleeding.

[526A] Figure 1.

526 Mechanical Lithotripsy: A Viable Modality for Endoscopic Gallstone Extraction in Bouveret Syndrome Syed Hasan1, Toseef Javaid, MD2, Nauman Siddiqui, MD1, Jamal Saleh, MD1, Ali Nawras, MD, FACG3. 1. University Of Toledo Medical Center, Toledo, OH; 2. University of Toledo, Toledo, OH; 3. University of Toledo Medical Center, Toledo, OH. Introduction: The creation of a bilioenteric fistula is a very rare complication of cholelithiasis which affects less than 1% of patients. The passage of a large gallstone through a cholecystoduodenal fistula and the subsequent impaction in the duodenum causing gastric outlet obstruction, also known as Bouveret Syndrome, is an even rarer occurrence. Given the relatively high mortality of 12-33%, and risk of stone migration causing mechanical small bowel obstruction or other morbidities as high 60%, it is important to diagnose it early and remove the stone safely. This can be done endoscopically, especially in patients who may otherwise be high risk for invasive procedures.


[526B] Figure 2.


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CLINICAL VIGNETTES/CASE REPORTS - ESOPHAGUS

527 “Downhill” Esophageal Varices Associated With Superior Vena Cava Obstruction: Case Report and Literature Review Michael Loudin, Sharon Anderson, MD, Barry Schlansky, MD, MPH. Oregon Health & Science University, Portland, OR. Case Presentation: A 22 year-old woman was hospitalized with black stools for 3 days followed by the acute onset of large-volume hematemesis. Her past medical history was notable for end-stage renal disease due to Henoch-Schönlein purpura, for which she underwent hemodialysis through a tunneled right internal jugular venous catheter. She had no prior history of liver disease or gastrointestinal bleeding. Physical exam revealed mild facial edema with no plethora, prominent abdominal and chest wall varices, and no ascites or hepatosplenomegaly. Vital signs were significant for tachycardia and normal blood pressure. Her hemoglobin was 7.5 g/dL, with normal platelets, liver tests and coagulation studies. Hospital Course: Urgent upper endoscopy revealed three bulging varices in the proximal esophagus that did not flatten with air insufflation, with a fibrin plug (nipple sign) and linear erythema (red wale sign). The mid and distal esophagus, stomach, and duodenum were normal. CT angiogram of the chest revealed a stenosis of the superior vena cava (SVC) at the distal aspect of the dialysis catheter, as well as prominent varices in the proximal esophagus and a severely dilated azygous vein acting as a shunt from the upper thorax to the abdomen, bypassing the SVC. Urgent angiography with catheter-directed balloon dilation of the stenotic SVC segment was performed, and she had no recurrence of bleeding at 3 months of follow-up after hospital discharge. Discussion: The venous drainage of the proximal 2/3rds of the esophagus is via the azygous, hemiazygous and inferior thyroid veins to the SVC. Obstruction of these vessels or the SVC may result in varices in the upper esophagus. Bleeding from “downhill” varices is a very rare cause of gastrointestinal bleeding (0.1% of all variceal hemorrhage), almost usually caused by SVC obstruction from mediastinal malignancy (thymoma, lung cancer) but rarely from a benign cause such as vascular stenosis/thrombosis related to an indwelling vascular prosthesis. The cornerstone of management of proximal esophageal varices is correction of the underlying vascular obstruction, typically with balloon dilation or stenting. When variceal bleeding is severe, successful hemostasis has been reported with endoscopic therapy including band ligation or sclerotherapy. Refractory bleeding may require surgical revision or bypass of the vascular obstruction.

[528A] Figure 1.

[527] Table 1. Reported Cases of Bleeding "Downhill" Varices Number of Cases

Etiology

Treatment

13

Central venous catheter

Angioplasty (5), stent (4), banding (4), sclerotherapy (1), vascular reconstruction (1), removal of CVC (1), conservative (1), not reported (1)

5

Malignancy

Sclerotherapy (1), banding (1), stent (1), surgical removal of cancer (1), conservative (1), not reported (1)

5

Mediastinal fibrosis

Conservative (2), steroids (1), Sengstaken-Blakemore tube (1), not reported (1)

4

SVC obstruction

Conservative (3), not reported (1)

3

Goiter

Banding (1), Sengstaken-Blakemore tube (1), surgical removal of goiter (1)

2

Behcets

Banding (1), conservative (1)

1

Upper extremity DVT

Banding, angioplasty and stent

1

Venulitits

Conservative

1

Cirrhosis

Diagnosis at autopsy

1

Post Fontan

Angioplasty, stent

1

Prior thyroidectomy

Sclerotherapy

1

Pulmonary hypertension

Conservative

1

HeRO graft

Banding

1

Ligation of SVC

Not reported

[528B] Figure 2.

CVC, central venous catheter; DVT, deep vein thrombosis; HeRO, Hemodialysis Reliable Outflow; SVC, superior vena cava.

[528C] Figure 3.

528 A Case of Acute Esophageal Necrosis (AEN) in a Hypothermic Patient: The Grave Prognosis of the Black Esophagus George Salem, MD, Sumit Ahluwalia, MD, Ralph T. Guild, III., MD, FACG. University of Oklahoma Health Sciences Center, Oklahoma City, OK. Introduction: Acute Esophageal Necrosis (AEN) is a syndrome characterized by diffuse, necrotic, circumferentially black distal esophageal mucosa on esophagogastroduodenoscopy (EGD) that ends at the gastroesophageal junction (GEJ).The exact etiology is unknown, with hypoperfusion predisposing the less vascularized distal esophagus to acute necrosis plays a rule. 70% of AEN cases present with upper


gastrointestinal bleeding (UGIB) and melena. We describe a case of AEN caused by severe hypothermia in an alcoholic patient presenting with UGIB. Case Report: 62 year-old lady with history of liver cirrhosis secondary to heavy alcohol intake presented with change in mental status and hematemesis. Vital signs were consistent with temporal temperature of 29.9 C, heart rate of 61 bpm, and blood pressure of 86/49. Bedside pulse oximetry recorded 84% on room air. She was confused, icteric with distended abdomen, and bilateral lower extremity pitting edema. She was admitted to the intensive care unit after intubation. Hemogram showed a hemoglobin of 5.1 g/dL, platelet count of 62, INR 7.2, total bilirubin 8.9, AST/ ALT 154/59, albumin 2.1. Model for End stage Liver Disease (MELD) score at presentation was 33. Patient was resuscitated with warm crystalloid fluids and 2 units of packed RBCs, and started on Octreotide and Pantoprazole drip. EGD showed normal looking


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proximal third of the esophagus, with diffuse mucosal ulceration of the middle and lower third of the esophagus (figures 1, 2) without varices, and sharp demarcation of affected areas noted in the GEJ (figure 3). Patient’s clinical condition deteriorated over the next 24 hours and she deceased despite aggressive supportive therapy with vasopressors, packed RBC, platelets, and fresh frozen plasma transfusion. Discussion: AEN is a rare syndrome with significant morbidity and mortality. It is found in patients undergoing upper endoscopy for evaluation of UGIB. EGD shows diffuse, circumferential, black pigmentation of the distal esophagus, ending sharply at the Z-line of the GEJ. Medical management is supportive with aggressive hemodynamic support, intravenous proton pump inhibitors, and treatment of underlying illness. Mortality rates in patients with AEN reported to range from 13 to 35%. Over 90% of death cases were secondary to their underlying serious illness. In our case, the patient’s clinical condition continued to deteriorate due to multi-organ failure despite aggressive medical intervention.

529 The Case of a Heartfelt Swallow Christopher Bach, MD, William Hale, MD. Norwalk Hospital, Norwalk, CT. Deglutition tachycardia is a rare disorder. There have been less sixty cases reported since it was first described in 1925 by Kasai et al. Here we present a case of deglutition tachycardia. The patient is a 56 year old man who presents with 2 weeks of palpitations associated with swallowing solids. He has no prior cardiac history. He reports transient (5-10 seconds) episodes of palpitations that would occur while swallowing solid food. He denied having symptoms when not eating, or swallowing liquids alone. His other past medical history includes hypothyroidism and myopia requiring retinal detachment 3 weeks prior to presentation. He reports only taking levothyroxine daily for hypothyroidism. On the day of presentation, while eating he began having palpitations that did not resolve and after 30 minutes he sought medical attention at the emergency department. In the emergency department he was found to have atrial fibrillation with rapid ventricular rate of 176 beats per minute. He was treated with diltiazem drip and metoprolol which converted his rhythm to normal sinus. Laboratory results were normal including hemoglobin and TSH. While admitted on continual telemetry he had short, 6-10 beats, bursts of atrial fibrillation with aberrant ventricular conduction (AVR) that occurred only during meal time. Echocardiogram and stress test during admission were normal. Gastroenterology recommended a barium esophagogram which showed no structural abnormalities but found that on 4 consecutive swallows a rhythm strip taken simultaneously revealed atrial fibrillation with AVR when the bolus passed the left atrium. He was discharged on metoprolol and had no further episodes. He later revealed that he was taking an anticholinergic eye drop for his retinal repair that he had started 3 weeks prior to presentation, and stopped shortly after discharge.

This patient experienced deglutition tachycardia from a combined effect of mechanical stimulation of the left atrial focus by the food bolus and the increased automaticity of the focus from the anticholinergic eye drop. Deglutition tachycardia though rare is important to recognize in a patient presenting with tachycardia associated with swallowing.

530 Esophageal Adenocarcinoma Masquerading as Hyperplastic Polyps Mustafa Musleh, MD1, Salma Akram, MD2. 1. Wright State University, Miamisburg, OH; 2. Wright State University/Dayton VAMC, Department of Gastroenterology, Dayton, OH. Introduction: We report a case with the rare occurrence of hyperplastic polypoid lesions in the background of Barrett’s esophagus in associated with invasive adenocarcinoma of the esophagogastric junction (EGJ). Case Report: A 65 year old Caucasian male with chronic acid reflux presented with progressive dysphagia and weight loss. Exam was unremarkable except for a body mass index of 37. Lab studies showed mild anemia with hemoglobin of 12.5 gm/dl. Esophagogastroduodenoscopy (EGD) revealed a diffuse, polypoid growth involving the distal 14 cm of the esophagus. Histological exam revealed glandular mucosa with elongated hyperplastic foveolar epithelium and cystic changes, consistent with hyperplastic polyp. EGD was repeated and tissue specimen collected with cold snare as well as multiple 4 quadrant biopsies every 1 cm, histology revealed hyperplastic polyps in the background of intestinal metaplasia without dysplasia. Endoscopic ultrasonography (EUS) showed that the growth was limited to the mucosal layer, positron emission test (PET) scan showed increased uptake only in the distal esophagus. Patient was referred to surgery and underwent esophagectomy with proximal gastrectomy. Esophago-gastric continuity could not be achieved, thus a left sided esophageal spit fistula was created. Surgical specimen showed moderately differentiated adenocarcinoma with tumor invasion through muscularis propria into the serosal fat at the EGJ and multiple lymph nodes involvement. Discussion: Epithelial polypoid lesions of the esophagus and EGJ are uncommon. Most of these lesions reportedly occur at the EGJ (67%) followed by distal esophagus (30%). Among these lesions, hyperplastic polyps are quite rare and usually occur in the setting of long-standing gastro esophageal reflux disease. In the largest reported case series by Abraham et al., among 27 patients with hyperplastic esophageal and EGJ polyps, only 15% had concomitant Barrett’s esophagus. There have been only two cases reported of hyperplastic polyps at EGJ where subsequent endoscopic mucosal resection showed foci of high grade dysplasia and adenocarcinoma. Our case is unique due to the presence of long segment Barrett’s esophagus with concomitant circumferential, villiform polypoid growth where multiple repeat mucosal biopsies showed reactive changes. Due to the diffuse extensive nature of the lesion it was not amenable to safe endoscopic resection and thus required surgical resection which revealed an invasive adenocarcinoma of the EGJ. This case highlights the extremely rare occurrence of the hyperplastic polyps in the setting of Barrett’s

[529A] Figure 1.



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[530A] Figure 1.

Case: A 30-year-old man with history of venous malformations in posterior chest wall and T7-12 paraspinal region requiring sclerotherapy was found to be anemic to 6.8 g/dl, with MCV of 61 fL and ferritin of 5.9 ng/mL. He denied any overt GI bleeding (OGIB). Upper GI endoscopy was unremarkable and colonoscopy revealed large VMs in the rectum, ascending colon, and cecum. Subsequent capsule endoscopy disclosed VMs in the terminal ileum. Computed tomography (CT) scan of abdomen showed diffuse wall thickening in cecum and proximal ascending colon; multiple tortuous blood vessels seen around the thickened bowel loops and splenomegaly. He underwent right hemicolectomy with re-anastomosis and the pathology from his cecum and colon confirmed VMs. His hemoglobin has been stable since surgery. We plan for a repeat colonoscopy in a year. Discussion: Vascular anomalies of GI tract are generally classified into three groups - Vascular tumors or angiomas (benign or malignant); anomalies associated with systemic or hereditary syndromes; and sporadic lesions. Sporadic angiodysplasia (AD) is commonly seen in patients >60 years of age, especially those with end stage renal disease, aortic stenosis, and von Willebrand disease (vWD), all excluded in our patient. Moreover, our patient had splenomegaly not attributable to any other systemic vascular malformation syndromes like blue rubber bleb nevus syndrome (BRBNS), Klippel-Trenaunay-Weber syndrome, Maffuci syndrome, and Osler-Weber-Rendu syndrome. Therapeutic modalities depend on degree of bleeding and size & number of lesions. Incidental lesions usually require no treatment. Endoscopic therapy with argon plasma coagulation (APC), band ligation, hemoclip placement, and injection sclerotherapy have been effective in reducing long-term bleeding from these lesions. Pharmacological agents may be considered if lesions are widespread or in a poor surgical candidate, with combination hormonal therapy or octreotide. If localized heavy load of VMs, surgery may be the best option, like in our patient. Future research should be directed towards effective pharmacologic agents with widespread action on systemic and GI vascular malformations.

532 Esophageal Bezoar as a Rare Cause of Dysphagia in Achalasia Jodie A. Barkin, MD1, Baharak Moshiree, MD, MS2, Michael J. Huang, MD2, Jamie S. Barkin, MD, MACG2. 1. University of Miami, Leonard M. Miller School of Medicine, Dept of Medicine, Division of Gastroenterology, Bay Harbor, FL; 2. University of Miami, Leonard M. Miller School of Medicine, Dept of Medicine, Division of Gastroenterology, Miami, FL.

[530B] Figure 2.

Dysphagia is a common presenting symptom in patients with achalasia. Recurrent dysphagia after successful endoscopic or surgical intervention is usually a sign of recurrent achalasia, reflux-induced strictures and esophagitis, or surgical complication. Our aim is to present a patient with worsening dysphagia due to an esophageal food bezoar who had a history of suspected achalasia. A 67 y/o woman presented with 3 weeks of acute dysphagia greater to solids than liquids, with ingestion of solids causing projectile vomiting, and minimal tolerance to clear liquids. She had a 40 year history of intermittent dysphagia to solids and liquids twice weekly, and post-prandial nausea and vomiting once to twice monthly, with stable weight. She had a suspected diagnosis of achalasia, and underwent 2 esophageal dilations 35 years ago. Endoscopy revealed pan-esophageal dilation with aperistalsis, a large distal esophageal food bezoar that was removed with a Roth net, and only mild resistance to passage of the endoscope through the lower esophageal sphincter (LES) (Figures 1 & 2). After removal of the bezoar, the patient’s acute dysphagia symptoms resolved to her prior baseline. A barium esophagram showed esophageal dilation with narrowing at the LES and delayed transit into the stomach. High resolution esophageal manometry confirmed a diagnosis of achalasia type II, with normal LES pressure of 13.5mmHg, high IRP of 28.8mmHg, failed swallows, and isobaric pressure patterns throughout the esophagus. She declined further intervention as her symptoms had improved to her baseline. Esophageal food bezoars typically present with acute dysphagia, and are primarily found in the presence of an underlying structural abnormality, i.e. esophageal rings or strictures. Motility disorders, i.e. achalasia, may predispose to an esophageal bezoar as in our patient, who had confirmed achalasia via high resolution esophageal manometry. There are 4 patients previously reported with an esophageal bezoar associated with achalasia, 2 of which underwent conventional esophageal manometry [Mamel JJ 1984, Shah SW 1997, Kim KH 2010, Liang JJ 2013]. In evaluating patients with acute worsening of dysphagia and history of achalasia, endoscopic visualization should be performed initially to offer potential diagnosis and therapy. In summary, esophageal bezoars should be included in the differential diagnosis of dysphagia in patients with esophageal motility disorders such as known or suspected achalasia.

[530C] Figure 3. esophagus and invasive adenocarcinoma of the EGJ. It also underscores the fact that malignancy in this setting should always be suspected even when mucosal biopsies are negative.

531 Co-existence of Gastrointestinal Vascular Malformations in Patients With Congenital Head/neck and Thoracic Vascular Malformations and Vascular Birthmarks Kshitij Chatterjee, MD, Jagpal Singh Klair, MD, Mohit Girotra, Aneet Kaur, Farshad Aduli. University of Arkansas for Medical Sciences, Little Rock, AR. Introduction: Vascular malformations (VMs) in GI tract are well-recognized etiology for both occult and overt bleeding. There exist good modalities for endoscopic diagnosis and but limited understanding on associations of GI vascular malformations with similar malformations elsewhere in the body.


[532A] Figure 1.


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mcl,PT 15.6,INR 1.4,PTT 31.5.Liver enzymes were normal.An EGD demonstrated a 6-7 mm healing ulcer in the mid esophagus with no evidence of active bleeding.The submucosa was not seen and no evidence of perforation was noted.She was discharged home with pantoprazole 40mg twice daily,sucralfate 1g four times daily and instructions to follow up in the GI clinic. Discusion: Esophageal injury is one complication of RFA therapy.This is due to the close anatomical proximity between the esophagus and the posterior LA wall which is estimated to be ≤ 5 mm in 40% of the population.The intestinal tissue is also far more susceptible to radiofrequency induced thermal injury than the muscular tissue of the heart.Therefore,direct contact of a probe is not required for thermal injury,as convection heat generated within the LA is enough energy to cause esophageal injury.Early diagnosis is vital to prevent fatal outcomes from complication such as perforation and fistula formation. Atrial fibrillation is projected to surge 2.5-fold in the near future due to the aging demographic leading to an increase use of RFA therapy. This may result in a higher incident of RFA related thermal esophageal injury.Further research is needed to identify risk factors,preventive strategies and optimal treatment for esophageal thermal injury related to left atrial RFA.

534 When Esophageal Varices Go Downhill

[532B] Figure 2.

533 A Case of Esophageal Thermal Injury Following Radiofrequency Catheter Ablation Therapy Mohsen Pourmorteza, MD1, John Litchfield, DO2, Larry E. Carter, DO3, Jason Mckinney, DO4, Mark Young, MD5. 1. Department of Internal Medicine, East Tennessee State University, Johnson City, TN; 2. East Tennessee State University, Department of Internal Medicine, Division of Gastroenterology, Johnson City, TN; 3. East Tennessee State University School of Medicine, Johnson City, TN; 4. East Tennessee State University, Johnson City , TN; 5. East Tennessee State University, Johnson City, TN. Introduction:Radiofrequency ablation (RFA) is a catheter based ablation technique used in patients with atrial fibrillation(AF) to achieve rhythm control.There is risk of esophageal thermal injury during RFA to the posterior left atrium given its close proximity to the anterior esophagus.We describe a case of thermal injury to the esophagus following RFA therapy to the left atrium. Case Report:A 69-year-old female with a history of hypertension,AF was seen with a two day history of melena.The patient’s melenic stools began one day following RFA therapy.The patient reported a “gassy feeling” in her stomach but denied abdominal pain,nausea,vomiting,chest pain,heartburn,dysphagia,o dynophagia,fever/chills.No history of GI bleed or change in stool consistency/color were reported in the past.On exam patient was afebrile,hypertensive(178/78) with heart rate of 80.Abdomen was soft/ nontender/nondistended with normoactive bowel sounds, no abdominal masses, organomegaly. Lungs were clear to ausculation as no abnormal heart sounds were noted. Lab results demonstrated Potassium 3.5mmol/L,Sodium 142mmol/L,Chloride 102mmol/L,hemoglobin 13.9 g/dL,platelet count 219 10(3)/

Joshua C. Berkowitz, MD1, Sumant Inamdar, MD, MPH2, Maurice A. Cerulli, MD2, Peter Shue, MD3, Deepak S. Desai, MD4. 1. North Shore-LIJ Health System, Department of Medicine, Lawrence, NY; 2. North Shore-LIJ Health System, Department of Medicine, Division of Gastroenterology, New Hyde Park, NY; 3. North Shore-LIJ Health System, Department of Medicine, Division of Gastroenterology, Great Neck, NY; 4. North Shore-LIJ Health System, Department of Medicine, Division of Gastroenterology, Manhasset, NY. Patient Presentation: A 32 year old female with ESRD secondary to mesangial proliferative glomerulonephritis, recurrent SVC catheters due to failed AVG’s, Mixed Connective Tissue Disorder and a failed renal transplant, presented with 2 days of melena and 2 episodes of hematemesis. There was no history of alcoholism, hepatitis, abdominal pain, NSAID or anticoagulant use. Physical examination was significant for tachycardia to 128 BPM, dilated superficial veins on the anterior chest wall, and melenic stool. There was no scleral icterus, abdominal distention, or hepatomegaly. The patient was transferred to the MICU. Work Up/Interventions: Laboratory studies were as follows: Hb 6.0 g/dL, Bilirubin 0.7, μmol/L, AST 7 U/L, ALT 6 U/L, INR 1.06 and Albumin 3.3 g/dL. The patient received transfusion of PRBC. EGD demonstrated F3 esophageal varices in the upper and mid-esophagus and presence of red wale signs and oozing blood. Endoscopic band ligation was performed. The melena resolved and the hemoglobin remained stable. Abdominal ultrasound demonstrated a normal liver. The portal veins were patent with normal direction of flow. The IVC and hepatic veins were patent. CT angiography of the abdomen demonstrated numerous abdominal wall collateral vessels. CT angiography of the chest revealed occlusion of the SVC along with numerous right-sided chest wall collaterals. The occlusion was at the junction of the SVC and the R brachiocephalic vein. A prominent azygous vein was seen. Diagnosis: Downhill esophageal varices secondary to SVC thrombosis due to multiple prior central venous catheters. Therapy: Balloon angioplasty of the SVC successfully improved flow. Subsequent EGD showed improvement of the esophageal varices. Definitive therapy consisted of right axillary vein to right atrium bypass graft.

[533A] Figure 1.



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535 Esophageal Mucosal Calcinosis Complicated by Upper GI Bleeding Navdeep Chehl, MD, Shubha Singh, MD, Bashar Almadani, MD, Sriram Jakate, MD, Salina Lee, MD, Rana Abraham, MD, Sohrab Mobarhan, MD. Rush University Medical Center, Chicago, IL.

[534A] Figure 1.

Calcium deposition in the gastrointestinal tract in the setting of hypercalcemia, while rare, is most commonly localized to gastric mucosa. We present, to our knowledge, the first reported case of esophageal mucosal calcinosis. The patient is a 51 year old female with past medical history significant for chronic kidney disease secondary to lupus nephritis (on immunosuppression), coronary artery disease s/p stent placement, abdominal aortic aneurysm s/p repair, pericarditis, transfusion-related hepatitis C, recurrent deep venous thrombosis (DVT- on warfarin), primary hyperparathyroidism and osteoporosis who was initially admitted for acute right lower extremity (RLE) DVT and two large RLE hematomas despite a therapeutic INR, s/p IVC filter placement, as well as a lupus flare requiring rituximab therapy. During her hospital course, she developed epigastric pain, dysphagia (initially to solids and progressing to include liquids), and odynophagia. Physical exam was significant for epigastric tenderness. Pertinent labs included creatinine 2.14 mg/dL and calcium (corrected) 11.0 mg/dL. EGD revealed severe acute esophagitis with extensive necrotic exudate in the distal esophagus, characterized by white, plaque-like lesions, as well as erosive gastritis with minor oozing in the gastric antrum and body. In addition to a twice daily proton pump inhibitor (PPI), fluconazole was started for presumed candidal esophagitis. Pathology did not show evidence of fungal infection. Symptoms did not improve and repeat EGD was performed, demonstrating a white, circumferential, plaque-like lesion with areas of ulceration, necrotic exudates, inflammatory granulation tissue and focal small calcific deposits. Pertinent labs included phosphorous 3.3 mg/dL, intact PTH 187 pg/mL, Vitamin D 25-OH 14. Fluconazole was discontinued. A few days later, the patient had massive hematemesis and rectal bleeding with hemoglobin 4.1 g/dL, tachycardia, and hypotension in the setting of a supratherapeutic INR. Emergent EGD revealed active arterial bleeding in the distal esophagus, stopped with epinephrine injection and two hemoclips. Interventional radiology then embolized a left gastric artery branch supplying the corresponding area of bleeding. Neck imaging failed to show evidence of a parathyroid adenoma. The patient had no further bleeding, her symptoms improved on the PPI and she was discharged home on calcium and vitamin D supplementation. She planned to follow-up with endocrine surgery for parathyroidectomy evaluation. This is a unique case of hypercalcemia from untreated primary hyperparathyroidism causing esophageal calcium deposition, ultimately leading to inflammation, necrosis, and bleeding.

[534B] Figure 2.

[535A] Figure 1.

[534C] Figure 3.

Discussion: Downhill esophageal varices cause less than 0.1% of all variceal bleeds. Occlusion of the SVC results in increased pressure to the azygous and hemiazygous systems responsible for drainage of the venous plexuses of the upper two thirds of the esophagus. If the occlusion does not interfere with azygous drainage to the SVC, only the upper two thirds of the esophagus will be involved, as in the present case. Occlusion of the azygous drainage into the SVC results in varices throughout the esophagus. Treatment of downhill varices focuses on restoring venous drainage. Options include balloon angioplasty, SVC stenting and open surgical therapies. Endoscopic options include proximal banding. Sclerotherapy is avoided due to concerns over embolization.


[535B] Figure 2.


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537

An Uncommon Subepithelial Lesion of the Esophagus

Dysphagia as the Sole Initial Presentation of Celiac Disease

Mohd Amer Alsamman, MD, Ashirf AlGhanoudi, MD, MPH, Alan Putrus, MD, Joshua Max, MD. Trihealth-Good Samaritan Hospital, Cincinnati, OH.

Andrew C. Berry, DO1, Rahman Nakshabendi, MD2, Hussein Abidali, DO3, Ozdemir Kanar, MD2, Danny Avalos, MD4, Aaron Baltz, MD5, James Kwiatt, MD5. 1. Department of Medicine, University of South Alabama, Muskego, WI; 2. University of Florida Health College of Medicine, Jacksonville, FL; 3. Department of Medicine, Banner-Good Samaritan Medical Center, Phoenix, AZ; 4. Department of Medicine, University of Miami Miller School of Medicine, Palm Beach Regional Campus, Muskego, WI; 5. GI Associates, Muskego, WI.

Introduction: A variety of esophageal lesions are encountered during endoscopic or radiologic evaluation. Many are asymptomatic and have little or no malignant potential. Nonetheless, establishing an accurate diagnosis and thereby formulating a management plan can be challenging. Case: A 49-year-old male presented for routine esophagogastroduodenoscopy (EGD) for chronic dyspepsia. He denied abdominal pain, odynophagia and dysphagia, weight loss or constitutional symptoms. EGD showed asmall pale submucosal nodule. It was biopsied and showedmild nonspecific esophagitis. An endoscopic ultrasound (EUS) showed a 1 cm yellowish esophageal subepithelial nodule at 35 cm from the incisors, the nodule was very difficult to identify with US due to the spastic nature of the esophagus, diminutive nature of the lesion, and single benign-appearing lymph node adjacent to the esophagus in the region of the lesion was seen. Because of diagnostic uncertainty, the decision was made to resect the lesion. A saline pillow was created and the lesion was resected with hot snare. The resultant mucosal defect was closed with 3 clips. Pathology showed cells with abundant granular eosinophilic cytoplasm in nests within the mucosa and smooth muscle bundles of the muscularis mucosa. The cells expressed S100 protein, consistent with a granular cell tumor of the esophagus. The tumor was not seen at the margins. A CT scan of the chest showed no lymphadenopathy or metastases. The plan is to survey the lesion with EGD in one year. Discussion: Granular cell tumors occur in the skin, tongue, breast, and gastrointestinal tract. Granular cell tumors of the esophagus are rare; their incidence in endoscopy series has been estimated at 0.033%, representing about 1% of benign esophageal tumors. Up to one-third of patients report dysphagia; the remainder of patients is asymptomatic. On endoscopy, lesions are typically sessile, yellowish-white, and are covered by normal-appearing mucosa. They feel firm or rubbery when prodded with a biopsy forceps. Mostly solitary lesions but up to 10% have two or more lesions.Interestingly, they have some malignant potential. Malignancy is more likely with large lesions and those that exhibit growth. In a review of 183 cases, eight lesions (4%) were malignant; all of these lesions were greater than 4 cm and had histological features of infiltrative growth. Therefore endoscopic resection is endorsed for all esophageal granular cell tumors. Small lesions can often be removed with a biopsy forceps, but lesions larger than 1 cm typically require endoscopic mucosal or submucosal endoscopic resection.

A 33-year-old Caucasian woman presented with 3 months of dysphagia to solids. She had “tightness” in her chest with eating bananas. She reported no weight loss, abdominal pain, or diarrhea. She had no heartburn symptoms. She also did not have any allergic rhinitis symptoms. There was no family history of eosinophilic esophagitis, inflammatory bowel disease, upper gastrointestinal cancers, or celiac disease. Due to her persistent dysphagia, an esophagogastroduodenoscopy (EGD) was performed revealing mild bulbar duodenitis, and scalloping in the 2nd and 3rd portions of the duodenum (Fig. 1, Fig. 2). Biopsies were taken from her mid esophagus, distal esophagus, stomach antrum, and 2nd and 3rd portions of the duodenum. Labs revealed a tissue transglutaminase IgA of >100 units. Serum IgA, vitamin A, folic acid, Vitamin B12, Vitamin D, thyroid stimulating hormone, iron studies, complete blood count, complete metabolic panel, and Helicobacter pylori IgG antibody were all within normal limits. Biopsies revealed no abnormalities in the mid esophagus, mild reflux esophagitis in the distal esophagus, mild gastritis with no evidence of H. pylori in the stomach antrum, and moderate to severe villous blunting and increased intraepithelial lymphocytosis consistent with Marsh 3 celiac disease in the 2nd and 3rd portions of the duodenum. Her esophagus was empirically dilated and dysphagia persisted post dilation. The patient was started on a gluten-free diet and three months later her dysphagia resolved. Follow-up tissue transglutaminase IgA at the time of resolution of the dysphagia was undetectable indicating resolution of the celiac disease. To the best of our knowledge, this case represents the first reported case of dysphagia as initial and sole presentation of celiac disease completely resolved by gluten-free diet. This patient did not have evidence of eosinophillic esophagitis, Plummer-Vinson Syndrome, or any other culprit for her dysphagia. She also did not complain of any other typical celiac disease symptoms, such as abdominal pain and discomfort, bloating, diarrhea, constipation, and irritable bowel-like symptoms. Laboratory testing of elevated tissue transglutaminase IgA level, followed by gluten-free diet with subsequent resolution of symptoms and normalization of tissue transglutaminase IgA confirmed the patient’s celiac disease course. Celiac disease is a diagnostic consideration in the evaluation of unexplained dysphagia. In patients presenting with solid food dysphagia, EGD remains the exam of choice. Whether celiac disease should be routinely excluded in patients presenting with dysphagia warrants further study.


[536B] Figure 2.


[537B] Figure 2. VOLUME 110 | SUPPLEMENT 1

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538 An Unusual Presentation of a Giant Squamous Papilloma in the Distal Esophagus Prince Philip, MBBS1, Jesse Sam2, Arathi Mohan, BS3, Karthik Reddy, MBBS4, Srinivas S. Vasireddi, MD5, Haig Minassian, MD6. 1. Advanced Digestive Center, Inc., Fords, NJ; 2. Windsor University School of Medicine, Lumberton, NJ; 3. Case Western Reserve University School of Medicine, Cleveland, OH; 4. Siddhartha Medical College, Karnataka, India, Long Branch, NJ; 5. Advanced Digestive Center, Inc., Metuchen, NJ; 6. BayShore Community Hospital, Red Bank, NJ. Introduction: Benign tumors of the esophagus account for 20% of the esophageal lesions. Many of these tumors are small and asymptomatic, and few lesions attract clinical attention1. Esophageal squamous papilloma is an uncommon epithelial polypoid tumor and is usually identified as a solitary lesion of the lower esophagus 2. These sometimes cause dysphagia and can rarely cause significant outcomes such as aspiration pneumonia and esophageal obstruction. Here we report a case of a large esophago-gastric junction polyp causing similar symptoms. Case description: A 54-year-old male was brought to the emergency room with complaints of fever, dyspnea and postprandial vomiting. He reported cough and dysphagia for the past few days. Physical exam showed rales on right lung base and tachycardia. Blood work and chest X-ray showed right lower lobe lung infiltrate and sepsis. He was put on an antibiotic regimen. The chest CT revealed distended debris that filled the esophagus with mass effect along the trachea. He complained of worsening dysphagia and throat irritation. Endoscopic evaluation showed copious food in the distal esophagus, which was gently pushed down into the stomach. Subsequent exam showed a large prolapsing pedunculated polypoid 2 x 3 cm mass (Figure 1a) at the EG junction with luminal occlusion. The mass was mobile and exerted

[538A] Figure 1.

a ball-valve effect in the esophageal lumen, thereby worsening food transit to stomach. The large polyp was removed with snare (Figure 1b) and histological examination was consistent with squamous cell papilloma (Figure 3), with no dysplasia or malignancy. Post procedure, the patient had complete relief. Follow up endoscopy after few weeks showed complete healing of the site. (Fig-2) The patient had no further recurrence of symptoms. Discussion: Benign esophageal lesions are common and can have a diverse spectrum of presentations in terms of clinical course and underlying pathologic features. They can sometimes cause chronic dysphagia and secondary achalasia leading to aspiration syndrome. A giant lesion causing dysphagia and aspiration as seen in our case is extremely rare. Endoscopic resection usually provides complete relief of symptoms. References: [1]. Tsai S, et al. Benign esophageal lesions: endoscopic and pathologic features. WJG 2015;21(4):1091-1098. [2]. Ferrari AP, Lanzoni VP, Kondo M, Lichtenstein DR, Carr-Locke DL. Esophageal squamous cell papilloma. A report of three cases. Diagnostic aspects. Rev Assoc Med Bras 41: 266-270.

539 Therapeutic Strategy for the Overlap Between GERD and Function Dyspepsia: Study of Additive Effect Acotiamide on Rabeprazole Toshihisa Takeuchi, MD, PhD, Yuichi Kojima, MD, PhD, Kazuhide Higuchi, MD, PhD. The Second Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan. Background: Proton pump inhibitors (PPIs), the first-choice agents for the treatment of gastroesophageal reflux disease (GERD), cure most GERD patients, but there are still patients in whom symptom improvement is poor despite remission of esophageal mucosal injury. Since the symptoms of such PPI-refractory GERD patients overlap with functional dyspepsia (FD). In Japan, acotiamide was approved as the world’s first drug for FD. Acotiamide is known to improve gastrointestinal tract motility by inhibiting acetylcholine esterase, but the therapeutic effect on the overlap between GERD and FD is unknown. A phase II study on acotiamide has been completed in the U.S. Objective: To study the improvement of symptoms when acotiamide was administered in addition to rabeprazole to treat the overlap between GERD and FD. Patients and methods: This study was conducted as a prospective, single-institution, open-label study. Twenty six patients were enrolled, who had a Grade A or higher mucosal injury according to the Los Angeles (LA) classification as judged by esophagogastroduodenoscopy (EGD) and remnant epigastric symptom, but in whom ECG indicated healing of mucosa after oral administration of 10 mg/day rabeprazole for 8 weeks or more. After examination of background factors, 300 mg/day acotiamide was added to 10 mg/day rabeprazole. The symptoms were examined again after 4 weeks to investigate the therapeutic effect. We used an Izumo scale questionnaire, which scores heartburn, epigastralgia, and epigastric fullness from 0 to 15 points each. Results: Twenty six subjects consisting of 11 males and 15 females were evaluated. Before and after adding acotiamide, heartburn scores were 4.2 and 3.0, respectively, demonstrating a significant decrease (improvement rate, 29%; p=0.044); epigastralgia scores were 3.8 and 3.1, respectively, indicating no significant difference (improvement rate, 18%; p=0.089); epigastric fullness scores were 7.0 and 3.8, respectively, demonstrating a significant decrease (improvement rate, 46%;p=0.0001); total scores of these three epigastric symptoms were 14.9 and 10.0, respectively, demonstrating a significant decrease (p=0.0002). Score decreased by 50% or more in 31% of subjects. Conclusions: Even if PPI administration improves mucosal injury, it is often difficult in clinical practice to treat the overlap between GERD and FD, with which epigastric symptom improvement with PPI treatment is poor. This study suggests that adding acotiamide to PPI is potentially effective in improving the symptoms in treating such patients.

540 An Uncommon Source of Upper Gastrointestinal Bleed: Epiphrenic Esophageal Diverticulum Chung Sang Tse, MD1, Neil P. Parikh, MD2. 1. Mayo Clinic, Rochester, MN; 2. Yale University School of Medicine, New Haven, CT.

[538B] Figure 2.

[538C] Figure 3.


Acute upper gastrointestinal bleeds (UGIB) are relatively common medical emergencies with an incidence of up to 150 per 100,000 people per year and a mortality rate of 7-14%. In this clinical case, we present a rare cause of UGIB that was successfully managed endoscopically. An 83-year old man with a history of HTN, AAA repair, daily NSAID use, and heavy alcohol use presented to the ED of a teaching hospital in New England in February 2015 with lightheadedness, multiple episodes of melena, and large volume hematemesis. He denied dysphagia, regurgitation, cough, or heartburn. On arrival, vitals were BP 118/67, HR 97, and positive orthostatic hypotension. Lab work showed Hgb/Hct 11.4/32.7, BUN 32, Cr 1.3, and BUN:Cr ratio of 24.6. The initial Rockall Score was 2 (out of 7). Initial management in the ED included volume resuscitation with normal saline boluses and continuous infusion of pantoprazole 8 mg/hr. He was admitted to the step-down unit. Subsequently, he had three additional episodes of hematemesis, Hgb/Hct trended down to 6.6/18.9, and BP reached a nadir of 60/30. He was started on a dopamine infusion and received three units of pRBC. Given the patient’s history, the etiology of the UGIB was suspected to be secondary to a peptic ulceration, mucosal tear, ruptured esophageal varix, or aortic-esophageal fistula. Urgent upper endoscopy performed 9-hours after admission revealed a broad-mouth, right sided diverticulum in the distal portion of the esophagus. Within the diverticulum, a blood clot was visualized and, once washed off, revealed an underlying bleeding vessel. Two hemoclips were applied to achieve hemostasis. The post-procedure Rockall Score was 7 (out of 11). Overnight, the patient had three additional episodes of melena but no hematemesis. The following day the patient was hemodynamically stable, off vasopressors, resumed an oral diet, and had Hgb/Hct of 8.5/24. He was discharged two days after the EGD and remained asymptomatic one month after. To our knowledge, this is the first case report of an UGIB from a bleeding epiphrenic esophageal diverticulum that was successfully managed endoscopically with hemoclips only. Prior case reports have used epinephrine injection, thermal coagulation alone, or thermal coagulation and hemoclips as endoscopic interventions. Esophageal diverticula have an estimated prevalence of 0.015% to 2%. While rare, our case serves as a reminder that bleeding epiphrenic esophageal diverticula can present as massive UGIBs and urgent endoscopic therapy can be life-saving.


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[540A] Figure 1.

541

[542A] Figure 1.

A Rare Case of Anaphylaxis to Botox Aakash Aggarwal, MBBS1, Badal Kalamkar2. 1. Mount Sinai St. Luke’s Roosevelt Hospital Center, Hartford, CT; 2. Baystate Medical Center, East Longmeadow, MA. Botulinum toxin (Botox) is a neurotoxin used as an off-label treatment of achlasia cardia since the 1990s in cases not responding well to conventional treatment. We present a case of severe anaphylaxis due to Botox. Anaphylactic reactions to Botox are virtually unheard of, and there was only one other case in the literature similar to ours. A 47-year-old male with endoscopically confirmed achalasia presented with progressive dysphagia. Previous treatments included surgical myotomy and pneumatic dilation with temporary relief. During the endoscopy (for Botox treatment), the patient was medicated with fentanyl 200 mcg IV and midazolam 5 mg IV. Notably, the patient had received both fentanyl and midazolam in previous endoscopies without any complications. During the procedure, 90 units of Botox (reconstituted in normal saline) was injected into LES. Soon after the injection, the patient’s eyes and face started swelling up. SBP rose into the 220s, and pulse was in the 120s. His oxygen saturation dropped into the 70s. Intubation was attempted, but was unsuccessful due to extreme vocal cord edema. An emergency cricothyroidotomy was performed. Simultaneously, the patient received 100 mg of hydrocortisone IV and 50 mg of diphenhydramine IV. The patient was then transferred to the ICU. In the ICU, the cricothyroidotomy tube was replaced with the endotracheal tube, and IV dexamethasone was used for the vocal cord edema. Eventually, the patient was extubated successfully and discharged home in stable condition. Botox has been subjected to rigorous clinical evaluation in numerous RCTs and open-label studies across a broad range of therapeutic indications. Most of the studies do not report any serious side effects to Botox. A large meta-analysis of 36 studies, including 2,309 subjects, did not report any systemic side effects to Botox. A systematic study of 20 randomized control trials was done on the adverse effects associated with the use of botulinum toxin for spasticity associated with cerebral palsy. No serious adverse effects were reported among 6 studies. Botox use was mostly associated with mild respiratory effects, falls, seizures, and unspecified pain. The usual complications of Botox injections included procedure-related like pain, ecchymosis, or idiosyncratic reactions. Only one other case of anaphylaxis due to Botox was found in the literature search. However, in that publication, the Botox was reconstituted in 1% lidocaine, which raises the question that the anaphylaxis may have been due to lidocaine instead of the Botox. Despite the reported safety of any drug, all drugs deserve preparation for an emergency reaction.

542 An Unusual Case of Upper Gastrointestinal Bleeding Laya Nasrollah, MD1, Camron Kiafar, DO, FACG2. 1. Banner - University Medical Center/Carl Hayden VAMC, Phoenix, AZ; 2. Carl T. Hayden VA Medical Center, Phoenix, AZ. A 63 year old man with history of diabetes mellitus presented with coffee ground emesis and was found to be in diabetic ketoacidosis (DKA). His coffee ground emesis was self-limited and his DKA was the result of failing to take his prescribed insulin. He denied any abdominal pain, NSAID use, alcohol ingestion, melena or hematochezia. His surgical history was significant for removal of a “benign cyst” from his esophagus. Hemoglobin and hematocrit levels on admission were 12.2 g/dL and 39.5%, respectively. Upper endoscopy was performed and showed a large epiphrenic diverticula with ulceration (image #3). The food content seemed to have eroded the mucosa of the diverticula and caused it to bleed. No visible vessel was found inside the diverticula. Barium esophagogram images confirmed enodsopic findings (Image #1-2 ). Epiphrenic diverticula are uncommon and has an incidence of 0.015% in the United States (7). Diverticulum of the esophagus can be seen in upper (Zenker diverticula), mid (Traction and Pulsion diverticula) and lower esophagus (Epiphrenic diverticula). 75% to 90% of patients with epiphrenic diverticula have


[542B] Figure 2.

an underlying esophageal motor disorder, rather than a primary anatomic abnormality, as an underlying cause. These motility disorders mainly comprise of achalasia, nut cracker esophagus and diffuse esophageal spasm (DES). Delay in the diagnosis and treatment of symptomatic epiphrenic diverticula can lead to severe complications; including cough, aspiration, gastrointestinal bleeding and malignancy (2).


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If the diverticula is found incidentally or if it is associated with mild symptoms, conservative management may be considered especially in high surgical risk patients. Surgery is recommended in severe symptomatic cases. The surgical procedure of choice is diverticulotomy plus myotomy and esophageal manomtery prior to any invasive procedure is recommended (3). The addition of an antireflux procedure after the myotomy is an area of ongoing research and debate. Surgery is associated with significant morbidity and mortality as high as 5-9% have been reported and should be performed at high volume centers.

543 Massive Esophageal Variceal Bleeding: A Rare Complication of Sickle Cell Anemia Malini Mathur, Mark Malamood, Gregory Bernstein, Zubair Malik. Temple University Hospital, Philadelphia, PA. Sickle Cell Anemia is a known hypercoagulable state.1 Thromboses in sickle cell anemia usually include deep venous thrombosis (DVT) or pulmonary embolism (PE). Thrombosis of the splanchnic venous system, however, is rarely seen with only two cases ever reported. We present a case of diffuse splanchnic venous thrombosis causing large esophageal varices, resulting in massive hemorrhage in a patient with sickle cell anemia. BM is a 24 year-old male with sickle cell anemia. He presented with fatigue, dyspnea on exertion, dark stools, and coffee ground emesis. His hemoglobin was 5.8 g/dl. Esophagogastroduodenoscopy (EGD) showed large esophageal varices throughout the esophagus (see Figures 1 and 2) with stigmata of recent bleeding. No other abnormalities were noted. During the EGD, BM developed massive variceal hemorrhage that was not amenable to banding or ethanolamine injection. A Blakemore tube was inserted with the goal of having an urgent transjugular intrahepatic portosystemic shunt (TIPS) procedure. Abdominal computed tomography noted complete thrombosis of the splenic vein, non-occlusive thrombus of the superior mesenteric vein extending into smaller mesenteric branches, and complete thrombosis of the left portal vein along with incomplete thrombosis of the right portal vein (see Figures 3 and 4). This eliminated TIPS as an option. Attempts at removing the Blakemore resulted in massive bleeding and the patient required 11 units of blood. After consultation with transplant surgery, hepatology, and interventional radiology, BM underwent embolization of the gastroesophageal variceal collaterals originating from the left gastric artery. Repeat EGD showed decompressed small esophageal varices with no active bleeding. The Blakemore tube was removed and did not need to be replaced.

[543C] Figure 3.

Due to alterations in the clotting cascade, patients with sickle cell disease (SCD) are hypercoagulable1-3. Most thrombotic events related to SCD involve DVT or PE.2,4,5 Thrombosis of the splanchnic venous system caused by SCD is exceedingly rare. A PubMed search revealed only two reported cases of splanchnic venous thrombosis attributed to SCD.6,7 Recognized risk factors for splanchnic venous thrombosis include myeloproliferative disorders/neoplasms, liver cirrhosis, abdominal malignancy, paroxysmal nocturnal hemoglobinuria, and inherited thrombophilias.8,9 BM had no suggestion of any of this based on thorough laboratory testing and imaging. Thus, as his only identified risk factor for hypercoagulability, sickle cell anemia was the cause of BM’s diffuse splanchnic thrombosis, large esophageal varices, and massive gastrointestinal hemorrhage. This is an incredibly rare association and only the third ever case reported.

544 A Rare Case of Non-Epstein-Barr Virus Associated Lymphoepithelioma-like Carcinoma of the Esophagus Treated With Endoscopic Submucosal Dissection David M. Pinn, MD1, Lionel S. D’Souza, MD2, Petros Benias, MD3, Abul Ala Syed Rifat Mannan, MD4, Songyang Yuan, MD, PhD5, David L. Carr-Locke, MD, FACG2. 1. Mount Sinai Beth Israel Medical Center, Department of Medicine, New York, NY; 2. Mount Sinai Beth Israel Medical Center, New York, NY; 3. Mount Sinai Beth Israel, Wayne, NJ; 4. Mount Sinai St. Luke’s Roosevelt Hospital Center, New York, NY; 5. Mount Sinai Beth Israel Medical Center, Flushing, NY.

[543A] Figure 1.


Lymphoepithelioma-like carcinoma (LELC), termed as such due to histopathological similarities to lymphoepithelioma of the nasopharynx, has been reported in multiple organs including stomach, liver and


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esophagus. Only 18 cases of esophageal LELCs have been reported in English literature, with only one in the United States. Diagnosis is made by the microscopic appearance of undifferentiated carcinoma with dense lymphoplasmacytic infiltration. Endoscopically, esophageal LELCs can appear as either mucosal or submucosal tumors covered with normal appearing epithelium. Esophageal LELCs may be associated with Epstein-Barr Virus (EBV) and pathologic findings also include positive p16, p63 and cytokeratin AE1/AE3. Based on prior case reports, LELC has been noted to have a more favorable prognosis compared to other undifferentiated carcinomas. Treatment varies widely from surveillance to surgical excision and chemoradiation. There have been no prior case reports discussing endoscopic submucosal dissection as a treatment modality. Case: A 69 year old asymptomatic woman undergoing endoscopic surveillance for Barrett’s esophagus was found to have an incidental nodule in the proximal esophagus. Biopsy showed invasive moderately to poorly differentiated squamous cell carcinoma. Staging with endoscopic ultrasound revealed thickening of the mucosa and muscularis mucosa without invasion of the submucosa (stage T1aN0). Lugol’s iodine staining was negative for synchronous lesions. Endoscopic submucosal dissection (ESD) of the lesion was successfully performed with confirmed tumor free margins. Histopathology revealed a poorly differentiated malignant neoplasm composed of sheets of epithelioid cells admixed with a dense lymphoplasmacytic infiltration, consistent with esophageal LELC. Immunohistochemical studies were positive for p16, p63 and cytokeratin AE1/AE3; in situ hybridization for EBV-encoded small RNA was negative. Wide Screen Spectrum HPV DNA typing by in situ hybridization was also negative. Surveillance EGD two months later was negative for recurrence. The patient has not required chemotherapy or radiation therapy and remains asymptomatic. Conclusion: LELCs may resemble common benign, or even malignant tumors, and a high clinical suspicion must be maintained for the diagnosis. While treatment options vary, our case report demonstrates the viability of ESD in treating esophageal LELC.

syncope. Colonoscopy showed fresh blood throughout the colon as well as terminal ileum without any source. EGD showed a large esophageal ulcer with active bleeding. Endoscopic clips did not stop the bleeding. A Sengstaken Blakemore tube was placed. Patient was taken to Interventional radiology suite where brisk active bleeding into the distal esophagus from esophageal branches of the left gastric artery was seen. The arteriogram showed saccular dilation/pseudo-aneurysms that were the source of bleeding (arrow, Figure 1). Gel-foam embolization of the left gastric and esophageal branches, coil embolization of the gastrohepatic trunk and particle embolization of the pseudo-aneurysms stopped the bleeding. Esophageal brushings showed active cytomegalovirus infection along with low complement levels consistent with active vasculitis from SLE and mixed connective tissue disease. The patient eventually underwent exploratory laparotomy with resection of a necrotic esophago-gastric junction as well as thoracic esophagectomy. Pathological evaluation showed submucosal hemorrhage, esophagitis with dysplastic Barrett’s mucosa and an ulcer containing cytomegaloviral inclusions. It is probable that the ulcer from cytomegalovirus eroded into the pseudo-aneurysm formed by the persistent SLE mediated vasculitis and lead to the refractory bleeding. We report the first case of arterial bleeding from peri-esophageal pseudo-aneurysms present in the aortoesophageal branches in the left gastric arcade. We also report the use of gel-foam and particle embolization for arterial bleeding in the esophagus.

546 A Rare Case of an Infected Mediastinal Cyst Resolving via Spontaneous Esophageal Fistula David M. Pinn, MD1, Simi Singh, MD2, Gil I. Ascunce, MD3. 1. Mount Sinai Beth Israel Medical Center, Department of Medicine, New York, NY; 2. Mount Sinai Beth Israel, New York , NY; 3. Icahn School of Medicine at Mount Sinai, New York, NY.

545 Peri-esophageal Pseudoaneurysms: Unique Cause of Refractory Arterial Bleeding Treated With Novel Technique Divyanshoo Kohli, MD1, George Smallfield, III., MD, MSPH2. 1. Virginia Commonwealth University, Richmond, VA; 2. Virginia Commonwealth University, Division of Gastroenterology, Richmond, VA. A 43 year old female with SLE and dysplastic Barrett’s esophagus (Prague class C8 M9) treated with radiofrequency ablation presented with hematemesis. An EGD showed esophageal ulcers without any active bleeding. After 2 days of conservative treatment, the patient had an episode of hematochezia and

Foregut duplication cysts are a congenital gastrointestinal malformation constituting 6-15% of primary mediastinal masses. Bronchogenic cysts comprise 7-15% of foregut duplication cysts and form at weeks 5-8 of gestation. Endoscopic ultrasound (EUS) is used for evaluation of duplication cysts by distinguishing solid and cystic lesions and identifying surrounding esophageal anatomy. Bronchogenic cysts typically appear as an anechoic, homogenous lesion with regular margins arising from the submucosal layer. When diagnosis is uncertain, fine needle aspiration (FNA) may be needed; risks include infections, mediastinitis and, rarely, fistulas. Surgical intervention is the treatment of choice for symptomatic cysts. We present a case of a hypoechoic bronchogenic duplication cyst that resolved via a spontaneous cystoesophageal fistula. Case: A 23 year old male with no past medical history presented with chest pain and a chest CT revealed a mediastinal mass. EUS showed a 34 mm x 18 mm hypoechoic, heterogeneous lesion in the mediastinum, juxtaposed to the esophageal wall. FNA cytology revealed abundant mucoid material and macrophages without lymphocytes or stromal cells, suggestive of an esophageal bronchogenic cyst. Five days post-FNA, the patient returned with progressive chest pain, vomiting, low grade fever and leukocytosis. The repeat CT scan showed the mediastinal lesion growing in size and density. Broad spectrum antibiotics were initiated for presumed infected cyst. The patient was taken to the OR for planned excision of the lesion via thoracotomy. Intraoperative EGD prior to the procedure demonstrated drainage of copious purulent fluid from a spontaneous cystoesophageal fistula. Operative repair was deferred, and repeat CT scan showed decompression of the cyst; leukocytosis resolved and the patient was afebrile. A PEJ tube was placed for alimentation. Follow-up esophagram revealed a small persistent esophageal diverticulum representing a small remnant cyst cavity. The patient improved and a regular diet was initiated. Conclusion: Our case highlights the importance of a broad differential when utilizing EUS to diagnose mediastinal cysts. Bronchogenic cysts typically present as anechoic and homogenous but, when inflamed, may appear on EUS as hypoechoic and heterogenous. Empiric antibiotics can be considered during FNA of suspected neoplasms of the mediastinum and endoscopic drainage of symptomatic mediastinal cysts may present an alternative to surgery.

547 Eosinophilic Esophagitis and Crohn’s Disease: An Unbalanced Co-Existence Felicia Humphrey, MD 1, Evan Atkinson, MD, MS2, Rashid Syed, MD3, Arnab Ray, MD1. 1. Ochsner Medical Center, New Orleans, LA; 2. Tulane University, Covington, LA; 3. Ochsner Medical Center, Metairie, LA.

[545A] Figure 1.


Eosinophilic Esophagitis (EoE) and Crohn’s Disease (CD) occurring simultaneously is rare. Our literature search revealed only two documented cases of co-existing EoE and CD, with very limited evidence supporting an association. We present two additional cases to demonstrate these distinct immunemediated diseases can occur together, and propose a unique hypothesis about their immunopathogenic relationship. Case 1: A 27 year old Caucasian female with a 4-year history of CD, whose biologic therapy had been held during pregnancy, presented to our hospital with an abdominal abscess and obstruction. After discharge, her biologic therapy was resumed. Two months later, she had improvement in her CD symptoms but reported new symptoms of solid food dysphagia. EGD revealed changes compatible with EoE. After an 8-week proton pump inhibitor trial, repeat esophageal biopsies showed persistent eosinophilia consistent with a diagnosis of EoE. Case 2: A 30 year old Caucasian male with a history of EoE well controlled on topical budesonide presented to our clinic for a second opinion regarding his 5-year history of fistulizing CD on methotrexate. EGD and colonoscopy confirmed quiescent EoE but active Crohn’s ileitis. History was remarkable for several failed CD therapies including immunomodulators and biologics, over which time his EoE remained well controlled. He was subsequently placed on vedolizumab for CD, and topical budesonide was continued for EoE. While it is accepted that CD and EoE are driven primarily by Th1 and Th2-mediated immune responses, respectively, much of the pathophysiology of these two conditions is not yet fully understood. These responses are fostered by differing and often competing cytokine profiles, and it is therefore conceivable that a Th1-mediated condition could help quell a Th2-mediated condition, and vice versa. This is supported by recent advances via epigenetics studies in patients with EoE and inflammatory bowel disease.


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Abstracts Our cases present two young, Caucasian patients with co-existent severe CD and EoE. In each case, one of the conditions is quiescent while the other is exacerbated. Patient 1, developed symptoms leading to the diagnosis of EoE only after her CD went into remission with aggressive biologic therapy. Patient 2 manifested treatment-refractory CD when his EoE was well controlled. Our clinical observation questions whether treating one condition can worsen the other as the immune response shifts between Th1 and Th2, or, possibly, whether EoE could be a marker for aggressive CD. As evidenced by recent epigenetics studies, the answers to these questions are undoubtedly complex. Until further advancements, it is important to recognize the potential interplay of diseases such as EoE and CD when managing these complex cases.

548 Not the Typical Chest Pain: Esophago-Atrial Fistula After Atrial Fibrillation Catheter Ablation Winnie Sheu Woc , MD, Abdalla Hassan, MD, Michael Flicker, MD. Advocate Illinois Masonic Medical Center, Chicago, IL. A 65-year-old male presented with sharp severe chest pain, worsened with respiratory movements. One day prior to admission, patient had catheter ablation due to persistent atrial fibrillation. He had no other medical history. Initial echocardiogram was normal and pericarditis treatment was started. Two days later, patient’s symptoms worsened: nausea and odynophagia. Repeat bedside echocardiogram showed pericardial effusion. Esophagogram with gastrografin was consistent with extravasation of contrast in left lateral distal esophagus. Chest computed tomography showed an esophago-pericardial fistula. Pericardial effusion was drained through median sternotomy. EGD revealed a medium-sized fistula in the middle third of the esophagus at 32 cm. A 20 mm x10 cm partially-covered controlled-release stent with a 25 mm flange under fluoroscopic guidance was deployed. Patient was kept NPO with broad spectrum antibiotics. Five days post stenting, repeat esophagogram did not show leakage and tube feeds through nasogastric tube started. Patient was transferred to inpatient rehabilitation program. One month post ablation, patient had new onset left sided paresthesia and weakness. Stroke workup was initiated, and echocardiogram showed a highly mobile left atrial mass. Accordingly, emergent left atriotomy was done. The thrombus was removed and a nickel-sized hole was found in the back of the left atrium which appeared to be fused with the esophageal wall outside the visible esophageal stent. Th e defect was repaired with autologous pericardium. Esophageal injuries after catheter ablation for atrial fibrillation are uncommon, incidence ranging between 0.05 to 1.5%. Timing of presentation varies, with a mean of 19 days post ablation. The mechanism for the fistula formation is still not completely understood but is highly suspected that the proximity of the esophagus and the left atrium with a thermal transmission may damage the tissues. Gastric acid reflux might also be implicated. Esophageal perforation treatments have been described , including insertion of covered or partially-covered stents, as in our patient. The stenting was successful, but the course was later complicated by an atrial perforation. Complications of these fistulas can be devastating if not treated early and physicians should be aware of such entity.

[549B] Figure 2.

549 A Rare Cause of Complete Esophageal Obstruction: Endoscopic Variceal Band Ligation Jonathan D. Weinberger, MD1, Seth Homer, MD1, Sam Serouya, MD2, Carl Guillaume, MD1, Petros Benias, MD3, David L. Carr-Locke, MD, FACG2. 1. Mount Sinai Beth Israel, New York, NY; 2. Mount Sinai Beth Israel Medical Center, New York, NY; 3. Division of Digestive Diseases, Beth Israel Medical Center, New York, NY. Introduction: Complications of endoscopic variceal band ligation (EVBL) include pain, dysphagia, infection and bleeding. We present a case of complete esophageal obstruction, a rare complication of EVBL, and the first ever reported successful endoscopic treatment of such an obstruction.

[549C] Figure 3.

Case: A 90 year-old woman with a history of Hepatitis C cirrhosis complicated by prior esophageal variceal hemorrhage requiring EVBL presented for outpatient EGD for evaluation of anemia and melena. The EGD revealed two columns of large varices in the lower third of the esophagus, with red wale signs, for which bands were placed with deflation of varices. The following day, she presented to the hospital with inability to tolerate any oral intake. A barium esophagram revealed complete lower esophageal obstruction. The patient was managed conservatively with IV fluids and observation, but her symptoms did not improve. An EGD was performed which demonstrated an area of obstruction in the mid esophagus.Three bands were seen attached to the esophageal lumen and the surrounding tissue was black and necrotic. The area of prior banding appeared to entrap the full circumference of the esophageal mucosa within the three bands. An attempt was made to remove all bands with rat tooth forceps, however only one band was successfully removed. A hot snare was then used to perform an endoscopic mucosal resection (EMR), removing the remaining two bands. Following this, the endoscope was easily advanced into the stomach. To prevent stricturing, a fully covered esophageal stent was placed. Following the procedure the patient’s diet was advanced and the patient was discharged home. The esophageal stent was removed four weeks later and the previous area of obstruction was healing well. Discussion: Complete esophageal obstruction is a rare complication of EVBL, described previously in only five published reports. Banding related tissue edema and necrosis may play a role, yet the exact etiology is unknown. This is the first reported case of a successful endoscopic approach to relieving such an obstruction. EMR, to our knowledge, has never before been attempted in this setting. There were no noted complications including bleeding, perforation or esophageal dissection. Given the frequency of EVBL cases, recognition of all possible complications is necessary. While conservative management has been successfully employed in prior reported cases, this report illustrates an additional approach to consider.

[549A] Figure 1.



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550 Getting Under Your Skin: A Case of Esophageal Cancer With Subcutaneous Metastases and Spontaneous Tumor Lysis Ami Panara, MD, Andrew Folick, PhD, Megan Walker, MD, Maneerat Chayanupatkul, MD, Clark Hair, MD. Baylor College of Medicine, Houston, TX. Introduction: Cutaneous metastases of esophageal and gastric cancer are rare but have been reported usually as late findings. We present a case of a stage IV adenosquamous carcinoma with rapidly progressing cutaneous metastases as the presenting finding, leading to the identification of a primary tumor at the gastroesophageal (GE) junction.

Case: The patient was a 62 year old male with chronic HCV (Hepatitis C), alcohol and tobacco abuse who presented with 1 month of decreased appetite with acute worsening over the last 4 days and the sensation of regurgitation without dysphagia or odynophagia. Over the previous 3 weeks he had noticed nodules in his skin, first on his scalp, and then on his abdomen, back and right arm. Vital signs were remarkable for tachycardia to 120. On physical exam the patient had multiple firm, mobile, non-tender subcutaneous nodules on his head, neck, back, abdomen and upper extremities with the largest palpable nodule on the left upper back measuring 2 cm in diameter. Labs on admission were remarkable for elevated creatinine, potassium, lactate dehydrogenase, transaminases, total bilirubin, and uric acid, all indicating tumor lysis syndrome. AFP was normal. CT scan of the abdomen and pelvis identified a large heterogeneous mass at the GE junction, a cirrhotic liver with multiple hypodensities, numerous subcutaneous nodules and extensive retroperitoneal lymphadenopathy. Biopsy of a subcutaneous nodule in the right parietal scalp showed metastatic poorly differentiated carcinoma with staining consistent with an adenosquamous carcinoma of upper GI origin. On esophagogastroduodenoscopy a large friable mass at the GE junction was visualized and biopsies showed the same morphology as the right parietal cutaneous lesion, suggesting an esophageal primary. Renal function worsened despite fluid resuscitation and the patient became oliguric and then anuric. On day 5 of hospitalization, he became hypotensive and passed away. Discussion: Regardless of the primary site, cutaneous metastases of gastrointestinal malignancy portend a poor prognosis, with several studies demonstrating median survival of less than six months. Spontaneous tumor lysis of solid tumors is even more rare and there are only 11 other cases described in the literature, 4 of which were gastrointestinal in origin. Spontaneous tumor lysis is seen more often, and should be considered in patients with advanced malignancy and electrolyte abnormalities.

551 Unusual Cause of Boerhaave Syndrome Treated With Novel Internal Wound Vacuum L. August Clark, MD 1, Jacqueline Rampy, MD1, Christopher Oguayo, MD2, Alicia Swink, MD1, Andrew Paulson, MD3, James Burdick, MD1. 1. Baylor University Medical Center, Dallas, TX; 2. Baylor University Medical Center, Dallas , TX; 3. Baylor University Medical Center, Dallas, TX, Canada. Introduction: This case highlights an atypical presentation of spontaneous esophageal perforation leading to the discovery of a gastrinoma. There has been one case report of spontaneous perforation due to

[550A] Figure 1.

[550B] Figure 2.

[550C] Figure 3.


[551A] Figure 1.

[551B] Figure 2. VOLUME 110 | SUPPLEMENT 1

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[551C] Figure 3.

gastrinoma. The typical management of esophageal perforation is esophagectomy associated with a high mortality rate whereas a novel endoscopic internal wound vacuum approach was successfully utilized in this case. Case Presentation: A 58 year-old man with history significant for esophageal stricture presented with complaints of severe abdominal and chest pain 10 days post dilation. CXR showed pneumomediastinum. The patient was intubated on mechanical ventilation and hypotensive requiring pressor support. Labs revealed leukocytosis, lactic acidosis, and elevations in gastrin and chromagranin A. Imaging confirmed paraesophageal pneumomediastinum, bilateral periesophageal fluid collections, and leftsided pleural effusion. EGD showed ulcerative esophagitis with bilateral perforations a few centimeters above the GE junction. A novel intervention of serial endoscopic debridement of bilateral abscesses and placement of internal wound vac was performed which resulted in complete closure without a stricture. An Octreoscan revealed an abnormal focus of radiotracer uptake localizing to the upper left abdomen which on cross-sectional imaging corresponded to a mass lesion in the uncinate process of the pancreas. Discussion: The estimated incidence of gastrinomas is 0.1 to 1 percent of patients with peptic ulcer disease. Less than 5 percent of patients present with an esophageal stricture. The diagnosis is made based on clinical suspicion, elevated fasting gastrin, and elevated chromogranin A. Treatment includes medical management with suppression of acid secretion usually with PPIs but also with somatostatin analogues in refractory cases. Resection can be curative in patients with sporadic gastrinomas. This patient was initially deemed too unstable for surgery and thus endoscopic wound vac therapy was initiated which has previously been used successfully for intra-thoracic leaks. Conclusion: This case provides an example of a novel approach for the treatment of esophageal perforation. Advancements in the recognition and treatment of gastrinomas have led to the decrease in morbidity and mortality associated with the disease. Atypical presentations such as refractory reflux disease require consideration of the diagnosis of a gastrinoma.

[553A] Figure 1.

552 WITHDRAWN

553 Scimitar Syndrome a Rare Cause of Isolated Esophgeal Varices Jagrati Mathur, MD, Manjunath Harlapur, MD, Jayanta Choudhury, MD. University of California San Francisco, Fresno, CA. We present a rare case of isolated esophageal varices arising from Scimitar syndrome, an anomalous connection of the right pulmonary vein to the Inferior vena cava (IVC). A 53 year old female with past medical history of Scimitar syndrome repaired at age 20, with dissection of the anomalous right pulmonary vein and connecting it to the right atrium, and then creating an intra-atrial pericardial baffle directing venous flow to the left atrium presented with epigastric pain. She denied history of gastrointestinal bleeding or chest pain. Vital signs and exam were normal. Labs were normal. CT Chest, abdomen and pelvis showed mild mediastinal enlargement, a small right pulmonary artery, loss of right lung volume and diffuse distal esophageal wall prominence. The liver, spleen & pancreas were unremarkable. For epigastric pain, she underwent an EGD showing H.pylori gastritis and grade III esophageal varices in the mid and distal esophagus. She was treated for H. pylori gastritis. Endoscopic US showed esophageal varices, a lymph node in the aortopulmonary region and normal flow in the portal and splenic veins. For further workup of her esophageal varices in the setting of Scimitar syndrome and in the absence of portal hypertension, she underwent a cardiac catheterization. The cardiac catheterization showed normal right atrial and left ventricular end diastolic pressures. Also right pulmonary venous hypertension was noted, with the pulmonary venous collaterals draining into the azygous venous system, intercostal veins and then into the para


[553B] Figure 2.

esophageal venous system producing esophageal varices. Blood flow in the baffle from the right lower pulmonary vein into left atrium was not visualized, suggestive of obstruction of the surgical baffle. The study concluded that the right pulmonary venous flow drained into the systemic circulation via the paraesophageal veins. Scimitar syndrome aka pulmonary venolobar syndrome is a rare congenital heart malformation, with a prevalence of 0.5-1%. It is characterized by partial


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[553C] Figure 3.

or complete anomalous drainage of the right pulmonary vein into the IVC, right lung hypoplasia and mediastinal shift. The ‘Scimitar sign’ is a curvilinear shadow resembling a curved Turkish sword ‘scimitar’ created by an abnormal right pulmonary vein draining into the IVC. The common causes of esophageal varices in an adult are portal vein thrombosis, liver cirrhosis, SVC obstruction, mediastinal tumors, thymoma or chronic fibrosing mediastinitis. Esophageal varices arising from an anomalous pulmonary venous return is very rare. In this case, obstruction of the surgical baffle resulted in esophageal varices without portal hypertension. Patient was referred to surgery for evaluation of right lower lobe pneumonectomy or creation of another surgical baffle which may diminish the esophgeal varices.

554 Isolated GI Aspergillosis Presenting as Dysphagia From an Esophageal Ulcer in an Immunocompetent Host

[554B] Figure 2.

appearing, 25-mm-wide, distal esophageal ulcer. Histopathology of ulcer biopsies demonstrated active esophagitis and superficial fungal organisms. A Gomori silver stain revealed true-septated hyphae with acute angle branching, highly consistent with Aspergillus (Figure 1). Barrett’s esophagus was also identified. Patient had no known malignancy and was HIV seronegative. Aspergillus galactomannan antigen was negative. He was treated with IV levofloxacin and then discharged to receive oral levofloxacin for suspected community-acquired pneumonia. Patient was discharged with oral omeprazole 40mg twice daily for 8 weeks. As per infectious disease and patient’s wishes, the patient was not administered antifungal therapy because the aspergillus was believed to represent superficial ulcer colonization. Chest x-ray and CT did not reveal evident pulmonary aspergillosis. Repeat EGD 4 months later showed a healed ulcer. Histology revealed no inflammation and no fungal organisms on special stains. Fungal culture was sterile. Discussion: This case of isolated esophageal aspergillosis in an immunocompetent patient represents the first case reported in the GI literature. The GI tract may represent a portal of entry for Aspergillus. Ulcer resolution with no aspergillus detected on repeat EGD with biopsies without antifungal treatment may indicate transient colonization in patients with underlying predisposing conditions, such as esophageal ulcer from GERD. Finding isolated esophageal aspergillosis in immunocompetent hosts may represent transient colonization not requiring antifungal therapy.

Dupinder Singh, MD, Ross Sage, MD, Mitual Amin, MD, Mitchell S. Cappell, MD, PhD. William Beaumont Hospital, Royal Oak, MI. Introduction: Isolated gastrointestinal (GI) aspergillosis is relatively rare, with all reported patients having underlying immunosuppression, from profound neutropenia, stem-cell or solid-organ transplantation, AIDS, or chronic granulomatous disease. A case is reported of isolated aspergillosis in an esophageal ulcer in an immunocompetent patient. Case Report: A 52-year-old-man with a history of hypertension, GERD, alcoholism, and COPD, presented with dysphagia and 10 kg weight loss, pharyngitis, and productive cough for 2 weeks. Physical examination revealed pharyngeal erythema, coarse crepitations in the lung fields bilaterally, and a normal abdominal examination. The leukocyte count=14.4 bil/L, Hg=8.9 g/dl, and creatinine=2.07 mg/dl. Chest x-ray revealed multilobular pneumonia. Nasopharyngeal swab revealed RSV. Chest MRI revealed circumferential distal esophageal thickening. EGD revealed a cratered, clean-based, benign-

[554A] Figure 1.


555 Acute Esophageal Necrosis, an Unordinary Cause of Upper Gastrointestinal Bleeding: Report of 2 Cases Mayurathan Kesavan, MD1, Hafiz M. Khan2, Moiz Ahmed, MD3, Ahsan Khan, MD4, Frank Gress, MD5, Liliane Deeb , MD6. 1. Staten Island University Hospital, Staten Island , NY; 2. Staten Island University Hospital, Staten Island, NY; 3. Siuh, Staten Island, NY; 4. Staten Island University Hospital, Bellerose, NY; 5. New York Presbyterian Hospital/Columbia University Medical Center, New York, NY; 6. Staten Island University Hospital/NorthShore LIJ Health System, Staten Island, NY. Acute esophageal necrosis (AEN) known as Gurvits syndrome, black esophagus or acute necrotizing esophagitis is a rare clinical entity that is poorly described in the medical literature. Once thought to be extremely rare, AEN is now more frequently diagnosed perhaps due to the widespread availability and utilization of endoscopy. It is a disorder characterized by a striking endoscopic image of diffuse circumferential black musosa in distal esophagus that stops abruptly at the gastroesophageal junction (GEJ). Pathophysiology is due to a combination of an ischemic insult notably in critically ill patients, added to decreased reparative ability of mucosal barrier systems in malnourished and debilitated states. Upper GI bleeding is the most common clinical presentation. Other manifestations include epigastric pain, retrosternal chest discomfort and dysphagia. We describe 2 cases of AEN in critically-ill diabetic patients who developed hematemesis and melena. Case1: 69 year old male with diabetes, kidney transplantation and heart disease was admitted with hypovolemic shock and DKA precipitated by a myocardial infarct. Days later, he develops hematemesis and endoscopy shows black esophagus starting at 25 cm and extending distally to stop abruptly at GEJ (Fig1). Biopsies revealed necrotic debris without viral inclusion bodies or fungal hyphae (Fig2). PPI and volume expansion were instituted and patient recovered completely on repeat EGD. Case2: 74 year old male with diabetes and vasculopathy presents with acute ischemic limb for which he underwent femoro-popliteal bypass surgery. This was complicated by a hypovolumic shock and subsequent upper GI bleeding. EGD shows black esophagus starting at mid esophagus with an abrupt cut off at the GEJ (Fig3). No biopsies were taken because of anticoagulation. Patient was managed with PPI and volume expansion to full recovery. AEN is an unordinary reason for GI bleeding and a diagnosis worth considering in the appropriate clinical setting. Diagnosis is made on endoscopy by the presence of diffusely black necrotic esophagus with sharp delineation of the GEJ. The distal third of esophagus is typically affected first given its watershed vascular supply, however proximal progression is not uncommon. Histopathology reveals tissue necrosis


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556 Black Esophagus: A Case of Acute Esophageal Necrosis Following Orthopedic Injury Brittney S. Zimmerman, MD1, Monica Saumoy, MD2, Robert Schwartz3, David W. Wan, MD2. 1. Mount Sinai Hospital, New York, NY; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 3. Weill Cornell Medical College, Newton, MA.

[555A] Figure 1.

Black esophagus or “Acute Esophageal Necrosis” (AEN) is a rare and often under-diagnosed cause of upper gastrointestinal bleed and melena in hospitalized patients. It is diagnosed by endoscopic findings of black discoloration and severe mucosal injury of the esophagus. Here we present a case of a 77-year-old female who developed AEN after presenting to the hospital with a left femoral neck fracture. A 77-year-old female was admitted to our hospital after a mechanical fall and was found to have a left femoral hip fracture. While in the emergency department, the patient became hypotensive with multiple episodes of melenic stool and one episode of hematemesis. Her hemoglobin dropped rapidly from 10.3 mg/dL to 7.3 mg/dL. The patient was transferred to the ICU and upper endoscopy was performed which revealed diffuse, severe mucosal abnormality with ischemic discoloration circumferentially around the middle and lower third of the esophagus. These endoscopic findings were consistent with AEN. The patient received supportive treatment in the ICU, with proton pump inhibitor therapy and oral intake rest. An inferior vena cava (IVC) filter was placed to prevent venous thrombosis because of the high risk of anti-coagulation in this patient. She subsequently underwent successful left hip hemi-arthroplasty for repair of the fracture. The patient recovered and had resolution of her AEN on repeat endoscopy, and was discharged to rehab. The etiology of AEN is not clearly identified, but various mechanisms have been proposed, including ischemia, chemical injury, esophageal infection, or underlying malignancy. Most patients with AEN, if identified by prompt upper endoscopy, receive supportive treatment with acid suppression therapy. Outcomes vary but mortality of over 35% has been reported in previous case series of over 50 patients with AEN throughout the United States. The cause of this patient’s hypotension was unknown, but may be related to a vasovagal pain response following hip fracture. This case adds to the growing body of literature about this rare entity by proposing orthopedic injury and subsequent hypotension as a possible inciting factor for the development of AEN.

557 Acute Esophageal Necrosis After Initiation of Hemodialysis in a Patient With Renal Failure Brittney S. Zimmerman, MD1, Monica Saumoy, MD2, Robert Schwartz3, David W. Wan, MD2. 1. Mount Sinai Hospital, New York, NY; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 3. Weill Cornell Medical College, Newton, MA.

[555B] Figure 2.

Acute esophageal necrosis (AEN, also commonly known as “black esophagus”) is a rarely described cause of upper gastrointestinal (GI) bleed, with an incidence of less than 0.01% in hospitalized patients. Here we present a case of a 72-year-old female who developed AEN after initiation of hemodialysis for acute on chronic renal failure. A 72-year-old female with a history of rheumatoid arthritis and chronic renal disease was admitted to our hospital for viral pneumonia. Her course was complicated by worsening renal function, requiring initiation of hemodialysis. She experienced two episodes of loss of consciousness during her first dialysis treatment, likely due to hypoperfusion. The following day, the patient developed multiple episodes of small-volume hematemesis and melena, with an acute drop in hemoglobin from 9 mg/dL to 5 mg/dL. Upper endoscopy revealed a black circumferential area of necrosis of the proximal esophagus. The patient received supportive treatment with nasogastric tube, proton-pump inhibitor therapy and oral intake rest. Follow-up endoscopy one week later showed complete resolution of her esophageal injury. The patient resumed oral intake without difficulty, and was discharged to rehab three weeks after admission. AEN is characterized by a circumferential, dark pigmented, black appearance of the esophagus with friable mucosa seen on upper endoscopy. AEN usually affects the distal 2/3 of the esophagus with sharp demarcation at the gastroesophageal junction, although it can affect the proximal esophagus as seen in this case. On pathologic examination of the tissue, mucosal and submucosal necrosis with heavy leukocyte infiltration is seen. Various mechanisms have been hypothesized for development of AEN,

[555C] Figure 3.

though biopsy is not required for diagnosis. Caution is advised with passage of nasogastric tube when needed, in order to avoid perforation. AEN carries a mortality of about 38%, hence, increased awareness of this syndrome is of utmost importance in order to take appropriate measures and prevent complications like esophageal stricture, perforation, and death. Treatment is basically focused on the underlying illness and involves fluid resuscitation, gastric acid suppression and parenteral nutrition when necessary.


[557A] Figure 1.


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[558B] Figure 2.

[557C] Figure 3.

including ischemia/hypoperfusion, impaired mucosal barriers, chemical injury, infection and underlying malignancy. Hypoperfusion resulting from dialysis treatment has been identified in recent literature as a possible cause of AEN in patients with renal failure. This case adds to the growing body of literature highlighting AEN as a consequence of hemodialysis, and should be considered as a possible complication of dialysis patients who present with upper GI bleed.

558 Iatrogenic Massive Gastrointestinal Bleeding: A Rare Cause Mihajlo Gjeorgjievski, MD1, Lohit Garg, MD2, Tusar Desai, MD3. 1. Department of Internal Medicine, Beaumont Health, Royal Oak, MI; 2. Department of Internal Medicine, Beaumont Health, Royal Oak , MI; 3. Department of Gastroenterology and Hepatology, Beaumont Health, Royal Oak, MI.

[558C] Figure 3.

A 58y.o. Male with past medical history of thoracic aortic aneurysm stent and repair presented with one month history of dark tarry stools. He denied abdominal pain, nausea, vomiting, constipation or diarrhea. On presentation, hemoglobin was 6.7 mg/dL; requiring transfusion of multiple units of packed red blood cells (PRBC). An esophagogastroduodenoscopy (EGD) revealed clotted blood in the gastric body and gastric fundus, but no active bleeding. Repeat EGD after 3 days revealed fibrin plug in stomach that was clipped. He had persistent melena and blood loss requiring transfusion of 17 units PRBC during his hospital stay. Tagged red blood cells scan did not reveal a site of active gastrointestinal bleeding. CT angiography revealed stable appearance of the thoracic aortic stent with significant edema in the superior mediastinum that seemed to separate the aorta with the stent from the esophageal lumen. A repeat

EGD on day 10 of admission showed extrinsic compression of the upper esophagus with superimposed blood clot, located 5cm below the upper esophageal sphincter. He underwent fluoroscopic placement of endograft over the source of the aorto-esophageal fistula (AE fistula) with subsequent resolution of the bleeding. He eventually underwent staged surgical correction with resection of the AE fistula. AE fistula represents a rare but life threatening complication of an endovascular repair of aortic thoracic aneurysm. Less than 500 cases of AE fistula have been reported in the literature so far with approximately



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Abstracts 30 cases of AE fistula after endovascular repair of aortic aneurysm. The mechanism of development of AE fistula after an aortic stent is not known. The current theories lean toward the possibility of stent protrusion through already developed part of the aortic aneurysm that does not contain adventitia. The risk is highest near the second esophageal constriction, where the esophagus is closest to the aortic arch. EGD is the most sensitive and specific test to diagnose AE fistula, although CT angiography could be helpful in some cases. Despite the negative CT angiography and tagged RBC scan, we made our diagnosis solely on the EGD findings. Direct pressure with Blakemore tube, endovascular restenting or embolization can provide temporary control of the bleeding. Operative repair is usually necessary for definitive treatment of AE fistula.

559 A Case of Plummer-Vinson Syndrome and Celiac Disease Nabeel Chaudhary, MD1, John Levey, MD2. 1. UMass Memorial Medical Center, Boston, MA; 2. UMass Memorial Health Care, Worcester, MA. Introduction: Plummer-Vinson syndrome is a triad of iron deficiency anemia, dysphagia, and cervical esophageal web. Celiac disease and Plummer-Vinson syndrome are both known to be associated with iron deficiency. There are very few reported cases of both being seen in the same patient. We report a case of a female found to have Plummer-Vinson syndrome along with celiac disase. Case report: We present a case of a 48 year old female with a long standing history of iron deficiency anemia. She had been following up with her primary care physician for a number of years for iron deficiency anemia and had extensive workup done. She required intermittent blood transfusions and was on B12 and Iron. She had been seen by gastroenterology 5 years prior to this visit, at that time it was recommended she have an upper endoscopy and colonoscopy which she refused due to being pregnant at the time. She was told to follow up with gastroenterology for an upper endoscopy and colonoscopy after her pregnancy was over. Years later she re-presented with anemia and dysphagia. An upper endoscopy and colonoscopy were scheduled. Upper endoscopy demonstrated a benign appearing intrinsic stenosis 24 cm from the incisors. A pediatric endoscope was required to traverse the web-like stenosis in the proximal esophagus. Duodenal biopsies were taken to check for celiac disease. Colonoscopy showed the entire colon to be normal. Duodenal biopsies were consistent with immune-mediated injury such as gluten sensitivity. She was thought to have Plummer-Vinson syndrome in the setting of iron deficiency anemia secondary to celiac disease. It was recommended that the patient adhere to a gluten free diet. The patient was scheduled for upper endoscopy for esophageal dilation but was again lost to follow-up. Conclusion: Plummer-Vinson syndrome is a triad of iron deficiency anemia, dysphagia, and a cervical esophageal web. Celiac disease and Plummer Vinson syndrome are rarely seen coinciding together in the same patient. Important point to remember is that if a patient is thought to have Plummer-Vinson syndrome they should be worked up for celiac disease as a cause of iron deficiency anemia. This case demonstrates this importance of keeping in mind that Plummer-Vinson syndrome and celiac disease can coexist in the same patient.

560 The Identification of Buried Glands by Optical Coherence Tomography (OCT) in Barrett’s Esophagus (BE) Presidential Poster Amit Desai, MD1, Nariman Gobara, MD, MS2, Felice Schnoll-Sussman, MD, FACG3. 1. New York Presbyterian Hospital/Weill Cornell Medical Center, New York City, NY; 2. Weill Cornell Medical Center, Houston , TX; 3. The Jay Monahan Center for Gastrointestinal Health, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY. A 69 year old male with a history of stage III colon cancer s/p right hemicolectomy and chemotherapy and paraesophageal hernia repair was referred for evaluation of a newly diagnosed long-segment Barrett’s esophagus with high grade dysplasia. An upper endoscopy with OCT and targeted biopsies was performed for further evaluation. On retroflexion, an intact wrap was noted. The esophagus and gastroesophageal junction (GEJ) were examined with white light and narrow band imaging from a forward and retroflexed view. There were mucosal changes consistent with long-segment Barrett’s esophagus extending from the upper extent

[560B] Figure 2.

[560C] Figure 3.

of the gastric folds at 40cm from the incisors to the Z-line at 29 cm. The NVision Volumetric Laser Endomicroscopy Imaging System (NinePoint, Cambridge, MA) was inserted. The 20 mm balloon was inflated to a pressure of 10 mmHg and a full scan was obtained. Given the long length of the BE segment, the process was repeated until the entire segment was adequately analyzed. The OCT images revealed loss of layering and atypical mucosal glands concerning for high-grade dysplasia at numerous segments (Figure 1). In addition, OCT uniquely revealed highly suspicious buried dysplastic sub-mucosal glands (Figure 2). Targeted biopsies were performed which confirmed high grade dysplasia and dysplastic buried glands (Figure 3). Buried dysplasia can be frequently missed on protocol BE biopsies1 . Buried glands, which may carry malignant potential, are very difficult to survey due to limited ability to obtain adequate specimens on standard biopsies. Protocol pinch biopsies frequently fail to identify buried glands in pre- and post-RFA treatment BE patients2. Furthermore, there may be no significant reduction in dysplastic buried glands post-RFA ablation treatment. Our case report highlights the benefits of OCT in the evaluation of BE, namely predicting and targeting biopsies to identify not only the presence and location of dysplasia, but also the presence of atypical buried glands. This case highlights the utility of OCT in the surveillance of patients with Barrett’s esophagus. OCT findings such as those found in this case may have significant implications in the ultimate treatment modality chosen. References: [1]. Gray et al AJG 2011 Nov; 106(11):1899-908. [2]. Zhou et al GIE 2012 Jul; 76(1):32-40.

561 Pseudoachalasia: Still a Tough Clinical Challenge Yi Jia, MD, PhD, Richard McCallum, MD, FACG. Texas Tech University Health Sciences Center, El Paso, TX.

[560A] Figure 1.


Background: The patients with a presentation of dysphagia with or without noncardiac chest pain can have the diagnosis of achalasia. Treatment of achalasia is focused on decreasing the lower esophageal sphinter (LES), by either pneumatic dilation (PD) or surgical myotomy. When patients symptomatically relapse after one or more PDs, then one explanation to consider is the possibility of pseudoachalasia as the diagnosis. Case Report: We present a rare sequence of events in an elderly patient with a presentation of chronic dysphagia, heartburn and severe weight loss, who initially had diagnostic findings consistent with achalasia. He subsequently responded very well to a series of PD (of 30-40 mm balloon size) without complications, but for only brief intervals. Further investigations finally uncovered esophageal adenocarcinoma with setting of Barrett’s esophagus by endoscopic ultrasound (EUS), thus making our patient an example of the entity “pseudoachalasia”. Conclusion: Pseudoachalasia secondary to an esophageal malignancy should be suspected when dysphagia progresses despite technically well performed PDs, and particularly suspicious in the setting of an elderly patient with marked weight loss and endoscopic evidence of mucosal inflammation. EUS is an excellent diagnostic tool for detecting and staging malignancy by obtaining diagnostic tissue and allowing appropriate therapy to be planned.


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Diffuse Extensive Esophageal Papillomatosis: A Rare Cause of Dysphagia

A Large Solitary HSV Esophageal Ulcer and Right-Sided Aortic Arch Causing Dysphagia in an Immunocompetent Host

Vipin Verma1, Dennis Nguyen, MD2, Barinder Chana, MD3, Suzan Ebrahimi4, Kushal Patel5, Sachin Patel, MD6. 1. MedStar Washington Hospital Center, Silver Spring, MD; 2. MedStar Georgetown University Hospital, Arlington, VA; 3. Internal Medicine, Georgetown University Hospital / Washington Hospital Center, Washington, DC; 4. Washington Hospital Center, Chevy Chase , MD; 5. Washington Hospital Center, College Park, MD; 6. MedStar Washington Hospital Center, Washington, DC. Esophageal squamous papilloma is a benign epithelial tumor, usually seen as a solitary, small, white or pink, sessile or polypoid mass. The true incidence of esophageal papillomatosis is unknown, however, various studies estimate the incidence between 0.007-0.43%1. Fifteen percent of papillomatosis cases are seen as multiple lesions and even fewer are extensive disease2. We present a case of diffuse extensive papillomatosis. A 69 year old African-American gentleman with hypertension, COPD and alcohol abuse who presented with 2-3 months of dysphagia, and 40 pounds of weight loss over 10 months. Esophagogastroduodenoscopy (EGD) revealed a partially circumferential/obstructing friable necrotic appearing mass in the mid-esophagus which was biopsied. Distal to the large mass were small, circumferential, pearly, wart/ finger-like exophytic growths which spared the very distal esophagus and the gastroesophageal junction. PET/CT scan revealed circumferential thickening and a hypermetabolic mid-esophageal wall over a length of 10cm, concerning for a primary esophageal cancer without evidence of metastatic disease. Initial pathology revealed no evidence of malignancy. The patient underwent two additional flexible EGDs with biopsies which were unrevealing. The patient finally underwent rigid esophagoscopy with biopsy with pathology revealing squamous papillomas. This was confirmed with pathology from a repeat EGD showing squamous papillomas without any evidence of malignancy. Our case is unique given the rarity of diffuse esophageal papillomatosis and highlights the challenges in diagnosing extensive disease as a non-malignant growth. Of note, 30 % of all lesions are associated with HPV and currently HPV on our patient remains pending. [1]. Syrjänen et al. Detection of human papillomavirus in esophageal papillomas: systematic review and meta-analysis. APMIS. 2013 May;121(5):363-74. [2]. Odze et al. Esophageal squamous papillomas. A clinicopathologic study of 38 lesions and analysis for human papillomavirus by the polymerase chain reaction. Am J Surg Pathol.1993 Aug;17(8):803-12.

Michael Hsu, MD, PhD, Peter J. Sargon, MD. Rush University Medical Center, Chicago, IL. Case Report: A 77-year-old African-American female with CAD, HTN, atrial fibrillation and GERD was admitted for further workup of dysphagia and weight loss. She developed dysphagia to solids suddenly 5 months prior. After 2 weeks of symptoms she presented to an outside hospital for pill impaction and underwent an EGD that found the pill in the mid-esophagus due to a 2-3 cm long stenosis without surrounding inflammation or mass lesion. The stenosis was dilated and afterwards was felt to be due to extrinsic compression. A fluoroesophagogram noted narrowing of the mid-thoracic esophagus, and a chest CT found an esophageal stricture with mild dilatation of the esophagus. Also noted was a R-sided aortic arch. She briefly benefited from dilation, but she presented again with pill impaction a month later and underwent an EUS along with a 2nd EGD. EUS revealed extrinsic compression of the mid-esophagus in the area of the stricture and there was an extraluminal hypoechoic lesion with internal hyperechoic strands consistent with calcifications. Four months later she was admitted to our institution with persistent dysphagia and weight loss. Chest CT was repeated and noted compression of the esophagus anteriorly by the heart and posteriorly by the anomalous descending thoracic aorta. A 1.7 x 1.0 cm soft tissue mass arising from the posterior esophageal wall was also seen. An EGD was performed and found a mid-esophageal stricture that prevented passage of a regular EGD scope. An ultrathin upper endoscope (“noodle scope”) was able to traverse the stricture which was found to be due to a hard, friable and nearly circumferential ulcerated mass. Biopsies of the mass showed extensive necrosis, severe acute esophagitis and viral inclusions consistent with herpes simplex virus. No neoplastic tissue was seen. The patient was subsequently started on acyclovir. Discussion: A R-sided aortic arch is a rare anatomical variant in ~0.1% of the population and has the potential to cause esophageal and/or tracheal compression. However, when the right aortic arch compresses the esophagus enough to cause symptoms of dysphagia, patients typically present during early childhood. Our patient had persistent dysphagia despite being immunocompetent. Furthermore, the endoscopic appearance was unusual for HSV esophagitis as she had a solitary large ulcer instead of numerous shallow ulcers. In our patient, her dysphagia was likely due to a combination of esophageal compression and HSV esophagitis.

564 A Rare Cause of Pill Esophagitis and Esophagitis Dessicans Superficialis Sam Serouya, MD1, Neeraj Mangla, MD2, Joseph Tawil, MD2, Aaron Walfish, MD2. 1. Mount Sinai Beth Israel Medical Center, New York, NY; 2. Mount Sinai Beth Israel, New York, NY.

[562A] Figure 1.

[562B] Figure 2.


Esophagitis dissecans superficialis (EDS) is a benign condition characterized by sloughing of portions of the esophageal squamous epithelium. It has been associated with particular medications as well as autoimmune diseases. We present the first known reported case of EDS caused by dabigatran. Our patient is a 38 year old man who had presented with acute onset of dysphagia and odynophagia. The patient was in his normal state of good health until two years prior, when he experienced a cerebrovascular accident. He was later diagnosed with a patent foramen ovale (PFO) and was started on clopidogrel and aspirin. One year later, while on aspirin and clopidogrel, the patient experienced a transient ischemic attack. His anticoagulation was changed to dabigatran which he would religiously take prior to dinner. He was subsequently scheduled for a transesophageal echocardiogram (TEE) for workup of possible closure of the PFO. On the evening prior to the TEE, due to unforeseen circumstances he took his dabigatran immediately prior to bedtime. The next morning he awoke with significant odynophagia with radiation to his back with all oral intake. Upon arrival for the TEE, his cardiologist cancelled the TEE and referred him to a gastroenterologist. He was started on carafate and a proton pump inhibitor and was scheduled for an esophagogastroduodenoscopy (EGD). The EGD was performed and demonstrated a superficial healing ulcer in the proximal esophagus, as well as plaque like whitish material with linear streaking consistent with esophagitis dessicans superficialis likely a secondary reaction to the pill esophagitis.


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[564B] Figure 2.

[565A] Figure 1.

[564C] Figure 3.

Esophagitis dissecans superficialis is an underreported rare condition of unknown etiology. Most patients may exhibit a variety of symptoms such as dysphagia, odynophagia, vomiting of tubular casts of esophageal mucosa, however, it is often asymptomatic and detectable only by endoscopy. EDS has been associated with bullous pemphigoid, pemphigus vulgaris, lupus, celiac disease, collagen vascular disorders, esophageal strictures, chemical ingestions, and hot beverages. Medications including bisphosphonates, NSAIDs, potassium chloride and iron supplements have also been associated with its development. We report the first known case of dabigatran induced EDS. Unlike other medications that may play a role in EDS, dabigatran is not known to interfere with swallowing, cause dry mouth, or known to cause esophageal injury. Further research is needed to elucidate the etiology of EDS due to dabigatran.

[565B] Figure 2.

565 Esophageal Pseudodiverticulosis: A Rare Case of Dysphagia Nupur Sanghavi, Giao Vuong, MD, Christine Hachem, MD. Saint Louis University, St. Louis, MO.

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Esophageal Intramural Pseudodiverticulosis (EIPD) is a rare condition that typically presents with dysphagia. We report a case of EIPD presenting with progressive dysphagia and odynophagia. Initial esophagram outlined a shaggy mucosal appearance and a long proximal stricture (Figure 1). Upper endoscopy revealed numerous small diverticula and white patches confirmed to be Candida on pathology (Figure 2). The patient was treated with a proton pump inhibitor and fluconazole which resolved his symptoms three weeks later. EIPD is a benign condition but complications such as strictures, bleeding, spontaneous perforation, mediastinal abscesses, or pleural effusions may require an esophagectomy.

Primary Esophageal Melanoma


Syed Amer, MBBS1, Nina Ngo, MD2, Jennifer L. Horsley-Silva, MD2, Christine O. Menias, MD2, Dora Lam-Himlin, MD3. 1. Division of Internal Medicine, Mayo Clinic, Phoenix, AZ; 2. Mayo Clinic, Phoenix, AZ; 3. Mayo Clinic, Scottsdale, AZ. An eighty-six year old male presented to the clinic with a chief complaint of heart burn. He was initially prescribed a proton pump inhibitor without improvement in his symptoms. Esophageal pH testing showed significant total acid exposure in both the supine and upright positions, and a decreased lower esophageal sphincter pressure.


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primary mucosal melanoma (Image 3). Given his advanced age, chemotherapeutic options were favored over surgical resection. However, due to severe toxicity after the first cycle of dacarbazine, he declined further chemotherapy and enrolled in hospice care. The patient expired nine months following diagnosis. Primary malignant melanoma of the esophagus is rare as it comprises only 0.1%-0.2% of all malignant esophageal tumors. It occurs predominantly in males aged 60-70 years. Dysphagia is the most common complaint followed by non-specific retrosternal pain and weight loss. Occasionally heartburn, hematemesis and melena are observed. Endoscopically, melanomas are characteristically polypoid and sometimes ulcerated. Because melanomas may be amelanotic, less than half of cases show pigmentation as seen in this example. Other diagnostic considerations for non-pigmented polypoid tumors of the esophagus include: leiomyoma, lipoma, fibroma, neurofibroma, sarcomas, small cell carcinoma, carcinosarcoma and metastatic melanoma, the diagnoses of which require biopsy. Primary esophageal melanomas are highly aggressive and metastasize early via hematogenous and lymphatic routes. Thoracic and abdominal computed tomography, barium swallow examination, EUS and fluorodeoxyglucose positron-emission tomography are useful staging methods. Treatment recommendations for patients are based almost exclusively upon small, retrospective studies; therefore, the optimal management remains unknown. Tumor size and location, presence or absence of metastases, age and comorbidities of the patient all affect treatment modality. Radical surgical resection is the only therapy option that might influence survival, as other modalities (radiotherapy & chemotherapy) are merely palliative. As the cancer is often quite advanced at the time of diagnosis, prognosis is exceedingly poor.

567 [566A] Figure 1.

The Unusual Coexistence of Achalasia and Scleroderma Romana Shehzadi, MD, Venkatasai Boda Eswara, Ankur Sheth, MD, FACG. Louisiana State University Health Sciences Center, Shreveport, LA. Scleroderma is an autoimmune disease characterized by excessive deposition of collagen and other connective tissue macromolecules in skin and multiple internal organs.It is called systemic Sclerosis(SS),when it involves internal organs.SS involves GI tract in 90% of the patients.Esophageal motility is the most

[566B] Figure 2.

[567A] Figure 1.

[566C] Figure 3.

Subsequent upper endoscopy showed a fungating mass with patchy black discoloration in the middle and distal esophagus (Image 1). CT of the thorax revealed a 3-cm esophageal mass and enlarged pretracheal lymph nodes (Image 2). Biopsy of the mass revealed a malignant neoplasm with features consistent with a


[567B] Figure 2.


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Abstracts for the majority of EC in the US. Volumetric laser endomicroscopy (VLE) is a safe and accepted method to visualize esophageal mucosa and submucosa in patients with suspected or confirmed Barrett’s esophagus (BE) or EAC with better resolution than endoscopic ultrasound (EUS). The application of VLE and optical coherence tomography (OCT) can be extended to the diagnosis and targeted therapy of ESCC. Case Report: 70 year-old female with a history of tobacco abuse and tongue SCC (status post partial glossectomy) was referred due to iron deficiency anemia. She denied gastrointestinal bleeding, dysphagia or alarm features. Physical exam showed partial glossectomy. Colonoscopy was unremarkable. Upper endoscopy revealed a 1 cm flat mucosal nodule in the upper one third of the esophagus that was not well visualized on subsequent EUS. VLE was used to obtain a 360-degree scan of the proximal esophagus to a depth of 3mm. This confirmed an upper esophageal lesion with changes suspicious of early ESCC (loss of layered architecture and inhomogeneous hyper-reflective surface). The lesion was resected via band ligation and snare mucosal resection with grossly clean margins. Pathology revealed SCC, moderately differentiated, with focal submucosal invasion but no perineural or lymphovascular invasion in a background of high grade squamous dysplasia. The deep margin was free of carcinoma. Discussion: ESCC is associated with significant morbidity and mortality in the US and globally. Risk factors in the US include tobacco and alcohol abuse. Pathogenesis of ESCC begins with epithelial dysplasia, followed by carcinoma in situ, and eventual invasive carcinoma. VLE has shown success in the evaluation of intestinal metaplasia (IM) and subsquamous IM of BE and early EAC. Prior Japanese studies demonstrated superiority of OCT versus EUS for assessing depth of tumor infiltration and preoperative staging of ESCC. We present the first US case of early stage ESCC in which VLE was utilized to facilitate diagnosis and guide targeted endoscopic resection. Larger US case series are needed to evaluate VLE as an efficient and minimally invasive modality to both screen and survey patients with ESCC.

569 Acute Esophageal Necrosis: A Very Rare but Potentially Fatal Medical Condition Francis Edeani , MD1, Alan Putrus, MD2, Mohd Amer Alsamman, MD1, Ashirf Al-Ghanoudi, MD, MPH3. 1. Good Samaritan Hospital, Cincinnati , OH; 2. Trihealth-Good Samaritan Hospital, Cincinnati, OH; 3. Good Samaritan Hospital, Cincinnati, OH. There are a few documented cases of acute esophageal necrosis. As of today, there are less than 100 cases reported in medical literature. Clinician should be aware of this disease because of the high morbidity and mortality reportedly associated with it. Early diagnosis and prompt treatment has been consistently associated with improved outcome. A 53 year old female with history of insulin-dependent diabetes, esophageal stricture, esophagitis and hypertension presented with multiple bouts of coffee ground emesis and diarrhea. She had stopped taking her insulin for about 6 months prior to onset of symptoms. Review of systems was positive for epigastric pain, polyuria and polydipsia. She was found to have DKA and her HBA1c was 11.3. An EGD showed diffuse, circumferential black distal esophageal mucosa with some large ulcers. Tissue biopsy was

[567C] Figure 3.

frequently affected function in GI tract.It classically manifests as reduced LES pressure and loss of distal esophageal body peristalsis.In comparison Achalasia is a primary esophageal motor disorder characterized by insufficient relaxation of the LES and loss of esophageal peristalsis.While Sclerdoerma leads to low LESP, Achalasia causes insufficient LES relaxation.Coexistence of the two is rare.We report a case of a Scleroderma patient presenting with Achalasia.A 62 years old African American woman with history of Scleroderma and Systemic Lupus Erythematosus overlap syndrome was evaluated by gastroenterology for dysphagia .She had worsening dysphagia to both solids and liquids for three to four years.She underwent EGD which showed dilated, sigmoid shaped esophagus with retained liquid and solid food. LES was found to be hypertensive and resistance was felt while entering stomach. .Barium esophagram showed dilated esophagus with narrowing at LES with bird beak appearance.So both studies were suggestive of Achalasia. Patient refused esophageal manometry at multiple occasions.Scleroderma occurs worldwide and affects all races but has higher general and age-specific rates in blacks with more severe disease and poorer outcomes than whites.GI tract involvement is very common and occurs early in the course of the disease. Esophagus is the most frequently involved internal organ causing symptoms of dysphagia, odynophagia,heartburn and regurgitation.Esophageal motility gets affected and is characterized by aperistalsis or low amplitude contractions, decreased or absent resting LES tone and lack of coordination between esophageal contractions and LES relaxations.Esophageal dysmotility in association with delayed gastric emptying results in impaired esophageal clearance of refluxed gastric contents and the development of reflux disease .In comparison Achalasia is characterized by absence of peristalsis in the distal two-thirds and elevated resting pressure in LES, typically above 45 mmhg along with failed LES relaxation with swallowing .LESP stays above 8 mmhg above gastric pressure.When the manometric characteristics of LES are compared, Achalasia is characterized by hypertensive LES and Scleroderma by hypotensive LES.Due to opposite changes in LESP, coexistence of Achalasia and scleroderma is extremely rare and so far only few cases have been reported .This case reports shows the rare coexistence of the two conditions making Achalasia one of differentials of dysphagia in Scleroderma patients.

568 Volumetric Laser Endomicroscopy to Diagnose and Guide Endoscopic Management of Early Esophageal Squamous Cell Carcinoma Sarah M. Hyder, MD1, Arifa Toor, MD2, Stuart R. Gordon, MD2. 1. Dartmouth Hitchcock Medical Center, Cranston, RI; 2. Dartmouth-Hitchcock Medical Center, Lebanon, NH. Introduction: Esophageal squamous cell carcinoma (ESCC) is prevalent worldwide, accounting for 70-90% of esophageal cancer (EC) in developing countries. Incidence of ESCC in the United States (US) has declined in the past 2-3 decades compared to esophageal adenocarcinoma (EAC), which accounts


[569A] Figure 1.


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[570A] Figure 1.

[569B] Figure 2.

obtained and histopathology confirmed tissue necrosis involving the mucosa and submucosa. Fungal and bacterial cultures were negative. Her management meant consisted of treatment of her DKA, nothing by mouth for the first 48 hours, IV proton pump inhibitors and Sucralfate. Patient’s symptoms resolved and she was discharged home on oral proton pump inhibitors and insulin. A follow up EGD a year later showed complete resolution of esophageal ulcers and restoration of normal pink mucosa. This case illustrates the need for a high index of suspicion for acute esophageal necrosis in high risk patients. According to available literature, risk factors include presence of chronic diseases especially diabetes, DKA, esophageal, stricture, esophagitis. In the event that these patients present with coffee ground emesis, an EGD should be obtained. Even though the reported prevalence is 0.001 to 0.2 %, overall mortality can be as high as 32%. The outcome has been good in patients with uncomplicated cases in which there was prompt diagnosis and treatment. Delay in diagnosis and treatment has been associated with complications such as esophageal stricture and perforation, with an attendant increase in morbidity and mortality.

570 A Case of Primary Malignant Melanoma of the Esophagus Hyun Ho Choi, Sang-Hyun Gil, Jihan Yu, Hyung-Keun Kim, Sang Woo Kim, Hiun-Suk Chae, Sung Soo Kim. Department of Internal Medicine, Uijeongbu St. Mary’s Hospital, College of Medicine, The Catholic University of Korea, Uijeong Bu-si, Korea, Republic Of. Primary malignant melanoma of the esophagus is a rare disease and aggressive tumor of the esophagus. Primary malignant melanoma represents 0.1% to 0.2% of all primary esophageal cancers. Hematogenous and lymphatic metastasis are common. The prognosis is quiet poor, so early dectection and accurate diagnosis should be made. We encountered a patient with a black esophageal lesion, which was histopathologically confirmed to be primary malignant melanoma of the esophagus. A 65-year-old men was admitted for evaluation of a black pigmentation at lower esophagus which was found at regular general physical exam. He had no symptoms, no history of any illness and no family history of cancer. Physical examination found no abnormal pigmentations of the skin or mucosa. Endoscopy revealed multiple scattered 0.4cm sized black pigmented ulcerative lesion at 37cm from the incisors (Figure 1). Pathological findings from endoscopy show melanin pigment deposition and melanophage infiltration (Figure 2). Immunohistochemical staining was positive for HMB45, Ki-67, S100 and melan-A. Computed tomography of chest and abdomen showed no evidence of discernible lesion in the stomach, lung and regional lymphadenopathy. Positron emission tomography demonstrated no regional or distant metastasis. He received esophagectomy and gastroesphagostomy. Muscularis mucosa was involved, but the surgical margin of the esophagus was free from tumors. And all regional lymph nodes were found free of tumor.


[570B] Figure 2.

571 Black and White Esophagus: Variants of Acute Esophageal Necrosis Santosh Reddy, MD1, Kimberly Kolkhorst, DO, MA2, Jonathan Keshishian, MD1, Patrick Brady, MD, FACG3. 1. University of South Florida, Tampa, FL; 2. University of South Florida, Department of Gastroenterology, Tampa, FL; 3. University of South Florida, Morsani College of Medicine, Tampa, FL. Acute esophageal necrosis (AEN) is a rare clinical syndrome that can be identified via esophagogastroduodenoscopy (EGD). The condition is described as circumferentially black appearing esophageal mucosa that affects the distal esophagus, and stops abruptly at the gastroesophageal junction. Depending on the stage, AEN will have a range of appearances, from the characteristic black necrotic appearance to circumferential ulceration with thick white exudates. Herein, we describe two cases of AEN that demonstrate this continuum. A 53 year-old male with diabetes mellitus type II presented to the hospital with a two-day history of vague epigastric pain with melena. Patient had blood glucose of 653 mg/dl with ketonemia which responded to therapy with insulin and IV fluids . EGD subsequently revealed diffuse severe esophagitis with a white-black appearance present from 25 cm to 40 cm and stopping abruptly at the gastroesophageal junction (Figure 1). Biopsies revealed acute necrotizing inflammation and fibrin neutrophilic crust material. The patient was treated with a PPI, and was able to tolerate oral feedings at the time of discharge. A 64 year-old female with multiple co-morbidities and significant vasculopathy was admitted for failure to thrive. Patient had decreased oral intake due to abdominal discomfort. EGD showed the patient had circumferential ulceration with white exudates seen extending from 25-35 cm and stopping abruptly at the gastroesophageal junction (Figure 2). Biopsies showed inflamed squamous mucosa and fragments of acute inflammatory necrotic debris from ulcer bed. Mesenteric angiogram revealed long segment occlusion of the main superior mesenteric artery with collateral flow from the celiac axis. Unfortunately, patient expired due to complications of her vasculopathy. Compared to the upper and middle esophagus, the distal esophagus is relatively hypoperfused. It receives blood flow from the branches of the celiac trunk. In DKA, dehydration leads to a low flow state that can compromise the distal esophagus. In an acutely diseased organ, AEN has a classic black appearance. The second case was a chronic insult secondary to combination of low fluid intake with increased demand from the celiac trunk due to occlusion of the SMA. The disease was in the healing stage, and


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[572A] Figure 1.

[571A] Figure 1.

[572B] Figure 2.

[571B] Figure 2.

had appearance of white esophagus due to exudates of necrotic debris. Although the clinical appearance and presentation of AEN is variable, the etiology can be attributed to hemodynamic compromise of the relatively hypovascular distal esophagus.

EGD showed a fistula between the esophagus and the left atrium with pulsatile mass, and clot the site of the fistula (Figure 2). Immediately following EGD, the patient had a recurrence of ST elevation on telemetry, became hypotensive and bradycardia. The working diagnosis was air emboli to the coronary and cerebral arteries secondary to the fistula. Patient was placed on Trendelenburg position, and supportive therapy was started to maintain the hemodynamics. She underwent emergent cardiothoracic surgical repair. However, she had severe coagulopathy following the surgery requiring massive blood transfusion. She rapidly progressed into septic shock and multiorgan failure. The patient passed away on the same day of operation. Discussion: Atrioesophageal fistula, a rare but life-threatening complication of pulmonary vein ablation therapy, has been reported in the literature with time of manifestation ranging from few days following the procedure to few weeks later. The clinical presentations includes pleuritic chest pain, signs of air emboli which depending of the vasculature involved could result in ischemic strokes and myocardial infarction, signs of upper gastrointestinal bleeding which may result in hemorrhagic shock and mediastinitis that starts as chemical and later evolves into septic mediastinitis, severe sepsis or septic shock. Establishing the diagnosis requires a very high index of suspicion. CT scan of the chest is the best method to make the diagnosis. EGD could provide therapeutic modalities such as esophageal stents however it carries a risk of massive air embolism and should not be used to establish a diagnosis. Emergent cardiothoracic surgery to isolate the fistula is the standard of care.

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573

When Esophagogastroduodenoscopy (EGD) Is Not the Right Thing to Do

Primary Esophageal Adenocarcinoma With Colon Metastases After Esophagectomy

Rami Khoury Abdulla, MD. William Beaumont Hospital, Royal Oak, MI.

Bonnie Patek , DO1, Hiral Shah, MD2, Shashin Shah, MD2. 1. Lehigh Valley Health Network, Macungie, PA; 2. Eastern Pennsylvania Gastroenterology and Liver Specialists, Allentown, PA.

A 63 years old female presented to the emergency room with symptoms of hematemesis of bright colored blood, generalized fatigue, non-specific chest pain and low grade fever. A month prior to presentation she had pulmonary vein isolation for refractory atrial fibrillation. Initial vitals: Blood pressure: 139/64, HR: 156, Temp: 38C. Physical Exam was remarkable for sick-appearing pale and lethargic patient. Pulse was irregularly irregular. Cardiac auscultation showed normal S1, S2, no murmurs. Abdominal exam was within normal limits. Laboratory findings includes: White count of 9400 cells/microliters with neutrophilic shift 8.8, lymphopenia 0.3, Hemoglobin of 10.9 (two weeks prior to presentation Hemoglobin was 13.9). Creatinine of 0.57, BUN: 15, Na: 139, K: 4.5. EKG upon admission showed ST elevation in inferior leads concerning for STEMI, these ST elevation resolved spontaneously within 5 minutes (Figure 1). Patient was admitted to the cardiac intensive care unit for monitoring. Shortly after admission, she had a seizure, CT scan of the brain showed two focal areas of edema in the right occipital and left temporal lobes.


Esophageal carcinoma is an aggressive cancer with predominance to squamous cell variation worldwide, but in the United States, adenocarcinoma is more common. Risk factors for esophageal adenocarcinoma (AC) include gastric acid reflux and tobacco use leading to an increase in oxidative stress resulting in inflammation and increase cellular turnover with metaplasia. Esophageal AC presents with manifestations of dysphagia, weight loss, malnutrition and advanced disease with dyspnea, cough or hoarseness. Esophageal AC can metastasize to the lung, liver, bone, celiac lymph nodes with rare spread to the colon. We present a case of primary esophageal AC status post chemoradiation and esophagectomy with metastatic disease found as asymptomatic colon polyps. Our patient is a 70 year-old male smoker presenting with dysphagia and weight loss of twenty pounds over 4 weeks. Esophagogastroduodenoscopy and endoscopic ultrasound revealed a nearly occlusive, friable mass invading the muscularis propria with celiac lymphadenopathy and biopsies confirming invasive, poorly differentiated AC without distant metastasis. Concomitant chemoradiation was initiated prior


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to surgical resection. An esophagectomy was performed with pathology consistent with prior biopsies. Routine CT scan four months later with enlarged para-aortic lymphadenopathy and liver lesions resulted in a colonoscopy to question the primary cancer. Colonoscopy exposed nodules throughout descending and ascending colon; biopsies consistent with similar immunoprofile as previous esophageal AC and liver lesions. Colon nodules were deemed consistent as metastasis from previous esophageal adenocarcinoma. Patient was started on FOLFOX therapy. Primary esophageal AC typically presents with advanced disease resulting in the likelihood of metastatic disease. Metastatic spread within the gastrointestinal tract, more specifically the colon, is rare with few case reports. Most case reports are of squamous cell carcinoma metastasizing, which can be explained by higher prevalence of disease worldwide. A definite challenge in this case is to determine the primary cancer. Colon nodules offer no differentiation from primary or secondary cancers with no particular features to be appreciated on imaging or endoscopy. Most nodules are asymptomatic and could be developing at the same time as the esophageal carcinoma. Treatment is based on the primary cancer with chemoradiation and surgical resection if applicable.

574 Lymphocytic Esophagitis and Dysphagia: Cause or Association? Yasser Alsamman, MD1, David W. Wan, MD2. 1. University Hospitals Case Medical Center, Cleveland Heights, OH; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY. Lymphocytic esophagitis (LE) is a histologic phenotype of chronic esophagitis. It is a rare condition characterized by intraepithelial lymphocytes in the peripapillary fields with few or no granulocytes in the esophageal mucosa. Here we report a case of lymphocytic esophagitis associated with dysphagia. An 87-year-old male presented to the clinic in 2014 with dysphagia. His past medical history included Barrett’s esophagus, chronic obstructive pulmonary disease, hypertension, right carotid endarterectomy, and chronic kidney disease. He complained of difficulty initiating swallowing with an inability to use his tongue to touch the roof of his mouth, which began after undergoing dental work 3 months ago. He stated that liquids were particularly difficult to swallow, and that it felt like a plug was stopping the flow of liquids, but not solids, from his esophagus to his stomach. Multiple swallows were required to finish a cup of water. He denied any odynophagia. As part of a workup for an unintentional 44-pound weight loss over several years, he had an EGD in 2009 only showing Candida esophagitis. Repeat EGD after fluconazole treatment was normal except for thickened folds. EUS at the time was normal. Colonoscopy in 2013 showed a small tubular adenoma. CT chest/abdomen/pelvis in 2009 was without obvious malignancy. A swallow evaluation was normal. Thus, given the worsening dysphagia, another EGD was performed which showed rings in the mid-esophagus and a mild Schatzki ring at the GEJ that was biopsied. The pathology was consistent with lymphocytic esophagitis at the GEJ and proximal esophagus and Candida esophagitis at the proximal esophagus. Afterwards, swallowed fluticasone was recommended, but the patient did not comply. He reported that the dysphagia resolved spontaneously. In a previous study, it was found that LE was present in 0.1% of esophageal biopsies.1 The etiology remains unknown, and no association has been found between LE and any clinical conditions. However, recent studies have shown that dysphagia is the most common presenting symptom in patients found to have LE. Although the incidence of LE has increased over the years, it is still unclear if it is a distinct clinical entity or a marker of another disease process. Further investigations are required to study the natural history of LE and to determine if an association exists between LE and dysphagia. References: [1]. Haque S, Genta RM. Lymphocytic oesophagitis: clinicopathological aspects of an emerging condition. Gut 2012; 61:1108.

[575B] Figure 2.

superficial sloughing of the mucosa. Biopsies revealed benign squamous mucosa with parakeratosis and necrosis without inflammatory reaction, consistent with diagnosis of Esophagitis Dissecans Superficialis. He was treated with Pantoprazole daily with no further vomiting, hematemesis, or pharyngeal dysphagia. Post EGD course was uneventful and had improved ability to safely tolerate oral intake without restriction. Discussion: Esophagitis dissecans is a disease characterized by sloughing esophageal mucosa, hence alternatively labeled as ‘sloughing esophagitis’. Our patient presented with hematemesis which has been reported in other case reports, including one of the earliest in 1954. The most common symptom is a globus sensation or dysphagia, and other manifestations may include chest pain, painful swallowing, and heartburn. He was an older debilitated nursing home resident which is also identified as typical demographic of the disease. Possible causes in our patient may have been Iron, Aspirin, Quetiapine, and Gabapentin, all of which were prior medications the patient had taken. Interestingly, in a recent study of 41 patients, the most common drug class used among those with esophagitis dissecans were psychoactive drugs, which were part of medication history in nearly ¾ of all patients, relating to our patient who had an atypical antipsychotic and gabapentin as prior drugs. In conclusion, esophagitis dissecans is a rare and fortunately frequently benign disease. Our case reinforces known qualities such as clinical presentation, endoscopic and histologic findings, and correlates well with newly emerging information concerning demographics, medication exposure, and functional status to better identify those most likely to be affected.

576 A Rare Cause of Odynophagia in a Healthy Adult

575 Esophagitis Dissecans Due to Quetiapine and Gabapentin? Vincent Petros, DO1, Bashar Hmoud, MD2, Matthew Maslonka, MD3, Michael Sedrak, MD2, Shehzad Merwat, MD2. 1. University of Texas Medical Branch, Texas City, TX; 2. University of Texas Medical Branch, Galveston, TX; 3. University of Texas Medical Branch, Galvetson, TX. Case: An 81 year old white male presented from his nursing home for hematemesis with no other gastrointestinal symptoms. He was anemic with hemoglobin 7.0 mg/dl and baseline 10 mg/dl, was transfused 1 unit packed red blood cells. On exam, oropharynx was clear, abdomen benign, stool brown but stool guaiac test positive. Prior medications included recent Quetiapine, Gabapentin, an 81 mg Aspirin but no other antiplatelet or anticoagulation, and no other history of alcohol use or liver dysfunction. Esophagogastroduodenoscopy (EGD) did not find any evidence active or prior bleeding, but did reveal diffuse


Umber Ahmad, DO1, Mustafa Musleh, MD2, Salma Akram, MD3. 1. Wright State University, Dayton, OH; 2. Wright State University, Miamisburg, OH; 3. Wright State University/Dayton VAMC, Department of Gastroenterology, Dayton, OH. Esophagitis caused by infectious etiologies are rare including Candida, Herpes Simplex Virus (HSV), and Cytomegalovirus (CMV). These esophageal infections are strongly associated with an immunosuppressed host and HSV esophagitis is exceedingly rare in the immunocompetent population. We present a case of a healthy male diagnosed with HSV esophagitis, with no evidence of immunosuppression.


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[576B] Figure 2.

[577B] Figure 2.

A 31 year old African American male presented with an 8 day history of chest pain, odynophagia, and dysphagia. Three days prior to developing symptoms, he reported fever, chills, arthralgia, and myalgia. He had no significant past medical or surgical history. He reports to be monogamous with single female partner and no history of sexually transmitted disease. On admission, he had a temperature of 101.7 F and tachycardia. There were no oropharyngeal lesions on exam. His White Blood cell count was 4.3 t/cmm. Serology for CMV, HSV I, HSVII, and HIV were all negative. Upper gastrointestinal endoscopy demonstrated severe ulcerative esophagitis with circumferential ulceration in the distal esophagus. Proximal to this lesion were multiple 2-4 mm well-circumscribed ulcerations. Esophageal biopsy revealed acute esophagitis, intra-nuclear inclusions, and ground glass nucleated giant cells, consistent with herpes simplex virus. A 10 day course of oral acyclovir was initiated, with complete resolution of symptoms at the end of treatment. HSV is a double stranded DNA virus which can causes infection of the visceral organs. Rarely, single organ can be involved of which esophagus is the most common. Similar to this case, HSV esophagitis in the immunocompetent is often a young male, under forty years old, with acute symptoms of odynophagia, fever, and substernal chest pain. They may present with weight loss, dysphagia, orolabial herpetic lesions, and prodrome of flu-like symptoms. Features consistent with HSV include punched out or coalesced lesions with cobblestone appearance. Esophageal involvement is often in the distal and midesophagus. Biopsy of esophageal ulcer edge with histopathology and viral culture is required to confirm diagnosis. Symptoms are expected to resolve by two weeks without treatment in an immunocompetent host. Systemic antiviral treatment is recommend. It is thought to reduce symptoms and prevent complications including esophageal perforation and gastrointestinal bleeding. A high index of clinical suspicion is key to diagnosis, followed by prompt endoscopy.

577 Percutaneous Endoscopic Gastrostomy Placement in a Patient With Anomalous Esophageal Anatomy Mel A. Ona, MD, MS, MPH, MA1, Lyna M. Campo, MD2, Tagore Sunkara, MD3, Andrea Culliford, MD4, Jay P. Babich, MD5. 1. The Brooklyn Hospital Center, Brooklyn, NY; 2. St. Barnabas Hospital, SBH Health System, Englewood, NJ; 3. St. Barnabas Hospital, New Rochelle, NY; 4. St. Barnabas Hospital, SBH Health System, New York, NY; 5. St. Barnabas Hospital, SBH Health System, Teaneck, NJ. Percutaneous endoscopic gastrostomy (PEG) placement is an effective way of providing enteral feeding to patients who have functionally normal gastrointestinal tracts but who cannot meet their nutritional

[577C] Figure 3.

[577A] Figure 1.


needs because of inadequate oral intake. The usual method for PEG tube insertion is the “pull through” method. A 76-years-old male, with history of non-small cell lung cancer status/post (s/p) resection, chemotherapy, and radiotherapy, presented to the hospital after being found unresponsive at home. Computerized tomography of the brain demonstrated hydrocephalus with periventricular edema. The patient was admitted to the intensive care unit for seizure and electrolyte abnormalities. His hospital course was complicated by hypoxemic respiratory failure due to pulmonary embolism and retroperitoneal hematoma due to anticoagulation. An inferior vena cava filter was placed. He remained ventilator dependent and underwent tracheostomy placement. A PEG tube was recommended for long-term enteral feeding. During the endoscopy, a large esophageal diverticulum was found just proximal to the gastro-esophageal junction. A 20-French PEG tube was inserted with ease per the usual endoscopic procedure and with no unplanned events. The patient tolerated the procedure well. (Figures 1-3) Epiphrenic diverticula are rare distal outpouchings of the esophageal lumen that are caused by a combination of an esophageal motility disorder and variations in lower esophageal pressure. Although up to 40% of patients with epiphrenic diverticula are asymptomatic, the majority of patients may experience dysphagia, chest pain, vomiting, and weight loss. Treatment is typically surgical intervention. Our patient was found unresponsive prior to hospital admission; therefore, it is unclear if he was symptomatic. Moreover, the indication of PEG placement was for long-term enteral access s/p tracheostomy due to failure to wean from the ventilator. The risk of perforating a distal esophageal diverticulum during guide-wire assisted insertion of the PEG


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through the esophagus and into the stomach is of concern. However, due to the soft and collapsible PEG bumper we found that a traction-retrievable PEG tube may be safely inserted endoscopically in a patient with this type of anomalous anatomical finding and no special technical skills or procedure modifications are needed.

578 Esophageal Mass: The Unusual Suspect Prathab Devaraj, Swapna Gayam. West Virginia University School of Medicine, Morgantown, WV.

[579C] Figure 3. A 93-year-old-male presented for outpatient dacryocystorhinostomy. Post-operatively, he reported sudden onset of severe odynophagia to liquids. He denied chest pain, nausea, vomiting, melena or hematochezia. He reported a history of dysphagia to pills requiring endoscopic esophageal dilation approximately one year prior to this presentation. He had chronic GERD treated with pantoprazole daily. His medical history included CAD, glaucoma and CVA for which he took aspirin 81 mg and Clopidogrel. Physical examination revealed no abdominal tenderness and normoactive bowel sounds. Esophagogastroduodenoscopy (EGD) demonstrated three discrete, exophytic, polypoid, ulcerated and friable mass like lesions each measuring approximately 2-3 cm x 1-2 cm. These lesions were concerning for malignancy based on their appearance. Pathologic examination of the biopsies revealed marked acute esophagitis with reactive changes but no evidence of malignancy. After further discussion with the pathologist, fungal staining was performed and demonstrated numerous fungal hyphae consistent with Candida. He was treated with Oral Fluconazole for 14 days. Repeat EGD 4 weeks later revealed significant improvement of the mass like lesions. Biopsies from the healing areas revealed no evidence of malignancy and no fungal elements confirming eradication of Candida confirming the diagnosis of Candidoma. Conclusion: Endoscopists should be aware that not all mass lesions are malignant and we report a case of Candidoma masquerading as esophageal cancer.

579 Complications of Barrett’s Radiofrequency Ablation in a Patient Treated With Chemoradiation for Esophageal Adenocarcinoma David DiCaprio, DO, Geethan Sivananthan, Niket Sonpal, David Robbins, MD. Lenox Hill North ShoreLIJ Hospital System, New York, NY. Barrett’s esophagus (BE) is the largest risk factor for esophageal adenocarcinoma (EAC), and the incidence of EAC has been increasing faster than any other malignancy in the US. Ablation after EAC is not well studied because treatments such as endoscopic resection and surgical esophagectomy, with or

without chemoradiation (CRT), are effective modes of treatment. The case below is the first reported case of radiofrequency ablation of dysplastic BE using the Barrx Halo catheter in a patient who has undergone CRT for EAC. A 68 year old male with GERD presented for surveillance EGD revealing nodular BE. EMR of one nodule revealed poorly differentiated adenocarcinoma extending into the muscularis mucosa and lateral margin of sample. Surgery was deferred in consideration of his previous bariatric surgery due to a higher perioperative risk. EUS and PET CT showed no nodal or metastatic disease, and the patient opted for chemoradiation. A post CRT EGD showed extensive neovascular changes (Fig 1), and a 12cm segment of Barrett’s esophagus. In consideration of the recent CRT, RFA for persistent BE was delayed 6 months. Using a Barrx probe, RFA was applied circumferentially at 12 joules/cm2 in the affected area (Fig 1). Immediately after RFA, the patient complained of substernal chest pain. He presented to the ED where a CXR was performed showing no evidence of perforation and he was discharged with analgesia. He came to the office one week later with worsening chest pain and dysphagia/odynophagia to solids. A CT scan revealed marked thickening of the distal two thirds of the esophagus (figure 2). The patient was given a steroid taper to reduce inflammation. Repeat endoscopy two weeks later showed inflamed, thickened mucosa corresponding to the ablated areas (Figures 3). There was marked granulation tissue, but no ulcers, active bleeding or strictures. His symptoms began to improve and repeat CT showed slight improvement of esophageal wall thickening. BE persists in up to 93% of patients who receive only CRT for EAC, leaving these patients vulnerable to metachronous EAC. RFA was chosen as an effective and affordable means for eradication of BE. The persistent inflammation and poor healing that followed, however, suggests acquired hypersensitivity from prior CRT. Based on current literature and our experience, we recommend against the routine use of RFA for Barrett’s ablation in patients with prior CRT for EAC.

580 Isolated Colonic Metastasis From Esophageal Adenocarcinoma Manraj Khosla, MD1, Madappa Kundranda2, Robert Whitehead3, Jeffrey Weber3, Toufic Kachaamy4. 1. St. Joseph’s Hospital and Medical Center, Phoenix, AZ; 2. Banner / MD Anderson, Gilbert, AZ; 3. Cancer Treatment Centers of America, Goodyear, AZ; 4. Cancer Treatment Centers of America, Phoenix, AZ. Esophageal Cancer is the eighth most common cancer worldwide with an increasing incidence. Prognosis is highly dependent on the stage. Common sites of metastasis (mets) include lymph nodes, liver, lungs, bones and the adrenal glands. Staging is by computerized axial tomography scan (CT) and endoscopic ultrasound (EUS) for non- metastatic disease. Positron Emission Tomography (PET) improves sensitivity for distant metastasis. Despite all the above imaging techniques, occult metastatic disease is sometime

[579A] Figure 1.

[579B] Figure 2.


[580A] Figure 1.


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[580B] Figure 2.

difficult to diagnose preoperatively. Isolated esophageal adenicarcinoma(EsoA)with mets to the colon have not been reported in the English literature. A 60 year old male with a history of Barrett’s esophagus presented with the complaint of dysphagia. An upper endoscopy (EGD) demonstrated an esophageal mass and biopsy was consistent with an adenocarcinoma, intestinal type, with foci of signet ring cell features. Staging with CT and EUS identified a T3N2M0 tumor. The patient was treated with neoadjuvant chemoradiation with the plan for an esophagectomy. His surgery was delayeddue to a new onset atrial fibrillation and stroke so chemotherapy was continued. Restaging PET/CT a year after presentation demonstrated no visible foci of mets. An esophagectomy with colonic interposition was considered so a preoperative colonoscopy was performed which demonstrated a colonic nodule with central ulceration in the proximal ascending colon. Biopsies were consistent with submucosal deposits of adenocarcinoma with signet cell features identical to the esophageal primary. Features that differentiate colonic mets from primary colonic adenocarcinoma include the submucosal location of the nodule and histologic characteristics consistent with the primary signet ring features. The finding of this colonic met avoided an unnecessary surgery, with significant morbidity and mortality, in a rather non curative setting. Extracolonic cancer with colonic mets are rare and have been reported in melanoma, breast cancer and lung cancer. They often are a manifestation of widespread mets . Metastatic esophageal squamous cell carcinoma to the colon has been rarely reported. This is the first reported case of an isolated colonic mets from esophageal adenocarcinoma not identified on prior imaging studies including PET/CT.

581 Systemic AL-Amyloidosis Initially Presenting as an Isolated Gastroesophageal Junction Amyloidosis

[581B] Figure 2.

amyloidosis. Subsequent bone marrow biopsy revealed plasma cell involvement of 4%. Electrophoresis and immunofixation results were consistent with AL amyloidosis. A repeat biopsy several months after revealed progression to diffuse gastrointestinal amyloidosis. Amyloidosis is a condition of extracellular fibrillar protein deposition, which is commonly associated with tissue damage and functional compromise. Primary amyloidosis usually represents an amyloidosis associated with immunocye dyscrasia and is caused by clonal proliferation of plasma cells that synthesize an immunoglobulin that is prone to form amyloid. Gastrointestinal amyloidosis without previously diagnosed inflammatory or plasma cell disorders is very rarely seen. It may be found as an isolated entity or as a part of multi-organ involvement. In the gastrointestinal tract, amyloid proteins (irrespective of the type) can deposit in various parts, resulting in a mixture of symptoms of: abdominal pain, dysmotility, diarrhea, liver injury or bleeding. Suspicion of gastrointestinal amyloidosis, irrespective of underlying etiology, always requires a direct biopsy of the part affected. The frequency of amyloid deposition in different anatomic parts of the gastrointestinal tract, in patients with gastrointestinal amyloidosis was established in a case series consisted of 37 patients. The highest frequency was in the duodenum, followed by stomach and colorectum. Some authors suggest that amyloidosis should always be considered in the differential diagnosis of hematemesis and gastric tumors, while others suggest high suspicion of amyloidosis in patients with multiple myeloma and obscure gastrointestinal bleeding.

Mihajlo Gjeorgjievski, MD1, Estela Mogrovejo1, Mitchell S. Cappell, MD, PhD2, Mitual Amin, MD3. 1. Department of Internal Medicine, Beaumont Health, Royal Oak, MI; 2. William Beaumont Hospital, Southfield, MI; 3. William Beaumont Hospital, Royal Oak, MI. A 55-year-old, African-American man with history of chronic abdominal pain, was admitted for progressive epigastric abdominal pain, anorexia and weight loss of 20 kilograms over the last year. Abdominal CT did not reveal any significant abnormalities. EGD revealed a cratered, non-bleeding, 10mm-wide, ulcerative-like lesion at the gastroesophageal (GE) junction. Two non-bleeding cratered gastric ulcers with no stigmata of bleeding were found in the gastric antrum as well as few, medium-sized non-bleeding erosions at the incisura and in the gastric antrum. Pathologic examination of the GE junction revealed amyloidosis with sample being positive for Congo red and crystal violet stain. An immunohistochemical stains revealed 3+ lambda staining and 1+ kappa staining, consistent with monoclonal lambda light chain AL amyloidosis. The gastric biopsy was positive for Helicobacter pylori, however did not reveal

582 Mitomycin C for the Treatment of a Recalcitrant Esophageal Stricture Xiaolu Carter, DO, Emuejevoke Okoh, MD, Craig Womeldorph, MD. SAUSHEC Department of Gastroenterology, San Antonio, TX. Background: Mechanical dilation is the most common treatment method for esophageal stricture. Rarely, a stricture may be refractory to combination therapy to including dilation, intralesional steroid injection, and esophageal stent therapy, which are all fairly common treatments for esophageal strictures. In the past decade, mitomycin-C has gained popularity for its use in treating refractory esophageal strictures with promising results mostly in pediatric patients. Design: Case report and literature review. Case: We present a 63 years old patient with complicated, recalcitrant esophageal stricture that failed to improve with multiple mechanical dilations, steroid injection, repeated esophageal stenting, and needle knife incisional treatment. The patient had intermittent and temporary relief of dysphagia with these treatments, but the symptom-free duration fluctuated between 1-4 weeks and dramatically dropped to 1-2 weeks after a complicated metal stent placement at the end of 2014. For this recalcitrant stricture, low dose topical mitomycin-C with mechanical dilation was used with good response. Conclusion: Mitomycin-C is a safe and effective treatment option for recalcitrant esophageal strictures; however, further study is needed to determine long term effects of topical application as well as optimal dosage and scheduling for this medication.

583 Flexible Endoscopic Zenker’s Mucomyotomy With the Carr-Locke Cap Presidential Poster Nathaniel Ernstoff, MD1, Simi Singh, MD1, David L. Carr-Locke, MD, FACG2. 1. Mount Sinai Beth Israel, New York, NY; 2. Mount Sinai Beth Israel Medical Center, New York, NY.

[581A] Figure 1.


Flexible endoscopic treatment of Zenker’s diverticulum is well-established using different techniques including freehand electrosurgical incision with or without a standard distal endoscope cap. The only purpose-designed accessory is a slotted overtube which is not available in the US. We describe our experience with a novel cap in performing cricopharyngeal mucomyotomy. An 85 year old man with a past medical history of subdural hematoma requiring two craniotomies, asthma and hypothyroidism presented with progressively worsening dysphagia, regurgitation and weight loss over two years. Social history was significant for cigar smoking for over forty years.


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Evaluations showed normal motility with the oropharyngeal phases of his swallowing mechanism, no cervical lymphadenopathy, and all cranial nerves were intact. Two esophagrams were performed over the course of six months which showed an enlarging 3 centimeter Zenker’s diverticulum on the posterior wall of the proximal esophagus. Otolaryngology evaluated the patient for stapler diverticulotomy. However, our patient had a limited ability to open his jaw with an inter-incisor distance of 28 millimeters. Thus, rigid endoscopic repair

could not be performed and surgical repair was recommended. Upon patient’s request, he was referred to gastroenterology for further evaluation. We performed a flexible endoscopic Zenker’s mucomyotomy using the Carr-Locke Cap. The mucomyotomy was performed without complication and the patient had complete recovery and symptom resolution at 1 month follow up. At that time repeat upper endoscopy showed a healed scar at the site of the mucomyotomy. The Carr-Locke Cap is a purpose-designed clear, soft, plastic distal attachment with one long and one short ‘blade’ placed on the end of the endoscope to help separate the esophagus from the Zenker’s diverticulum. The cap allows isolation of the cricopharyngeal ‘septum’ in the slot between the blades, permits advancement of the endoscope and cap as one unit and automatically determines when the incision is complete by passage of the cap into the esophagus with the endoscope. This endotherapy technique was successfully performed in eight patients with 100% clinical success at one month and with no adverse events. No patients reported symptom recurrence and no repeat treatments were required. This technique may become the new standard for endotherapy of Zenker’s diverticulum.

584 Rendezvous With a Twist: Novel Guide Wire Manipulation Helps Traverse a Tortuous Esophageal Stricture Eric Yoon, MD1, George Protopapas, MD2, Weizheng Wang, MD2. 1. Rutgers New Jersey Medical School, Bloomfield, NJ; 2. Rutgers New Jersey Medical School, Newark, NJ.

[583A] Figure 1.

The management of tortuous esophageal strictures can often pose a technical challenge. Esophageal strictures may confer morbidity in the form of medical, nutritional and psychiatric disease. A 33-year-old man with history of caustic inhalational injury had progressive dysphagia to solids and liquids causing undesired weight loss. Serial attempts at endoscopic esophageal dilatation were attempted yet unsuccessful, necessitating percutaneous enterocutaneous gastrostomy (PEG) tube placement for feeds. The emerging popularity of retrograde endoscopy and rendezvous techniques, also known as combined anterograde retrograde dilation, or CARD, has provided an additional tool in our armamentarium in the therapeutic intervention of esophageal strictures. While reaching the esophageal stricture is half of the battle, traversing the stricture comprises the other half of the challenge. We describe how the simple bowing and external rotational movement of a guidewire can help create additional tension within a guidewire, which was necessary for successful navigation through a long zig-zag stricture. Ultimately this technique, as if operating a rotating crankshaft, allowed for a return to a life of normalcy as far as nutritional intake is concerned as the patient was able to resume oral intake for nutrition and weight gain.

[583B] Figure 2.

[583C] Figure 3.


[584A] Figure 1.


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Abstracts lowed by myotomy of the longitudinal muscle. The POEM procedure was initiated with the mucosal tunnel starting at 10 cm and the myotomy at 8 cm above the gastroesophageal junction (GEJ) and was continued for 2 cm distal to the GEJ. Given this patient’s presentation with Type III Spastic Achalasia, the myotomy was extended 5 cm to increase the length of the myotomy to 13 cm. We used SURGIFLO, an absorbable hemostatic gelatin, to fill the submucosal tunnel. Post procedure the patient had an upper esophogram, which did not show any extravasation of contrast, and hemodynamic parameters were all within normal limits. SURGIFLO mixed with thrombin solution (from human plasma) is indicated in surgical procedures as an adjunct to hemostasis when control of bleeding by ligature or cautery is impractical. The gelatin matrix consists of cross linked gelatin granules allows for coagulation. It is an easy, inexpensive and safe modality that can be incorporated for use in POEM. We think this product may protect against delayed bleeding by providing a good sealant effect in the submucosal tunnel before closing the mucosal entrance with hemostatic clips. A prospective randomized study is needed to evaluate the efficacy of SURGIFLO during POEM procedure.

586 Triple Lumen Esophagus Arooj Babar, MD1, Moaz M. Choudhary, MD1, Jose Churrango, MD2, Sami Samiullah, MD2, Weizheng Wang, MD3. 1. Rutgers New Jersey Medical School, Bloomfield, NJ; 2. Rutgers New Jersey Medical School, Newark, NJ; 3. Division of Gastroenterology, Department of Medicine, Rutgers New Jersey Medical School, Newark, NJ.

[584B] Figure 2.

A 55 year-old-lady with history of HIV (CD 4+ count 268/ μL) was evaluated for a one day history of hematemesis. She had long-standing history of dysphagia and had history of G tube placement as a child. EGD on admission revealed ulcerated and friable distal esophageal mucosa. Blood was seen in the stomach and the area could not be examined well due to blood clots. Biopsy specimens from esophagus showed acute and chronic inflammation. Candida was seen however the stains for CMV, HSV I and II were negative. AFP smear and cultures were negative. An Esophagram was performed which showed collection of contrast material at aortic arch, likely secondary to contrast within a fistulous connection. There were also a few linear collections of contrast in the expected location of the gastroesophageal junction, also likely within tiny fistulous tracts. [Figure 1A]. Follow up EGD at 10 weeks showed a long mucosal bridge in the mid esophagus, giving esophagus a shape of double lumen [Figure 1B] .The distal esophagus near the GE junction separated into three lumens. [Figure 1 C] One was true GE junction and other two were fistulous tracts. The gastroscope itself could not be traversed through the fistulous tracts. Retroflexion showed openings of both fistulous tracts into stomach evident from secretions coming out of fistulous tracts. [Figure 1D]. Biospy specimens from the mucosal bridge in mid esophagus showed squamous mucosa with atypia and parakeratosis. Esophagogastric fistula is a rare condition. Term double lumen esophagus has been used for esophagogastric fistulas in literature when a neo-lumen is formed in the esophagus due to fistula. Only a few cases have been reported in literature. Our patient has two esophagogastric fistulas giving rise to a triple lumen esophagus. Typically patients with EG fistulas present with symptoms of dysphagia and have history of GERD, esophageal ulcers, strictures and dilations. Esophageal Crohn`s disease, carcinoma, fungal and viral infections needs to be ruled out in these patients with biopsy specimens and special staining. Treatment options include aggressive control of reflux disease and treatment of specific etiologies, which may be responsible for fistulas. Surgery remains the last option since these patients are generally poor surgical candidates due to repeated interventions and presence of inflammation.

[584C] Figure 3.

585 SURGIFLO® in the Tunnel: A Novel Technique to Decrease Post-POEM Bleeding Niket Sonpal, MD1, Sherif Andrawes, MD2, Gregory Haber, MD3. 1. Lenox Hill Hospital, Happauge, NY; 2. Staten Island University Hospital, Staten Island, NY; 3. Lenox Hill Hospital, New York, NY. In Peroral Endoscopic Myotomy (POEM) the creation of large wound surfaces can be a risk for delayed bleeding. Delayed bleeding in the submucosal tunnel is another rare complication and the bleeding can be concealed in the submucosal tunnel making diagnosis difficult. Proper POEM technique includes meticulous coagulation of all submucosal vessels with monopolar coagulation forceps. Substantial intraprocedural bleeding is one of the most feared potential complications. We present a case of a POEM procedure in which post 50 year-old diagnosed with Type III spastic Achalasia according to the Chicago classification presented for a POEM procedure. An esophageal manometry demonstrated abnormally increased resting pressures of the lower esophageal sphincter with simultaneous high-pressure spasm. It was then decided to proceed with a POEM procedure. Normal saline mixed with methylene blue was injected to raise the mucosal layer, which was dissected with a 1.5 dual knife at the 5 o clock position. Keeping the plane of the dissection in perspective the triangular tip (TT) knife was used to dissect the submucosal layer. Once the submucosal plane was dissected at the level, a submucosal tunnel was created along the line of the esophagus towards the distal esophagus into the lesser curvature. Upon completion of the submucosal dissection the scope was brought back to the lumen of the esophagus and positioned at in the submucosal window. Linear myotomy involving the circular muscle layer was performed fol-


[586A] Figure 1.


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Our patient was treated with PPI BID. She has improved symptoms of dysphagia. She is scheduled for a CT scan of chest and abdomen and a repeat EGD to access for healing and repeat biopsies. References: [1]. Samiullah S, Samad F, Tang YM, Abdullah N, Marium M, Shaikh Z, Brelvi Z, Wang W. Double lumen esophagus: a rare complication of gastroesophageal reflux disease. Dig Endosc. 2014 Mar;26(2):282-4. doi: 10.1111/den.12041. Epub 2013 Mar 5. PubMed PMID: 2346177.

587 Fixing a Rare Complication: Broncho-Esophageal Fistula in Late-Stage Squamous Cell Carcinoma Alexander Perelman, DO, MS1, Scott Harrison, BS2, Neil Sharma, MD3. 1. Yale University School of Medicine, New Haven, CT; 2. Indiana University School of Medicine, Indianapolis, IN; 3. Parkview / indiana University, Fort Wayne, IN. Case Summary: A 57-year-old male with a past medical history of alcohol and tobacco abuse presented with a cough and unintentional weight loss of 25 pounds. He reported a six-month history of dysphagia, to solids, and has had multiple episodes of aspiration pneumonia (PNA) in that time period. A Chest CT was preformed and demonstrated a left sided subcarinal mass occluding the bronchus and extending 2 cm into the left lower lobe. Bronchoscopy confirmed a nearly complete occlusion of the left lower lobe bronchus by the mass. Biopsy was consistent with non-keratinizing squamous cell carcinoma. Upper GI fluoroscopy showed dilation of the proximal esophagus with an apple-core lesion at the level of the carina. Esophagogastroduodenoscopy (EGD) with biopsy of the esophageal lesion was consistent with squamous cell carcinoma. Endoscopic ultrasound (EUS) confirmed the stage (IV) and helped to define the anatomy. Self-expandable metallic stents (SEMS) were placed in the esophagus and left bronchus, permitting closure of the airway-esophageal fistula (AEF.) The patient underwent chemotherapy and radiation with a good outcome. Discussion: The development of an airway-esophageal fistula (AEF) in advanced esophageal or lung cancers, though rare, is a dangerously debilitating condition. The AEF may also result secondary to

[587C] Figure 3.

patients undergoing radiation or chemotherapy treatment. AEF may lead to poor nutrition, deterioration of the airway, and pulmonary sepsis, threatening patient survival and inevitably diminishing quality of life. Modern advanced interventional endoscopy has enabled the precise placement of esophageal and bronchial stents, while reducing complications in the treatment of AEF. After stent insertion, there is immediate relief of dysphagia symptoms and termination of airway-ablating aspiration. Although plastic or silicone stents have been used in years past, SEMS have become the gold standard as they tend to better seal large defects, experience lower rate of migration, and demonstrate a greater increase in post-operative quality of life. In our patient with non-keratinizing squamous cell carcinoma of the esophagus, SEMS were used to effectively seal off an AEF successfully relieving him of dysphagia symptoms and recurring PNA.

588 Unusual Esophageal Presentation of Atherosclerosis of Thoracic Aorta Muhammad I. Ahmad, MD1, Yezaz A. Ghouri, MD2, Sushovan Guha, MD, PhD2. 1. University of Texas Health Science Center, Houston, TX, Tuvalu; 2. University of Texas Health Science Center, Houston, TX.

[587A] Figure 1.

[587B] Figure 2.


Introduction: Ischemic changes can occur in almost any segment of the GI tract but ischemic necrosis of esophagus is uncommon. The upper, middle and lower third of esophagus are supplied by the inferior thyroid artery, thoracic aorta, and left gastric artery respectively. Case Report: A 74-year-old woman with a history of hypertension, hyperlipidemia and diabetes presented to emergency room (ER) after being found down with severe lethargy and pre-syncope. She had an episode of vomiting and complained of chest pain. Initial physical exam was non-contributory and laboratory data showed consistent elevation in troponin I levels and a hemoglobin of 9.1 g/dL. She was initially evaluated with a CT angiogram of the chest which showed no evidence of pulmonary embolism but revealed diffuse atherosclerotic calcification of thoracic aorta. Subsequently a coronary angiogram was performed which showed non-occlusive coronary artery disease. She was incidentally found to have a deep vein thrombosis (DVT) in right lower extremity and was started on low-molecular weight heparin. She was also started on aspirin and clopidogrel for her underlying coronary artery disease. One

[588A] Figure 1.


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Abstracts day after her discharge she presented to the ER with hematemesis, nausea, and epigastric pain. Aspirin, clopidogrel and heparin were discontinued and she was started on an intravenous pantoprazole infusion. Upper GI endoscopy showed necrotic and friable mucosa with oozing of blood noted in upper and middle third of the esophagus (Figure 1). Rest of the endoscopic exam was normal. Histopathology of random biopsies of mid-esophageal necrotic areas showed frank necrosis with inflammatory/reactive changes. Subsequently hematemesis resolved as she was placed on oral pantoprazole and sucralfate. IVC filter was placed for her underlying DVT and low dose aspirin was started on discharge. Discussion: Atherosclerotic calcifications of the thoracic aorta can be indicative of ongoing ischemia of its esophageal branches which primarily supply the middle third and possibly lower part of upper onethird of the esophagus. A catheter based intervention like a coronary angiogram can dislodge atherosclerotic plaques which can potentially form atheroembolic occlusion of the esophageal branches of thoracic aorta leading to necrosis of primarily the middle third of the esophagus.

DNA PCR was elevated. Treatment was initiated with valganciclovir. The patient improved and her bleeding subsequently resolved. Discussion: CMV infection is common among donors and recipients prior to transplantation. Risk of CMV disease is elevated with transplant between CMV+ donor and recipient which increases with use of lymphocyte-depletion induction therapy, as seen in our case. In such patients primary prophylaxis with antiviral therapy decreases the incidence of significant CMV disease. It usually presents as mononucleosis-like illness and other organs can be involved. GI bleeding is caused by erosions or ulcerations however life threatening bleed is rare. Our case stresses the need to recognize invasive

589 A Case of a Bullet Penetrating the Esophagus Rebecca Tsang, MD1, Anoop Appannagari2, Jack Leya2. 1. Loyola University Medical Center, Chicago, IL; 2. Loyola University Medical Center, Maywood, IL. Purpose: We present a case of a bullet visualized during endoscopy after gun shot wound in which no surgical or endoscopic intervention was needed for a good outcome. Results: Patient is a 21 year old female with recent gun shot injury who came to emergency room complaining of epigastric pain. One month ago, she presented with gun shot wounds and was found to have three bullet fragments in her body—two fragments in her left leg and one large fragment between the esophagus and aorta without extravasation from heart, aorta or great vessel. Barium swallow study did not show any esophageal injury at the time. She had multiple medical complications during that hospitalization, including pneumomediastinum, right hemothorax and pneumothorax, and posterior mediastinal hematoma. Surgical removal of this bullet fragment was not done due to difficult positioning and risk associated with operative intervention. During the most recent admission, the patient presented with epigastric pain and nausea that became progressively worse the last few days. Swallowing exacerbated the pain. She denied difficulty protecting her airway, dysphagia, emesis, hematemesis, or hemoptysis. Initial CT scan was concerning for shift in position of bullet compared to previous imaging. Gastroenterology team was consulted, as it was difficult to discern if the bullet penetrated the esophagus. EGD was performed and the bullet was seen embedded in mucosa of the lower esophagus. Gastrograffin esophagram did not show any contrast extravasation. Aortogram showed no focal aortic or arterial injury. The surgery team discharged the patient without surgical intervention, as she was tolerating a diet and did not have evidence of vasculature injury. Few weeks later, plain films showed the bullet having migrated into the small intestine. One week later, the bullet was in the left colon. EGD and flexible sigmoidoscopy were performed without retained bullet. Esophageal mucosa was completely normal without any abnormalities. Conclusion: This is a case of a bullet that fully penetrated the esophagus over time without any complications. No surgical or endoscopic intervention was required, with the esophageal mucosa healing completely on its own.

[590A] Figure 1.


590 Case of Massive Gastrointestinal Hemorrhage Post Renal Transplant: A Diagnostic Conundrum Dhruv Lowe, MD, Shreya Sinha, Muhammad O. Arif, MD, Savio John, MD, Alfredo Valente. SUNY Upstate Medical University, Syracuse, NY. Introduction: CMV infection is a major cause of morbidity and mortality in immunocompromised patients. Renal transplantation confers an increased risk of UGI bleed however invasive CMV disease causing life threatening hemorrhage is a rarer entity. We describe a case of recurrent massive GI bleed due to invasive CMV disease which responded remarkably to timely antiviral treatment. Case: 34 yo female w/PMH of ESRD due to HTN was admitted for elective deceased donor transplant. Both the patient and donor were CMV +. Post transplant induction therapy with TAG-basilixumab was done followed by MMF-tacrolimus for maintenance. Further hospital course was complicated by renal vein thrombosis (s/p thrombectomy) and intestinal ischemic necrosis (s/p resection of 60 cm of jejunum). While in recovery, she had multiple episodes of melena and drop in hematocrit. PPI drip was initiated and EGD showed severe esophagitis, gastritis with large antral clot limiting further exam. Bleeding continued to recur and PRBC transfusions were needed. Angiogram was non-diagnostic however gastroduodenal artery was embolized without any success. Repeat EGD showed esophagitis with multiple duodenal ulcers, anastomosis site was clean. Esophageal biopsy was consistent with invasive CMV disease, serum CMV


[590C] Figure 3.


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CMV disease as an important cause of UGI bleed in renal transplant patients. Diagnosis is made with lab tests in appropriate clinical setting. In our patient with e/o esophagitis, duodenal ulceration, diagnosis was confirmed with elevated CMV DNA PCR levels and demonstration of CMV inclusions on biopsy. Treatment includes antiviral therapy such as ganciclovir or valganciclovir with reduction of immunotherapy. Conclusion: Our case highlights the importance of recognising invasive CMV disease as a causative agent of significant GI bleed in renal transplant patients. Also to recognize the importance of appropriate patient selection for primary prophylaxis against CMV disease to limit its incidence and associated morbidity post renal transplant.

591 Squamous Cell Carcinoma in the Achalasia Population: Case Series of Two Patients Kirbylee K. Nelson, MD1, Steven B. Clayton, MD2, Cynthia Harris, MD 3, Khaldoun Almhanna, MD 3, Jon Finan, MD, PhD4, Prasad Kulkarni, MD, FACG 5, Joel Richter, MD, MACG2. 1. Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL; 2. University of South Florida, Tampa, FL; 3. Moffitt Cancer Center, Tampa, FL; 4. Tampa General Hospital, Tampa, FL; 5. James A. Haley Veterans Hospital, Tampa, FL. Delayed esophageal emptying in achalasia leads to food stasis and mucosal irritation predisposing patients to an increased risk of developing squamous cell carcinoma (SCC). Currently, there are no guidelines regarding surveillance endoscopy. We present two cases of longstanding achalasia with subsequent development of SCC of the esophagus. A 56-year-old female with achalasia diagnosed at age 18 status post myotomy presented with a twomonth history of fatigue, weight loss, and burning upper abdominal pain. She had previously undergone dilations every few years as needed for dysphagia and regurgitation. She appeared cachectic but her physical exam was otherwise unremarkable. Computed tomography (CT) showed a dilated esophagus with debris and retained contrast with a large hiatal hernia and multiple radiopaque densities. Esophagogastroduodenoscopy (EGD) was notable for a large, friable, necrotic biopsy proven invasive SCC. Endoscopic ultrasound (EUS) revealed invasion beyond the muscularis propria and positron emission tomography (PET) confirmed metastasis. She underwent radiation and palliative chemotherapy but died of complications from extensive disease burden.

[591C] Figure 3.

A 62-year-old male with achalasia status post Nissen fundoplication performed 36 years ago presented with a painful, enlarging right submandibular mass. He suffered longstanding dysphagia requiring repeated dilations and was restricted to a soft liquid diet. Exam was notable for a firm, tender mass in the submandibular triangle with diminished tongue mobility due to mass effect. Fine needle aspiration was consistent with SCC. PET scan performed to locate the primary malignancy was notable for a suspicious lesion in the esophagus. Barium swallow and EGD confirmed massive esophageal dilation with a multifocal large segment area of filling defects in the distal esophagus and areas of mucosal ulceration. Biopsies were consistent with moderately differentiated SCC. He continues to receive palliative chemotherapy. The risk of SCC in achalasia ranges from 16 to 140-fold. The presence of a mega-esophagus with poor emptying is the most important factor in these patients having food stasis and secondary carcinoma. Age and duration of disease are merely surrogate markers for this critical physiological and anatomic aberration. We recommend initiating surveillance endoscopy in patients with achalasia 15 years after the development of symptoms with concomitant esophageal dilation or tortuosity.

592 An Incidental Finding of Esophageal Parakeratosis Daniel J. Waintraub, MD, Sam Serouya, MD, Caren Waintraub, MD, Emilio Madrigal, DO, Lan Sun Wang, MD. Mount Sinai Beth Israel Medical Center, New York, NY.

[591A] Figure 1.

Esophageal parakeratosis is an uncommon endoscopic finding of unknown clinical significance. We present a case of esophageal parakeratosis found in a 72 year-old male presenting with anemia and dark stools.

[591B] Figure 2.

[592A] Figure 1.



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Abstracts 593 Cricopharyngeal Muscle Hypertrophy: “Bar”rier Causing Upper Esophageal Food Impaction Padma Chamarthy, MD1, Hadie Razjouyan, MD2, Sita Chokhavatia, MD3. 1. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ; 2. Rutgers Robert Wood Johnson Medical School, Eaton Town, NJ; 3. Rutgers Robert Wood Johnson Medical School, Paramus, NJ. Introduction: Esophageal food impaction occurs in 13 per 100,000 people, usually in the distal esophagus due to luminal compromise from a peptic stricture or obstructing Schatzki’s ring. Impactions in the upper third of the esophagus are less common and can occur due to cricopharyngeal muscle (CPM) dysmotility, cervical spur, Zenker’s diverticulum, or esophageal webs. Antegrade bolus propulsion occurs when adequate pharyngeal pressure propels ingested bolus in the presence of coordinated relaxation of the CPM. Management of proximal esophageal food impaction is a challenge given the proximity of the impacted bolus to the airway and technical difficulties encountered during disimpaction maneuvers with a flexible endoscope. Case Report: 59 year old female with a history of hypertension, alcohol and drug abuse, cervical spine injury presented an hour after choking on pork. She reported similar symptoms and intermittent dys-

[592B] Figure 2.

[593A] Figure 1.

[592C] Figure 3.

A 72 year-old man with a past medical history of paroxysmal atrial fibrillation on anticoagulation, diabetes mellitus type two, stage four chronic kidney disease and iron deficiency anemia on iron supplementation presented with anemia and black stools for 3 days. He also reported chronic abdominal distention and constipation. He denied any use of non-steroidal anti-inflammatory drugs, alcohol intake, or history of gastrointestinal bleeding. Physical exam was notable for a soft, mildly distended abdomen with mild tenderness to palpation diffusely without rebound or guarding. The digital rectal exam was unremarkable. Lab work was significant for a hemoglobin (Hb) of 5.2g/dL (baseline Hb – 7.5g/dL), MCV of 91.7FL, platelets of 275,000/uL, INR of 2.1 and a positive fecal occult blood test. Computed tomography of the abdomen showed diverticulosis and possible diverticulitis. Th e patient was started on piperacillin-tazobactam and an esomeprazole drip. He was transfused one unit of packed red blood cells. When hemoglobin levels were stable, he underwent upper endoscopy which did not demonstrate a source of bleeding, however it was significant for non-bleeding erosive gastropathy and stripes of dark thickened mucosa in the distal esophagus and gastroesophageal (GE) junction (Figure 1), which was biopsied. Pathology revealed squamous esophageal mucosa with detached parakeratotic superficial mucosa (Figures 2 and 3). The patient improved clinically and was discharged home. Esophageal parakeratosis has been described endoscopically as multiple strips of linear plaques or mucosal thickening with orderly displayed rings and furrows. This endoscopic appearance can mimic that of esophageal dysplasia or malignancy. Parakeratosis has been associated with esophageal cancer and alcoholic cirrhosis, however no clear correlation is known. In the clinical setting, gastroenterologists must be aware that while the endoscopic appearance of parakeratosis may mimic neoplastic lesions, its clinical significance and malignant potential are unknown.

[593B] Figure 2. © 2015 by the American College of Gastroenterology


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phagia to solids for many years without prior endoscopic evaluation. Occasional solid food impaction was usually completely relieved after drinking copious amounts of fluids or Heimlich maneuver delivered by her husband. She visited emergency room after none of the previous interventions provided relief. She had been drooling since the choking event, but was able to talk in full sentences. She did not have a laryngeal stridor. Vital signs and oral exam were unremarkable. Chest xray and lateral neck X ray did not reveal opaque intraluminal esophageal density. Neck CT showed a food bolus in upper third of esophagus, figure 1. At endoscopy, solid food bolus was encountered just below the upper esophageal sphincter (figure 2). Zenker’s diverticulum was not seen either on CT or endoscopy. The impacted food bolus was removed piecemeal using multiple endoscopic accessories including Roth net, snare and tripod. The adult gastroscope was switched to a pediatric endoscope and the remaining food bolus was pushed into the distal esophagus and subsequently the stomach. Following removal of the impacted bolus, a barium swallow to rule out esophageal injury showed CPM hypertrophy (hypopharyngeal bar), figure 3. As the patient’s dysphagia relieved, she had immediate travel plan, she elected to defer further evaluation for her dysphagia with a modified barium swallow and esophageal manometry. Discussion: CPM hypertrophy should be considered in patients who present with food bolus impaction in the proximal esophagus. Cricopharyngeal bar causing dysphagia is encountered more commonly in the older adult. Treatment options include endoscopic or surgical myomectomy, botulinum toxin injection, or esophageal dilatation.

594 Primary Pemphigus Vulgaris of the Esophagus Christopher Nguyen, DO1, Michael Baek, DO2, Gati Goel, MD, PhD1. 1. Loma Linda University Health, Loma Linda, CA; 2. Loma Linda University Health, Loma Linda, CA. Pemphigus vulgaris (PV) is an autoimmune blistering disease associated with symptomatic involvement of the skin and mucous membranes. Most patients present with fragile, bullous oral lesions. Though the esophagus is lined with stratified epithelium, PV rarely involves the entire esophagus1. Prior study has shown that patients with esophageal involvement manifest as dysphagia (57%) and odynophagia (21%), whereas hematemesis is seen in only 3.5% cases2. Here we describe an atypical case of PV isolated to the esophagus wherein endoscopy was critical in diagnosis. A 48 year-old male with no significant medical problems presented with a 2-month history of dysphonia and pharyngeal discomfort with associated 20-pound weight loss. He described severe, sharp pain localized to the posterior tongue and pharynx, worse with swallowing. He had tried Azithromycin without improvement in symptoms causing him to seek further care. His exam showed injected conjunctiva, palatal and pharyngeal erythema with white exudates on the tongue. He was started on Nystatin for presumed fungal esophagitis, laryngoscopy showed oropharyngeal white patches, but with negative cultures. Initial EGD showed friable, erythematous mucosa with severe esophagitis; biopsies were consistent with Herpes Simplex, thus the patient was started on Acyclovir. He had persistent symptoms on week 2 of Acyclovir treatment. This prompted a repeat EGD which revealed circumferential erythema, mucosal sloughing involving almost the entire esophagus to the gastroesophageal junction (Figure 1). The biopsies showed suprabasilar acantholysis with papillomatous features and scattered dyskeratotic cells most consistent with PV (Figure 2). Subsequently he was seen by dermatology, who initiated steroid therapy resulting in a dramatic response. This case highlights the importance of endoscopy in the diagnosis of primary esophageal PV, especially in the absence of skin lesions. Dysphagia and odynophagia are common presenting symptoms in esophageal PV, similar to infectious esophagitis. Physical exam is often nonspecific resulting in an incorrect diagnosis and improper treatment. Evaluation with upper endoscopy is prudent in patients with unclear diagnosis in order to properly guide management.

595 Dysphagia After Total Gastrectomy Hadie Razjouyan, MD1, Amy Tilara, MD2, Sita Chokhavatia, MD3. 1. Rutgers Robert Wood Johnson Medical School, Eaton Town, NJ; 2. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ; 3. Rutgers Robert Wood Johnson Medical School, Paramus, NJ. Introduction: Dysphagia after total gastrectomy can occur in 60-70% of patients post operatively due to alkaline reflux (20-50%), esophageal dysmotility (80-90%) and iatrogenic damage to the vagus nerve, recurrence of gastric cancer (70%), and anastomosis stricture (4.1 %), or paraneoplastic syndrome. Case report: A 73 year old woman was diagnosed withgastric body adenocarcinoma (T3 N2) in February 2012. She underwent neoadjuvant chemoradiation therapy followed by a total gastrectomy on July 2012. Two months after surgery, she developed progressive dysphagia to solids and eventually liquids. The patient subsequently had her first endoscopy 2 months post surgery. A nonobstructing benign anastomotic stricture was dilated up to 18 mm with a TTS CRE balloon dilator for symptom management. Dysphagia symptoms improved for a short period of time after each procedure; however, her symptoms would recur within weeks despite empiric dilation of the anastomosis. She was unable to meet daily caloric requirements and given her significant weight loss, enteral access was then obtained via a percutaneous endoscopic jejunostomy. A PET scan, tumor markers and CT scans did not reveal recurrence of her gastric cancer. The patient eventually was unable to swallow her saliva and hospitalized for further management. A repeat upper endoscopy revealed a widely patent anastomosis. A modified barium swallow showed silent aspiration with thin liquids and retention of contrast in the lower esophagus above the esophagojejunal anastomotic site, figure 1. High resolution manometry (HRM) was performed to evaluate the severe esophageal dysmotility. The diaphragmatic pinch was seen on inspiration, aperistalsis in the lower two thirds of the esophagus, figure 2. The saline bolus during HRM failed to clear on impedance testing. Dietary interventions to add thickeners to fluids and swallow rehabilitation were subsequently initiated. The patient during this hospitalization, three years after initial diagnosis, was found to have metastatic disease in the retroperitoneum and patient elected hospice care. Conclusions: Our patient had a complicated course with early post-gastrectomy dysphagia. The benefit of empiric dilatations of a nonobstructing esophagojejunal anastomotic stricture was short-lived. The treatment options of esophageal dysmotility due to presumed vagus nerve injury is limited. The severe worsening of her dysphagia could be either due to unfortunately recurrence of gastric cancer or paraneoplastic syndrome as well. In patients with gastric cancer, management of postoperative dysphagia can be a challenge and etiologies could be multifactorial, as in our case. Benign and malignant causes need to be considered as they may occur synchronously.


596 Esophageal Foreign Body: The Case of the Missing Tooth Julia Shor, MD1, Hadie Razjouyan, MD2, Sita Chokhavatia, MD3. 1. Rutgers Robert Wood Johnson University Hospital, Highland Park, NJ; 2. Rutgers Robert Wood Johnson Medical School, Eaton Town, NJ; 3. Rutgers Robert Wood Johnson Medical School, Paramus, NJ.

[594B] Figure 2.


Introduction: Esophageal foreign bodies (FB) in adults are usually accidental rather than intentional ingestion of FB which may include fish bones (9-45%), bones (8-40%), and dentures (4-18%). Dental injury is one of the adverse effects of anesthesia, occurring in 1 in 5000 cases, more commonly in those with poor dentition or difficult laryngoscopy/intubation. Endoscopic removal of FB is recommended if the object size or shape or sharp edge poses risk of complication, is causing esophageal obstruction or a small FB remains in esophagus or stomach for over 24 hours or FB is considered valuable. We present a case of accidental dislodgement of partial denture during intubation for surgery which necessitated endoscopic retrieval in perioperative period.


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[595B] Figure 2.


Case Report: 43year old female underwent elective lumbar spine fusion with allograft and plates with screws due to L3-4 foraminal and extraforaminal herniated disc. Upon recovery from uneventful surgery under general anesthesia, she noted missing one post of molar tooth which she recalled. Patient expressed her displeasure to the anesthesiologist at the loss of expensive dental work. Chest X-ray confirmed the presence of esophageal FB consistent with the reported missing dental (the radiopaque post was seen at the level of the mid esophagus), figure 1. Although the patient was asymptomatic of chest


pain, dysphagia, odynophagia and handling secretions well, as the repeat imaging performed 4 hours and 6 hours later revealed no propagation of the FB. Emergent endoscopic retrieval of impacted mid esophageal FB was successfully performed using a Roth net, figure 2. The impacted post was returned to the patient.


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Discussion: Comprehensive preoperative examination includes oral exam for airway and should include dental examination for presence of loose teeth and dental implants in addition to attention to removable dentures. Dislodgment of dental implants during endotracheal intubation or endoscopic procedures (EGD, ERCP) can occur and may require emergent endoscopic FB retrieval. References: [1] Venkataraghavan K, Anantharaj A, Praveen P, Rani, SP. Accidental ingestion of foreign object: systematic review and report of a case. Saudi Dent J. 2011 Oct; 23(4):177-81. [2]. Warner ME, Benenfeld SM, Warner MA, Schroeder DR, Maxson PM. Perianesthetic dental injuries: frequency, outcomes, and risk factors. Anesthesiology 1999, 90(5);1302-5. [3]. Tang SJ. Endoscopic management of foreign bodies in the gastrointestinal tract. Video journal and encyclopedia of GI endoscopy 2013, 1(1);35-8. [4]. Management of ingested foreign bodies. Gastrointestinal endoscopy 2011 73(6) 1085-91

Severe Hyponatremia Associated With the Use of Pantoprazole

bleeding. This combination achieved HS for around 8 months after which he presented with recurrent melena. A second attempt at treatment with APC achieved initial hemostasis but bleeding recurred 2 days later. Cryo was offered to him to aid with his dysphagia and possibly hemostasis. On EGD a fungating tumor oozing blood was seen in the distal third of the esophagus. Cryo was performed with 15 second freeze cycles. The patient experienced significant improvement in his dysphagia and resolution of his melena. The patient expired 2 months later due to newly diagnosed brain metastasis without recurrence of his melena. ET of GIMB continues to be a challenge. Multiple modalities can be tried including standard hemostatic maneuvers. Bleeding often recurs and can become refractory. Hemospray has been reported to be effective in these situations but is not available in the United States. Cryo, proven effective in refractory benign bleeding and approved for tumor ablation was used successfully in this patient. Cryo effect at standard application duration is limited to the superficial 5 mm of tissue. In addition to tumor necrosis has the theoretical advantage of forming crystal in the microvasculature leading to thrombosis and possibly hemostasis. This is a case of long term hemostasis achieved by cryotherapy in a patient with refractory tumor bleeding. A prospective study is needed to determine whether these effects can be reproduced in other patients.

Jagdish Nachnani, MD1, Deepti Bulchandani, MD2, Sheetal Bulchandani3. 1. Sumner Regional Medical Center, Hendersonville, TN; 2. Sumner Medical Group, Gallatin, TN; 3. LT Medical College, Mumbai, India.

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Background: Many consider proton pump inhibitors (PPIs) to be devoid of adverse effects; however, PPIs can cause serious side effects. This case highlights a case where the patient kept getting PPIs and causing severe hyopnatremia leading to multiple hospitalizations. Case report: A 48 year old Caucasian male complaining of reflux and dysphagia was seen in clinic. The patient underwent an esophagogastroduodenoscopy (EGD) and was found to have a stricture which was dilated as well as Grade D esophagitis. In view of the same, the patient was started on Pantoprazole 40mg orally twice a day. Patient was admitted to the hospital in five days following that with mental status changes due to severe hyponatremia. He was treated with fluid restriction and discharged after the sodium was better. He underwent an extensive workup for the hyponatremia which included CT scans of the head, chest and abdomen but no reason was found for the same. He was admitted with a sodium of 108 mmol/L during that admission and tt was thought that this sodium was related to primary polydipsia. The patient was discharged again on Pantoprazole and was readmitted to the ICU with a low sodium after a week with similar symptoms. He had multiple admissions in a course of two months without any specific cause being found. Finally his Pantoprazole was discontinued and patient did not have any more exarcebations with low sodium or hyponatremia. Conclusion: This case highlights this rare adverse drug reaction of proton pump inhibitors, but given its ubiquitous use is normally not thought of in the differential of hyponatremia. As our patient developed hyponatremia multiple times without considering this reason, this case highlights the importance of this adverse drug effect.

Signet Ring Cell Adenocarcinoma of Esophagus: Case Report and Review of Literature Ami Panara, MD, Ashish Sharma, MD, Milena Gould. Suarez, MD. Baylor College of Medicine, Houston, TX. Introduction: There is an increasing prevalence of signet ring cell (SRC) type tumors in United States since the 1970s, with stomach being the most common site in the GI tract. However, SRC carcinoma of the esophagus and GEJ (gastro-esophageal junction) is infrequent. There is a paucity of published literature specifically relating to the biologic factors and overall prognosis of esophageal SRC carcinoma. Here we present an interesting case of esophageal SRC carcinoma, and review current literature regarding its epidemiology and prognosis. Case presentation: A 70 year old white male with history of long standing GERD, cigarette smoking, BMI of 32, compensated cirrhosis from Hepatitis C and alcohol presented with one month of dysphagia to solids. He denied odynophagia, and endorsed decreased appetite and a 30 lb. weight loss. Exam was significant for bilateral lymphadenopathy in the cervical and supraclavicular chains and poor air movement of bilateral lungs. CT imaging was significant for thickening of the distal esophageal wall, extensive and significant mediastinal, left axillary and proximal abdominal lymphadenopathy. PET scan

598 Successful Endoscopic Hemostasis with Cryotherapy for a Case of Refractory Esophageal Cancer Bleeding Manraj Khosla, MD1, Jeffrey Weber2, Tess Magat2, Weiss Glen2, Toufic Kachaamy3. 1. St. Joseph’s Hospital and Medical Center, Phoenix, AZ; 2. Cancer Treatment Centers of America, Goodyear, AZ; 3. Cancer Treatment Centers of America, Phoenix, AZ. Gastrointestinal malignancy bleeding (GIMB) can be a clinical challenge. Options for treatment include surgical resection, radiation, angiography with embolization and endoscopic treatment (ET). Currently there is no standard of care for ET of GIMB. Modalities tried in the past include epinephrine injection, contact thermal devices, argon plasma coagulation (APC) and hemoclip (HC) placement. Cryotherapy (cryo) is a modality used for tumor ablation. It has also been successfully used in treatment of benign bleeding such as radiation proctitis and gastric antral vascular ectasia. There is one case report of cryo use in refractory GIMB leading to short term hemostasis (HS). We present a case of long term HS achieved by cryo in a patient with refractory GIMB. A 51 year old male with a history of metastatic esophageal adenocarcinoma presented with melena. He was successfully treated with APC and was then referred for external beam radiation to prevent further

[598A] Figure 1.


[599A] Figure 1.

[599B] Figure 2.


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[599C] Figure 1.

demonstrated linear, intense FDG uptake with diffuse distal esophageal thickening from the carina extending to the esophagogastric junction. PET scan confirmed extensive bilateral mediastinal, left axillary and proximal abdominal wall lymphadenopathy, and also showed increased uptake in multiple bones in the axial and appendicular skeleton. EGD was performed and showed diffusely ulcerated mass in distal mass in the vicinity of esophageal varices. A 3 cm hiatal hernia was also present. Careful esophageal biopsies taken from distal esophagus showed poorly differentiated adenocarcinoma with SRC histology. Discussion: SRC is a rare histologic variant of esophageal adenocarcinoma that has been recently increasingly reported in the literature. Esophageal tumor location independently predicts poor prognosis in GEJ SRCs. Recent studies show that patients with a SRC of the esophagus or GEJ responded poorly to induction chemo-radiation therapy, and had decreased overall survival compared with patients with non-SRC histology. The SRC infiltrative characteristics may lead to a later onset of dysphagia compared with non-SRCs, and may explain the worse prognosis. Staging laparoscopy should be performed and an extended resection should systematically be attempted to achieve an R0 resection, which remains a major prognostic factor.

[600B] Figure 2.

600 Blood Brothers: Concurrent Duodenal Ulcer and Acute Esophageal Necrosis Illuminates the Pathogenesis of Black Esophagus Ryan A. McConnell, MD, Priya Kathpalia, MD, Michael Korn, MD. University of California San Francisco, San Francisco, CA. Introduction: Acute esophageal necrosis (AEN), also known as black esophagus, is a rare condition that tends to afflict older men with multiple comorbidities. Hypoperfusion is thought to be a key trigger in disease pathogenesis, with resultant heightened susceptibility to mucosal injury. Methods: We present a case of AEN with concurrent duodenal ulcer, which highlights the hypothesized vascular pathogenesis. Results: An 84 year-old man presented with nausea and severe sepsis from Klebsiella bacteremia. Medical history included insulin-dependent diabetes, hypertension, cerebrovascular disease, sple-

[600C] Figure 3.

nectomy, bladder cancer, and recurrent urinary infections. He developed hematemesis and painless hematochezia with 7-gram hemoglobin drop and 60 mmHg systolic blood pressure decrement. Risk factors for bleeding included occasional ibuprofen use and acute kidney injury. Esophagogastroduodenoscopy revealed circumferential black esophageal mucosa with white exudates extending continuously from 20 cm beyond the incisors to the gastroesophageal junction (Image 1). There was an abrupt transition to normal mucosa entering the stomach (Image 2). A 1.5 cm ulcer with adherent clot resistant to vigorous irrigation was found in the posterior duodenal bulb (Image 3). Esophageal biopsy revealed necrotic tissue with acute inflammation and no fungal organisms. Bleeding persisted despite gastroduodenal artery embolization, requiring 15 units of packed red cells. Bleeding ceased following duodenotomy with ulcer imbrication. The patient had no antecedent esophageal symptoms and did not develop dysphagia or odynophagia in the convalescent period. Following a normal upper GI barium series, he tolerated dietary advancement and was discharged on proton pump inhibitor therapy. Discussion: Duodenal bulb pathology often co-occurs with AEN owing to a common blood supply arising from branches off the celiac axis. As a relative watershed area, the distal esophagus is susceptible to ischemic injury in patients with underlying vasculopathy. We hypothesize that a flow-limiting celiac axis lesion may contribute to this concurrent pathology, and could predispose to recurrence with hypotensive events. In this case, the bleeding duodenal ulcer may have either caused the hypoperfusion or resulted from it. Sepsis preceded the bleeding and is a known co-factor in the development of AEN. Gastric outlet obstruction from bulb edema may promote further esophageal injury, but was not observed in this case.

[600A] Figure 1.



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601 Bullous Bleeding: Esophagitis Dissecans Superficialis in a Patient With Bullous Pemphigoid Jigar Bhagatwala, MBBS, MPH1, Muhammed Sherid, MD1, Siegfried Yu, MD2, Zunair Afghani1, Sumanth Daram, MD1. 1. Georgia Regents University, Augusta, GA; 2. Georgia Regents University, Evans, GA. Introduction: Esophagitis Dissecans Superficialis (EDS), characterized by sloughing of the esophageal epithelial lining, is a rare endoscopic finding. Causes include medications, hot beverages, celiac disease, collagen vascular diseases, idiopathy, and autoimmune bullous dermatoses (ABDs), such as Bullous Pemphigoid (BP) and Pemphigus Vulgaris (PV). Symptoms include dysphagia, odynophagia, and heartburn; vomiting of mucosal casts and hematemesis rarely occurs. We present a patient with BP and EDS with upper gastrointestinal bleeding (UGIB). Case: A 54 year-old female with a medical history of end stage renal disease, due to hypertension, status post renal allograft transplant, with graft failure on hemodialysis, presented to the emergency department (ED) with hematemesis. For 2 weeks she had worsening oral ulcerations and hematuria and 6 hours prior, she had severe nausea, burning chest pain, and 4-5 episodes of bright red vomitus. With 1 episode, she saw a “½ foot” long grayish-white soft tissue-like material. In the ED, she was hypertensive and tachycardic, with cutaneous blisters at various stages of healing. Hemoglobin was 7.1 g/dL, from 8.1 g/dL 2 weeks prior. An urgent EGD revealed mucosal sloughing involving the entire esophagus and posterior oro-pharynx, with associated clots and bleeding. Biopsy was deferred. Further history indicated she had a 4 month history of skin blisters and oral ulcerations, occurring after her transplant immunosuppresants were withdrawn, and was diagnosed with BP. Workup revealed a BP180 IgG > 150 units (normal < 9) and skin biopsy showed linear basement membrane pattern staining for IgG and C3 antibody. Her esophageal findings were attributed to her underlying BP. With PPI therapy, high-dose methylprednisolone, and mycophenolate mofetil she had significant improvement with resolution of hematemesis. A repeat endoscopic evaluation was declined. Discussion: Hematemesis with vomiting of esophageal mucosal casts is a rarely reported presentation of EDS. EDS has many potential causes, and recently, the pathophysiology and relationship between EDS and ABDs such as BP and PV have been increasingly acknowledged in the literature. Conclusion: EDS should be considered in patients who present with hematemesis and/or report of vomiting esophageal mucosal casts; endoscopic findings of exfoliative esophagitis support the diagnosis. These clinical findings should lead to consideration of ABDs as an etiology, to guide appropriate management decisions.

[602B] Figure 2.

602 A Unique Case of Alpha-Fetoprotein-Producing Esophageal Adenocarcinoma Jeremy Wang, MD1, Wendy Liu, MD2, Keyur Parikh, MD2, Anthony Post, MD2. 1. Ronald Reagan UCLA Medical Center, Fremont, CA; 2. University Hospitals Case Medical Center, Cleveland, OH. Alpha-fetoprotein (AFP)-producing esophageal adenocarcinoma (EAC) is a rare occurrence. Elevation of serum AFP is commonly associated with hepatocellular carcinoma and yolk sac tumors, but has also been reported in patients with other malignancies, most notably of gastrointestinal origin. However, the organs of origin typically include gastric, pancreatic, and biliary, but rarely esophageal. Here, we report a case of an AFP-producing EAC. A 51 year-old previously healthy man presented with new onset severe acid reflux and a weight loss of 35 pounds over a 2 week duration. He also endorsed 2 days of non-bloody emesis, but denied dysphagia or regurgitation of undigested food. Physical exam was only remarkable for right upper quadrant tenderness. The patient was slightly anemic with a hemoglobin of 12.8 g/dL. Elevated labs included: AST 66 U/L, ALT 81 U/L, CEA 6.4 ug/L, CA 19-9 317443 U/mL, and AFP 2524 ng/mL. Hepatitis B surface antigen and hepatitis C antibody were non-reactive. Computed tomography (CT) scan of the abdomen revealed abnormal thickening of the esophagus and multiple masses throughout the liver consistent with metastatic disease. CT-guided biopsy of one of the masses revealed CDX-2 positive adenocarcinoma, suggesting gastrointestinal origin. Subsequent upper endoscopy revealed a large, partially-obstructing mass in the lower third of the esophagus, the assumed primary source. Biopsy of the mass revealed ulcerated glandular mucosa with high grade dysplasia, with

[602C] Figure 3.

likely underlying malignancy. One month later, the patient underwent palliative esophageal stent placement. He was scheduled to begin FOLFOX/Herceptin therapy, but expired a week later. EAC is typically found in the lower third of the esophagus, and is associated with Barrett’s esophagus, smoking, obesity, and epidermal growth factor polymorphisms. A previous study attempting to determine possible tumor markers in patients with esophagus cancer reported serum AFP levels >5 ng/mL in up to 18% of EACs, with the highest reported AFP level being 320ng/mL. However, to the best of our knowledge, our case is only the 14th AFP-producing EAC to be thoroughly described in the English literature. Patients with EAC and cirrhosis often share common risk factors that make the differential diagnosis of liver masses and elevated AFP challenging. Some AFP-producing EACs contain cells resembling hepatic cells and are termed hepatoid EAC. Although not possible in our case, serial measurement of serum AFP level may be useful for monitoring clinical status and response to treatment. Most cases are treated with surgery and adjuvant chemotherapy but with disappointing results given the advanced presenting stage, high liver metastatic potential, and poor prognosis of AFP-producing EAC.

603 A Unique Case of Esophageal Leiomyoma Sabrina Jones, MD, Jennafer Ottenheimer, MPH, PA-C, Peter J. Sargon, MD, A. Aziz Aadam, MD. Rush University Medical Center, Chicago, IL.

[602A] Figure 1.


Introduction: Esophageal leiomyomas are rare in the GI tract, but the are most common mesenchymal tumor affecting the esophagus. Leiomyomas constitute less than 1% of esophageal neoplasms.


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Abstracts Case Report: A 31 year old female presented to an outside hospital with three months duration of chest pain and shortness of breath. She also endorsed intermittent dysphagia to solids and liquids, night sweats, and fatigue. Her past medical history was notable for an eight pack year smoking history. A barium esophagram was performed and was unremarkable. CT scan of the chest was obtained and showed a mediastinal mass either immediately adjacent to or arising from the esophagus that was creating mass effect on the trachea. A CT guided biopsy was performed revealing squamous cell carcinoma of the lung. The patient was referred to our academic center for further evaluation and management. The patient’s pathology specimens were reviewed and only fragments of squamous epithelium with inflammatory atypia were identified and there was no evidence of malignancy. An EGD was performed and a subepithelial lesion was identified in the cervical esophagus which was compressing the lumen. Endoscopic ultrasound (EUS) was notable for a 6cm anechoic, cystic lesion without any solid component that appeared to arise from the submucosal layer of the esophagus. Given its classic appearance, the lesion was thought to be a duplication cyst and biopsy was not performed due to infection risk. Because of the symptomatic nature of the lesion, patient ultimately underwent thoracotomy with enucleation of the esophageal mass and pathology was consistent with leiomyoma. The patient’s symptoms resolved following surgery. Discussion: This case illustrates a rare endoscopic appearance of esophageal leiomyoma. Leiomyomas generally appear as hypoechoic, well circumscribed lesions in the muscular propria or muscularis mucosae. These lesions are more commonly in the mid to distal esophagus and occur more commonly in men. This lesion was unusual as it was anechoic on EUS, which is often a characteristic of a duplication cyst. References: Shami, Vanessa M., and Michel Kahaleh. Endoscopic Ultrasound. New York: Humana, 2010.

604 HIV-Associated Idiopathic Esophageal Ulcers Roger Nehaul, MD1, Ashley H. Davis-Yadley, MD2, Miguel Lalama, MD, MPH3, Sahab Mustafa, MD2, Haim Pinkas, MD4. 1. University of South Florida, Morsani College of Medicine, Valrico, FL; 2. University of South Florida, Morsani College of Medicine, Tampa, FL; 3. Digestive Diseases and Nutrition, Morsani College of Medicine, University of South Florida, Brandon , FL; 4. Digestive Diseases and Nutrition, Morsani College of Medicine, University of South Florida, Tampa, FL. While thought to be a rare diagnosis and one of exclusion, HIV-associated idiopathic esophageal ulcers may be more prevalent than initially thought. A small study of 51 patients with HIV showed 49% of esophageal ulcers were idiopathic in nature, as opposed to approximately 1.1% in immunocompetent patients.6 Underdiagnosis may be due to lack of endoscopic evaluation in patients with ulcer symptoms as well as high mortality in patients with the degree of immunosuppression needed to develop such ulcers.1 We present the case of a 32-year-old male with no significant past medical history presenting with atypical chest pain. The pain was described as crampy, midsternal pain exacerbated by eating over one month accompanied by dysphagia to solids and liquids. The patient was ruled out for acute coronary syndrome. Initial laboratory testing revealed pancytopenia with eosinophilia and lymphopenia. HIV testing was positive with a CD4 count of 12. He was started empirically on fluconazole for suspected candida esophagitis. After no improvement, an EGD was performed showing numerous ulcers throughout the esophagus with no signs of bleeding. Biopsies were negative for CMV, HSV, fungal infection or neoplasia. The diagnosis of HIV-associated idiopathic esophageal ulcers was made. He was started on prednisone 40mg daily for 1 week with a taper over 1 month, pantoprazole 40mg twice daily and GI cocktails (Maalox™, viscous lidocaine, donnatal) for symptomatic relief. Follow-up EGD two months later revealed healing ulcers significantly improved from prior examination. Idiopathic esophageal ulcers in HIV-infected patients may be underdiagnosed and should be considered in patients who presenting with dysphagia and immunosuppression who do not respond to empiric treatment for infectious causes. When found, treatment includes antiretroviral therapy in combination with corticosteroids or thalidomide.2,3 Thalidomide is thought to stimulate the production of T cells, inhibiting HIV by interfering with TNF and mRNA.4 In patients with severe neutropenia, however, thalidomide is not an option and steroids may be used. Although, the mechanism is unknown, steroids have been demonstrated as an effective treatment option.3,5


[604B] Figure 2.

605 Esophageal Leiomyoma Presenting as Achalasia

[603B] Figure 2.

Rahul Kataria, MD1, Ashil Gosalia, MD1, Baharak Moshiree, MD, MS2, Amar R. Deshpande, MD3. 1. University of Miami/Jackson Memorial Hospital, Miami, FL; 2. University of Miami, Leonard M. Miller School of Medicine, Dept of Medicine, Division of Gastroenterology, Miami, FL; 3. University of Miami, Leonard M. Miller School of Medicine, Dept of Medicine, Division of Gastroenterology, Miami Beach, FL. A 26-year-old woman with a history of Down syndrome presented with nausea and vomiting for 5 months duration. The family noted difficulty initially with solids, which then progressed to liquids. Vomiting occurred immediately after any oral intake along with a 50-pound weight loss over several weeks with some volume depletion prompting hospital admission. Barium swallow revealed near complete tapering of the distal esophagus at the level of the gastroesophageal junction (GEJ), with



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[605A] Figure 1.

[605B] Figure 2. [605C] Figure 3. no passage of contrast seen. Upper endoscopy revealed a dilated, boggy, and aperistaltic esophagus with a tight lower esophageal sphincter (LES) and no evidence of extrinsic compression or mass in the cardia or esophagus. Neonatal endoscope was required to traverse the LES. High resolution esophageal manometry was performed showing an increased LES pressure of 104.8 mmHg, IRP of 73.8 mmHg, and aperistalsis consistent with type 1 achalasia (Image 1). With such an elevated LES pressure and IRP, there was concern for a possible extrinsic esophageal mass. Contrast chest CT demonstrated a possible submucosal soft tissue mass at the level of the GEJ concerning for pseudoachalsia (Image 2). Endoscopic ultrasound (Image 3) showed thickening of the distal esophagus and a lesion in layer 4. Core biopsy of the mass was consistent with leiomyoma. Laparoscopy was then performed with resection of lower esophageal leiomyoma, stricturoplasty, Heller cardiomyotomy and Dor fundoplication. Although the above presentation has been shown in previous case reports, it has been done in association with Alport’s Syndrome, a hereditary disease that has been found to co-exist with diffuse leiomyomatosis. Demonstration of an isolated esophageal leiomyoma presenting as pseudoachalsia on high resolution esophageal manometry and upper endoscopy has only been shown in one previous case. (Katzka et al, 2012). This case highlights the importance of differentiating achalasia versus pseudoachalasia even in the absence of a cardial mass. With an elevation in both IRP and LES pressure, as well as difficulty traversing the GEJ with a neonatal scope, an extrinsic mass must be considered as part of the differential.


The importance of utilizing multiple diagnostic modalities to correctly manage and diagnose motility disorders is shown, as pseudoachalasia can very closely mirror achalasia findings. A rare presentation of a benign tumor could very easily be mistaken for true achalasia.

606 Esophageal-Pericardial Fistula: A Rare Complication of Atrial Fibrillation Catheter Ablation Treated Successfully With an Esophageal Stent Vipin Verma, MBBS1, Poonam Bhyan, MD2, Jigar M. Patel , MD3, Vipul Madhwani, MBBS2, Gustavo S. Guandalini, MD4. 1. Internal Medicine, Georgetown University Hospital / Washington Hospital Center, Silver Spring, MD; 2. MedStar Washington Hospital Center, Washington, DC; 3. MedStar Washington Hospital Center, Hyattsville, MD; 4. MedStar Washington Hospital Center, New York, NY. Esophago-pericardial (EP) fistula is a rare complication of atrial fibrillation (AF) ablation, with an incidence reported as < 0.05%.1 Surgery is the mainstay of treatment, but there are few cases treated with


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Abstracts 5/5 foot plantar and dorsiflexion. The patient had intact sensation, cranial nerves, and mental status. Lumbar puncture showed a mild lymphocytic pleocytosis, negative cultures, and normal glucose and protein. Additional testing including CSF VDRL, Lyme and Borrelia PCR, and paraneoplastic antibodies were negative. The Centers for Disease Control and Prevention (CDC) was contacted and the botulism antitoxin was delivered and administered on the fourth day post-procedure. She was also trialed on pyridostigmine. Unfortunately, the patient developed bulbar symptoms and her muscle strength continued to worsen, reaching 0/5 in all extremities, with gross hyporeflexia and hypotonia. She had a lengthy and complicated hospital course marked by multiple intubations and infections. Ultimately, her family elected to withdraw care and the patient died soon thereafter. Current treatment guidelines for achalasia recommend either graded pneumatic dilation or laparoscopic surgical myotomy with partial fundoplication. Patients who are not candidates for those procedures can receive botulinum toxin therapy and if they fail that, should receive pharmacological therapy. Botulism has been observed as a complication in other uses of botulinum toxin. With supportive care, there can be significant improvement of symptoms within weeks to months. We hypothesize that the inadvertent injection of toxin into a nearby blood vessel at the esophageal sphincter caused systemic circulation of the toxin, resulting in severe botulism. To our knowledge, this is the first case of botulism as a complication of endoscopic BTI. Hospital Course:

[607]

Patient presents with coffee ground emesis. Upper endoscopy shows clean-based gastric ulcers as well as possible achalasia.

Days 4–9

Upper GI series confirms the diagnosis of achalasia. Patient receives repeat upper endoscopy with injection of 80 units of botulinum toxin. Within one day of injection, patient begins to develop signs of botulism.

Days 10–13

Lumbar puncture shows mild lymphocytic pleocytosis, negative cultures, normal glucose, and normal protein. The CDC is contacted as the patient’s clinical status deteriorates. The antitoxin is delivered and administered and the patient is also trialed on pyridostigmine.

Week 2

Patient’s respiratory status worsens and she is intubated for impending respiratory failure.

Weeks 3–17

Patient eventually receives a tracheostomy and PEG tube. Her hospital course is complicated by a critical illness polyneuropathy as well as multiple hospital-associated infections. The patient’s family ultimately elects to withdraw care and the patient dies after an approximately seventeen week hospitalization.

[606A] Figure 1.

esophageal stenting. We present a case of EP fistula developed after AF ablation and treated with esophageal stenting. An 80 year old woman presented with shortness of breath, fever, confusion and hypoxia three weeks after AF ablation. During this procedure, she underwent pulmonary vein isolation and ablation of complex fractionated electrograms. Besides persistent AF, she also had COPD and GERD. She had similar symptoms ten days prior to this presentation, when she was empirically treated for pneumonia with only minor improvement. Her home medications were apixaban, diltiazem, digoxin, and albuterol inhaler. Initial laboratory analysis showed leukocytosis (WBC 15k/μL), hypoxemia (PAO2 60 on 3L NC), cardiomegaly and left pleural effusion on chest X-ray. Echocardiogram revealed severe pericardial effusion, for which she underwent pericardiocentesis. Pericardial fluid was exudative, with WBC 5,300/mm3 with 92% neutrophils, amylase 204 and Candida albicans on culture. The patient was intubated for hypoxic respiratory failure, and a chest CT with oral contrast revealed the EP fistula in the mid to distal esophagus, as well as small pneumopericardium and moderate left pleural effusion. Flexible esophagoscopy showed anterior esophageal perforation at 32 cm from the incisors. A covered esophageal stent (Alimaxx 18 x 100 mm) was deployed and a left sided chest tube were placed. The patient was treated with antifungal and antibiotics during hospitalization, with significant improvement and discharge home within 10 days. EP fistula is associated with very high morbidity and mortality, so early diagnosis with immediate intervention is critical2. As AF ablation becomes more commonly performed, we should expect an increased incidence of its complications; EP fistula is more associated with complex fractionated electrogram ablation. Our case is unique given it is a rare complication of AF ablation and successful treatment of EP fistula with esophageal stenting. References: [1]. Cappato R et al. Updated worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circ Arrhythmia Electrophysiol 2010;3:32-8. [2]. Dagres N et al. Rapid detection and successful treatment of esophageal perforation after radiofrequency ablation of atrial fibrillation: lessons from five cases. J Cardiovasc Electrophysiol 2006;17:1213-5.

607 Botulism in a Patient Treated With Intrasphincteric Botulinum Toxin for Achalasia Ahmed Khan, MD1, Geoffrey You, MD2, Gary Forester, MD3, Hatim Youssef, DO4. 1. Rutgers Robert Wood Johnson Medical School, Bloomfield, NJ; 2. Rutgers Robert Wood Johnson Medical School, Newark, NJ; 3. University Medical Center of Princeton at Plainsboro, Plainsboro, NJ; 4. University Medical Center of Princeton at Plainsboro, Kendall Park, NJ. Intrasphincteric botulinum toxin injection (BTI) is used as a treatment for achalasia as it theoretically brings the lower esophageal sphincter back to a resting tone by blocking presynaptic release of acetylcholine. We present a rare case of botulism in a patient who received a botulinum toxin injection for achalasia. The patient was a 90-year-old female with a past medical history of coronary artery disease and gastroesophageal reflux who initially presented with coffee-ground emesis. Upper endoscopy found two non-bleeding linear gastric ulcers but also retained food in the stomach, suggestive of achalasia. This was confirmed on a subsequent barium swallow. Due to the patient’s overall frail condition, she received a botulinum toxin injection instead of pneumatic dilaton or myotomy. Within one day, the patient began to develop a worsening descending paralysis, which was more pronounced proximally. Initial neurological exam revealed bilateral muscle strength was 0/5 deltoids, 3/5 biceps, 2/5 triceps, and 4/5 in the wrists and intrinsic hand muscles. Leg strength was 3/5 iliopsoas, 4/5 hamstrings, 4/5 quadriceps, and


Table 1. Hospital Course

Days 1–3

608 Curative Therapy of an Acid Secreting Inlet Patch Producing Chronic Sore Throat Mehnaz A. Shafi, MD, FACG1, David Y. Graham, MD, MACG2. 1. University of Texas MD Anderson Cancer Center, Houston, TX; 2. Baylor College of Medicine, Houston, TX. A 27 year man presented for evaluation of chronic sore throat which had been present for more than one year. On endoscopy a single 1 cm inlet patch was seen. Biopsies show hetrotrophic gastric type mucosa with parietal cells present consistent with the diagnosis of inlet patch in the proximal esophagus. The remainder of the EGD including the EG junction was unremarkable. A BRAVO pH capsule was attached in the upper esophagus one cm distal to the inlet patch and 20 cm above the LES. The patient had stopped all acid suppressing medicines a week prior. The BRAVO readings showed abnormal acid exposure in the proximal esophagus on day 1. A total of 78 reflux episodes were reported. One reflux episode was > 5 min. The longest episode of reflux was 8 minutes. Total time pH was. Therapy: A month later the patient underwent a second endoscopy and the ectopic gastric mucosa was completely ablated using argon plasma coagulation at 0.8 L/min and 30 Watts. No residual inlet patch was seen post APC. A month after the ablation a BRAVO pH capsule was attached again in the upper esophagus in the same location as before. The patient was off acid suppression. He noted no episode of heartburn, dysphagia, or sore throat following the inlet patch ablation and during the test. The BRAVO readings did not show abnormal acid exposure Total reflux episodes seen were 40 and 56 on day 1 and day 2 respectively. No reflux episode > 5 min was seen on either day. The longest episode was 1 min and 2 min on day 1 and day 2 respectively. Total time pH was < 4 min was 18 min and 24 min on day 1 and day 2 respectively. % time pH was below 4 was 1.4 and 1.8 on day 1 and day 2 respectively. Discussion: An inlet patch is a congenital anomaly consisting of heterotopic gastric mucosa in the upper esophagus. The prevalence varies from 0.1% -10%. If parietal cells are present, the inlet patch may be associated with globus and throat pain. Treatment with acid suppressing medicines is often only partially successful. Here we report a patient with a resolution in abnormal pH exposure after ablation of the inlet patch. The patient also reported complete relieve of symptoms. Conclusion: Ablation of the inlet patch appears to be an effective therapy for alleviation of symptoms from acid-secreting inlet patch and should be considered as it may be curative and obviate the need for long term acid suppressing medications.

609 “Stack of Coins” on Manometry: Type 3 Achalasia Complicated by Severe Esophageal Diverticulosis Jonathan Pourmorady, MD, Mark Pimentel, MD, Siamak Tabib, Ali Rezaie, MD. Cedars-Sinai Medical Center, Los Angeles, CA. A 58 year old female presented to clinic complaining of uncontrolled acid reflux symptoms for the past twenty years. She was previously diagnosed with gastroesophageal reflux disease (GERD) and was taking proton pump inhibitors twice daily without significant response. She endorsed frequent episodes of chest pain, heartburn, regurgitation, and dysphagia, noting episodes of food getting stuck in her throat. Barium swallow esophagram revealed a tapered narrowing in the distal esophagus, multiple pulsion diverticula, and marked stasis of barium contrast in the distal esophagus. Endoscopy was then performed which revealed distal esophageal diverticula (Fig 1), a tight gastroesophageal junction, and a dilated


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[609A] Figure 1.

proximal esophagus suggestive of achalasia. She subsequently underwent high resolution esophageal manometry which revealed a lower esophageal sphincter with normal pressure at rest which failed to relax with wet swallows (Lower esophageal sphincter (LES) relaxation residual pressure 20 mmHg). All wet swallows were followed by vigorous non-peristaltic contraction compatible with type 3 achalasia. On further assessment of the esophageal contractions and increasing the pressure range to 300 mmHg revealed a peculiar reproducible pattern depicting a “stack of coins” on manometry (Fig 2 & 3) that corresponded to the patient’s esophageal diverticula. In our case report, we describe a patient with an extensive history of poorly controlled GERD symptoms and dysphagia ultimately found to have type 3 achalasia with esophageal diverticula. Achalasia associated esophageal diverticula is a rare occurrence with a previously described prevalence of less than 5% and is associated with a higher risk of complications with dilatation and surgical interventions. Our case report identifies a “stack of coins” appearance on manometry as a new finding in patients afflicted with achalasia complicated by esophageal diverticula. To our knowledge, this appearance on esophageal manometry corresponding to achalasia with esophageal diverticula has not been previously described in the literature. After ruling out secondary causes of achalasia, our patient ultimately underwent Heller myotomy and partial (Dor) fundoplication with significant improvement in her symptoms post-operatively.

610 The Blackened Esophagus Tyson H. Collazo, MD1, Mitesh Bhalala, MD2, Yuriy Israel, MD3, Brad M. Dworkin, MD, FACG4. 1. New York Medical College/Westchester Medical Center, Bronx, NY; 2. Westchester Medical Center, Yonkers, NY; 3. Westchester Medical Center, White Plains, NY; 4. New York Medical College/Westchester Medical Center, Valhalla, NY.

[609B] Figure 2.

Introduction: Acute Esophageal Necrosis (AEN) is a rare cause of upper GI bleeding characterized by circumferential black esophageal discoloration. The etiology of AEN is likely multi-factorial: tissue hypoperfusion , impaired local defense barriers, and influx of gastric contents, leading to direct injury and necrosis. Case: A 65 year old man with a history of Renal Cell Carcinoma treated by left nephrectomy, presented to a community hospital with hematemesis and melena. He was found to have acute liver injury, acute renal failure, sepsis, and severe lactic acidosis, and was transferred to Westchester Medical Center for further management. He was hemodynamically stable at the time of transfer. Physical exam was notable for hepatomegaly. Labs upon transfer were notable for: WBC 29.7; Hgb 9.7; Bicarbonate 9; BUN 55; Cr 2.4; AST 579; ALT 222; Direct Bilirubin 6.8; Total Bilirubin 8.3; Alkaline Phosphatase 428; Lactate > 15.6. A non-contrast CT scan was negative for esophageal perforation, but showed hepatomegaly and innumerable hepatic lesions that likely represented metastases. On upper endoscopy, the entire esophageal mucosa was blackened and had areas of white exudate. There was a sharp transition to pink mucosa at the gastro-esophageal junction. The gastric mucosa was pink, but nodular in appearance, and there were multiple, non-bleeding ulcers found in the duodenal bulb. Esophageal biopsies revealed fibroconnective tissue with necrosis and acute inflammation. These findings were consistent with AEN. The patient was placed on intravenous pantoprazole and Sucralfate. He was later able to tolerate a liquid diet, his hemoglobin remained stable, and his melena resolved. However, he remained in persistent severe lactic acidosis and sepsis, requiring dialysis, bicarbonate drip, and broad spectrum antibiotics. Unfortunately, he passed away on hospital day 10.

[609C] Figure 3.



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Abstracts Discussion: AEN is rare, with an estimated prevalence of 0.2 %. Other causes of blackened esophageal mucosa include: caustic ingestion, melanocytosis , malignant melanoma, acanthosis nigricans, and coal dust deposition of the esophagus. The mortality rate associated with AEN is 13-35%, but is typically due to the another underlying disease rather than AEN itself. With supportive care, intravenous proton pump inhibitors, and treatment of the underlying illness, resolution of endoscopic findings occurs in most patients. Complications of AEN include esophageal strictures and perforation.

611 Black Esophagus: A Lurking Marker of Illness Severity Patrick Coleman, MPH1, Ryan Haley, MD2, Brian Cohee, MD2, Noah Hall, MD2, Nisha Shah, MD2, Patrick Young, MD, FACG2. 1. Uniformed Services University of the Health Sciences, Bethesda, MD; 2. Walter Reed National Military Medical Center, Bethesda, MD.

[610A] Figure 1.

Introduction: Acute esophageal necrosis, or “black esophagus”, is a rare finding on esophagogastroduodenoscopy. It is identified by characteristic diffuse circumferential black mucosa in the distal esophagus with an abrupt transition to normal appearing tissue at the gastroesophageal junction. Underlying causes are typically multifactorial, but the finding is associated with high mortality. Case: A 72-year-old African American male with end stage renal disease, cirrhosis, diabetes mellitus, deep vein thrombosis, and atrial fibrillation presented with altered mental status. He was hypotensive and diagnosed with sepsis from spontaneous bacterial peritonitis and left leg cellulitis. The patient’s international normalized ratio was elevated. Hypotension persisted despite fluid resuscitation and broad-spectrum antimicrobials. On hospital day 4, he experienced large volume coffee ground emesis and worsening mental status. He was intubated and his coagulopathy was corrected. Esophagogastroduodenoscopy revealed circumferential black, friable, mucosa in the distal esophagus and no other bleeding source. The patient was started on high dose intravenous proton pump inhibitors and was kept nil per os in the ensuing days while an aggressive search for an unaddressed etiology for illness was undertaken. He was ultimately found to have extensive osteomyelitis of the left lower extremity with multi-drug resistant Pseudomonas aeruginosa that required an above knee amputation to achieve source control. Discussion: Acute esophageal necrosis is usually seen in the context of multiple medical comorbidities and acute illness with hypoperfusion. The distal esophagus is a watershed area for vascular supply, and systemic hypoperfusion affects this part of the organ first, leading to loss of barrier protection from

[610B] Figure 2.

[611A] Figure 1.

[610C] Figure 3.


[611B] Figure 2.


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gastric acid. The finding is associated with approximately 30% mortality, presumably due to the severity of the underlying illness. Treatment is focused on the underlying illness, and supportive care includes proton pump inhibitors and avoidance of oro- or nasoenteric tubes and oral intake. Recognition of this clue to illness severity led the team to search harder to find an underlying cause, which ultimately turned out to be osteomyelitis. Clinicians should be aware of this finding and its significance in prognosis and management.

612 Squamous Cell Carcinoma of the Esophagus Presenting as a Submucosal Mass Deepshikha Nag Chowdhury, MD1, Youssef Botros, MD2, Matthew Grossman3, Walid Baddoura, MD3. 1. St. Joseph’s Regional Medical Center/Seton Hall University School of Health and Medical Sciences, Hackensack, NJ; 2. St. Joseph’s Regional Medical Center, Paterson, NJ; 3. St. Joseph’s Regional Medical Center, Paterson, NJ. Introduction: Subepithelial lesions (SELs) of the GI tract originate from below the epithelial layer and most are found incidentally during EGD; however, some may be symptomatic. SELs of the esophagus are usually benign. We present a patient with dysphagia due to an esophageal subepithelial mass, ultimately diagnosed as an esophageal squamous cell cancer. Case report: A 61 year-old male with a history of hypertension and coronary artery disease presented to the emergency department with a 3-week history of progressive dysphagia to solids and subsequently liquids. He also reported a 15-pound weight loss. He had a 60 pack-year smoking history, and quit 1 year prior to presentation. He also stated excessive alcohol use in the past. Family history included a brother with lung cancer and an uncle with esophageal cancer. Physical examination was unremarkable. Hemoglobin was 11.5 g/dl and albumin 3.9 g/dl. CT of neck showed an upper esophageal mass with an enlarged left supraclavicular node. EGD showed a large intraluminal submucosal esophageal mass at 20 cm, with near-complete occlusion of the lumen. The gastroscope could not be passed beyond the lesion. “Deep-well” biopsies of the mass were obtained which showed normal squamous epithelium. Subsequently, he underwent an endoscopic ultrasonography (EUS) revealing a poorly circumscribed hypoechoic subepithelial mass, measuring 4.3 x 3.2 cm, originating from the submucosa with an intact muscularis propria. No adjacent lymphadenopathy was identified at the level of the lesion. Cytology obtained by fine-needle aspiration (FNA) was consistent with squamous cell carcinoma (SCC). CT of chest and abdomen showed mediastinal, axillary and celiac axis lymphadenopathy, without any distant organ metastases. The patient underwent a surgical gastrostomy tube placement with a plan for chemoradiation therapy. Discussion: Differential diagnoses of esophageal SELs include leiomyoma, leiomyosarcomas, gastrointestinal stromal tumor, granular cell tumor, glomus tumor, lipoma, carcinoid tumors, cysts, varices or extrinsic compression. Forceps biopsies are inadequate for diagnosis due to normal overlying mucosa thus necessitating EUS/FNA which has a diagnostic accuracy reaching 80%. Esophageal SELs are rarely malignant and are treated only when symptomatic with endoscopic/surgical excision. While SCC is primarily mucosal in origin presenting with an ulcerating lesion, intramural SCC is an exceedingly rare condition, with only a few cases reported in the English literature. As our case illustrates, esophageal SELs can be a very atypical presentation of SCC that could be included in the differential diagnosis.

613 A Case of Esophagogastric Outflow Obstruction From Aortic Impingement Shubha Singh, MD, Rana Abraham, MD, Jennafer Ottenheimer, MPH, PA-C, Peter J. Sargon, MD, A. Aziz Aadam, MD. Rush University Medical Center, Chicago, IL. Introduction: Patients with impaired esophagogastric junction (EGJ) relaxation and some preserved peristalsis are considered to have a variant of achalasia termed esophagogastric junction outflow


obstruction (EGJOO). Anatomic variations may correspond to pressure abnormalities visualized on high resolution manometry. Case Report: A 71 year old female with a two year history of progressive chest pain, dysphagia, and dyspepsia presented to outpatient gastroenterology clinic after an unremarkable esophagogastroduodenoscopy (EGD) at another facility. The patient had a negative recent cardiac evaluation. Past medical history was significant for coronary artery disease and previous tobacco abuse. Her physical exam was unremarkable. An esophagogastroduodenoscopy (EGD) revealed mild distal esophagitis and a 2 cm hiatal hernia.. High resolution manometry (HRM) of the esophagus revealed presence of a hiatal hernia, normal lower esophageal sphincter (LES) pressure, elevated integrated relaxation pressure (IRP) of 17 mmHg (normal < 15 mmHg), strong vascular signal, and intact peristalsis. High IRP with preserved peristalsis and strong vascular signal suggested esophagagastric junction outflow obstruction (EGJOO), after which the patient was referred for endoscopic ultrasound (EUS). EUS revealed normal thickness of the EGJ with asymmetric external compression visualized from the aorta on the gastroesophageal junction (GEJ), consistent with aortic impingement at the GEJ. CT chest was negative for aortic aneurysm. A trial of a tricyclic antidepressant for visceral hypersensitivity was unsuccessful since she was unable to tolerate the medication due to side effects. She was then referred for a trial of hypnotherapy for her continued symptoms. Her dysphagia resolved and she is receiving ongoing treatment for her dyspepsia. Conclusion: EGJOO is defined by elevated IRP with intact to weak peristalsis.1-3 . The anatomy associated with HRM findings is innately unknown, which is why EUS should be considered in patients with EGJOO to identify extrinsic compression or malignancy4. EUS is most useful in patients with a strong vascular signal on HRM or personal history of malignancy. This case exemplifies the utility of EUS in patients with HRM findings suggestive of strong vascular signal, normal peristalsis, and increased IRP from aortic impingement.

614 Dysphagia Lusoria - An Unusual Cause of Dysphagia Jigar M. Patel , MD1, Dennis Nguyen, MD2, Lauren Halvorson, MD3, Seper Dezfoli, MD4, Zone-en Lee, MD4. 1. MedStar Washington Hospital Center, Hyattsville, MD; 2. MedStar Georgetown University Hospital, Arlington, VA; 3. MedStar Georgetown University Hospital/Washington Hospital Center, Silver Spring, MD; 4. MedStar Washington Hospital Center, Washington, DC. A 54 year old female with past medical history of hypothyroidism presented to the emergency department by EMS after an episode of choking after drinking Gatorade. Heimlich maneuver was performed which relieved her symptoms. Detailed history revealed that the patient had a similar episode about 5 months ago while having dinner; it was relieved after a Heimlich maneuver. She reported having episodes of dysphagia for the past 4 years, about once a month in frequency which progressively worsened in with both frequency and severity. Over time she developed anxiety associated with swallowing. Contrastenhanced CT of the neck and chest demonstrated an aberrant right subclavian artery, a third branch of the aortic arch with a common origin of the common carotid arteries. It coursed posterior to the esophagus. EGD was done to exclude an intrinsic etiology of her symptoms. It showed a moderate-sized area of extrinsic compression in the upper third of the esophagus at 20 cm from the central incisors with evidence of pill residue at the site. Barium swallow demonstrated a smooth extrinsic mass effect upon the esophagus at the level of the transverse aorta.. In I761, Dr. David Bayford made his discovery of esophageal compression by an aberrant right subclavian artery in a fatal case of ‘obstructed deglutition’ for which he coined the term ‘dysphagia lusoria’ [1]. The prevalence of an aberrant subclavian artery in the general population is estimated at 0.4% to 0.7% in published literature [2]. In his characterization of the syndrome, Bayford described that the act of deglutition will not be accompanied with pain or soreness, but extreme anxiety and violent palpitations of the heart [1]. Our patient over time had developed anxiety due to dysphagia. In patients who present at an advanced age, decreased vascular compliance is thought to be the most predominant factor [2]. A barium swallow and CT scan of the chest are highly valuable in the diagnosis of dysphagia lusoria. Surgical correction is indicated in symptomatic cases. Our patient underwent right carotid-subclavian bypass with Dacron graft. Right subclavian artery embolization with amplatzer plug was aborted because the right brachial artery was too small in diameter. Instead ligation and extraction of the anomalous right subclavian artery was performed the next day. After surgery she was able to swallow without any difficulty.


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[614A] Figure 1.

[615A] Figure 1.

[614B] Figure 2. [615B] Figure 2. References: [1]. Asherson, N., David Bayford. His syndrome and sign of dysphagia lusoria. Ann R Coll Surg Engl, 1979. 61(1): p. 63-7. [2]. Bennett, A.L., et al., Dysphagia lusoria: a late onset presentation. World J Gastroenterol, 2013. 19(15): p. 2433-6.

615 Severe Achalasia Presenting With Lung Abscess Tahmina Sikder, MD1, Nina Kello2, Raghav Bansal3, Joshua Aron4. 1. Elmhurst Hospital Center, Icahn School of Medicine at Mount Sinai, Flushing, NY; 2. Queens Hospital Center, Jamaica , NY; 3. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), Elmhurst, NY; 4. Elmhurst Hospital Center, Elmhurst, NY. Introduction: Achalasia is an idiopathic disorder of esophageal aperistalsis and chronic lower esophageal sphincter (LES) contraction, resulting in dysphagia to solids and liquids, regurgitation and associated chest discomfort. The most common extraesophageal manifestations of achalasia are pulmonary complications secondary to microaspiration. Recurrent microaspiration can lead to diffuse aspiration bronchiolitis, broncho- pneumonia, obliterative pneumonitis, mediastinitis or lung abscess as in the case of our patient. Case presentation: A 31-year-old male with no past medical history who presented with a 5-day history of productive cough with associated night sweats and generalized weakness along with 1-year history of intermittent reflux and dysphagia . On admission, he was febrile to 102.6F with decreased breath sounds and dullness in the left upper lobe . Initial chest x-ray (image 1) showed a thickened wall cavity in the left lung apex, concerning for lung abscess and a markedly dilated esophagus. CT chest with I/V contrast (Image 2) revealed an abnormal air collection , surrounded by pleural thickening in the left upper lobe cavity and a markedly distended esophagus with air-fluid levels. Patient was ruled out for tuberculosis and started empirically on ampicillin-sulfbactam for lung abscess deemed secondary to aspiration from presumptive achalasia .Barium swallow (image 3) revealed marked dilated esophagus


[615C] Figure 3.


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with eccentric tapering and delayed filling of the stomach. EGD revealed a dilated esophagus with food in the mid and distal portions. Manometry confirmed the diagnosis of achalasia. The patient underwent Heller myotomy with Dor fundoplication. Patient improved clinically and was discharged home after 8 weeks of antibiotics. Discussion: Both structural and functional changes in the lungs can be seen in patients with achalasia. Serious pulmonary complications such as aspiration pneumonia, lung abscess, and empyema can develop in less than 10% of untreated patients with achalasia. Atypical mycobacteria particularly Mycobacterium fortuitum can cause disease in the setting of dysphagia. The possibility of an underlying and causative œsophageal lesion should be considered in every case of pulmonary inflammation of obscure etiology and the appropriate investigations should be carried out. .Our case emphasizes the severity of untreated achalasia and its extraesophageal manifestations. The treatment of lung abscess in the setting of achalasia includes management of the pulmonary issues and treatment of achalasia. Medical treatment of achalasia is temporary and suboptimal at times. Surgical approaches offer longer-term solutions but many patients are not candidates due to medical co-morbidities.

616 Lichen Planus: Esophageal Involvement Ashirf Al-Ghanoudi, MD, MPH1, Khaled Shawwa, MD1, Mohd Amer Alsamman , MD2, Alan Putrus, MD3, Francis Edeani, MD3. 1. Good Samaritan Hospital, Cincinnati , OH; 2. Good Samaritan Hospital, Cincinnati, OH; 3. Trihealth-Good Samaritan Hospital, Cincinnati, OH. Case Presentation: A 71-year-old white female with a past medical history of gastroesophageal reflux disease presented with intermittent dysphagia to solid food and odynophagia that had been progressing for the past few months. She also reported unintentional weight loss. Patient has history of erosive lichen planus that was causing ulcers in her oropharynx three years ago and it was treated with topical steroids. All her initial laboratory tests were normal, this includes CBC, BAMP, LFTs. Barium sallow was performed and showed narrowing in the proximal one-third of the esophagus. Subsequent upper endoscopy revealed ulcerated circumferential stricture in the proximal esophagus just 2 cm below the cricopharyngeal muscle. Upper endoscopy also showed moderate mid and distal esophageal strictures (Figure.1). Esophageal biopsies were consistent with acute erosive esophagitis with lymphocytic predominance and with minimal eosinophils. Based on the presence of oral lichen planus, our patient’s endoscopic apperance and the biopsy findings, the patient was diagnosed with esophageal lichen planus. She had undergone multiple esophageal dilatations since the initial presentation. She had also received a course of systemic steroids. On follow-up, the patient was clinically stable and had denied worsening of her symptoms. Discussion: Lichen planus is a common idiopathic disorder involving skin, nail, and mucosal membranes. It is characterized by immune response attacking an antigen in the basal cells of squamous epithelium. Esophageal lichen planus is a relatively rare condition and the prevalence is unknown. The diagnosis can be challenging due to the subtle clinical findings and lack of characteristic histologic features. Esophageal lichen planus usually affects the upper and mid esophagus; in addition, it often spares the gastroesophageal junction when compared to reflux esophagitis. The history of oral lichen planus, endoscopic images and site of esophageal involvement are very helpful in differentiating between the latter two entities. Esophageal lichen planus has a tendency to be chronic disease with the potential risk of malignancy. Topical and oral steroids are the mainstay of treatment but to date there are no wellestablished guidelines. Conclusions: Oropharyngeal lichen planus is a chronic disease that can lead to recurrent esophageal stricture. Endoscopic findings and pathology may not be specific; however, clinicians should be aware of this entity and appropriate referrals should be made as patients might need repeated interventions to have a relief in their symptoms.

Case: We report a 77 year old woman a history of sick sinus syndrome and a ventricular pacemaker who presented to the hospital with multiple syncopal episodes associated with eating. On physical exam, her vitals were stable with no orthostatic changes. Cardiovascular system exam showed normal regular heart sounds with an ejection systolic. Electrocardiogram showed sinus rhythm with ventricular pacing, and Echocardiogram revealed severe aortic stenosis. Brain CT scan with perfusion was negative for ischemia. Electroencephalogram was normal. Barium esophagogram and video swallow testing did not show any pathology. The patient did not have any episodes of syncope while eating in the hospital bed. Her syncopal episodes were attributed to the reduction in cardiac output secondary to swallow induced vegally mediated vasodilation that was augmented by aortic stenosis. Her symptoms were alleviated by having small bites and leg elevation during meals to increase preload. Successful transcatheter aortic valve replacement (TAVR) was performed few months later. Relief of LV outflow obstruction provided benefit and complemented conventional therapy. She did not report any syncopal episodes thereafter. Discussion: Deglutition syncope is a rare type of neuro-cardiogenic syncope. Literature review reported highest association with gastrointestinal diseases (31cases). Bradyarrythmias were associated with most of the cases (68 cases). Different mechanisms play role in the pathophysiology. Deglutition induced vagal reflex is believed to be the major factor in cardiovascular inhibition leading to bradyarrythmias and vasodilation which reduces cardiac output and ultimately causes cerebral hypoperfusion. Left ventricular outflow obstruction can contribute as well. Although dietary modifications play an important role in the treatment, understanding and treating the underlying mechanism is paramount.

618 An Unusual Cause of Dysphagia: Pancreatic Pseudocyst Jigar M. Patel , MD1, Lauren Halvorson, MD2, Dennis Nguyen, MD3, Suzan Ebrahimi4, Mitesh Patel, MD, FACG5. 1. MedStar Washington Hospital Center, Hyattsville, MD; 2. MedStar Georgetown University Hospital/Washington Hospital Center, Silver Spring, MD; 3. MedStar Georgetown University Hospital, Arlington, VA; 4. Washington Hospital Center, Chevy Chase , MD; 5. MedStar Washington Hospital Center, Washington, DC. A previously healthy 41-year-old man presented with intermittent dysphagia with solids for 2 weeks. The food felt as if it was stuck in the lower third of his chest and was associated with constant, non-radiating epigastric discomfort, described as a pressure sensation which was worsened by eating. He denied weight loss, odynophagia, or constitutional symptoms. Further history from the patient which revealed he is an avid competitive bicyclist who fell over the handlebars and sustained blunt trauma to the abdomen about 3 months ago. Abdominal examination was significant only for mild epigastric tenderness. Esophagogastroduodenoscopy showed extrinsic compression in the distal esophagus but no obstruction. Gastric exam revealed localized severely congested mucosa on the lesser curvature of the antrum, biopsies of overlying mucosa were unrevealing. Computed tomography of abdomen with contrast showed a large 3.5 cm, thick-walled cystic structure adjacent to the esophagus at the hiatus, a similar smaller structure on the left side of the porta hepatis, and a larger cystic structure, 5.7 x 3.7 cm, in the lesser omentum. The lesions were not within the liver and the pancreas was normal. EUS showed irregularly shaped anechoic structure in periesophageal space, FNA deferred due to intervening vasculature. Management was expectant in our case and his symptoms completely resolved 2 months later. Repeat MRI showed near complete resolution of peripancreatic inflammatory changes.. Dysphagia is rarely the presenting symptom of a pancreatic pseudocyst. Mediastinal pancreatic pseudocysts are rare but life threatening complications of pancreatitis [1]. An adult series of pseudocyst reported trauma as the etiological factor in only 3-8% of patients [1]. Most pseudocysts (90%) are single, and multiplicity is found significantly more often in patient with acute alcoholic pancreatitis than in all groups combined (47% vs. 19%) [1]. Our case is unique in that it represents a rare presentation of pancreatic pseudocyst. The ideal management of mediastinal pseudocysts is controversial and depends on the underlying ductal anatomy, size of the pseudocyst, presence of complications and available expertise [2]. Management was expectant in our case and his symptoms completely resolved 2 months later. Repeat MRI showed near complete resolution of peripancreatic inflammatory changes.. References: [1]. Andren-Sandberg, A. and C. Dervenis, Pancreatic pseudocysts in the 21st century. Part I: classification, pathophysiology, anatomic considerations and treatment. JOP, 2004. 5(1): p. 8-24. [2]. Panackel, C., et al., Pancreatic pseudocyst presenting as dysphagia: a case report. Saudi J Gastroenterol, 2008. 14(1): p. 28-30.

[616A] Figure 1.

617 Deglutition Syncope in a Patient With Aortic Stenosis Hussein Al-Hamid1, Shwan Jalal, MD2, Thomas LaLonde, MD2. 1. Providence Hospital, Southfield, MI; 2. St. John Hospital and Medical Center, Grosse Pointe Woods, MI. Introduction: Deglutition or swallow syncope is a rare type of neuro-cardiogenic syncope defined as a brief period of loss of consciousness during or immediately after deglutition of food. To date about 81 cases were described. Literature review shows highest association with gastrointestinal diseases. Our case describes other possible contributing mechanism.


[618A] Figure 1.


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[618B] Figure 2.

[619A] Figure 1.

had any complications or recurrence. Endoscopic mucosal resection is a low-risk, efficacious treatment that can be used to resect GCTs confined to the mucosal and submucosal layers, providing resolution of symptoms and improved quality of life, as in the case of our patient.

620 Endoscopic Management of Recurrent Food Impactions and Dysphagia in a Patient With Allgrove’s Syndrome Thomas R. McCarty, MD1, Tarun Rustagi, MD2, Mena Bakhit, MD3, Ali M. Ahmed, MD4, Mayra Sanchez2. 1. Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, Yemen; 2. Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT; 3. Department of Internal Medicine, Yale University School of Medicine, New Haven, CT; 4. Yale University School of Medicine, New Haven, CT.

[618C] Figure 3.

Clinical Vignette: A 23-year-old male with Allgrove’s syndrome complicated by multiple esophageal strictures with esophageal diverticula, and recurrent food impactions presented with dysphagia. He was diagnosed with achalasia in infancy and was previously treated by Heller myotomy and fundoplication. Endosopcy was performed and a gastroscope could not pass an esophageal stricture, just below the upper esophageal sphincter. Instead, an ultraslim nasal scope was successfully used and a jagwire was passed under fluoroscopic guidance into the stomach. The jagwire then assisted scope navigation through the esophagus. A long stricture was identified from 30 cm to 40 cm with a food

619 Endoscopic Mucosal Resection of Granular Cell Tumors in the Esophagus Alexander Perelman, DO, MS1, Colin Linke2, Neil Sharma, MD3. 1. Yale University School of Medicine, New Haven, CT; 2. Lincoln Memorial University, DeBusk College of Osteopathic Medicine, Bolingbrook, IL; 3. Parkview / Indiana University, Fort Wayne, IN. Case Summary: A 24-year-old female with a past medical history of type one diabetes mellitus and a seizure disorder was admitted to the hospital for chief complaint of vomiting, dysphagia, and pain in the chest and epigastric regions. Her outpatient gastroenterologist, who had performed three esophagogastroduodenoscopies (EGD’s) over the course of three months, referred her for evaluation of esophageal changes he noted on his workup. An esophageal nodule and mucosal changes indicative of eosinophilic esophagitis were noted on the first EGD. The second EGD confirmed eosinophilic esophagitis, discovered a ringed esophagus, and confirmed the nodule to be a Granular cell tumor (GCT). Pathologic analysis showed the lesion to stain positively for PAS and S100, which is consistent with GCT. The patient was therefore referred to us for endoscopic mucosal resection (EMR) of the lesion. An endoscopic ultrasound(EUS) was performed, which confirmed a 1 cm oval lesion within the mucosa of the esophagus, located at 20 cm from the incisors. However, due to the strictures within the upper esophagus, the EMR device could not be passed, and the procedure was aborted after dilation of the stricture. Endoscopic mucosal resection was successfully performed one month later, with one margin of resection being positive. The accompanying figure depicts the gross morphology of the GCT after EMR. A repeat EGD 6 week’s status post resection did not demonstrate any recurrence at the location of the previous lesion. Biopsies of the area with pathologic analysis failed to demonstrate any residual GCT tissue. Discussion: Granular cell tumors are extremely rare lesions that can affect the esophagus. Although our patient presented with gastrointestinal symptoms, it is likely that GCTs are much more prevalent than what is documented in the literature, given the indolent nature of GCTs. We were able to utilize EMR as a safe and effective treatment option for this patient GCT. Although our follow-up is limited, she has not



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bolus located proximally and removed by Roth net. The stricture was serially dilated using a TTS CRE balloon from 4 to 6 mm (Image 1). The nasal scope was then advanced distally to 40 cm where another food bolus was fragmented using biopsy forceps and deposited into the stomach. The patient tolerated the procedure well and his diet was advanced. He was discharged with outpatient follow-up for stricture dilation. Discussion: Allgrove’s syndrome is a rare autosomal recessive disorder characterized by a triad of adrenal insufficiency, achalasia, and alacrima often associated autonomic dysfunction. Esophageal abnormalities are similar to idiopathic achalasia caused by a thickening of the intramuscular layer, loss of the myenteric ganglia and decreased nitric oxide signaling. Traditional treatments include Heller myotomy and endoscopic dilation. The most frequently used dilators for achalasia are the wire-guided polyvinyl dilators (Savary-Gilliard) and the TTS CRE balloon dilators. The Savary-Gilliard dilator exerts a radial force as it gradually passes distally, though the dilating force is transmitted longitudinally secondary to shearing effects. In contrast, the balloon dilators lack longitudinal force and deliver the radial force instantly. Longitudinal force and lack of visualization pose a significant risk for perforation and are contraindicated in multiple, long, or complex strictures, or when diverticula are present. Our patient has a complex esophageal stricture due to asymmetry, diameter < 12mm, and inability to pass the endoscope. While no clear advantage has been demonstrated among dilator types, this case highlights the benefit of endoscopic visualization with the CRE balloon dilator to accurately position the balloon across the stricture.

[622A] Figure 1.

621 Endoscopic Ultrasound-Guided Fine Needle Aspiration (EUS-FNA) and Biopsy (EUS-FNB) for Evaluation of Mediastinal Masses Causing Esophageal Obstruction: A Case Series Ashirf Al-Ghanoudi, MD, MPH1, Mohd Amer Alsamman , MD2, Alan Putrus, MD3, Francis Edeani, MD3, Joshua Max, MD1. 1. Good Samaritan Hospital, Cincinnati , OH; 2. Good Samaritan Hospital, Cincinnati, OH; 3. Trihealth-Good Samaritan Hospital, Cincinnati, OH. Case 1: A 77-year-old female with a history of squamous cell carcinoma of the lung status post chemotherapy presented to our hospital with persistent dyspnea and hypoxemia. She also noted mild dysphagia. CT chest revealed circumferential thickening of the esophageal wall at the level of the carina with a soft tissue mass in the subcarinal region. The patient underwent an esophagogastroduodenoscopy (EGD) that showed extrinsic compression in the mid-esophagus with a small mucosal break containing a fistulous tract. EUS-FNB was performed and biopsies confirmed squamous cell carcinoma. The patient will be started on palliative chemotherapy and radiation and hospice care was initiated. Case 2: A 50-year-old male admitted to our hospital with decreased appetite, weight loss and pain and numbness involving the right upper extremity. CT chest confirmed a large right lung mass extending into the mediastinum and causing superior vena cava syndrome. The patient underwent EGD showing an extrinsic compression in the proximal and mid-esophagus. EUS-FNA was performed and pathology confirmed small cell lung carcinoma. The patient commenced chemotherapy and radiation for limited stage small cell carcinoma. Case 3: A 56-year-old male was admitted to our hospital with dysphagia. A CT chest revealed a large mediastinal mass as well as extensive mediastinal lymphadenopathy. On EGD there was an extrinsic compression of the proximal esophagus. EUS confirmed a large hypoechoic mediastinal mass with subcarinal and aortopulmonary adenopathy. FNA was performed with pathology showing small cell lung carcinoma. The patient was started on palliative chemotherapy and radiation but passed away less than two months after the EUS. Discussion: In this case series we describe three patients presenting with esophageal obstruction due to lung cancer. Esophageal obstruction is an uncommon complication of mediastinal masses occurring with extrinsic compression into the esophageal lumen. While EUS-guided fine needle sampling of mediastinal masses has been well-described, to our knowledge few if any reports exist of this technique for patients with overt esophageal obstruction. In our experience, EUS-FNA/FNB provides a minimally invasive approach with a high diagnostic yield in these patients (Table 1). EUS-FNA/FNB results:

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Table 1. EUS-FNA/FNB results Needle used

Pathology

[622B] Figure 2.

beats per minute. Pertinent labs revealed a hemoglobin of 6.3gm/dl compared to a baseline of 10.9gm/ dl. An esophagogastroduodenoscopy (EGD) revealed large amount of blood clots in the stomach (Figure 1a), nodular ulcerating lesions throughout the entire stomach (Figure 1b) and an esophagogastric fi stula (Figure 2) on retroflexion. Multiple samples of the necrotic lesions in the stomach were obtained for biopsies. Pathology showed squamous mucosa, acute and chronic candida esophagitis, papillomatosis with parakeratosis and fibrinous exudates. Repeat EGD and biopsies of gastric mucosa showed similar findings and pathology. Patient was treated with fluconazole but was persistently unable to tolerate oral intake thus she underwent open jejunostomy tube placement. Although rare, esophagogastric fistulas should be considered in patients with recurrent GERD symptoms who have predisposing risk factors such as long standing reflux disease or esophagogastric procedures. The optimal therapeutic approach is not well defined.Management involves acid suppression therapy in the setting of long standing GERD. Surgical options should be considered when medical management fails.

Age/sex

EGD findings

77 y/o female

Extrinsic compression of the midesophagus with a fistulous tract

22 gauge FNB

Squamous cell lung carcinoma

50 y/o male

Extrinsic compression of the proximal and mid-esophagus

25 gauge FNA

Small cell lung cancer

623

56 y/o male

Extrinsic compression of the proximal esophagus

22 gauge FNA

Small cell lung cancer

Achalasia-Like Findings on Barium Esophagogram in Systemic Sclerosis (SSc): A Case Series

622 Esophagogastric Fistula: A Rare Complication of Chronic Candida Esophagitis and Repaired Esophageal Atresia Nneoma O. Okoronkwo, MD1, Gustavo Churrango, MD2, Weizheng Wang, MD3. 1. Rutgers New Jersey Medical School, Belleville, NJ; 2. Rutgers University, Berkeley Heights, NJ; 3. Division of Gastroenterology, Department of Medicine, Rutgers New Jersey Medical School, Newark, NJ. Esophagogastric fistulas can develop as a rare potential complication of prolonged gastroesophageal reflux disease (GERD), any form of esophagogastric surgery such as fundoplication, esophageal carcinoma or esophageal ulcer.Here, we describe an interesting case of esophagogastric fistula in the setting of chronic esophagitis and a history of esophageal manipulation. A 55 year old female with a history of repaired esophageal atresia, HIV with a CD4 count of 268 presented with five episodes of hematemesis. On physical exam, she was tachycardic with a heart rate of 108


Shamiq Zackria, MD1, Nitin Aggarwal, MD2, Prashanthi Thota, MD3. 1. CMEF/Cleveland Clinic, Canton, OH; 2. Cleveland Clinic, Cleveland, OH; 3. Department of Gastroenterology and Hepatology, Cleveland Clinic Foundation, Cleveland, OH. Background and Aims: The hallmark feature of esophageal involvement in SSc is absent peristalsis or ineffective esophageal motility. These findings are reported in up to 70-90% of patients with SSc. With the widespread use of barium esophagogram and availability of high resolution esophageal manometry (HREM), a variety of atypical esophageal findings are seen. Our aim was to see if the atypical findings on barium are confirmed on HREM Methods: Charts of SSc patients with findings suggestive of achalasia on barium esophagogram were reviewed and the following variables collected: Age, gender, race, comorbidities and findings on barium esophagram, HREM, upper endoscopy, esophageal pH monitoring and autoantibody panel. Results: Patient 1 is a 48 year old male who was undergoing lung transplant evaluation for interstitial lung disease (ILD). Patient 2 is a 41 year old African American female with scleroderma and pulmonary fibrosis. She was undergoing lung transplant evaluation secondary to her pulmonary fibrosis. Patient 3 is a 74 year old Caucasian female with a PMH significant for diabetes mellitus, scleroderma and pulmonary hypertension who presented with dysphagia.


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[623]

Table 1. Summary of Test Results in Scleroderma with Achalasia like findings on Barium Esophagogram

Variable

Patient 1

Patient 2

Patient 3

Patient 4

Patient 5

Patient 6

Barium Esophagogram findings: Dilated Esophagus

Normal

Present

N/A

Present

Present

Present

Aperistalsis

Present

Present

Present

Present

Present

Present

Delayed esophageal emptying

Absent

Absent

Present

Absent

Present

Present

Impaired LES relaxation

Present

N/A

Present

Present

Absent

Present

Reflux

Absent

Absent

Absent

Absent

Present

Absent

0.3

HREM Findings: Basal LES pressure (mm Hg)

5

0.5

1.2

2.6

−4.9

Mean IRP of LES

2.7

1.2

3.8

12

0.3

0

Peristalsis

Absent

Absent

Absent

Absent

Absent

Absent

Motility Disorder

Absent contractility






Normal

N/A

N/A

Normal

N/A

pH testing

Normal

Upper endoscopy

N/A

N/A

Normal

HH, Esophagitis, Schatzki ring

HH

Markedly dilated esophagus

Anti ENA panel

N/A

Elevated CRP and ANA titers

- Elevated CRP and ANA titers - Scleroderma IgG Antibody positive

- Elevated ANA titers - SS-A Antibody positive

- ANA positive - negative for antimitochondrial antibody

- Elevated CRP

ANA, Antinuclear antibody; CRP, C-reactive protein; HH, Hiatal Hernia; IRP, integrated relaxation pressure; LES, lower esophageal sphincter; N/A, not available.

Patient 4 is a 58 year old African American male with a history of SSc with skin, joints, lung and gastrointestinal tract involvement, heart failure, chronic kidney disease- stage II, pericardial window secondary to pericardial effusion who presented with dysphagia for solid foods, weight loss and failure to thrive. Patient 5 is a 51 year old Caucasian male with a PMH of pulmonary hypertension, scleroderma and interstitial lung disease who presents for a lung transplant evaluation. Patient 6 is a 74 year old Hispanic female with a long standing history of rheumatoid arthritis who presents with dysphagia to solid food and heartburn. The findings on barium esophagogram, HREM, upper endoscopy, pH testing and antibody panel are presented in Table 1. Conclusion: All the 6 patients in this series had findings suggestive of achalasia on barium esophagram but had absent contractility with low LES pressures on HREM.

624 A Unique Case of an Esophageal Perforation That Cannot Be Missed Nicholas Battista1, Emily Tommolino2, Ahmad Daraghmeh2, Christian Machado, MD2. 1. St. John Providence Hospital, Canton, MI; 2. St. John Providence Hospital, Southfield, MI. Esophageal injury following radioablation of atrial fibrillation is among the more rare and fatal complications of such procedures. Our patient’s case illustrates an array of the clinical variability, diagnostic challenges, and dreaded sequela associated with these gastrointestinal complications, in particular esophageal perforation and esophago-pericardial fistula. We present a case of a 74 year-old male who presented to our emergency department complaining of chest discomfort 19 days status post radioablation for atrial fibrillation. His chest pain was initially mild, however, 3 hours later, he had abrupt onset of severe, substernal chest pain complicated by hemodynamic instability. Following a negative bedside echocardiogram, performed to rule out cardiac tamponade, the patient was taken for a stat CT Thorax/Abdomen. Computed tomography revealed air adjacent to the mid esophagus and in the anterior pericardial space with a small amount of pericardial fluid consistent with esophageal perforation. Given these findings, our patient was taken for immediate cardiothoracic surgery where he underwent exploration of the mediastinum via right thoracotomy, drainage of the pericardial effusion, and an equivocal intraoperative esophagram. Following surgery, it was felt the most likely mechanism to describe our patient’s clinical conditions was thermal injury to the esophagus, due to radioablation of the left atrium, resulting in perforation and fistula formation where esophageal contents escaped into the pericardial space. Postoperatively, our patient was managed in the intensive care unit through an interdisciplinary approach with general supportive measures, intravenous antibiotics and chest tube drainage. While thoracostomy fluid remained culture negative, pericardial biopsies grew Peptostreptococcus and Streptococcus Oralis. He was eventually discharged with a right upper extremity PICC line for continuation of sensitive antibiotic therapy. Eight days following his discharge, our patient was back in the emergeny room unresponsive and in septic shock. An MRI Brain eventually displayed innumerable acute, bilateral cerebral and cerebellar infarctions suggesting possible septic emboli. The patient’s autopsy later revealed a right atrial thrombus leading us to believe the septic emboli were dislodged from an infected PICC line, that had been previously withdrawn one hour prior to his clinical deterioration, and traveled paradoxically to the patient’s brain. This case not only demonstrates the rare and life threatening gastrointestinal complications associated with atrial fibrillation ablation but the sequela these complications carry themselves. It will only become more imperative to maintain a high index of suspicion for these complications as the number of radiofrequency ablations performed continues to increase.

625 Cerebral Air Embolism Complicating Esophageal Dilation Muhammad S. Mansoor, MD1, Ashar Usmani, MD2. 1. Department of Medicine, Yale-New Haven Hospital, Yale University School of Medicine, Hamden, CT; 2. Department of Medicine, Yale-New Haven Hospital, New Haven, CT. A 57-year old man with history of HIV (undetectable viral load) and compensated liver cirrhosis underwent an elective upper endoscopy for a yearlong history of mid-sternal solid food dysphagia. The EGD was performed under conscious sedation. He was found to have severe mid and distal esophagitis with white patches and a tight esophageal stricture at 34 cm through which an adult gastroscope was unable to pass. With help of a pediatric endoscope length of the stricture was determined to be 1 cm. A through-the-scope controlled radial expansion balloon (TTS-CRETM, Boston Scientific) was advanced through stricture with guidewire. Serial balloon dilations were performed (6-7-8mm) with post dilation oozing seen above the stricture site that resolved spontaneously. His post-procedure course was complicated by oxygen desaturation, tachycardia and hypotension. He failed to recover from propofol sedation and despite getting naloxone remained unresponsive to verbal or painful stimuli. Physical examination revealed non-reactive pupils, absent corneal and gag refl exes, flaccid muscle tone and positive Babinski sign bilaterally. He was immediately transferred to ICU for ventilator and vasopressor support. CT-head revealed multiple small foci of pneumocephalus overlying the vertex and bilateral frontal lobes without intravascular gas (Image 1). On CT-chest the esophagus had diffuse distal wall thickening with associated fat stranding but no evidence of esophageal rupture. A transthoracic echocardiogram did not reveal any intra-cardiac shunt. The patient underwent an MRI revealing diffuse cortical laminar necrosis and hypoxic-ischemic encephalopathy (Image 2), marked cerebellar edema with mass effect upon the midbrain and pons with early ascending trans-tentorial herniation (Image 3). Due to his hemodynamic instability he could not be transferred to another facility for hyperbaric oxygen therapy. His neurologi-

[625A] Figure 1.



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cal status remained unchanged and the family decided to focus on his comfort along with withdrawal of life support. Only a handful cases have been reported of cerebral air embolism during esophageal dilation. Patients usually present with coma, seizures or upper motor neuron signs. Air is thought to enter the arterial vasculature during insufflation though the disrupted mucosa. Air embolism can also occur through venous system via arteriovenous shunts or pulmonary capillary bed. Air embolism results in ischemia, vascular endothelial damage, edema and platelet aggregation. Patients are mainly treated with hyperbaric oxygen or high-flow oxygen, left-lateral decubitus or Trendelenburg’s position and supportive care. Morality is >90% for untreated patients but can be reduced to 7% with hyperbaric oxygen though survivors often have neurological deficits.

626 Bronchoesophageal Fistula in a Female With History of Crohn’s Disease and Small Cell Lung Cancer Soumil Patwardhan, MD1, Krunal Patel, MD1, Christopher Marshall, MD2, Karl Uy, MD1, Julien Fahed, MD1. 1. University of Massachusetts Medical School, Worcester, MA; 2. UMass Memorial Health Care, Worcester, MA. Background: Airway-esophageal fistulas are serious complications of lung or esophageal tumors. They arise either as a result of progression of lung or esophageal malignancies or manifest as a complication of chemoradiation therapy. They can also be a rare complication of Crohn’s disease of the esophagus. There is limited literature on bronchoesophageal fistulas in lung cancer patients with Crohn’s disease. This is a


[626C] Figure 3.


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Abstracts description of a case involving a middle aged female with history of Crohn’s disease diagnosed with small cell lung cancer presenting with dysphagia who was found to have a bronchoesophageal fistula. Case Description: This is a 47 year old female who was diagnosed to have stricturing and fistulizing Crohn’s disease 15 years ago, treated in the past with mesalamine (Asacol), prednisone, azathioprine, and infliximab on no current maintenance medications for five years who presents to clinic in December 2014 with dysphagia, nausea and vomiting. Imaging revealed a large mass in the left lower lobe abutting the mediastinum and the carina which was confirmed to be small cell lung cancer by bronchoscopy. She completed 4 cycles of cisplatin and etoposide following which she presented to clinic in May 2015 with fever, tachycardia, and hypotension as well as nausea, vomiting, cough and dysphagia. An upper endoscopy was performed revealing a large esophageal ulcer and bronchoesophageal fistula. She subsequently underwent esophageal stenting with a covered esophageal stent and open gastrostomy tube placement. Discussion: We investigate this case of a bronchoesophageal fistula in a patient with prior history of Crohn’s disease and small cell lung cancer. Airway-esophageal fistulas are a known complication of tumor growth or recurrence in lung or esophageal tumors. They can also arise secondary to chemotherapy or radiation. Rarer causes include Crohn’s disease, laser therapies, biologics like Bevacizumab and pressure necrosis from esophageal stents. Mean survival is 1-6 weeks. Common causes of death are respiratory infections and malnutrition. Esophageal stenting relieved symptoms in 80% of patients, was more effective (p=0.001) and led to better survival (p=0.07) and better quality of life (p=0.01) in multivariate analyses as compared to bypass or resections. Self expanding metallic stents are preferred over silicone or plastic stents.

627 Thinking Outside of the Granuloma: An Unusual Cause of Upper Abdominal Pain Alya Ahsan, DO1, Nicole Gentile, MD2, David Labowitz, DO3. 1. University of Chicago, NorthShore Campus, IL; 2. University of Chicago, NorthShore Campus, Evanston, IL; 3. North Shore University Health System, Evanston, IL. Case: A 27-year-old Indian male with history of H. pylori presented to clinic with intermittent, progressive, upper-quadrant abdominal pain for four months. The pain was persistent despite treatment of the H. pylori infection. EGD demonstrated chronic gastritis and one linear, non-bleeding esophageal ulcer. Biopsies of the ulceration revealed a non-caseating granuloma and were negative for CMV and HSV. This finding raised the concern for sarcoidosis or Crohn disease. MR Enterography and ACE level were checked, which were unremarkable. Further evaluation included a CT Chest, which showed tree-in-bud lung nodularities, focal infiltrates with central cavitations, left axillary adenopathy, along with a thoracic paraspinal abscess. These findings were concerning for Tuberculosis (TB). Quantiferon gold and mycobacterium cultures were found to be positive, clinching the diagnosis of disseminated TB. His case was reported to the department of public health, and he was started on RIPE therapy. Discussion: In general, the differential of a non-caseating granuloma includes sarcoidosis and Crohn disease. However, non-necrotizing granulomas can occur alone or alongside necrotizing lesions in TB. It is also important to note that all granulomas begin as non-caseating granulomas before transforming into their necrotizing forms. Thereby, as was demonstrated in this case, the finding of a non-necrotizing granuloma does not and should not exclude an infectious etiology. Mycobacterium tuberculosis is well known to present with pulmonary symptoms, but in its disseminated form, extrapulmonary TB can manifest itself at any organ site. Gastrointestinal TB is rare in developed countries, with most cases being reported in those who are immunocompromised, homeless or immigrants from endemic countries. Esophageal TB accounts for only 1% of the reported gastrointestinal tuberculosis cases,which may present with symptoms of epigastric and retrosternal pain, dysphagia and odynophagia. EGD typically reveals ulcerative lesions in the middle portion of the esophagus (1). This unique case demonstrates that the differential for a non-caseating granuloma should include TB. The case also demonstrates that disseminated TB can present with the complaint of upper abdominal pain. Since the prevalence of disseminated TB is decreasing, in order to maintain a high index of suspicion, it is important to be aware of these atypical manifestations. Citation: Khan R, Abid S, Jafri W, Abbas Z, Hameed K, Ahmad Z. Diagnostic dilemma of abdominal tuberculosis in non-HIV patients: an ongoing challenge for physicians. World J Gastroenterol 2006; 12:6371- 6375

628 IgG4-Related Esophagitis Mihir Bikhchandani1, Guy A. Weiss, MD2, Jeffrey Conklin, MD3. 1. David Geffen School of Medicine at UCLA, Los Angeles, CA; 2. UCLA, Los Angeles, CA; 3. UCLA, Division of Digestive Diseases, Los Angeles, CA. Purpose: IgG4-related disease is an emerging condition characterized by dense lymphocytic inflammation consisting of IgG4 plasma cells and storiform fibrosis, affecting multiple organs, but rarely the upper GI tract. We present two patients with IgG4 esophagitis: one who developed an esophageal stricture and the other who developed esophagitis dissecans and then invasive squamous cell carcinoma. The latter is the first report of IgG4 esophagitis associated with malignancy. Case 1: An 87 year-old female presented to our motility clinic with progressive dysphagia to solids for 1 year that was refractory to sucralfate, H2 blockers and PPI. Upper endoscopy showed an esophageal stricture at 27cm that was subsequently pneumatically dilated. Biopsy of the stricture showed ulcerative esophagitis with an underlying dense chronic inflammation. Immunohistochemical staining revealed a focal population of IgG4-positive plasma cells in the lamina propria, numbering up to 25/HPF. The patient was started on swallow inhaled fluticasone, which provided minimal relief, and repeat biopsy after three months showed increased inflammation with 50 IgG4-positive plasma cells/HPF. Over two years, the patient underwent 12 stricture dilations that provided only temporary relief. Case 2: A 65 year-old man presented to our clinic with worsening dysphagia and odynophagia. Endoscopy showed diffuse narrowing of the esophagus with friable mucosa that easily peeled away with minimal trauma. Biopsy showed diffuse lymphocytic esophagitis with a focal plasma cell infiltrate in the


[628A] Figure 1.

[628B] Figure 2.

lamina propria of the proximal esophagus. The region of plasma cell infiltrate correlated with esophageal wall thickening seen on endoscopic ultrasound. Staining showed polyclonal plasma cell infiltrate with mostly IgG4-positive plasma cells. The patient was started on steroids, but 6 months later returned with worsening symptoms. Repeat endoscopy revealed an esophageal stricture at 20cm and proximal esophagitis dissecans, as evidenced by sloughing of the esophageal mucosa with minimal trauma. Soon after, the patient developed white lesions on his tongue and buccal mucosa and was diagnosed with cicatricaial pemphigoid. However, this diagnosis was lifted after a subsequent endoscopy showed an invasive squamous cell carcinoma at the proximal esophagus. His tumor was moderately differentiated, invading through the muscularis propria and into the adventita. The patient underwent an esophagogastrectomy thereafter.

629 Eosinophilic Esophagitis or Hypersensitive Esophagitis Ranje (RJ) Mohamadameen, DO1, Michael Valladares, DO1, Joseph Salhab, DO2, Javier Sobrado, MD1. 1. Nova Southeastern University-Larkin Hospital, Miami, FL; 2. Nova Southeastern University-Larkin Hospital, Tampa, FL. Eosinophilic Esophagitis (EoE) is a localized eosinophil predominant inflammation of the esophagus. It’s an atopic inflammatory disease that has become increasingly recognized over the last decade. It’s even referred to “asthma of the esophagus” due to the similarities in their characteristics. Although present in most of the GI tract, the esophagus is unique in that it’s void of eosinophils in healthy individuals. However, pts with EoE have eosinophils which infiltrate the esophagus, contributing to tissue damage and inflammation. Dx requires clinical manifestations and histological findings. It’s characterized by >15 eosinophils per HPF on biopsy and absence of other causes of esophageal eosinophilia such as GERD.


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Common sxs include dysphagia, food impaction, heartburn, and regurgitation. Tx consists of dietary modifications, pharmacologic therapy, and mechanical dilation of the esophagus. 18 y/o M presents to ER after feeling impaction of steak he ate from night before and inability to swallow. We were called by ER physician who stated a CXR was performed and was WNL. We recommended pt be given IV Glucagon and Reglan with a CT of neck and soft tissues to r/o foreign body. We were called back at 4:30 A.M. with news that pt remains symptomatic despite negative CT. The decision was then made to proceed with emergent endoscopy for extraction of foreign body. At 15 cm, there was food bolus that appeared to be steak. It was gently advanced into the stomach. As we withdrew the scope back into the esophagus, there was erythema and edema with oozing of blood around impaction site. No evidence of stricture. The remainder of the esophagus had scalloping and furrowing with small nodules consistent with eosinophlic microabscesses. Multiple biopsies were taken of proximal, middle, and distal esophagus. Results indicated many eosinophils within the acanthotic squamous epithelium, surface, and muscularis propria. With clinical history taken into account, Dx of EoE was made. Pt was started on PPI BID dosing, elimination diet, and close f/u appt made for further mgmt. We would like to propose the term “hypersensitive esophagitis” to explain this reactive inflammatory condition of the esophagus as it shares characteristics with asthma. Classic presentation often includes a young man with h/o food or allergies, asthma, or atopy with dysphagia or food impaction. We stress the importance of endoscopic findings paired with clinical history to trigger the suspicion of a Dx such as EoE. Discussion with pathologist may be of benefit. While there have been new developments in the last decade, we advocate further research for the optimal mgmt. One theory is to inject topical corticosteroids during endoscopy once the diagnosis is made and repeat endoscopy for further tx/biopsy to assess response.

630 A Rare Cause of Dysphagia to Consider: Calcific Tendinitis of the Longus Colli Muscle Dominic M. Colella, DO1, Fiorella Calderón Sandoval, MD2, David W. Powers, DO3, Seth Rosen, MD1, Javier Sobrado, MD1. 1. Nova Southeastern University-Larkin Hospital, Miami, FL; 2. Universidad de Ciencias Medicas, Cartago, Costa Rica; 3. Nova Southeastern University-Larkin Hospital, South Miami, FL. Calcific tendinitis of the longus colli muscle is an acute inflammatory condition caused by the deposition of calcium hydroxyapatite crystals in the muscle’s superior insertion point. It is a rare condition with a reported incidence of 1.31 per 100,000 person-years that most commonly presents during the third through sixth decades of life. Symptoms consist of acute neck pain characterized as stiffness with associated odynophagia; the condition is less frequently associated with dysphagia. A mild leukocytosis is typically present, which should prompt investigation to rule out other infectious etiologies first. Characteristic radiographic findings include calcifications in the superior fibers of the longus colli muscle tendons at the level of C1 or C2. This self-limiting condition usually resolves spontaneously with nonsteroidal anti-inflammatory agents. A 44-year old female patient with a medical history of gastroesophageal reflux disease, gastric ulcers, gastritis, gastric polyps, Schatzki ring, hiatal hernia, and benign thyroid nodules presented to the hospital with the complaint of progressive dysphagia to solid foods. This dysphagia developed after an isolated incident of food aspiration four weeks prior to her presentation. Three weeks after this event, she experienced persistent odynophagia with associated left-sided occipital headaches and neck pain radiating to the left ear and mastoid process. Physical examination was remarkable for decreased range of motion with neck flexion and extension, bilateral neck soft tissue tenderness to palpation, and thyromegaly. Laboratory data revealed a hemoglobin of 11.5, hematocrit of 34.8, and WBC of 11.88. An upper gastrointestinal series with barium swallow confirmed the presence of the patient’s known Schatzki ring and hiatal hernia. A CT scan, MRI, and MRA of the brain was negative for acute abnormalities, however the CT scan of her neck was positive for calcified longus colli tendons just below the anterior ring of the C1 vertebrae. After an infectious etiology was ruled out, she underwent a trial of oral corticosteroids and NSAIDs that quickly improved her dysphagia and odynophagia. Though exceedingly rare, calcific tendinitis of the longus colli muscle must be considered in a differential diagnosis once the more common etiologies of acute dysphagia and odynophagia have been ruled out or do not correlate with the clinical presentation and/or patient’s history. Since this patient’s symptoms were progressive, persistent, and associated with a decreased range of motion in her neck along with soft tissue tenderness to palpation, her symptoms were not solely due to the presence of a Schatzki ring. These symptoms did indeed support the final diagnosis of calcific tendinitis of the longus colli muscle.

The esophageal relationship with the surrounding structures makes EUS-FNA an ideal diagnostic tool for mediastinal tumors. The use of doppler allows for avoidance of blood vessels and safe FNA of lesions. EUS-FNA has been shown to be 97% sensitive and 100% specific for malignant mediastinal lesions 1; benign lesions can also be accurately diagnosed. . Conclusions: To our knowledge, there have been only two previously reported cases utilizing EUS-FNA for the diagnosis of a mediastinal schwannoma2, 3. Most mediastinal lesions are easily and safely accessible with EUS-FNA and the modality has high diagnostic accuracy. This approach should be considered before more invasive mediastinoscopy is perfomed for diagnosis. . References: [1]. Savides TJ. EUS Diagnosis of Posterior Mediastinal Masses, Lymph Nodes, and Cysts. In: Hawes RH and Fockens P, editors. Endosonography. Philadelphia: Saunders; 2006: 85-94. [2]. McGrath KM, Ballo MS, Jowell PS. Schwannoma of the mediastinum diagnosed by EUS-guided fine needle aspiration. Gastrointest Endosc. 2001; 53(3): 362-365. [3]. Pakseresht K, Reddymasu SC, Oropeza-Vail MM, Fan F, Olyaee M. Mediastinal Schwannoma Diagnosed by Endoscopic Ultrasonography-Guided Fine Needle Aspiration Cytology. Case Rep Gastroenterol. 2011 May-Aug; 5(2): 411–415..

632 A Rare Case of Esophagopericardial Fistula With Development of Hydropneumopericardium: An Unusual Complication of Esophageal Cancer Nauman Siddiqui, MD1, Toseef Javaid, MD2, Syed Hasan, MD2, Jamal Saleh, MD1, Arunkumar Baskara, MD3, Ali Nawras, MD, FACG4. 1. University Of Toledo Medical Center, Toledo, OH; 2. University of Toledo, Toledo, OH; 3. University Of Toledo Medical Center, Perrysburg, OH; 4. University of Toledo Medical Center, Toledo, OH. Esophagopericardial fistula (EPF) is an abnormal tract between the esophagus and pericardium. EPF is mostly related to benign esophageal diseases, esophageal ulcers, reflux esophagitis, foreign body impaction and esophageal perforation. Esophagopericardial fistula and hydropneumopericardium are rare but serious complications of esophageal cancer and carries a grave prognosis. We report a case of EPF leading to hydropneumopericardium in a patient with known esophageal cancer. A 75-year-old white American male known to have esophageal adenocarcinoma previously treated with chemotherapy and radiation presented with altered mental status and two day history of worsening chest pain associated with shortness of breath. The patient was hemodynamically unstable and was admitted to intensive care unit and was placed on a mechanical ventilator. Initial chest x-ray showed a large left pleural effusion and air overlying the heart within the pericardial sac (image1b). CT scan showed erosion and fistula formation between esophageal lumen and posterior pericardium (image1a) with subsequent development of complex pericardial effusion with air. Interventional gastroenterology was consulted for placement of esophageal stent to control esophageal leak as patient was not a good surgical candidate. Before placement of stent, cardiothoracic surgery was consulted for an immediate pericardial catheter insertion to drain air and fluid to prevent cardiac tamponade which can result from air insufflation during the stent placement. As the catheter entered the pericardial sac significant amount of air was released. Left side chest tube was also placed for the complicated pleural effusion. Although the patient was stabilized, the family opted to withdraw life sustaining treatment given the overall poor quality of life and prognosis. Esophagopericardial fistula is a rare complication of locally advance distal esophageal adenocarcinoma. In patients with esophagopericardial fistula, placement of a pericardial catheter before any endoscopic intervention is essential to prevent cardiac air tamponade from air insufflation.

631 Diagnosis of Mediastinal Schwannoma With Endoscopic Ultrasound-Guided Fine Needle Aspiration

[632A] Figure 1.

Vinaya C. Maddukuri, MD, Carol Weida, MD, Andrew Dries, MD. Carolinas Medical Center, Charlotte, NC. Introduction: Endoscopic Ultrasound (EUS) is a minimally invasive modality that can be used for the evaluation and diagnosis of most mediastinal lesions. We present here an uncommon use of EUS and fine needle aspiration (FNA) for the diagnosis of a mediastinal Schwannoma. Case: A 66 y/o man with newly diagnosed prostate cancer underwent CT scan of the chest and abdomen for staging which revealed a 2.5 cm mass in the lower mediastinum. Evaluation by linear scanning EUS revealed a 35mm x 29mm, partially cystic heterogeneous mass adjacent to the distal esophagus and FNA was performed. Four passes were made with a 22 gauge needle under doppler guidance. No other lesions were identified and patient tolerated the procedure well. Cytopathology revealed bland spindle cells that stained positive for S-100 but negative for CD117, Actin and Desmin which is consistent with a Schwannoma. Discussion: Schwannomas are the most common neurogenic mediastinal tumors arising from peripheral nerves. They are typically slow-growing, benign and asymptomatic. They are generally found incidentally on imaging. Imaging may reveal calcifications, cysts and hemorrhage. It is important to differentiate Schwannomas from other mediastinal tumors. Resection is the treatment of choice as they could grow over time and also because of low risk of malignant transformation.


633 Successful Treatment of Kommerell’s Diverticulum: A Rare Cause for Massive Upper Gastrointestinal Bleed Krunal Patel1, Hemant Chatrath, MD2, Eugene Trowers, MD, MPH3. 1. Banner - University Medical Center, Trumbull, CT; 2. Banner - University Medical Center, Tucson, , AZ; 3. Banner - University Medical Center, South Campus, Gastroenterology, Tucson, AZ. Introduction: Kommerel’s diverticulum is a rare anomaly of the distal aortic arch. The bulbous outpouching at the anomalous origin of the left subclavian artery is described in most cases. We describe a primary rupture of Kommerel’s diverticulum as a cause for aortoesophageal fistula and an upper gastrointestinal bleed. Case description: A 79-year-old male presented to an outside hospital for a massive upper gastrointestinal bleeding. He was transferred for tertiary care. Outside CT scan images were reviewed which showed


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[633A] Figure 1.

[634A] Figure 1.

[633B] Figure 2.

the presence of a mass in the mediastinum surrounding the aorta with pockets of gas. An EGD was performed which showed the presence of a clot in the middle third of the esophagus. The patient was taken to the OR for endovascular intervention. A 40 x 15 mm Gore endovascular thoracic graft was placed and the origin of the diverticulum was sealed. No bleeding was identified on the first day post operatively. The patient had massive rebleeding on the second day requiring multiple transfusions and a subclavian embolization was performed. The bleeding stopped. Further treatment was held and palliative measures were ensued per the patient’s request. Discussion: Burckhard Friedrich Kommerell first described Kommerel’s diverticulum in 1936. In this anomaly, the left subclavian artery arises from the right-sided aortic arch as the 4th branch and passes behind the esophagus to the left arm. The incidence of this anomaly is not exactly known and is considered very rare. Most patients with these anomalies remain asymptomatic. Kommerell’s diverticulum is well described in the literature as a cause of dysphagia and also bronchial obstructions. Reyes et al have described a case of an upper GI bleed where the patient presented after thoracic trauma. According to our search, we have described the only case where this anomaly has been responsible for an upper GI bleed. In theory, the aneurysmal dilation could cause erosions of the surrounding structures. It remains unclear if the presence of this anomaly increases the risk for aortoesophageal fistula. As with other causes of aortoesophageal fistulas our patient had an infection with an abscess that possibly eroded the aneurysmal wall. Conclusion: Kommerell’s diverticulum is a rare cause for massive upper GI bleeding. The mortality for an upper GI bleed from an aortoesophageal fistula is very high. Prompt attention is required for a successful outcome.

634 Dysphagia in a Patient With Bullous Pemphigoid Ashref Mohamed , Ariwan Rakvit, MD, Haithem Mazek. Texas Tech University Health Sciences Center, Lubbock, TX. Bullous pemphigoid is an acquired autoimmune skin disease that predominantly affects elderly. It is characterized by the presence of blisters resulting from defect of the adhesion of the basal epidermal layer with the basement membrane. It affects any part of the skin. Mucus membranes are rarely affected. Esophageal involvement has only been reported in a few cases.


[634B] Figure 2.

56 Years old farmer male with medical history of Bullous Pemphigoid diagnosed three years ago presented with odynophagia and progressive dysphagia to solid foods for one year. Bullous lesions involved his upper and lower extremities and worsens with friction from work in his farm. He also had mouth ulcers, but denies any genital or anorectal lesions. No weight loss. His medications were Prednisone, Cellcept and Methotrexate. Skin exam revealed multiple widespread, symmetrically distributed Bullous lesions involving his upper and lower extremities. Complete blood count, and complete metabolic panel were unremarkable. Esophagram showed esophageal stricture. Upper endoscopy showed esophageal stricture extending from 25-40 cm from the incisors. Balloon dilation was performed. Pathology showed evidence of acute and chronic inflammation. Patient was started on Proton Pump inhibitor and reported improvement of symptoms. Bullous pemphigoid is an autoimmune disease associated with circulating antibodies against hemidesmosomes that leads to disruption of the adhesive material which leads to intraepithelial bullous formation. It is predominantly affects the skin. In contrast to Pemphigus vulgaris, mucosal involvement is rare and extra oral involvement is exceptional. Our case is interesting as the disease presents with severe esophageal involvement with subsequent dysphagia. Esophageal involvement has been only reported in few cases. Our patient has severe esophageal disease with very long stricture. This case highlights the


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importance of considering esophageal disease in those patients with suggestive symptoms. Early diagnosis could reduce the risk of esophageal strictures development.

636 Dysphagia: An Unusual Primary Presentation of SCLC Shreya Sinha, Dhruv Lowe, MD, Sheila Lemke. SUNY Upstate Medical University, Syracuse, NY.

635 Esophagitis Dissecans Superficialis: An Uncommon Endoscopic Diagnosis Timothy Chen, MD, Jesse Liu, MD. California Pacific Medical Center, San Francisco, CA. A 72 year old female with a history of cervical nerve impingement presented with sudden onset of odynophagia. On presentation to the emergency room, the patient reported 6 hours of severe odynophagia which was dull at rest but spastic with swallowing. Of note, the patient had recently started taking cyclobenzaprine at bedtime and had completed a course of prednisone three weeks prior for neck pain attributed to her cervical nerve impingement. She denied fevers, chills, nausea, vomiting, regurgitation, dyspepsia and abdominal pain. She had no prior surgeries. Physical exam revealed an afebrile woman in no apparent distress with normal oropharyx, pulmonary and abdominal exam. Initial laboratory studies revealed CBC and CMP within normal limits. Plain films of the neck revealed no radiopaque foreign bodies or soft tissue swelling. EGD showed long strands of friable tissue paper-like mucosa overlying normal appearing esophageal mucosa. There were no signs of esophageal narrowing or retained food. Biopsies showed diffuse superficial necrosis of the squamous mucosa with separation of the necrotic upper portion from the unremarkable viable deeper layers. Additionally, few intraepithelial eosinophils were noted. These findings were most consistent with esophagitis dissecans superficialis(EDS). The patient completed a month course of twice daily proton pump inhibitor with complete resolution of her symptoms. EDS is a desquamative disorder of the esophagus with a benign natural history that is under-recognized with less than 100 published cases. Currently the etiology of EDS is poorly understood and it has a wide range of associations. The most common pathogenesis is thought to besecondary to injury of the esophageal mucosa, specifically from medications and other caustic agents. Case reports previously had focused on the histological constellation of parakeratosis, strips of epithelium with distinct necrotic edge, and lack of inflammatory infiltrates. More recent studies have proposed a clinicopathologic diagnosis of EDS with the major diagnostic criteria being 3 key endoscopic findings of the esophageal mucosa: (1)strips of sloughed esophagus, (2)normal underlying mucosa, (3)lack of ulceration/friability of adjacent esophageal mucosa. Increased awareness of the clinical, endoscopic, and histologic features of EDS should result in greater detection rates, which will prevent unnecessary investigation and therapies while aiding in the understanding of its etiology.

Introduction: Small cell lung cancer usually presents with weight loss, cough and chest pain however dysphagia as its first presentation is extremely rare. Extrinsic compression from enlarged mediastinal structures is a known and rare cause of mechanical esophageal dysphagia usually from vascular rings or thyroid enlargement. We describe an unusual case of small cell lung cancer invading into the mediastinum leading to dysphagia as the first symptom resulting in its diagnosis. Case: We present a case of a 54 yo female with past history of DM, hypothyroidism and 30 PY smoking history who presented with dysphagia to solid foods of 1 months duration accompanied by chest pain, but no odynophagia. She was only able to tolerate pureed foods and liquids. She had lost around 20 lbs in 4 months. On exam she had decreased breath sounds b/l and mild lower extremity edema. CXR showed large left sided mass. CT thorax revealed a 14.7cmx11.8cmx10.4cm mass causing compression and deviation of the trachea and esophagus to the right. Biopsy revealed SCLC and the patient was started on cisplatin and etoposide. Radiation therapy was subsequently started to relieve compressive symptoms. Discussion: Small cell lung cancers are rapidly expanding, centrally occurring tumors. The most common presentation is cough (50-75%), hemoptysis (20-50%), or chest pain due to mediastinal, pleural or chest wall extension (20-40%). Dysphagia is a rare presenting complaint, but when present, is due to metastasis to the GI tract and not due to extrinsic compression. SCLC is an unusual but important differential of dysphagia given the rapidly expanding nature of the tumor and different treatment course. Our case is different in that the dysphagia was due to extrinsic tumor compressing the esophagus. Diagnosis is dependent on imaging. Treatment includes chemo and radiation therapy by decreasing tumor burden. Conclusion: Dysphagia is an alarm symptoms for GI malignancies and work up includes fluoroscopic imaging and EGD. In a patient with dysphagia and a history of weight loss, it is important not only to


[635B] Figure 2.


[636B] Figure 2.


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Abstracts and clear liquid diet was initiated. PPI drip was changed to oral 40 mg PPI twice daily and the patient was discharged on liquid diet. Discussion: Various endoscopic modalities such as endoscopic band ligation, hemoclipping, and local epinephrine injection have been described for management of Mallory-Weiss tear. Our case was unique with respect to the extent and depth of the tear. We suggest the use of BICAP cautery as another modality in the armamentarium for management of Mallory-Weiss tear.

638 Dysphagia for a Different Reason Vinod Kumar, MD1, Shobha Shahani, MD2, Nelson Moy, MD3. 1. University of Illinois at UrbanaChampaign, Internal Medicine Residency Program, Champaign, IL; 2. University of Illinois at UrbanaChampaign, Champaign, IL; 3. Carle Clinic, Urbana, IL.

[636C] Figure 3.

Case: 32 years old female presented with right sided chest discomfort going on for 2 weeks, worse on deep inspiration. She also had developed progressive odynophagia and dysphagia, initially to solid but then progressed to liquids as well. She was given proton pump inhibitors but it continued to worsen. Esophagogastroduodenoscopy was done which showed a esophageal mass at 24 cms, ulcerating in the center and obstructing about 75% of the lumen of the esophagus. Biopsy from the nodule showed neutrophilic and eosinophilic infiltrate but was negative for malignancy. Endoscopic ultrasound showed a large hypoechoic mediastinal mass measuring 39.6 x 24.2 compressing the esophagus and causing ulceration and abutting the right pleura. Multiple hyperechoic non shadowing foci were noted inside the mass. Fine needle aspiration and biopsies also showed squamous mucosa with ulcer and granulation tissue with

consider GI etiologies, but also lung pathology, especially centrally located tumors like small cell that can cause extrinsic compression on the esophagus. This differential needs to be recognized for early intervention and follow up.

637 Extensive Mallory-Weiss Tear Managed With Bipolar Circumactive Probe (BICAP) Cautery Vivek Kesar1, Prashant Mudireddy, MD1, Varun Kesar, MBBS2, Arun Swaminath, MD1, Gregory Haber1. 1. Lenox Hill Hospital, New York, NY; 2. Lenox Hill Hospital/ Mount Sinai Hospital, New York, NY. Introduction: Mallory-Weiss (MW) syndrome is defined by an upper gastrointestinal bleed from vomiting/retching induced mucosal tear. Patients with active hematemesis or hemodynamic instability need endoscopic or surgical approach to achieve homeostasis. We report a case of deep and extensive MW tear managed by use of bipolar circumactive probe (BICAP) cautery. Case: A 41 yr old male with past medical history of alcohol abuse presented to emergency department (ED) with hematemesis. The patient endorsed food impaction followed by retching, prior to his first episode of hematemesis. On presenting in ED, the patient had three more episodes of hematemesis each approximately 100 – 150 cc. Patient denied any recent alcohol intake, NSAID or anti-coagulant use or known liver problems. The patient’s vitals in the ED revealed tachycardia. The initial physical exam was unremarkable. Subsequently, the patient was intubated for airway protection. The patient was given PPI (IV) bolus followed by drip, 2 liters of IV normal saline, 2 units of packed RBC, one bag of fresh frozen plasma, and octreotide IV bolus followed by drip. The initial labs revealed hemoglobin 14.2 gm/dl (13 -17 gm/dl) and normal coagulation panel. The patient was transferred to ICU and an emergent bed-side upper endoscopy was preformed. The endoscopy revealed a deep muscularis propria tear of the esophagus, extending 32 cm to 38 cm from incisors. There was an adherent clot interspersed with areas of active bleeding overlying the tear. The clot was gently snared and active bleeding was noticed. The hemostasis was achieved by using BICAP cautery. The settings used on BICAP cautery was power of 45 watts. Post BICAP cautery, complete hemostasis was achieved. CT chest, abdomen and pelvis with contrast was done which ruled out any evidence of esophageal perforation. The patient’s hospital course was complicated by aspiration pneumonia which was managed with IV Clindamycin. Eventually, the patient was extubated

[637A] Figure 1.


[638A] Figure 1.

[638B] Figure 2.


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phyria was found, but not the kind that presents with abdominal pain. In the meantime, the pathology report from panendoscopy returned with findings consistent with eosinophilic enterocolitis; another rare disease, but one that finally explained his current symptoms. After ruling out celiac disease, patient was started on food elimination diet to identify trigger foods since the major cause of eosinophilic enterocolitis is food sensitivity.

640 Belching: When It’s Not So Normal Nisha Shah, MD1, Lavern Belle, BS1, Harold Wain, MD1, Fouad J. Moawad, MD2. 1. Walter Reed National Military Medical Center, Bethesda, MD; 2. Walter Reed National Military Medical Center, Kensington, MD.

[638C] Figure 2.

marked acute and chronic inflammation with scattered multinucleated giant cells, histiocytic aggregates and focal granulomas. CT chest abdomen and pelvis followed, showing the same mass compressing the esophagus. As the biopsies had been negative for malignancy and suggested infectious etiology, infectious work up was sent which came out positive for Histoplasma Antibodies confirming the diagnosis of Histoplasmosis causing the mediastical mass and compressing on the esophagus. Discussion: Histoplasmosis is caused by dimorphic fungus histoplasma Capsulatum. Histoplasmosis usually is self limited in immune competent patients. GI tract involvement is rare and usually seen in disseminated cases with colon and small bowel are most commonly involved. Esophageal ulceration and dysphagia due to mediastinal mass compression is very rare presentation of histoplasmosis and usually seen in immune-compromised patients. It can cause dysphagia, obstruction and fistula formation. Treatment involved systemic antifungal agents or surgery in case of fistula formation.

Eructation is a normal physiologic event. However, when it occurs in excess, it can become problematic for patients and affect their quality of life. The differential diagnosis for excessive belching includes GERD, functional dyspepsia, rumination syndrome, aerophagia, as well as, isolated excessive belching which can be further categorized into supragastric versus gastric belching. Supragastric belches involve air being injected or sucked into the esophagus without esophageal peristalsis, unlike aerophagia where there is esophageal peristalsis with swallowing of air. Both behaviors are learned, but the latter presents with abdominal distention and discomfort as the predominant symptom rather than excessive belching. We present a 63-year-old female with a history of morbid obesity and gastroesophageal reflux disease who presented for evaluation of excessive belching and chest pain. The belching occurred approximately one hundred times per day. It was not related to food and had been steadily worsening over the last two years. A trial of acid suppressive therapy did not improve her symptoms. She denied drinking carbonated beverages, rarely used straws for sipping, and denied chewing gum. She described her chest pressure as a substernal sensation occurring several times per day. It was not exacerbated by meals, exertion, nor position but was actually relieved with belching. She denied dysphagia, heartburn, regurgitation, and weight loss. Her EGD was normal. She underwent an esophageal manometry (EM) with a 24 hour pH/Impedance study off PPIs. Her EM was normal (normal LES and 10/10 wet swallows propagated). Her total pH score was normal. During the study, she recorded 86 belches with a symptom index of less than 50%. On careful review of her belches using multi-channel intraluminal impedance, it was noted that she had over 50 supragastric belches. The patient is currently working with a behavioral therapist using diaphragmatic exercises to help reduce the numbers of supragastric belches. Although 10 sessions may typically be required before results are seen, she has noted after her second visit that the number of belches has decreased. Although functional disorders appear benign to the spectator, it can create a calamity for those who cannot participate in social environments due to the embarrassing nature of the disorder. As these behaviors can be untrained, detection by using techniques such as impedance is important to establish a diagnosis as illustrated in this case.

CLINICAL VIGNETTES/CASE REPORTS FUNCTIONAL BOWEL DISEASE

639 The Challenging Case of a Patient With Recurrent Unexplained Abdominal Pain: A Journey Through Cronh’s, Porphyria, Nephrolithiasis, Shingles, and Other Zebras Ekaterina Kostioukhina, MD1, Gaurav Singh, BA2, Andrew Fischer, MD2, Cristina Bunton, MD2. 1. University of Miami Miller School of Medicine Regional Campus, Fort Lauderdale, FL; 2. University of Miami Miller School of Medicine, Atlantis, FL. We present a patient with recurrent abdominal pain and a challenging journey to find an answer to his debilitating symptoms. Through years of struggling with pain and diagnostic dilemmas, we were faced with a history of appendectomy, cholecystectomy, episodes of pancreatitis, nephrolithiasis, abdominal shingles, Crohn’s disease, concern for drug seeking behavior, Irritable Bowel Syndrome, depression, recurrent hospitalizations, multiple colonoscopies, innumerable negative stool studies, a rare diagnosis of porphyria (but not the abdominal pain causing type), and finally, this arduous chase yielded a diagnosis of eosinophilic enterocolitis, another rare disease. 36 year old male with history of Crohn’s disease, multiple hospitalizations for abdominal pain, cholecystectomy, and appendectomy was admitted for yet another recurrence of abdominal pain and worsening of chronic diarrhea. Objective diagnostic work-up, including an abdominal CT and other bloodwork, did not show supportive evidence for Crohn’s flare. Tenderness on light touch and multiple requests for Dilaudid alerted the medical team for drug seeking behavior. However, other objective findings triggered a broader differential: a low MCV without anemia, elevated iron with normal ferritin, dark urine, history of recurring photosensitivity facial rash, a clean record on Eforcse, and the patient’s long journey to find an answer for his gastrointestinal disturbances. On further review of outside records: a series of panendoscopies with no major findings, intestinal biopsies showing intermittent signs of diffuse chronic inflammation, extensive testing for chronic diarrhea, cholecystectomy of a non-inflamed and acalculous gallbladder, appendectomy, abdominal shingles, pancreatitis, nephrolithiasis and multiple frustrated doctor’s notes, the answer to our enigma was thought to be found in the form of a positive porphyria work up! However, the test for acute exacerbation returned with undetectable porphyrin levels while the patient continued to be symptomatic. Despite our current disappointment, the diagnosis of porphyria was confirmed reliably at two different occasions in the past, with testing to rule-out other causes of elevated porphyrins and a pathologist interpretation of Porphyria Cutanea Tarda. In the quest to uncover the etiology to his chronic abdominal pain, por-


[640A] Figure 1.

641 Black Cohosh-Induced Abdominal Pain: Sometimes More Than Just a Supplement Umair Sohail, MD1, Imran Ashraf, MD1, Ashraf Almashhrawi, MD1, Rubayat Rahman, MD, MPH1, Douglas Nguyen, MD2, Matthew Bechtold, MD, FACG1. 1. University of Missouri, Columbia, MO; 2. University of California Irvine, Anaheim Hills, CA. Introduction: Black cohosh, Cimicifuga racemosa, is a North American plant. Extracts of the plants have been used for treatment of symptoms associated with menopause. Although adverse effects of black cohosh are mild and usually reversible, a few severe side effects including hepatic, cardiac and musculoskeletal have been documented but without a clear causal relationship. We report a case of black cohosh-induced abdominal pain. Case: 48 year-old female with past medical history significant for hypertension, anxiety, and uterine fibroids was referred to gastroenterology clinic for evaluation of abdominal pain going on for almost 3 months. The pain was located in the hypogastric area with no radiation, intermittent, and crampy in nature. Patient denied nausea, vomiting, constipation, diarrhea, hematemesis, melena, hematochezia, or weight loss. Abdominal cramps got worse during bowel movements. Upon examination her vitals were stable. Her examination was normal including gastrointestinal exam showing soft, non-tender,


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Abstracts non-distended, normal bowel sounds with no organomegaly. Her routine labs and CT scan of the abdomen ordered by her PCP was unremarkable except for diverticulosis. She had a pelvic ultrasound which showed two small fibroids and was thought not be causing her abdominal pain. Upon further history, she recently started an OTC menopausal product (black cohosh) for hot flushes and sleep disturbances and her symptoms started 3 weeks after starting black cohosh. She stopped taking it and noticed improvement in her symptoms of abdominal cramps. Discussion: Black cohosh was traditionally used by Native Americans of Canada and the eastern United States to treat malaria, impaired kidney function, sore throat, rheumatism, menstrual irregularities, and pain during childbirth. Recently, there has been interest in its use in the treatment of menopausal symptoms. The exact mechanism by which it exerts its action is unknown. The most common side effects are mild and reversible, such as headache, nausea, vomiting, and abdominal pain. There have been case reports mentioning severe side effects, including fulminant hepatic failure, bradycardia with heart block, and myopathy. However, causal association could not be established in these cases. This case demonstrates the need to perform a thorough history of all OTC supplements patients ingest since some may be harmful and mistaken for other diagnoses.

642 Use of Serum-Derived Bovine Immunoglobulin/Protein Isolate (SBI) for the Management of DMARD-Induced Chronic Loose and Frequent Stools Mark Anderson, MD1, Mitchell Mah’moud, MD, FACG2, Hayley Young, PhD3. 1. Boice-Willis Clinic, Rocky Mount, NC; 2. Duke University School of Medicine, Rocky Mount, NC; 3. Entera Health, Cary, NC. Serum-derived bovine immunoglobulin/protein isolate (SBI) is a prescription medical food intended for the dietary management of gastrointestinal disorders that present with chronic loose and frequent stools, namely IBS-D, IBD, and HIV enteropathy. As a medical food, SBI provides distinctive, specially formulated proteins in the form of immunoglobulins not attainable in the normal diet that bind microbial components. This results in a downstream reduction in inflammatory markers and up-regulation of tight junction proteins, thus decreasing permeability and increasing barrier function. These actions assist in managing underlying components associated with gastrointestinal conditions. Furthermore, SBI has been well-tolerated in fragile populations and has no contraindications with other medications. Due to its mode of actions, safety, and supporting clinical reports, SBI was used for the management of intractable diarrhea in an elderly female suffering from a variety of co-morbid conditions. Her response was retrospectively collected. This patient is a 61 year old African American female with a past medical history of systemic lupus erythematosus (SLE), type II diabetes, COPD, and depression. In addition to standard therapeutics to treat her co-morbid conditions, she had been given methotrexate, a disease-modifying antirheumatic drug (DMARD) to treat her SLE. However, this patient developed diarrhea due to the anti-folate drug and discontinued therapy. She was subsequently given leflunomide, another DMARD, but again discontinued after 2 weeks due to worsening of stool frequency and consistency which persisted even after she stopped the drug. Diagnostic colonoscopy results were negative for microscopic colitis and stool tests were negative for infectious agents, including C. difficile. At this time, SBI 5 g BID was initiated. Within 1 month, this patient reported management of stool frequency and consistency and continues on therapy. This patient, who developed persistent, chronic loose and frequent stools induced by methotrexate treatment, was able to manage her condition upon administration of SBI. This case highlights the applicability of this medical food for the management of chronic loose and frequent stools in patients who may have DMARD-induced diarrhea.

643 Serum-Derived Bovine Immunoglobulin/Protein Isolate (SBI) Provides Management for Patients With Longstanding Intractable Diarrhea William Salt, MD1, Fred Fowler, MD, MBA2, Mitchell Mah’moud, MD, FACG3, Hayley Young, PhD4, Raymond M. Panas, PhD5. 1. Ohio Gastroenterology Group, Westerville, OH; 2. Carolina Digestive Health Associates, Harrisburg, NC; 3. Duke University School of Medicine, Rocky Mount, NC; 4. Entera Health, Cary, NC; 5. Entera Health, Washington, DC. Serum-derived bovine immunoglobulin/protein isolate (SBI) is a prescription medical food intended for the dietary management of enteropathy including diarrhea-predominant irritable bowel syndrome (IBS-D). SBI provides specially formulated immunoglobulins not found in the diet in sufficient quantities to manage the enteropathy of IBS-D. We propose that SBI should be considered an early management option as illustrated by the following cases: A 40 y/o Caucasian female had a 5 yr history of diarrhea, postprandial abdominal pain, bloating, and distention diagnosed as IBS-D. She had failed various other treatments; colesevelam and low FODMAP diet and estimated that she had only a 35% reduction in symptoms. In a second case, a 68 y/o Caucasian female with a 3 yr history of diarrhea presenting as 6-8 watery stools/day including frequent episodes of incontinence was diagnosed with IBS-D. She refused eating at restaurants because of stool urgency. Traditional therapies had failed to resolve her symptoms. The third case involved an 18 y/o African-American male experiencing chronic diarrhea lasting several months in duration and involving 3-4 loose stools/day; he was diagnosed with IBS-D after excluding other causes. Recent reports and clinical experience support the efficacy of SBI in the management of enteropathies including IBS-D. As such, SBI was added to the therapy of these patients in an effort to manage their conditions. For Patient #1, SBI 5g BID for the first two wks was incorporated into the therapeutic regimen and then maintained at 5g QD. For Patient #2, SBI was added into the patient’s regimen at 5g QD and maintained at this level. Patient #3 was started and maintained at 5g BID as a monotherapy. The first patient had significant improvement within the first 4 wks with at least a 75% reduction in overall symptoms. Her quality of life had improved significantly including durable ability to eat without fear of triggering bouts of urgent diarrhea. The second patient reported a similarly substantial improvement of quality of life including the enjoyment of eating at restaurants due to 1-3 formed stools/day without incontinence. The third patient reported no further episodes of loose stools and is doing remarkably well on SBI therapy. These three cases add to the accumulating evidence that the prescription medical food, SBI, is an effective management option for the enteropathy of IBS-D.

644 Management of Antibiotic-Associated Diarrhea After C. difficile Infection With a Serum-Derived Bovine Immunoglobulin Preparation Michael LeVine, MD1, Bruce Burnett, PhD2, Larry Good, MD3. 1. Atlanta Gastroenterology Associates, Smyrna, GA; 2. Entera Health, Cary, NC; 3. State University of New York, Lynbrook, NY. Clostridium difficile infection (CDI) has a high mortality, morbidity and large economic cost and can cause mild diarrhea to a fulminant, life threatening colitis. Antibiotics, though effective can lead to antibiotic-associated diarrhea (AAD). Serum-derived bovine immunoglobulin (SBI) has been shown to bind/neutralize toxins A&B from hypervirulent ribotypes in vitro and reduce CDI-induced mortality by 50% in a low-protein fed mouse model. Due to these activities and its reported efficacy in managing chronic loose and frequent stools, SBI was administered to 4 patients with CDI experiencing AAD. Patient 1 (89 yrs Caucasian female) had a history of severe CDI in 2012 unresponsive to metronidazole requiring vancomycin for 2-wks and a 1-mo taper. Following a urinary tract infection resolved with antibiotics, CDI reoccurred and was resolved with additional vancomycin, but the patient had AAD unresponsive to loperamide. Patient 2 (76 yrs Caucasian male) had CDI-induced colitis treated with a 20-day course of metronidazole, but had continued diarrhea. Probiotics had no effect. Patient 3 (59 yrs Caucasian female) had a history of chronic IBS-C, controlled by lubiprostone. After an upper respiratory tract infection treated with amoxicillin/clavulanic acid, she developed severe, watery, foul smelling stools (8-12/d) within 48 hrs. The patient was switched to azithromycin and discontinued lubiprostone. Despite switching to azithromycin, it did not stop her diarrhea and was found to be CDI positive by PCR. Patient 4 (89 yrs Caucasian male) had myelodysplatic syndrome, ASCVD s/p CABG, was hospitalized with acute exacerbations of COPD treated with IV piperacillin/tazobactam, and developed diarrhea on day 4. PCR stool analysis revealed CDI and the patient was switched to oral vancomycin. Post-discharge, his diarrhea persisted after 5 days of vancomycin therapy. Patient 1 was given SBI 5g BID and after 1-week had improved stool consistency/frequency and a better sense of well-being. Patient 2 received SBI 5g TID for 9-d and it managed chronic loose and frequent stools. Patient 3 dosed with SBI 5g BID had normal stool frequency/consistency within 72 hrs. He was maintained asymptomatically on SBI for 30-d. Despite a positive CDI stool test by PCR, routine colonoscopy 6-wks later revealed no clinical signs of disease. Watery stools in Patient 4 were managed with the combination of 200mg fidaxomicin BID and SBI 5g BID after 48 hrs. After the 10-day course of fidaxomicin, SBI was continued for an additional 14-d with no recurrent symptoms. It is hypothecized that SBI may help restore normal barrier function by binding to microbial components produced after antibiotic therapy, thereby reducing immune activation which degrades the intestinal barrier. These cases suggest that SBI is useful in helping nutritionally manage AAD.

645 Hypertrophic Myopathy of the Anal Sphincter Muscle in a Patient With Chronic Proctalgia Xiaolu Carter, DO1, Kulthep Rattanakovit, MD2, Satish Rao, MD3. 1. SAUSHEC Department of Gastroenterology, San Antonio, TX; 2. Georgia Regents University, Bangkok, Thailand; 3. Medical College of Georgia at Georgia Regents University, Augusta, GA. Introduction: Chronic proctalgia is a rare functional anorectal disorder. Levator ani syndrome (LAS) and unspecified functional anorectal pain are two subtypes of chronic proctalgia. Literature review reveals two case reports of internal anal sphincter myopathy causing proctalgia fugax with possible hereditary contribution, however never observed in chronic proctalgia patient. Case: We are presenting a 54 year old African American female with over 10 years history of constant rectal pain, constipation with intermittent severe spasm. She is status post hysterectomy for possible large fibroid that cause constipation, and diverting colostomy with colostomy bag after multiple stool impactions. Her MRI studies of cervical and lumbar spine were benign. Electromyography study showed chronic left S1 radiculopathy. Her anorectal manometry showed hypertensive fluctuating anal sphincter tone with usual pattern of cyclical increase in resting sphincter tone, maximum pressure of over 300 mmHg with each spasm. She has severe dyssynergic defecation and failed balloon expulsion. Anal ultrasound showed severe hypertrophic anal sphincter muscles. Her translumbar and transacral nerve conduction tests showed bilateral anorectal neuropathy. Flex sigmoidoscopy showed a small fissure and mild colitis of distal colon blind pouch, for which she was treated with metronidazole for possible diverting colitis and topical diltiazem for the fissure. Discussion: Treatment of LAS includes topical agent, digital massage of the levator ani muscles, sitz baths, muscle relaxants, botulinum toxin A, electrogalvanic stimulation, sacral neurostimulation,



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647 Multifactorial Etiology of Worsening Gastroparesis in a Patient With Ehler’s Danlos Winnie Szeto, MD1, Lauren M. Fine, MD2, Allan Levi, MD, PhD2, Lucy Chen, MD1, Syeda U. Abbas, MD1, Baharak Moshiree, MD, MS3. 1. University of Miami Miller School of Medicine, Miami, FL; 2. Miami Miller School of Medicine, Miami, FL; 3. University of Miami, Leonard M. Miller School of Medicine, Dept of Medicine, Division of Gastroenterology, Miami, FL.

[645B] Figure 2.

biofeedback training, local steroid injection and surgery. Her anorectal pain did not improve with treatment of her small fissure and colitis. The likely causes of her rectal pain include LAS with possible anorectal neuropathy causing chronic spasm of the sphincter muscles. However, anal sphincter muscle hypertrophy has not been described in the past in patients with LAS. Her anorectal neuropathy, chronic pain, and straining might contribute to, or be the result of her hypertrophic sphincter muscle. She has failed conservative medical treatment. Repetitive nerve stimulation treatment was scheduled for her but has not yet started. Conclusion: Chronic proctalgia is a rare and difficult condition to treat. Different treatments have been tried in the past but with mixed effects. Anal sphincter muscle hypertrophy can be either the cause or result of chronic proctalgia and repetitive nerve stimulation treatment can be a useful treatment option.

A 27 yo female with a history of dystonia, chronic migraines, motor tics, Ehler’s Danlos Syndrome and Chiari malformation presented with persistent nonbilious emesis, headaches, nausea and early satiety. The patient had a posterior fossa craniotomy with placement of a DuraGen dural graft matrix 6 weeks prior, and lost 15 pounds due to severe nausea and vomiting with inability to tolerate liquids or solids. On MRI of the head she was found to have a stable suboccipital craniotomy. She also underwent a lumbar puncture with negative cultures. A NM gastric emptying study was performed which demonstrated significant retention of gastric contents calculated to be 25% at 4 hours. Endoscopy with botox injection of the pylorus was performed. Over the next few months her nausea and vomiting persisted despite treatment with ondansetron, prochlorperazine maleate, trimethobenzamide, dexamethasone, domperidone, dronabinol, anti-migraine medications, IV caffeine drip and promethazine. A jejunostomy tube was placed given ongoing malnutrition. During this time, she developed a pruritic urticarial rash at the site of her cranial decompression. In order to control her pruritus she required high doses of diphenhydramine, given lack of response to hydroxyzine; 100mg oral 3-4 times a day. An allergic reaction to the prolene sutures or gortex dura graft was suspected with the recent posterior fossa craniotomy. Allergy skin testing was performed with placement of prolene sutures and a gortex patch on the patient’s forearm. She was positive for a prolene allergy and was subsequently taken to the operating room with removal of her prolene sutures. As the urticaria and pruritus resolved she no longer required diphenhydramine. Her nausea and vomiting resolved and she gained 28 pounds. She no longer required J tube feedings. This case emphasizes the importance of medication-induced delay in gastric emptying from anti cholinergic agents. Medication induced gastroparesis should be considered even in patients with EDS in whom an etiological diagnosis of gastroparesis is common. It is critical to discontinue narcotics and other medications that affect gastric emptying at least 48 hours prior to a gastric emptying test. Once diagnosis is confirmed, management should include assessment and correction of nutritional state, relief of symptoms, improvement of gastric emptying, and glycemic control in diabetics.

CLINICAL VIGNETTES/CASE REPORTS - IBD

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Chronic Idiopathic Intestinal Pseudo-Obstruction: Revisiting Neurogastroenterology

Is an Ileal Phlegmon Always Crohn’s Disease?

Ankush Kalra, MD, Anthony J. DiMarino, Jr., MD. Thomas Jefferson University Hospital, Philadelphia, PA.

Juan M. Marques-Lespier, MD1, Rocio Feliu, MD2, Miguel Noy3, Jose J. Muñoz4, Roberto Osorio2, Yomarid Quiñones2, Carmen Gonzalez, MD5, Juan J. Lojo, MD6, Roman Velez, MD7, Irene S. Villamil, MD2, Esther A. Torres, MD, MACG8. 1. University of Puerto Rico, Guaynabo, Puerto Rico; 2. University of Puerto Rico, San Juan, Puerto Rico; 3. University of Puerto Rico-RCM, San Juan , Puerto Rico; 4. University of Puerto Rico, San Juan , Puerto Rico; 5. University of Puerto Rico School of Medicine, San Juan , Puerto Rico; 6. School of Medicine, University of Puerto Rico, San Juan, Puerto Rico; 7. School of Medicine, University of Puerto Rico, Guaynabo, Puerto Rico; 8. University of Puerto Rico School of Medicine, San Juan, Puerto Rico.

Chronic intestinal pseudo-obstruction (CIP) is a rare and disabling motility syndrome, yet one that demands an extensive review of digestive motility and peristaltic pathophysiology. Symptoms are often slowly progressive and diagnosis requires the presence of symptoms for at least six months. RC is a 75-year-old male with no significant past medical history. His story begins with mild symptoms, limited to constipation relieved with over the counter laxatives. After two brief admissions for small bowel obstructions (SBOs) that resolved with nasogastric tube (NGT) decompression, RC presented months later with an SBO that persisted after NGT placement. A CT scan demonstrated multiple dilated loops of small bowel with a transition point in the proximal ileum. During exploratory laparoscopy, the entire small bowel and colon demonstrated no abnormality. Ultimately, an ileocecectomy was performed and RC underwent a thorough diagnostic workup. CIP is categorized as either idiopathic or secondary. Secondary CIP was ruled out with lab testing for collagen vascular diseases, hypothyroidism, diabetes and celiac disease. A thorough paraneoplastic workup was unremarkable, including Ho, Yu, and neuronal nuclear antibodies, as well as workup for thymoma, lung cancer, thyroid cancer, and testicular cancer. The ileocecectomy specimen demonstrated small bowel mucosa with prominent reactive lymphoid hyperplasia. While nonspecific, this pathology is most consistent with an inflammatory neuropathy. Treatment began with an ileocecectomy and gastrostomy tube for venting. With continued symptoms and radiographic pseudo-obstruction after ileocecectomy, RC was started on total parenteral nutrition. After failure of stool softeners, laxatives, and lubiprostone, success was achieved with a regimen of linaclotide, octreotide and rifaximin. RC resumed regular bowel movements and maintains a gastrostomy tube for intermittent venting. Inflammatory neuropathies are the most common cause of CIP, defined by myenteric plexus ganglionitis. Octreotide has been demonstrated to generate migrating motor complexes in CIP secondary to scleroderma. While bowel stasis generates a cycle of small intestinal bacterial overgrowth (SIBO) causing mucosal inflammation and further dysmotility, octreotide and rifaximin have both been proven to reduce SIBO, measured by breath hydrogen excretion. Linaclotide is believed to maintain intestinal mucosal integrity via guanylate cyclase C agonism. The medical community must continue to inquire about such targeted therapies for CIP and other functional gastrointestinal disorders. It is essential that failed and successful treatment regimens be shared and discussed, and that the pathophysiological basis of treatments used in these cases continues to be a key focus of research.


Introduction: There are 4800 new cases of small bowel adenocarcinoma each year in the USA, of which adenocarcinoma of the ileum accounts for only 18% of cases. Crohn’s disease is the greatest risk factor with a relative risk between 15 and >100. The risk does not begin until at least 10 years after onset of Crohn’s disease and typically occurs after more than 20 years. Clinical Case: This is a 47 y/o male diagnosed with Crohn’s disease in 1989 after presenting with abdominal pain, non-bloody diarrhea and weight loss. Diagnosis was confirmed bye endoscopic evaluations, and small bowel series. Treatment consisted of prednisone 30mg daily and mesalamine at the beginning, however it was discontinued due to poor tolerance. He continued on steroids with clinical improvement until 2010. In 2011, the patient developed multiple abdominal symptoms including RLQ pain, and follow up abdominal CT scan showed significant progression of disease in the ileum despite chronic therapy with prednisone. He was prescribed adalimumab in 2013, however due to social problems therapy was postponed. Follow up imaging in July 2013 showed worsening disease in the ileum, with evidence of phlegmonous process and active disease in the terminal 56cm of ileum. Patient refused hospitalizations for condition and finally started adalimumab in February 2014. Clinical symptoms deteriorated, developing malnutrition, anemia, marked weight loss, and hypoalbuminemia. In September 2014, the patient was admitted to the UPR Center for IBD. He was placed on bowel rest, parenteral nutrition and antibiotics. An exploratory laparotomy was performed after his nutrition had improved and the inflammatory process had decreased. Extensive inflammation around the ileum and ascending colon and a perforation were identified. 66cm of small bowel were removed, including multiple fistulas, a contained perforation and adhesions. An end ileostomy and colonic mucous fistula were left in place. Pathologic exam showed Ileum adenocarcinoma T4NX. Distant metastasis was not found. Conclusion: Adenocarcinoma of the ileum is a rare disease. However, long standing Crohn’s disease is a risk factor. The failure of a stricture or inflammatory process to respond to appropriate medical therapy over a reasonable time period should prompt the consideration of surgical resection. The decision for surgery requires a well-integrated team approach and expert clinical judgment. The possibility of an underlying malignancy must be kept in mind, and the inability to exclude cancer, as well as the refractoriness of the disease to medical therapy, are clear indications for surgery.


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Multiple Enteroenteric Fistulas: Crohn’s Disease

Primary Varicella Infection During Infliximab Treatment for Fistulizing Crohn’s Disease

Faizan Sheraz, MD1, Hasnain Abbas Dharamshi2, Maliha Shakil, MD, MBBS3, Shaista Noor Mohammad, MBBS, MD4, Bushra Ehsanullah, MBBS, MD5, Nawal Muazam, MD, MBBS6. 1. Army Medical College, Pearland, TX; 2. Karachi Medical and Dental College, Karachi, Pakistan; 3. Ziauddin Medical University, Spring, TX; 4. Vydehi Institute of Medical Sciences, Naperville, IL; 5. Baqai Medical University, Des Plaines, IL; 6. Army Medical College, Bensalem, PA.

Thu Pham, MD1, Sasha Taleban, MD2. 1. University of Arizona, Santa Ana, CA; 2. University of Arizona, Tucson, AZ.

A 39 years old Pakistani male with a past history of significant crohn’s disease since last 18 years presented to ER with severe supra pubic abdominal pain, dysuria, pneumaturia and fecal contamination of urine. He had occasional nausea and vomiting, crampy abdominal pain with bloating associated with meal intake and occasional diarrhea leading to significant weight loss of 15 pounds over the previous 1-2 months.He was medically managed on infliximab for approximately 10 years but switched later to cetolizumab due to episodes of exacerbation between the doses. The next drug also failed after 1-2 months as he started having acute episodes in the last few months. He had pre-operative colonoscopy, a year ago, after that exploratory laparotomy was recommended with possible resection of diseased bowel and stricturoloplasty by his primary GI physician but he denied it. He completed a 2 week course of ciprofloxacin plus metronidazole and a week course of prednisone for his symptoms and became asymptomatic with the treatment. One week after completion of symptomatic treatment he became symptomatic again and has been progressively getting worse. CT scan with contrast showed moderately distended small bowel, compatible with small bowel obstruction, due to significant inflammatory edematous thickening of the terminal ileum. There was evidence of multiple enteroenteric fistulas. Also there was an inflamed small bowel loop inseparable from the superior wall of bladder with presence of gas in the urinary bladder demonstrating evidence of enterovesicular fistula. The overall configuration suggested complications related to chronic inflammatory bowel disease. Colonoscopy a year ago showed classic features of chronic inflammatory disease with tubulization in the cecum, ascending colon and proximal transverse colon as well as sigmoid colon and rectum. The distal transverse colon and the entire descending colon appeared to be free of obvious disease. A flat carpet like polyp was also seen at ano-rectal junction. Crohn’s disease involves the gastrointestinal tract from mouth till anus. Skip lesions, fistula formation and transmural involvement of colonic wall are features of the disease. Adequate medical and surgical treatment can keep the disease in remission and prevent acute exacerbations. This case reports multiple eneteroenteric and enterovesicular fistulas in asian patient suffering from long term crohn’s disease however this disease is very rare in asian population with such an advanced involvement of gastrointestinal tract involving urinary tract as well.

Background: Anti-TNF therapies are important in the prevention and treatment of complications in moderate to severe Crohn’s disease. The risk of viral infections is increased in immunosuppressed patients. The herpes viruses are the most common viruses complicating immunosuppressed inflammatory bowel disease (IBD) patients. Compared to the general population, the risk of varicella virus is increased in IBD. Primary varicella virus is particularly important in immunosuppression as it can lead to disseminated disease and death. To our best knowledge, there have been very few reported cases of primary varicella infection in IBD patients while on anti-TNF therapy. Case Description: We report a case of a 21-year-old female with a history of internal fistulizing Crohn’s disease of the colon that was diagnosed in 2006 who first presented to our clinic in 2014. She was first started on Infliximab in 2011 and was continued at 5 mg/kg every 8 weeks. Of note, she lives with her father who recently had active singles. She presented to our clinic with vesicular eruptions on her back, abdomen, and trunk. Her varicella vaccination status is unclear. Clinical Outcome: Infectious disease was consulted and patient was started on oral Acyclovir. Due to endoscopic remission of her disease, Infliximab was held. She completed her course of antiviral and her varicella skin lesions gradually healed. Discussion: Although varicella infection is generally a benign disease in children, it can pose serious threats to immunocompromised individuals. It is important that physicians ask patients with inflammatory bowel disease regarding their vaccination history and VZV exposure at the first visit in the event they may require immunosuppressive therapy and may need appropriate vaccinations prior to commencing such therapy. Unfortunately, obtaining a history may not be adequate as a study done by Melmed et al revealed 11% of IBD patients did not reliably recall a history of chicken pox or varicella vaccination. Conclusion: Primary varicella infection appears to be a relatively uncommon occurrence in IBD patients. Patients should undergo serology testing for VZV IgG to determine the need for vaccination prior to initiating immunosuppressive therapy. If varicella infection occurs during therapy, prompt diagnosis and treatment with Acyclovir is important. With disseminated varicella infection, immunosuppressive therapy should be stopped. In varicella infection isolated to the skin, the decision to continue immune suppression should be made on a case-by-case basis.

651 Isolated Gastroduodenal Crohn’s Disease: Masked as a Malignancy Rukevwe Ehwarieme, MD1, Suhag Patel 2, Murray Ehrinpreis, MD3, Kartikkumar Jinjuvadia2. 1. McLaren Flint, Flint, MI; 2. Harper Hospital, Detroit, MI; 3. Department of Gastroenterology, Wayne State University School of Medicine, Detroit, MI.

[649A] Figure 1.

Crohn’s disease is a chronic idiopathic inflammatory disease of the GI tract which is usually associated with ileo-colonic and colonic/rectal involvement. The stomach and duodenum are rarely the sole predominant site of Crohn’s disease. We report such a case where gastroduodenal Crohn’s was interpreted as a malignancy. A 26 year-old male was referred to our clinic for a second opinion by an oncologist following an abnormal abdominal CT scan showing an antral mass suggestive of a malignancy, and an endoscopy with biopsy which showed atypical cells. He complained of intermittent epigastric pain and post-prandial nausea and vomiting for over 9 years. His symptoms had failed to respond to proton pump inhibitors and diet modification. He also reported unintentional weight loss of over 60 lbs within a period of 6-7 years. He denied smoking or alcohol abuse. He had no other medical conditions, and he denied any family history of intestinal tract malignancy or bowel disease. He was cachectic and in mild distress from epigastric discomfort. He was hemodynamically stable. Abdominal examination revealed mild epigastric tenderness on deep palpation. There were no oral ulcers, lymphadenopathy, or anal fissures or fistulas. The remainder of his physical examination was normal. He had a microcytic anemia and a normal complete metabolic profile. Tests for TB and HIV were negative. Chest x-ray was normal. Colonoscopy with terminal ileoscopy was unremarkable. An endoscopic ultrasound revealed diffuse thickening of the antral wall with no other abnormality. An upper endoscopy showed markedly abnormal granular, edematous, friable, and ulcerated mucosa involving the antrum, pre-pyloric region, and the pylorus, with mild gastric outlet obstruction. The duodenal bulb and second portion were also involved. There was extensive superficial ulceration and overlying exudate. Biopsy showed chronic inflammation with granulation tissue and multinucleated giant cell formation. Stain for H. pylori was negative. He was started on a proton pump inhibitor, sucralfate, and prednisone with marked resolution of symptoms. This case demonstrates a rare presentation of isolated gastroduodenal Crohn’s disease mimicking a gastric malignancy. Gastroduodenal Crohn’s can easily be confused with other diseases, including peptic ulcer disease and, as in our patient, malignancy. The characteristic findings on endoscopy and adequate biopsies usually aid the diagnosis. Close follow up is suggested as up to one third of these patients develop distal disease over time. Although management remains controversial, initiation of steroids and proton pump inhibitors have been shown to be helpful symptomatically.

652 A Novel Presentation of 6-Mercaptopurine Toxicity in a Patient With IBD Zachary C. Junga, MD1, Nisha Shah, MD2, John Betteridge, MD3. 1. National Capital Consortium, Walter Reed National Military Medical Center, Rockville, MD; 2. Walter Reed National Military Medical Center, Bethesda, MD; 3. Walter Reed National Military Medical Center, Kensington, MD.

[649B] Figure 2.


Pancreatitis and drug fever are well-known idiopathic side effects of the immunomodulatory drugs. Erythema nodosum (EN) and episcleritis are well-known extra intestinal manifestations of Inflammatory Bowel Disease (IBD). We present a unique case of 6-MP induced pancreatitis, drug fever, episcleritis, and erythema nodosum in a patient with IBD. A 30-year-old female with Ulcerative Colitis status post proctocolectomy with an IPAA re-presented with inflammatory arthritis and diarrhea. Endoscopy showed proximal ileitis consistent with Crohn’s. She was


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653 Ustekinumab in the Successful Treatment of Refractory Esophageal Crohn’s Disease Presidential Poster Jodie A. Barkin, MD1, Amar R. Deshpande, MD2. 1. University of Miami, Leonard M. Miller School of Medicine, Dept of Medicine, Division of Gastroenterology, Bay Harbor, FL; 2. University of Miami, Leonard M. Miller School of Medicine, Dept of Medicine, Division of Gastroenterology, Miami Beach, FL.

[652A] Figure 1.

Esophageal involvement in Crohn disease (CD) is rare; a segment of this population is refractory to conventional CD therapies. Ustekinumab, a human monoclonal antibody against IL-12 and 23, is an emerging biologic agent in the management of patients with CD. Here we present a case of refractory esophageal CD that responded to ustekinumab. A 23 year old man presented for follow up of his CD complaining of odynophagia and oral ulcers. He had a 15 year history of aggressive, primarily stricturing colonic and perianal CD, status post subtotal colectomy with end ileostomy. Prior to colectomy, he failed conventional therapies including mesalamines, steroids, thiopurines, methotrexate, and anti-TNF agents; he also failed to respond to unconventional therapies including thalidomide, worms, GM-CSF, and stem cells. Post-operatively he did well on certolizumab pegol for a few years before the proximal alimentary tract symptoms occurred. Upper endoscopy revealed oral aphthae and multiple esophageal ulcers, biopsies showing ulceration and inflammation negative for viruses. Otolaryngology empirically treated for herpes simplex virus with valacyclovir and prednisone; symptoms rapidly improved but recurred after tapering off prednisone with poor oral intake leading to a 30 pound weight loss. He continued to have intermittent oral and esophageal symptoms despite high-dose prednisone, swallowed fluticasone, aggressive acid suppression, and certolizumab pegol. He declined natalizumab given JC virus positivity, vedolizumab was not yet approved and he did not meet study entry criteria, and thalidomide had previously led peripheral neuropathy. He was therefore switched from certolizumab pegol to ustekinumab at 90mg subcutaneously every 8 weeks; over the next several months he achieved prolonged symptom remission off all steroids and acid suppression. Repeat upper endoscopy revealed complete resolution of oral and esophageal ulceration (pre- and posttreatment in Figures 1 and 2 respectively). Ustekinumab has been shown to have promise in the treatment of refractory, typically intestinal CD [Gastroenterology 2008;135(4):1130-41. N Engl J Med 2012;367(16):1519-28]. To our knowledge, there are no prior reports on the successful use of ustekinumab in esophageal CD. We previously reported on the successful use of thalidomide for esophageal CD [Am J Gastroenterol 2013;108(5):855-7]. Most new therapies have focused on ileocolonic disease, including the anti-integrins; ustekinumab should be considered as a possible management strategy in patients with esophageal CD.

[653A] Figure 1.

[652B] Figure 2.

started on combination immunosuppression with adalimumab and 6-MP. She later presented to clinic with six days of epigastric pain, vomiting, fevers, and scleral injection. Three days prior she had developed multiple red, tender, non-pruritic nodules on her anterior tibia bilaterally. Her bowel frequency had improved from 12 to 4 stools per day. She was febrile with an elevated lipase, CRP, and a neutrophil predominant leukocytosis. She was diagnosed with pancreatitis and admitted. Liver enzymes were not elevated and imaging was negative for biliary disease. There was no history of alcohol consumption. Blood, urine, and stool cultures were negative and her stool was negative for c. difficile. Dermatology concluded the lesions were consistent with EN and ophthalmology concluded the scleral injection was consistent with episcleritis. The 6-MP was stopped and the patient improved rapidly. By hospital day 2, she was tolerating a normal diet and her leukocytosis had resolved. The lower extremity rash also rapidly improved. Throughout the patient’s hospitalization, there was no change in the character or frequency of the patient’s bowel movements. While pancreatitis and EN are documented side effects of 6-MP, the combination along with episcleritis and presence of fever make for a novel presentation of 6-MP toxicity in a patient with IBD. Although IBD flare was on the differential as well as inflammatory panniculitis secondary to pancreatitis, the improvement in baseline Crohn’s symptoms with medical therapy, the timing of new symptoms related to initiation of 6-MP, as well as rapid improvement in symptoms after discontinuation of 6-MP are all indicative of a drug-related etiology. While this is a very unique case, its importance lies with appropriate management of thiopurine toxicity which includes quick clinical recognition and discontinuation of the medication which can be challenging in such complicated patients.


[653B] Figure 2.

654 Case Vignette: Palmar Plantar Erythrodysesthesia (PPE) Resulting From Mesalamine C. Gregory Albers, MD, FACG1, Ketan Shah, MD, MBA2. 1. University of California Irvine Medical Center, Orange, CA; 2. University of California Irvine Medical Center, Irvine, CA. A 68-year old Korean male with a history of diabetes mellitus, dyslipidemia, latent TB status post treatment, and prior hepatitis B exposure was diagnosed with Crohn’s colitis in 2010. He was treated with multiple agents, including but not limited to multiple anti-TNF agents, rotating antibiotics, and topical mesalamine. Anti-TNF therapies appeared to be associated with leukopenia and other complications and hence needed to be discontinued. The patient was in clinical remission and had a low fecal calprotectin level while on low-dose suppressive ciprofloxacin and oral MMX-mesalamine 1.2 grams twice daily. Two months after starting mesalamine, he developed a pruritic rash on his palms and soles associated with dysesthesia that persisted despite administration of high-potency topical steroids and discontinuation of


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Abstracts capecitabine, 5-fluorouracil, liposomal doxorubicin, and sorafenib. We report a case of PPE related to the administration of mesalamine, of which only a few cases have been reported in the literature. The rash quickly resolved after discontinuation of mesalamine.

655 A Rare Case of Persistent Lichen Planus in the Setting of Tumor Necrosis Factor (TNF) Alpha Inhibitor Use Meredith R. Sherrill, MD, MS1, Jordan J. Karlitz, MD2, Ardalan Minokedeh, MD, PhD3. 1. Tulane University Internal Medicine Residency, Jefferson, LA; 2. Tulane University School of Medicine, New Orleans, LA; 3. Tulane University Dermatology, New Orleans, LA.

[654A] Figure 1.

HPI: A 41 yo woman with Crohn’s disease (CD) presents with a diffuse rash that began 1 month after starting certolizumab. It began as “spots” on her hands, progressing to feet, buttocks, chest, abdomen and back. The “spots” became raised, erupted, and bled, often at joints, causing pruritus and pain. She started a topical cream but the rash worsened, so certolizumab was stopped after 6 months of treatment. Other medications include acetaminophen and triple antibiotic cream. Prior CD medications included infliximab, steroids and mesalamine. PMH: Fistulizing CD, requiring bowel resections and multiple perirectal abscess drainages. PE: Multiple hyperkeratotic violaceous papules on the dorsal hands, palms, feet, soles, vagina and rectal area with fissuring. Some papules coalesce into plaques, especially on the dorsal hands and forearms. Isolated 7-9 mm papules on her right lower abdominal quadrant and middle back. Nails showed dorsal pterygium. Laboratory: WBC (14.3), Hgb (8.5) and Plt (579,000). Biopsy: 4 mm punch biopsy from left dorsal hand consistent with lichenoid drug eruption: lichenoid irregular acanthosis, hypergranulosis, hyperkeratosis with focal parakeratosis as well as superficial dermal perivascular and interstitial lymphocytic infiltrate with rare eosinophils. Hospital and Outpatient Course: She was given a topical steroid. As an outpatient, she started adulimumab, with mild resolution of the rash over 6 months. Discussion: TNF alpha inhibitors block TNF alpha, an active participant in the inflammatory cascade, and are used in autoimmune disorders such as rheumatoid arthritis, infl ammatory bowel disease, and psoriasis. Interestingly, there have been multiple cases of cutaneous side effects, both common (psoriasis) and rare (lichenoid eruption). Lichen planus-like reactions have been reported with certolizumab, etanercept and infliximab. As the rash occurs on a continuum from clear psoriasiform eruption to full lichen planus, histological evaluation from punch biopsy is usually needed for diagnosis.

[655A] Figure 1.

[654B] Figure 2.

ciprofloxacin. The rash was an impressive erythematous, eczematous rash with extensive lichenification, cracking, and crusting (see images). It was isolated to the bilateral palms and soles with clear demarcation between normal and abnormal skin. Skin punch biopsy demonstrated eosinophilic spongiosis consistent with an eczematous drug reaction, which we felt to be consistent with palmar plantar erythrodysesthesia (PPE) related to mesalamine. Three months after development of the rash, mesalamine was eventually discontinued and replaced by delayed-release oral budesonide. Soon thereafter, the rash rapidly improved and completely resolved. He was bridged with oral corticosteroids and oral metronidazole to vedolizumab and is currently doing well. Palmar plantar erythrodysesthesia (PPE), also known as hand-foot syndrome, is a known and common toxicity and possible adverse drug effect related usually to chemotherapy agents, most often with



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[655C] Figure 3.

[656B] Figure 2.

This paradoxical reaction, when an anti-inflammatory agent causes an inflammatory reaction, is theorized to be due to up-regulation of other pro inflammatory agents in the body, such as interferon-alpha, in the setting of decreased TNFa. The reaction develops over weeks to months. Various treatments include total cessation of TNFaI, initiation of alternative TNFaI, and topical +/- oral steroids. Improvement of the rash varies from mild improvement to full resolution and can take weeks to months. Regardless of treatment approach, it is important to recognize and treat early as these cutaneous side effects can exacerbate and complicate already existing fistulizing CD.

656 T-Cell Lymphoma in a J-pouch After IPAA Navdeep Chehl, MD1, Edwin McDonald, MD1, Bashar Almadani, MD1, Garth Swanson, MD, MS1, Michael Brown, MD, FACG1, Shriram Jakate, MD1, Ali Keshavarzian, MD2. 1. Rush University Medical Center, Chicago, IL; 2. Rush Univeristy Medical Center, Chicago, IL. Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) with an ileal reservoir in a J configuration (J-pouch) is the surgical treatment of choice for many patients with intractable ulcerative colitis (UC). Malignancy of the ileal pouch, especially lymphoma, rarely occurs after IPAA. We present, to our knowledge, the first reported case of T-cell lymphoma (TCL) occurring within a pouch following IPAA. The patient is a 51 year old male with PMH significant for UC, diagnosed in 1992, s/p subtotal colectomy with IPAA and a J-pouch in 2005. He presented in April 2014 with worsening abdominal pain, increased watery bowel movements with occasional blood, 20-lb unintentional weight loss, oral ulcers and fever in the setting of hypoalbuminemia and elevated ESR/CRP. EGD and sigmoidoscopy revealed severe inflammation with ulcerations in the neo-terminal ileum and pouch mucosa; pathology was consistent with Crohn’s disease. He was treated with IV steroids and started on infliximab; methotrexate was soon added. He was readmitted due to persistent symptoms in June 2014, with associated fever, leukocytosis, iron-

[656C] Figure 3.

deficiency anemia, thrombocytosis, hyponatremia, and elevated CRP. CT abdomen/pelvis showed wall thickening in the distal small bowel and rectum. Repeat EGD and sigmoidoscopy demonstrated severe inflammatory changes of the neo-terminal ileum and pouch mucosa with deep fissured ulcers, loss of vascularity, erythema, and severe nodularity; in addition to mild duodenal Crohn’s disease, pathology showed necrosis with highly atypical lymphoid cells consistent with a T-cell lymphoproliferative disorder in the pouch. NIH review of the slides confirmed the diagnosis of TCL. CT staging, bone marrow biopsy and flow cytometry failed to show evidence of lymphomatous involvement. The patient underwent a diverting ileostomy and was discharged on a steroid taper and TPN. He subsequently received 6 cycles of CHOP chemotherapy and underwent an autologous stem cell transplant. Repeat sigmoidoscopy revealed mild erythema of the pouch mucosa consistent with pouchitis; pathology was negative for lymphoma. The patient currently remains in remission and is without any further inflammatory bowel disease activity despite the lack of maintenance therapy. This is a unique case of a patient developing T-cell lymphoma in a J-pouch. Pouchitis is the most common complication in UC patients who have undergone IPAA, and chronic pouchitis is a known risk factor for neoplastic transformation. Clinicians must consider the possibility that persistent pouchitis may herald the development of lymphoma, thus placing the utmost importance on ensuring a high-quality biopsy specimen is obtained and thorough analysis is performed.

657 Herpetic Whitlow as a Clue to HSV Colitis in a Patient With Ulcerative Colitis: A Case Report Haroon Shahid, Aaron Martin, MD, Kunjal Gandhi, MD, Christina Tofani, MD, Patricia Kozuch, MD. Thomas Jefferson University Hospital, Philadelphia, PA.

[656A] Figure 1.


55-year old woman, diagnosed with ulcerative colitis (UC) proctitis, received rectal mesalamine for one week, followed by one month of hydrocortisone enemas and oral prednisone 20 mg daily. Her symptoms


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Abstracts did not improve and repeat colonoscopy one month after diagnosis showed colitis involving two thirds of the colon. Prednisone was increased to 80 mg BID and Infliximab (IFX) 5 mg/kg and 6-mercaptopurine 50 mg daily were started. After three doses of IFX she developed worsening rectal bleeding. On admission she had normal vital signs. Physical exam was notable for circumferential perianal ulcers extended 5 cm onto the intergluteal fold and cleft. A group of coalesced vesicles with ulceration was noted on her right index finger. Labatory findings: hemoglobin 10.5 g/dL, ESR 53 mm/hr, CRP 0.7 mg/L. Infectious stool studies were negative. Intravenous (IV) methylprednisolone started on admission. Colonoscopy revealed a large ulceration in the descending colon and several circular superficial clean-based ulcers throughout the sigmoid colon which were biopsied. Dermatology biopsied the perianal ulcerations. The sigmoid and perianal biopsies showed multiple herpes simplex viral (HSV) inclusions and a single CMV inclusion . The patient’s finger ulceration was clinically consistent with herpetic whitlow. IV ganciclovir was started to treat HSV and CMV colitis. The patient’s symptoms of hematochezia improved within 7 days of IV ganciclovir. She was discharged on oral valgancyclovir and a prednisone taper. Both IFX and 6-MP were stopped indefinitely given the opportunistic infection. HSV colitis is rare with only a few reported cases, but it can cause major morbidity especially in patients with IBD. 2009 ECCO guidelines recommended against routine screening for latent HSV prior to starting immunomodulating IBD therapy. However, we believe that patients should routinely be asked if they have a history of orolabial, genital, or ophthalmic HSV infection prior to starting immunomodulating therapy. Patients with recurrent attacks should also be considered for prophylactic antiviral therapy. This is the first reported case of HSV colitis presenting with herpetic whitlow and perianal ulcerations. Our patient’s unique presentation stresses the importance of a thorough physical exam, including skin and the perianal area, in all patients with suspected IBD relapse as it may suggest an easily overlooked opportunistic infection.

lobe bullous changes. The patient was started on antibiotic and antifungal therapy. His liver enzymes were uptrending throughout his hospitalization. A urine histoplasma antigen returned positive and therapy was adjusted to liposomal amphotericin B followed by oral itraconazole. A lumbar puncture showed no evidence of central nervous system (CNS) involvement and oral itraconazole therapy was continued. The patient improved steadily on therapy and was in remission when evaluated a few months later. Discussion: While the majority of Histoplasma infections are clinically silent in patients with a normal immune system, patients in endemic areas receiving anti–TNF-α therapy are at an increased risk for developing severe histoplasmosis infection.² The treatment-related impaired cellular immune response, can allow disseminated histoplasmosis to occur, resulting in multi-organ failure or even death.¹³ As histoplasmosis is an endemic fungal infection, further research should focus on 1) determining which patients are at highest risk and 2) the role of antifungal prophylaxis.

659 A Diagnostic Dilemma: Diarrhea and Dermatitis Noa Krugliak Cleveland, MD1, Jami A. Kinnucan, MD2, John Hart, MD1, David T. Rubin, MD1. 1. University of Chicago Medicine, Chicago, IL; 2. University of Chicago Medicine, Ann Arbor, MI. Introduction: Clarifying the diagnosis in a patient with bowel and skin inflammation can be a challenge. The differential diagnosis includes conditions such as Henoch-Schönlein Purpura (HSP) and inflammatory bowel disease (IBD). We describe a patient who presented with GI and skin inflammation and discuss the approach to diagnosis and treatment. Case Description: A 29-year-old non-smoking female presented with two weeks of LLQ abdominal pain and 10 BMs/day with occasional blood and mucus. She also described a new painful and pruritic macular rash on her legs and feet (Fig 1a). She denied other systemic symptoms or weight loss. She was admitted to the hospital with presumed IBD and possible erythema nodosum, and empiric IV steroids were initiated. Colonoscopy revealed diffuse inflammation and friability of the entire colon, and an endoscopically normal terminal ileum. Biopsies showed acute inflammation and crypt architectural distortion consistent with a diagnosis of active chronic ulcerative colitis (Fig 2a-b). However, skin biopsy identified a leukocytoclastic vasculitis, and direct immunofluorescence (DIF) revealed an IgA deposition, consistent


658 Disseminated Histoplasmosis Associated With Anti-Tumor Necrosis Factor Alpha Therapy: A Case Series Lara Dakhoul, MD1, Keyur Parikh, MD2, Anthony Post, MD2, Jeffry Katz, MD2. 1. University of Illinois at Chicago/Advocate Christ Medical Center, Oak Lawn, IL; 2. University Hospitals Case Medical Center, Cleveland, OH. Introduction: Anti-tumor necrosis factor alpha (anti–TNF-α) therapy is effective and widely used in the treatment of inflammatory bowel disease and autoimmune rheumatic disease. The immunosuppressive effects of anti-TNF agents are well known; however, in rare cases disseminated fungal infections have been reported.¹ We present two patients who developed disseminated histoplasmosis after initiation of anti–TNF-α therapy. Case 1: A 47 year old male, who was recently initiated on methotrexate followed by adalimumab for psoriatic arthritis, was admitted for fever, cough and transaminitis. No clear etiology was ascertained and he progressed to acute respiratory failure and acute liver failure. A computed tomography (CT) of his chest reported diffuse ground-glass opacities. Antivirals, antifungals, including amphotericin B, and steroids were added to antibiotics without improvement. Given the unclear etiology of his multi-organ failure, a liver biopsy was performed; however, the patient expired the following morning. A urine Histoplasma antigen returned positive two days after. The biopsy demonstrated poorly formed granulomas with yeast forms, consistent with Histoplasma capsulatum. Case 2: A 30 year old male, on infliximab and 6-mercaptopurine for his Crohn’s disease, was hospitalized for fever and dyspnea. Initial labs indicated leukopenia. A chest x-ray (CXR) demonstrated right upper


[659B] Figure 2.


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with HSP (Fig 1b). Our patient experienced significant improvement of both the rash and diarrhea with IV solumedrol and was discharged on oral steroids. By 3 months, there was complete resolution of her rash and diarrhea, and the steroids were tapered. At 6 months, she was clinically well with no evidence of a recurrent rash. Flexible sigmoidoscopy revealed normal colonic mucosa and biopsies were normal (Fig 2c-d). However, at 12 months she had increased BMs and an elevated fecal calprotectin. Flex sigmoidoscopy and pathology revealed moderate active colitis with negative IgA staining. Anti-TNF treatment was initiated with significant relief of her symptoms. Discussion: We report a case of a patient who met the diagnostic criteria for HSP, with DIF showing an IgA-mediated vasculitis, along with rapid resolution of her symptoms after steroid therapy. However, the recurrence of her symptoms and endoscopic and histologic inflammation on repeated sigmoidoscopy confirmed the diagnosis of UC instead. This case describes an IgA positive leukocytoclastic vasculitis in IBD, which has classically been a characteristic of HSP. Although the acute treatment for both conditions is similar (steroids), the prognosis and management differences for these two conditions demonstrate the importance of an accurate diagnosis.

660 Ileal DALM in Crohn’s Disease: An Overlooked Entity? Brian L. Huang, MD1, Michelle Vu, MD1, Neal Kaushal, MD1, Karen Zaghiyan, MD2, Joanne Rutgers, MD3, Andrew Ippoliti, MD2, Stephan Targan, MD2, Ali Rezaie, MD4. 1. UCLA, Los Angeles, CA; 2. Cedars-Sinai Medical Center, Los Angeles, CA; 3. Cedars-Sinai Medical Center, Irvine, CA; 4. CedarsSinai Medical Center, West Hollywood, CA. Background: Patients with inflammatory bowel disease (IBD) are at an increased risk for developing neoplasia. Dysplasia associated lesions or masses (DALMs) are traditionally described in the colon and may represent underlying malignancy. Current surveillance protocols for malignancy generally require colonic biopsies. Small bowel malignancy among patients with Crohn’s Disease (CD) has been described, but surveillance protocols for these patients have not been well defined. Case Report: We report here a 62 year old male with a history of umbilical hernia repair who presented with abdominal pain, nausea, and vomiting. He was previously diagnosed with mixed-pattern irritable bowel syndrome and had two episodes of small bowel obstructions (SBO) that were attributed to adhesions and managed conservatively. He had a heavy smoking and NSAID use history. The patient had never had a colonoscopy before and denied a family history of IBD or GI malignancy. Physical exam was significant for a distended abdomen. CRP was elevated at 3.82 mg/dL (normal < 0.5 mg/dL) and ESR was normal. A CT scan showed partial SBO with a long segment of ileal wall thickening. Colonoscopy showed fistulae at 45 and 55 cm from the anal verge. Abnormal polypoid lesions were seen in the terminal ileum (Fig 1) and biopsies showed tubulovillous-like lesion with low grade dysplasia, located within the distal portion of inflamed ileum compatible with DALM (Fig 3). A definitive diagnosis of CD could not be made and hence no medical therapy was started. CT enterography showed inflammation involving 20 cm of the distal ileum. A retrograde double balloon enteroscopy was performed, but the ileum could not be reached. As malignancy could not be ruled out, the decision was made for exploratory laparotomy that showed creeping fat and severe distal ileitis with enter-entero and entero-sigmoid fistulas. The patient underwent ileosigmoid fisula closure, and ileocolic resection with primary ileo-ascending colon anastomosis. Gross pathology confirmed severe Crohn’s ileitis with tubulovillous-like lesions in TI with low grade dysplasia compatible with DALM in the distal ileum (Fig 2,3). No colitis was appreciated. Conclusion: This case report demonstrates a DALM that affected the distal ileum in the setting of severe untreated ileal Crohn’s. This brings into question the role for endoscopic surveillance and possible need for obtaining tissue to evaluate for malignancy among patients with CD with small bowel involvement.

[660B] Figure 2.

[660C] Figure 3.

661 Sterile Seroma After Drainage of Pyogenic Muscle Abscesses in Crohn’s Disease: 2 Cases Lara Dakhoul, MD1, Natasha Shah, MD1, Jelena Andrejic, MD2, Charles Berkelhammer, MD, FACG1. 1. University of Illinois at Chicago/Advocate Christ Medical Center, Oak Lawn, IL; 2. Southwest Gastroenterology, Oak Lawn, IL.

[660A] Figure 1.


Introduction: Crohn’s disease (CD) can result in purulent musculoskeletal complications related to abscesses and fistulas. This has been described in 4% of patients with CD. We present 2 rare cases in which a pyogenic skeletal muscle abscess in CD transformed into a sterile seroma after drainage of the abscess. Case 1: A 24 year old female with a history of Crohn’s ileitis presented with right flank pain. She was 31 weeks pregnant. Magnetic resonance imaging (MRI) showed a 7x5 cm iliacus muscle abscess. Ultrasound-guided aspiration of 90 ml of purulent fluid cultured enteric organisms. She was treated with intravenous antibiotics and percutaneous drainage, with abscess resolution on MRI. An iliacus muscle fluid collection recurred 2 months later. A computed tomography (CT) scan did not reveal any contrast extravasation into the fluid collection. She underwent percutaneous drainage, followed by ileo-cecal resection. Again, 3 weeks post-operatively, a 6x5 cm fluid collection recurred. Percutaneous aspiration revealed no organisms on gram stain or culture. An abscessogram revealed the iliacus muscle cavity. Her sterile seroma was treated with a prolonged course of percutaneous drainage, followed by sclerotherapy of the residual fluid collection cavity. Case 2: A 29 year old female with Crohn’s ileitis presented with a chronic psoas muscle abscess. A small bowel follow-through x-ray revealed a fistula from the ileum to the right psoas muscle. She underwent ileo-cecal resection and surgical drainage of the psoas muscle abscess. Three years later, she was found to have a large fluid collection in the right psoas muscle in the same area as the previous pyogenic muscle abscess. CT-guided aspiration did not reveal any organisms. She was treated with a prolonged course of percutaneous drainage, followed by sclerotherapy of the residual fluid collection cavity.


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Abstracts Discussion: Pyogenic skeletal muscle abscess can occur as a complication of fistulizing CD. We describe 2 cases in which purulent abscesses involving the iliacus muscle (Case 1) and the psoas muscle (Case 2) transformed into sterile seromas after percutaneous and surgical drainage. Sterile seromas occur in the “dead-space” created by the previous pyogenic abscess. Sterile seroma requires differentiation from a purulent muscle abscess, as its etiology, septic risk and treatment differ. Awareness of this phenomenon is necessary to avoid confusion from a recurrent pyogenic abscess.

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The introduction of vedolizumab has provided an alternative agent for the IBD patients with moderate to severe active IBD. Although vedolizumab is still in its infant stages with just over 10,000 patients recieving therapy in the United States, there have been to date no therapy related cases of psoriasis reported. Switching a patient with @-TNF driven psoriasis to vedolizumab should be considered early in the management strategy in those patients who do not respond to topical treatment or switching to another @-TNF agent. Our patient who had been tried on multiple @-TNF agents, vedolizumab resolved her psoriasis and maintained clinical and endoscopic remission. Vedolizumab should be consider in the patient with @TNF induced refractory psoriasis that has not respond to standard therapy.

Vedolizumab Resulted in Resolution of Anti-tumor Necrosis Factor Psoriasis and Sustained Clinical and Endoscopic Remission of Crohn’s Colitis

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Betty White, RN, BSN, MN , NP-C1, William Holderman, MD2. 1. Digestive Health Specialists, Maple Valley, WA; 2. Digestive Health Specialists, Tacoma, WA.

Across the Divide: A Rare Case of Ulcerative Colitis in Colonic Interposition for Esophageal Atresia

Psoriasis is a well-documented complication of anti- tumor necrosis factor (@-TNF) therapy (1). Cumulative incidence of psoriasis as reported by Guerra was 1.62%; 95% CI 1.06%-2.47%. The cause of this side effect is unknown. Management includes switching @-TNF agent or topical therapy. However, in many, these strategies do not lead to resolution of dermatological symptoms. Severe psoriasis may lead to the patient discontinuing the @-TNF agent.Vedolizumab, an integrin receptor antagonist,has recently been approved for achieving clinical response and steroid free remission in Crohns disease.To date there are no reported cases of drug induced psoriasis (2). We report a case of a patient with @-TNF induced psoriasis in which dermatological symptoms did not respond to standard treatment. She had rapid and complete resolution of her psoriasis with induction and maintenance of vedolizumab. 17 y/o female with Crohn’s colitis requiring @-TNF agents since 2008. She was induced and maintained in a steroid free remission with 5mg/kg infliximab .4/2009 after being in clinical remission on infliximab (8 doses) ,dermatology confirm psoriasis to the palms of hands and soles of feet related to @-TNF, started on topical steroids. 7/2009 she was switched to certolizumab after failure to improve with topical treatment. 2/2011 clinically well, colonoscopy showed moderate to severe active disease, her psoriasis remained active. 7/2012 switched to adalimumab and 6mp was added. 2012-2014 lost to follow up. 6/2014 active Crohn’s symptoms, psoriasis now active with complete loss of hair and ulceration of fingernail beds. 7/2014 started on vedolizumab within 4 months had complete resolution of psoriasis with new hair and nail growth. 3/2015 colonoscopy revealed quiescent Crohns disease.

Hafiz Muhammad Sharjeel Arshad, MD1, Eula Tetangco, MD1, Imad Elkhatib, MD2. 1. University of Illinois at Chicago/Advocate Christ Medical Center, Oak Lawn, IL; 2. Advocate Christ Medical Center, Oak Lawn, IL. Colonic interposition as esophageal replacement is an established treatment for long-gap esophageal atresia. These patients need long term follow up because complications can arise decades after surgery. We present a case of ulcerative colitis developing in a colonic conduit placed for esophageal atresia. A 38-year old male with Hepatitis B, a remote history of colonic interposition for childhood esophageal atresia in Jordan, presented with one day of dysphagia to both solids and liquids and abdominal pain. Esophago-gastroduodenoscopy (EGD) showed that the 7-cm segment of native esophagus appeared normal. The esophago-colonic anastomosis was at 25 cm and appeared circumferentially ulcerated. The colonic conduit was diffusely erythematous with overlying exudate, mucous and regions of severe ulceration. A colo-gastric anastomosis at 35 cm appeared normal. The stomach and duodenum appeared normal. Pathology showed colonic mucosa with architectural disarray with crypt

[663A] Figure 1.

[662A] Figure 1.

[662B] Figure 2.


[663B] Figure 2.


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665 D-Lactic Acidosis Triggered by a Carbohydrate Load in a Patient With Crohn’s Disease Allison Yang, MD, William Mantyh, MD, Amy Oxentenko, MD, FACG. Mayo Clinic, Rochester, MN.

[663c] Figure 3.

distortion, paneth cell metaplasia, acute inflammatory exudate and granulation tissue, suggestive of inflammatory bowel disease. Infectious workup including colonic aspirate was negative. CT angiography did not show vascular stenosis or signs of ischemia. A preceeding colonoscopy also showed segmental colonic ulceration with similar findings on biopsy. The patient was started on oral balsalazide 4.8g daily, pantoprazole, and sucralfate. With minimal improvement in symptoms after 4 weeks, budesonide 9mg qday was started for three weeks, then prednisone for two weeks.Follow up EGD two months after diagnosis revealed remarkable improvement in mucosal ulceration and inflammation of the colonic conduit. In this case, the combined endoscopic and histologic findings of both the colonic conduit and remnant colon and exclusion of other causes was used to make the diagnosis of ulcerative colitis. Ulcerative colitis (UC) is thought to arise from the combination of exposure to infection or toxins and the genetic susceptibility of the host, in part due to defective down regulation of the inflammatory process with subsequent tissue destruction and fibrosis.It has been hypothesized that inflammation in one intestinal site may trigger ulcerative colitis at a different site, as suggested by appendiceal inflammation as a skip lesion in ulcerative colitis that histologically resembles inflammatory bowel disease rather than acute appendicitis. There have been case reports of ulcerative colitis developing in colonic transpositions for vaginal reconstruction, but to the authors’ knowledge, there has been no published literature on ulcerative colitis in colonic conduits for esophageal atresia.

664 A Rare Case of Ulcerative Colitis Diagnosed After Pelvic Radiation Therapy and the Role of Early GI Evaluation in Patients With Gastrointestinal Symptoms Post-Radiation Steven Shamah, MD1, Gary Romaka, DO2, Megha Kothari3, Arun Swaminath, MD3. 1. North Shore-LIJ Lenox Hill Hospital, New York , NY; 2. North Shore-LIJ Lenox Hill Hospital, New York, NY; 3. Lenox Hill Hospital, New York, NY. Introduction: Gastrointestinal complications after radiation therapy are common. The causes and treatments of these are variable. Here we present a rare case of ulcerative colitis diagnosed in an elderly patient after pelvic radiation for prostate cancer. The case demonstrates that endoscopic and histologic examination should be considered early in the course of disease to establish a diagnosis and effective treatment plan. Case: A seventy-four year old man was referred to the gastroenterology clinic for evaluation of a twomonth history of persistent and occasionally bloody diarrhea with greater than four episodes per day. He had been treated eleven months prior to presentation with pelvic radiation therapy for prostate cancer. The patient had been prescribed oral loperamide by his urologist for symptomatic relief of presumed radiation colitis, but his symptoms had persisted. Physical exam revealed moderate left-sided abdominal tenderness to palpation but was otherwise normal. Colonoscopy was performed and revealed circumferential mucosal inflammation and ulceration from the rectum to the hepatic flexure without telangiectasias. Biopsies were taken and confirmed the diagnosis of ulcerative colitis. The patient was started on an oral mesalamine preparation with improvement in his symptoms. Discussion: This case demonstrates a very unusual occurrence of ulcerative colitis diagnosed in an elderly patient after exposure to pelvic radiation therapy for prostate cancer. To date, no cases have described newly-diagnosed inflammatory bowel disease (IBD) following radiation therapy, but there is much evidence that radiation can exacerbate pre-existing quiescent IBD, which is likely what occurred in this case. Radiation is a common treatment for several malignancies, but its benefits are offset by harmful adverse effects that can severely diminish patients’ qualities of life. The phenomenon of gastrointestinal complications after radiation therapy is a well-described entity. The clinical presentation of radiationinduced bowel injury can mimic several other common pathologies that have varying treatments. Colonoscopic exam and biopsies are often necessary to establish a diagnosis and effective therapy. In this case, the lack of a proper diagnosis led to inappropriate initial treatment and increased suffering for the patient. Specialist evaluation should be considered early in the disease course of any patient presenting with GI symptoms after pelvic radiation.


Case: A 54-year-old man with Crohn’s disease who was status-post multiple intestinal resections, with 100 cm of remaining small bowel, was transferred from an outside facility for ataxia and altered mental status. He had initially presented with word-finding difficulties, hallucinations, personality changes and ataxia after eating a large pasta meal. Initial labs showed serum pH 7.15, HCO3 14 mmol/L and normal lactate. Head and abdominal imaging were unrevealing. Due to concern for Wernicke’s encephalopathy, he was initiated on IV thiamine with mild improvement, but four days later, he had recurrent dysarthria, hallucinations and ataxia. Bicarbonate and metronidazole were started. Upon transfer, he was unable to recall events of preceding days. Exam showed paresthesias of his upper extremities and face and difficulties with word finding. He was continued on a bicarbonate drip, with subsequent resolution of neurologic symptoms and acidosis. The etiology of his presentation was attributed to D-lactic acidosis due to severe metabolic acidosis, episodic nature of neurologic symptoms, and history of short bowel syndrome. Discussion: D-lactic acidosis is an uncommon form of lactic acidosis, which occurs in patients with short bowel syndrome when dietary carbohydrates are metabolized by colonic bacteria to D-lactic acid. D-lactate cannot be metabolized by L-lactate dehydrogenase (which normally converts L-lactate to pyruvate). D-lactic acid is increased in short bowel syndrome due to increased delivery of carbohydrates to the colon due to reduced short bowel length and overgrowth of gram-positive anaerobes. Patients present with episodic metabolic acidosis (often after high carbohydrate meals) and neurologic abnormalities, including confusion, cerebellar ataxia, slurred speech and memory loss. The diagnosis can only be confirmed by special enzymatic assays that use D-lactate dehydrogenase. Management involves sodium bicarbonate infusion in the acute setting. For short bowel syndrome leading to D-lactic acidosis, oral antimicrobials may decrease the number of organisms that produce D-lactate, and a low carbohydrate diet can decrease carbohydrate delivery to the colon. This patient was treated with a low-carbohydrate diet and rifaximin to decrease the bacterial load in the colon. He was also initiated on Imuran and Remicade for treatment of his Crohn’s disease. At last followup, he had not had recurrence of symptoms.

666 Histoplasma Meets Crohn’s: A Rare Case of New Onset Ascites Charles Bosshardt, MD, Joseph Swingle, MD, Nilesh Lodhia, MD. Medical University of South Carolina, Charleston, SC. Learning Objectives: 1) Recognize Crohn’s Disease patients on immunosuppressive therapy are at increased risk of serious adverse events. 2) Recognize isolated Histoplasma peritonitis as a rare opportunistic infection in a Crohn’s Disease patient on immunosuppressive therapy. 3)Discuss therapeutic options for Crohn’s Disease in the setting of opportunistic infections. Case Description: A 53 yo male with history of Crohn’s Disease presented to the ER with abdominal pain and fatigue of one month duration. He had associated fever, chills, and 15lb weight loss. He denied any nausea, vomiting, or diarrhea. His Crohn’s Disease management was intermittent prednisone tapers and adalimumab. On presentation, vital signs were normal. Labwork was significant for WBC 8.8, ESR 39, CRP 13, and albumin 2.7. A CT Abdomen revealed wall thickening of the terminal ileum and cecum and moderate volume abdominal ascites. A paracentesis revealed yellow, hazy fluid with 6287 nucleated cells (7% neutrophils, 38% monocytes, 55% lymphocytes), total protein 4.5, and albumin 2.2. His serum-ascites albumin gradient was 0.5. Ascitic fluid bacterial culture, AFB smear and cytology were negative. Further labwork revealed a weakly positive urine and serum histoplama antigen. A diagnostic laparoscopy for peritoneal biopsy showed metastatic caking of the omentum and abdominal wall. Peritoneal biopsies revealed Histoplasma peritonitis. Peritoneal fluid was positive for histoplasma capsulatum. No evidence of disseminated Histoplasmosis was found in his lungs, central nervous system, or adrenal glands. Our patient completed two weeks of IV liposomal amphotericin B and was transitioned to oral itraconazole. Adalimumab was stopped and he was started on azathioprine and vedolizumab. With treatment, patient noticed remarkable improvement in abdominal symptoms and fatigue. Discussion: Crohn’s Disease patients on immunosuppressive therapy are at risk for opportunistic infections. We present a Crohn’s patient with intermittent prednisone use and adalimumab therapy with new onset non portal hypertensive ascites. To our knowledge, this is the first reported case of histoplasma peritonitis associated with immunosuppression in a patient with Crohn’s Disease. Our patient was treated with vedolizumab, which has a lower serious infection profile and may be an alternative therapeutic option for Crohn’s disease with opportunistic infections.

667 Mesenteric Fibromatosis in Crohn’s Disease: A Novel Case and Potential Effects of Adalimumab Abdelhai Abdelqader, MD1, Eren Taydas, MD2, Albert Fleisher, MD2. 1. MedStar Franklin Square Medical Center, Rosedale , MD; 2. MedStar Franklin Square Medical Center, Baltimore, MD. Desmoid tumor is a monoclonal proliferation of myofibroblasts. To our knowledge, this is the first case where a female with Crohn’s disease, but no common risk factors developed a mesenteric desmoid tumor (DT) after initiating tumor necrosis factor-α (TNF-α) therapy. We explore the plausibility of TNF-α therapy and its association with malignancy in the setting of Crohn’s disease (CD). 36-year-old female with no past medical history presented with unexplained weight loss. A CT scan showed segmental small bowel wall thickening, suggestive of CD, but no mass. CD was later diagnosed via several endoscopic studies. She was started on anti-TNF-α therapy, adalimumab, and tolerated it until nine months later when she lost 11lbs. Repeat CT showed a 7x8x8 cm mass and a possible necrotic center on PET CT. A CT-guided biopsy revealed mesenteric fibromatosis (MF). Due to further weight loss and benign pathology, adalimumab was continued. Several months later, repeat CT showed the mass had enlarged (Figure 1). She underwent an exploratory laparotomy and had 107 cm segment of small bowel resected with en block tumor resection (Figure 2). The histology suggested focal origin from the small bowel wall rather than an infiltrative process (Figure 3). Resected small bowel had histological changes also consistent with Crohn’s.


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Abstracts A year post-resection, she remains off adalimumab, improved weight, and no mass recurrence seen on surveillance CT. Some etiological associations of CD with the development of MF are history of familial adenomatous polyposis and after any abdominal surgery1. We hypothesize our patient did not have a pre-existing mesenteric tumor based on lack of clinical and radiographic evidence, rather possibly elicited by adalimumab. We explored the literature and found very limited supporting evidence relating MF and TNF-α therapy. A meta-analysis shows a 0.36% increased incidence of cancer events, about 4.5 times higher compared to the control group within 6 months of treatment with adalimumab2. Another metaanalysis of rheumatoid arthritis patients initiated on adalimumab found there was a dose-dependent increased incidence of solid malignancies as early as 6-12 months3. Differences in study populations, study practices and data reporting create challenges in conclusively determining the relationship of antiTNF-α therapy and malignancy in CD. Despite the low incidence of new neoplastic events, this case underscores the need for close surveillance and action by the physician in the management of patients with CD and anti-TNF-α therapy, even in the absence of risk factors for malignancy. This case suggests the possible association of new DT with initiation of adalimumab in CD.

[667A] Figure 1.

668 Tracheobronchitis in a Patient With Crohn’s Disease Christopher Henry, MD1, Vincent Yeung, BA2, Anusha Ganesh, MD1, Sanaa Somalya, MD1. 1. Thomas Jefferson University/Thomas Jefferson University Hospital, Philadelphia, PA; 2. Jefferson Medical College/ Thomas Jefferson University, Philadelphia, PA. Introduction: We describe a 63-year-old female who presented with one month of non-productive cough and non-bloody diarrhea, 15 years after her diagnosis of Crohn’s disease (CD), who was subsequently found to have erythematous ulcerations and nodularity of her trachea. Case Report: A 63-year-old non-smoking female with CD diagnosed at age 47 with only colonic involvement presented with a one month duration of worsening cough and diarrhea. On admission, she was febrile to 100.4 F and tachycardic to 119 beats per minute. Labs were significant for an elevated white count of 13.3 cells/mcL, and a hemoglobin of 8.6 grams/dL. A full infectious work-up was negative. Erythrocyte sedimentation rate was elevated to 105 mm/hour. Colonoscopy confirmed moderately active colitis in her terminal ileum, as well as pan-colitis, consistent with CD. Bronchoscopy revealed erythematous and edematous ulcerations throughout her trachea, as well as nodular mucosa, and pathology showed a squamous papilloma. She was started on intravenous Solumedrol and tapered to prednisone 40 mg twice daily with significant improvement in both her diarrhea and her cough. Discussion: Although clinically significant airway disease is rare in inflammatory bowel disease (IBD), the most common pulmonary manifestations are bronchiectasis and chronic bronchitis, both of which are accompanied by large amounts of sputum production. Typically, when airway disease occurs, ileal/ colonic Crohn’s is inactive.1 Pulmonary manifestations do not typically mirror disease activity, and many case reports have even described pulmonary complications developing after colectomy.2,3 Chest imaging may show circumferential or nodular narrowing of the trachea or the bronchi, but bronchoscopy remains the gold standard for diagnosis.4 Our patient is unique in that she presented with a non productive cough during an acute flare of her CD with no obvious lung pathology on chest imaging. On bronchoscopy, however, her mucosa was characteristically nodular and almost “cobblestoned”, and the trachea ulcerated and covered by a layer of fibrin. Treatment for patients with CD with upper airway disease usually involves oral and inhaled corticosteroid therapy, which is effective in improving both respiratory and gastrointestinal symptoms. In this patient, we chose oral steroids over just inhaled given her concurrent gastrointestinal flare, which proved to be effective. Conclusion: Tracheobronchitis is a rare manifestation of IBD that should be considered in CD patients presenting with persistent non-infectious cough.

[667B] Figure 2.

[668A] Figure 1.




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669 Ergotomine-Induced Ulcerative Colitis Diana Whitehead, MD1, Corey A. Siegel, MD2. 1. Dartmouth-Hitchcock Medical Center, New London, NH; 2. Dartmouth-Hitchcock Medical Center, Lebanon, NH. Migraine headaches are commonly treated with ergotamines. Serotonin-1 5-hydroxytryptamine (5-HT 1) receptor agonists are first line agents for migraines. Intravenous dihydroergotamine (DHE) is sometimes used for refractory migraines. Previously published case report have suggested an association between 5-HT 1 receptors and onset of ulcerative colitis, however, this was dismissed as an unlikely cause. We report a case of a new diagnosis of ulcerative colitis associated with intravenous DHE use for refractory migraine. A 45-year-old female with a past medical history of severe migraines presented with a two month history of bloody diarrhea and abdominal pain. Her home medication regimen included naproxen and naratriptan. She was admitted to the Dartmouth-Hitchcock Medical Center (DHMC) a month prior for intractable migraines, where she received seven treatments of IV dihydroergotamine (DHE). During her second infusion of DHE, she developed severe abdominal cramps with associated bloody diarrhea. Infectious workup including stool for C. Difficile was negative. She was subsequently treated for infectious colitis with ciprofloxacin/metronidazole and discharged home. Two month post-discharge, she represented to DHMC for ongoing symptoms of abdominal pain, and bloody diarrhea (10-12 bloody bowel moments daily). In the Emergency Department she had a hemoglobin of 11 and C-reactive protein of 18.5 without an associated leukocytosis. An extensive infectious stool evaluation was negative. Sigmoidoscopy was performed and showed mild to moderate colitis extending from anal-rectal verge to 40 cm (the extent of the examination). The mucosa was characterized by diffuse erythema, edema, complete loss of the normal vascular pattern, granularity, contact friability and superficial ulceration (figure 1). Histopathology confirmed mildly active chronic colitis consistent with ulcerative colitis, without evidence of infection (Figure 2). She was treated with hydrocortisone 100mg IV q8hr with a rapid dramatic improvement in her symptoms. She was subsequently transitioned to prednisone with a planned taper and mesalamine 4.8g daily. Repeat colonoscopy four months later showed complete mucosal healing (Figure 3). There has being one case report of ergotamine induced ulcerative colitis in the literature. Since ergotamines are used wildly for the treatment of migraines, it is important to understand if there is a true association with inflammatory bowel disease. The mechanism of ergotamine inducing ulcerative colitis is not completely understood. However, the hypothesis is that vasoconstriction leads to ischemia triggering a pro-inflammatory state. We report this case to raise awareness of this possible association so that it can be identified and studied further in the future.

[669A] Figure 1.

[669C] Figure 2.

670 Calcified Foreign Body Causing Intestinal Obstruction in a Patient With Crohn’s Disease Umair Sohail, MD1, Imran Ashraf, MD2, Fazia Mir, MD2, Zihao Wu, MD3, Hazem Hammad, MD2. 1. Division of Gastroenterology/Hepatology, University of Missouri, Columbia, MO; 2. University of Missouri, Columbia, MO; 3. Division of Surgical Oncology, University of Missouri, Columbia, MO. Introduction: Crohn’s disease (CD) is a chronic inflammatory disease involving any part of the gastrointestinal tract. Within 20 years of diagnosis, about 50% of patients will have intestinal complications, such as strictures or fistulas. Optimizing the medical treatment to prevent the occurrence or recurrence is the best strategy for managing strictures in CD patients. We report an unusual case of a patient with history of crohn’s disease presenting with intestinal obstruction secondary to a calcified foreign body. Case: A 62 year old male with history of CD disease for the last 35 years. He also reported a bout of small bowel obstruction 30 years ago requiring ileocecectomy. Patient has been doing relatively well without any medical treatment. He presented to our hospital with 2 day history of nausea, vomiting and lower abdominal pain. He denied having any flare ups of his Crohn’s disease since his surgery. Physical examination was remarkable for abdominal distension, hypoactive bowel sounds, and generalized mild tenderness to palpation. His labs were unremarkable. CT scan of abdomen showed small bowel obstruction with a 3 cm ring-like hyperdense mass just proximal to the region of the ileocolonic anastomosis suggestive of a calcified foreign body. Attempts to evaluate this further and potentially retrieve the foreign body were started with colonoscopy. This showed mild narrowing of the ileocolonic with mild superficial ulcerations. The scope went through with minimal resistance and was advanced under fluoroscopy to about 10-15cm from the anastomosis. No foreign bodies were seen. Further advancement was not successful. Subsequently, laparoscopy was performed and showed a palpable stricture in the ileum approximately 30 cm proximal to the ileocolonic anastomosis with an impacted large fecalith just proximal to the stricture. Removal of the large impacted fecalith was performed along with resection of 12 cm of ileum. Discussion: Intestinal obstruction due to impacted fecalith is a rare condition. This typically occurs in patients with history of multiple abdominal surgeries, radiation exposure or strictures due to inflammatory bowel disease. In patients with history of crohn’s disease, optimizing medical management is important in preventing the development and recurrence of strictures. Foreign body impaction either external or de novo should be in the differential diagnosis of a patient with crohn’s disease who presents with signs of intestinal obstruction.

671 Ulcerative Colitis Flare or Infection: Sometimes Difficult to Know With Immunosuppression Ashraf Almashhrawi, MD1, Imran Ashraf, MD1, Umair Sohail, MD1, Rubayat Rahman, MD, MPH1, Jared Coberly, MD1, Douglas Nguyen, MD2, Matthew Bechtold, MD, FACG1. 1. University of Missouri, Columbia, MO; 2. University of California Irvine, Anaheim Hills, CA.

[669B] Figure 2.


Introduction: Ulcerative colitis is a chronic disease characterized by inflammation of the colonic mucosa that results in symptoms of diarrhea, passing blood per rectum, and in severe cases, abdominal pain, colonic distension, and other signs of toxicity including fever. However, other etiologies have similar symptoms resulting in increasing difficult diagnosing flares versus infections, especially given the use of immunosuppressives. We present a case of a patient with ulcerative colitis who experienced multiple infections as a result of immunosuppression. Case: 67 year-old male presented with severe bloody diarrhea. Colonoscopy revealed colonic mucosa ulcerations, loss of vascularity, and bleeding compatible with inflammatory bowel disease and biopsies revealed chronic colitis. After excluding infectious causes a diagnosis of pancolonic ulcerative colitis was made. Over a course of a year, he was treated with mesalamine and several courses of prednisone (intravenous and oral). Two months into therapy he had worsening in his symptoms. His stool was positive for Clostridium difficile and he was treated with metronidazole for two weeks. Repeat testing for clostridium


| OCTOBER 2015

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Abstracts was negative. Repeat colonic mucosa biopsies were positive for inclusion bodies and positive staining for cytomegalovirus (CMV). He was treated with gancyclovir for three months. Unfortunately, his symptoms would relapse every time steroids were tapered down. Once gancyclovir was stopped, he was admitted with another episode of worsening of his diarrhea and repeat colonic biopsies showed CMV again. At this time he developed shortness-of-breath and CT scan of the chest revealed pulmonary embolism for which he had to be anticoagulated. He was started on infliximab with no immediate relief. The patient elected at that point to proceed with surgical management and he underwent a laparoscopic total proctocolectomy with terminal ileostomy. Discussion: Ulcerative colitis clinical course can be severe and complicated in some patients. Health-care providers should be aware of other etiologies that mimic ulcerative colitis flare-like symptoms, especially in these patients who have received immunosuppression.

672 Attempted Salvage Therapy Through Inpatient Initiation of Vedolizumab in Two Patients With Refractory Active Ulcerative Colitis Matthew J. Sullivan, DO1, Paola Blanco, MD2, Shashin Shah, MD3, Hiral Shah, MD4. 1. Lehigh Valley Health Network, Hellertown, PA; 2. Lehigh Valley Health Network, Eastern Pennsylvania Gastrointestinal and Liver Specialists, Allentown, PA; 3. Eastern Pennsylvania Gastroenterology and Liver Specialists, Allentown , PA; 4. Lehigh Valley Health Network; EPGI, Center Valley, PA. Background: The management of ulcerative colitis (UC) has changed greatly due to the introduction of tumor necrosis factor-alpha (TNF-α) antagonists such as adalimumab and infliximab. However, there is a subset of patients with moderate to severe disease who are refractory to these medications. Vedolizumab, an α4β7 integrin inhibitor resulting in a “gut selective” anti-inflammatory effect, has recently been approved for use in this population. Case 1: A 40 year-old male with UC progressed to pancolitis over the course of a few months with worsening abdominal pain, bloody diarrhea, and intolerance to oral intake. During that time period he was initiated on infliximab without significant improvement to his symptoms and was referred to colorectal surgery to discuss surgical options. As his symptoms progressed he was admitted for generalized weakness and malnutrition. Colonoscopy revealed severe diffuse UC. Due to the severity of his refractory disease it was decided to initiate the patient on vedolizumab during his stay. Unfortunately, he did not respond and required total colectomy during the same hospitalization. Case 2: A 75 year-old female with a three year history of UC was admitted with increased stool frequency and bloody bowel movements shortly after completing a steroid taper. She had been initiated on infliximab at the time of her diagnosis but this was discontinued due to intolerance. Colonoscopy revealed severe diffuse colitis. She preferred to avoid surgery and the decision to initiate vedolizumab was made. She received her first dose as an inpatient and her stool frequency stabilized enough to allow discharge. However, three weeks later she was readmitted and required total colectomy with end ileostomy. Discussion: Clinical trials such as GEMINI I have shown that vedolizumab is safe and effective in patients with moderate to severe UC, including those who have previously failed anti-TNF-α therapy. A 2005 study of 181 adults with active UC demonstrated a clinical remission rate of 33% by six weeks after infusions at days one and 29. However, patients in that study were naïve to anti-TNF-α agents. Our patients were initiated on vedolizumab as inpatients during active disease flares for attempted salvage therapy after failing anti-TNF-α agents and neither was able to avoid surgery. More studies of vedolizumab are required in this difficult to control population where it has potential great benefits to disease control and patient quality of life.

674 The Utility of Anti-TNF Therapy in Treating Clostridium difficile Infections in Inflammatory Bowel Disease: A Case Series Henry Jen, MD1, Neal Joseph, MD1, Arun Swaminath, MD2, Burton Korelitz, MD3, Alexandra Feathers, MPA, MPH2. 1. Lenox Hill Hospital, New York , NY; 2. Lenox Hill Hospital, New York, NY; 3. Lenox Hill Hospital, NY. Background: Incidence of Clostridium difficile infections (CDI) has been increasing in patients with Inflammatory bowel disease (IBD). CDI may precipitate flares of underlying IBD. The complex interplay between colonic inflammation from infection versus the underlying IBD process itself presents a clinical dilemma in deciding between immunosuppressant medications and antibiotics. Current recommendations against the escalation of immunosuppressant therapy for active CDI in IBD are based on very limited data. Aim: The aim of our case series is to present the potential utility of anti-TNF therapy in treating CDI in IBD. Methods: Patients hospitalized with CDI and IBD, treated with antibiotic therapy and anti-TNF therapy in the same hospitalization were identified through a search of hospital records. Inpatient and outpatient records were reviewed for inpatient and eight week outpatient outcomes. Results: Five patients met the inclusion criteria. Four patients had Ulcerative Colitis while one had Crohn’s Disease. All patients showed evidence of pancolitis at initial presentation. One patient presented with severe CDI. Two patients were admitted with a history of recurrent CDI. Mean time from

[674]

Table 1. Background Demographic and Clinical Characteristics Patient 1

Patient 2

Patient 3

Patient 4

Patient 5

Age

67

48

35

27

62

Sex

M

M

M

M

F

Ulcerative Colitis

+

+

+

+

Antibiotic use in prior 3 months

−

−

−

−

−

Proton pump inhibitor use in prior month

+

−

+

−

−

Smoking history

+

+

+

−

−

Prior history of CDI

+

−

−

+

−

• Aminosalicylates

−

+

−

+

+

• Corticosteroids

+

+

+

−

+

• Immunomodulators (AZA, 6-MP)

+

−

+

−

−

• Anti-TNFs

−

−

−

−

−

Crohn's Disease

Prior IBD treatments

673

[674]

UC, CMV, PE, Why Me?

Hospital Course Information

Joshua Rubin, MD, Derek Patel, MD. University of California San Diego, San Diego, CA. Introduction: Patients with ulcerative colitis (UC) are at risk for complications including CMV colitis and thromboembolic disease. CMV complicating UC typically occurs in severely active or steroidrefractory colitis. Thromboembolic events in UC are usually associated with disease flares and steroid use. We present a case of systemic CMV infection and thromboembolism in a patient with previously quiescent UC. Case Description: A 42-year-old woman with pancolonic UC presented with 2 weeks of fever, shortness of breath, constipation and rectal bleeding. Her UC had been in clinical, endoscopic and histologic remission on infliximab, 6-mercaptopurine (6MP) and mesalamine. She elected to discontinue infliximab 6 months prior to presentation and remained asymptomatic. Two weeks after travelling to Indonesia, she experienced the onset of fevers, constipation, and later, scant hematochezia. An evaluation for infectious causes was negative. Due to progressive symptoms, the patient returned to the USA and a sigmoidoscopy revealed ulcerative proctitis limited to the distal 5cm of the rectum. She was hypotensive and hypoxemic and was referred to the emergency department (ED) for further evaluation. In the ED, she was febrile to 103.7o F with a WBC of 3.6 with lymphopenia and a hemoglobin of 10.7. AST and ALT were elevated at 38 and 51. A CT of the chest showed multiple pulmonary emboli (PE). Rectal biopsies showed mild chronic active proctitis with CMV. Serum CMV IgM and IgG were positive. A plasma CMV DNA PCR was elevated at 5074. She was admitted to the hospital for anticoagulation and symptomatic treatment. She received IV gancyclovir and SQ low molecular weight heparin, and was transitioned to valgancyclovir and rivaroxaban on discharge. 6MP was discontinued and infliximab was restarted. On follow-up, her fevers, cytopenias, liver enzyme abnormalities and hematochezia had resolved. Discussion: CMV colitis and thromboembolism complicating severe UC are well described in the literature. This patient developed systemic CMV reactivation and bilateral PE with only limited proctitis, no recent UC flare and no steroid use. CMV reactivation with systemic manifestations is a rare occurrence, but should be considered in UC patients who have systemic symptoms out of proportion to the activity of their colitis. This case also highlights the multiple interacting risk factors (including CMV infection itself) for PE in patients with UC.


+

Table 2. Hospital Course Information and Outpatient Outcome Measures Patient 1

Patient 2

Patient 3

Patient 4

Patient 5

CDI treatments used • Oral Vancomycin

+

+

+

+

+

• Oral Metronidazole

−

+

−

−

−

• Intravenous Metronidazole

+

+

−

+

−

• Oral Rifaximin

−

+

−

−

−

• Intravenous Immunoglobulin Time from last positive CDI test to initiation of anti-TNF

−

+

−

−

−

5 days

7 days

3 days

7 days

10 days

Morbidity and mortality data after anti-TNF administration • Death

−

−

−

−

−

• Sepsis

−

−

−

−

−

• Colectomy

−

−

−

−

−

• Ileus

−

−

−

−

−

• Megacolon

−

−

−

−

−

• Need for ICU level care

−

−

−

−

−

8 days

5 weeks

15 days

7 days

12 days

Hospital length of stay Outpatient Outcome Measures CDI recurrence Severity of IBD per physician assessment Re-hospitalizations within 8 weeks

−

−

−

−

Not available

Improved

Improved

Improved

Improved

Not available

−

−

−

−

Not available


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last positive CDI test to initiation of anti-TNF treatment was six days. Four of the five patients showed initial improvement on CDI antibiotic treatment prior to starting anti-TNF. One patient failed to improve despite multiple CDI treatments before ultimately improving on anti-TNF therapy. There were no cases of worsening CDI defined as worsening sepsis, need for colectomy, need for ICU level care, or death. Post-hospitalization colonoscopy reports were available for three of the five patients which all showed improvement in inflammation and mucosal healing. There were no cases of CDI recurrence or IBD-related re-hospitalizations within the follow up window. Conclusions: Research on the safety of anti-TNF administration in the setting of active CDI is limited and data on outcomes of recurrent CDI in IBD after initiation of anti-TNF therapy is unknown. We describe five successful cases of CDI and IBD flare where anti-TNF medications were initiated during the same hospitalization. We also present two cases of recurrent CDI managed with escalation of IBD therapy to successfully avoid recurrent CDI. Further research is needed to elucidate the safety and efficacy of a combination approach of anti-TNF therapy and antibiotics for treating patients with IBD and CDI.

675 Pulmonary Manifestations of Inflammatory Bowel Disease (IBD) in Patients With Late-Onset IBD Neil Marya, MD1, Scott Ferrara2, Andrew Moraco3, David R. Cave, MD, PhD4, Scott Kopec3. 1. University of Massachusetts Medical School, Northborough, MA; 2. University of Massachusetts Internal Medicine Residency Program, Worcester, MA; 3. University of Massachusetts Department of Pulmonary and Critical Care Medicine, Worcester, MA; 4. University of Massachusetts Medical Center, Worcester, MA. Background: pulmonary manifestations are uncommon in IBD. We report 3 different pulmonary manifestations in patients with late onset IBD to show that they may be more prone to pulmonary complications. Patient #1: A 45 year old male developed frequent loose stools with streaks of blood. Colonoscopy demonstrated diffuse colitis extending from the distal colon to the distal ascending colon. Biopsy demonstrated chronic active colitis with extensive ulceration and inflammation. The patient was diagnosed with Ulcerative Colitis and started Mesalamine. Over a 3 month period the patients symptoms continue to worsen despite increased doses of Mesalamine and a trial of oral corticosteroids. The patient was started Azathioprine. Two weeks later the patient presented for dyspnea and was diagnosed with a pulmonary embolus. He was discharged from the hospital on Warfarin. He continued Warfarin therapy for 12 months with no further reported evidence of thrombus formation. Patient # 2: A 71 year old male developed hematochezia. 71. A flexible sigmoidoscopy demonstrated ulcerated mucosa concerning for IBD. He was started on mesalamine for 3 months without benefit, so it was stopped. He then developed a perianal fistula, requiring fistulotomy 14 months later. Colonoscopy showed segmental colitis in the sigmoid. The patient developed dyspnea and was referred to the pulmonary clinic. Pulmonary function tests showed mild restrictive disease and a CT chest showed bibasilar and right middle lobe honeycombing. The patient remained off medications for colitis and had spontaneous symptomatic improvement of his shortness of breath. A chest x-ray 16 months later showed no evidence of interstitial disease. Patient #3: A 51 year old male, with ulcerative colitis, was on prednisone and mesalamine for approximately for 7 years with good control. Because of a flare he was started on azathioprine, but developed fever and dyspnea. A chest x-ray showed bibasilar consolidation and a CT chest showed extensive ground glass opacities bilaterally in the upper lobes. He underwent broncho-alveolar lavage (BAL) and transbronchial biopsies. The BAL cultures showed Staph aureus without symptoms; the transbronchial biopsies showed cryptogenic organizing pneumonia. Azathioprine was stopped, prednisone and mesalamine were continued. Prednisone was tapered and follow up CT chest showed a near resolution of his organizing pneumonia Discussion: Patients #1 and #2 developed pulmonary symptoms close to diagnosis. Patient #3 developed symptoms nearly 7 years after diagnosis, during a flare. These cases demonstrate the importance of looking for pulmonary symptoms in older patients diagnosed with IBD, especially during onset and acute flares.

[676A] Figure 1.

[676B] Figure 2.

676 Cytomegalovirus Ileitis in a Patient With Longstanding Crohn’s Disease Ami Panara, MD, Ashish Sharma, MD, Jason Hou, MD. Baylor College of Medicine, Houston, TX. Introduction: Cytomegalovirus (CMV) is known to complicate inflammatory bowel disease (IBD), possibly because of a tropism of CMV to sites of inflammation. It commonly affects the colon; small bowel involvement of CMV is not common described. Here we present a case of ileal Crohn’s disease (CD) complicated by isolated CMV ileitis. Case presentation: The patient is a 55 year old African American male with a 25 year history of stricturing and fistulizing CD with 2 prior bowel resections. He was previously treated with mesalamine, azathioprine, and infliximab. At the time of current presentation, the patient had a recent increase of gastrointestinal symptoms typical of a CD flare with 10-12 liquid bowel movements a day, nocturnal bowel movements, hematochezia, and rectal urgency. He was on azathioprine at the time of presentation. Colonoscopy showed diffuse erythema and edema with mild stricturing in the ileum; however the colon was endoscopically normal. Histology and immunohistochemistry from ileal biopsies showed evidence of CMV but negative for herpes simplex 1 and 2. Stool PCR was negative for clostridium difficile. Random colonic biopsies showed no evidence of CMV colitis. The patient did not have pancytopenia or signs of disseminated CMV. The patient was admitted for intraveneous ganciclovir with improvement of diarrhea within 3 days. He was then transitioned to oral valganciclovir to complete a 2 week course. Discussion: While awareness of CMV colitis has increased with recommendations for sigmoidoscopy as part of practice guidelines in severe ulcerative colitis (UC), the impact of isolated ileal CMV is much less established. CMV can affect any part of the digestive tract, however CMV has a predilection for the colon and esophagus. As demonstrated in our case, ileal involvement of CMV may be missed if only sigmoidoscopy is performed. A full ileocolonoscopy with biopsies of the terminal ileum may be required to rule out isolated CMV ileitis. In our case presentation, the patient had a marked clinical improvement


[676C] Figure 3.

after anti-viral therapy suggesting CMV ileitis was the cause of clinical symptoms. In conclusion, ileocolonoscopy with random biopsies of the ileum and colon may be required to evaluate for CMV in ileal CD patients with an exacerbation of gastrointestinal symptoms.


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Abstracts 677 Salmonella and Crohn’s: Continued Debate of Colitis Scott Liu, MD1, Rashad Wilkerson, DO2. 1. Naval Medical Center Portsmouth, Norfolk, VA; 2. Naval Medical Center Portsmouth, Portsmouth, VA. Introduction: Limited data exists regarding the association of Salmonella typhimurium and Crohn’s disease (CD). We present a case of newly diagnosed inflammatory ileocolonic CD associated with S. typhimurium infection. Case: A 22 year-old female with a 2 year history of oral aphthous ulcers, intermittent post-prandial abdominal pain and hematochezia presented to the emergency room with a 4 day complaint of progressive, severe abdominal pain, diarrhea and hematochezia. She was empirically treated for infectious colitis

with oral ciprofloxacin and metronidazole and discharged home once stool cultures were obtained. After 2 days with no improvement she was admitted to the hospital. On admission, her vital signs were normal. There was diffuse abdominal tenderness and a normal rectal examination. Her hemoglobin was 10.8 g/dl, ESR 18 mm/hr and CRP 27 mg/L with a normal WBC. Stool studies revealed fecal leukocytes. There was rectosigmoid to distal descending colon wall thickening without abscess, stenosis, or fistula on contrast enhanced abdominal CT scan. Colonoscopy revealed moderate colonic inflammation with skip lesions. The terminal ileum appeared endoscopically normal. The patient was diagnosed with CD and prednisone 40 mg was initiated with symptomatic improvement 2 days later. Although the terminal ileum was endoscopically normal, biopsies returned as chronic active ileitis with cryptitis. Colonic biopsies revealed chronic active colitis with surface erosions cryptdestruction and crypt abscess formation. After discharge, stool cultures revealed S. typhimurium, sensitive to sulfamethoxazole/trimethoprim (SMX-TMP). She was treated for 2 weeks with SMX-TMP while continuing steroid therapy. Although clinical remission was induced, our patient declined biologic or immunomodulator therapy and pursued a Paleo diet with mild clinical improvement. She subsequently became pregnant and initiation of treatment has been delayed until delivery. Discussion: Our patients’ clinical presentation, endoscopic and histologic findings are consistent with an initial inflammatory Crohn’s ileocolitis flare triggered by concomitant S. typhimurium infection, necessitating treatment of both. Patients with CD are at a higher risk for infectious colitis. Although salmonella has been postulated as a trigger for the onset of CD, in genetically susceptible individuals, her presentation does not fit that model. Our case underscores the importance of stool cultures in these patients.

678 Jamaican Me Toxic: An Unusual Presentation of Crohn’s Disease in a 43-Year-Old Jamaican Man Lance D. McLeroy, MD1, Jennifer Seminerio-Diehl, MD2. 1. Medical University of South Carolina, Johns Island, SC; 2. Medical University of South Carolina, Charleston, SC. This is a case of a 43 year-old Jamaican male with no significant past medical history who presented to the emergency department with a four week history of abdominal pain and profuse, watery diarrhea that began two weeks after returning from a trip to Jamaica. Upon admission he was found to be afebrile and

[677A] Figure 1.

[677B] Figure 2.

[678A] Figure 1.

[678B] Figure 2.



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tachycardic with diffuse abdominal tenderness. Labs were significant for a hgb of 5.5, WBC count of 22K and platelet count of 571K. A CT abdomen and pelvis with contrast was performed that showed colonic inflammation and a colonic diameter of 5cm. Multiple stool studies were sent to further evaluate what was believed at the time to be an infectious etiology and empiric treatment for c.diff was started. He later developed toxic megacolon with colonic diameters approaching 13cm. He was made NPO and had both a NG tube and rectal tube placed. His TMC and symptoms failed to improve and a flex-sigmoidoscopy was eventually performed in an effort to decompress his colon. Multiple large circumferential ulcerations suspicious for CMV were found. Biopsies were taken that were negative for CMV but positive for a pattern consistent with Crohn’s disease. Solumedrol was started once all infectious serologies were negative. He experienced marked improvement in his symptoms with resolution of his toxic megacolon. An MR enterography was subsequently performed that showed findings consistent with pancolitis. Colonoscopy showed pancolitis with rectal sparing, ulcers throughout the entire colon, and a normal ileum. He was started on azathioprine and was discharged home on azathioprine and prednisone. Upon follow-up visit he reported continued improvement of his symptoms. Crohn’s disease can present with a wide variety of clinical manifestations. Endoscopic findings usually show cobble stone appearance with longitudinal ulcers. Larger, circumferential, heaped-up ulcers, like those found in this case, are rarely found in Crohn’s disease, and are more commonly seen in CMV colitis. Furthermore, toxic megacolon rarely occurs as the initial presentation of Crohn’s disease. Case reports have documented pathologic evidence of CMV in patients with a classic endoscopic appearance of Crohn’s disease but there is scant evidence of Crohn’s disease presenting with an endoscopic appearance similar to CMV. Without a biopsy-proven diagnosis the use of immunosuppressant therapy can exacerbate CMV as well as other infectious causes of colitis that often masquerade as Crohn’s. This case demonstates a unique presentation of Crohn’s disease, illustrates the difficulty physicians may sometimes face in diagnosing Crohn’s disease, and highlights the importance of obtaining a tissue biopsy to rule out infectious causes before initiating immunosuppressive therapy.

679 An Unusual Case of Isolated Ampullary Crohn’s Disease Brett Sadowski, MD1, Manish B. Singla, MD2, Scott Cunningham, MD2, Patrick Young, MD, FACG1. 1. Walter Reed National Military Medical Center, Bethesda, MD; 2. Walter Reed National Military Medical Center, Bethesda , MD. Crohn’s disease (CD) is a chronic, inflammatory disorder that can affect the entire gastrointestinal tract. Ampullary involvement of the disease is rare, and can lead to ampullary incompetence or stenosis. A 64-year-old female with a 14-year history of penetrating ileocolonic CD presented with epigastric abdominal pain, fever, and leukocytosis. She had undergone ileocecectomy and a subsequent ileal resection, and was in endoscopic remission on infliximab. She was a non-smoker and taking no NSAIDS. Her history included nonalcoholic steatohepatitis and an episode of pancreatitis associated with ruptured duodenal diverticulitis. Her abdominal pain began 3 weeks prior to presentation and was associated with non-bloody diarrhea and intermittent subjective fevers. Notable laboratory findings included a white blood cell count of 20,000/μL, and normal liver enzymes, lipase, coagulation studies, inflammatory markers, and fecal calprotectin. Infliximab was held due to concern for infection. Computed tomography of the abdomen showed an 11 mm common bile duct with intrahepatic duct dilation without stones or masses. A search for infectious causes of her fever and leukocytosis was negative, including blood cultures. Endoscopic ultrasound showed a dilated bile duct with a smooth taper to the ampulla with no obstructing lesion. Endoscopic retrograde cholangiography showed a prominent, erythematous ampulla with multiple small ulcerations and papillary stenosis consistent with ampullary CD. The remainder of the duodenal mucosa appeared normal. Biopsies demonstrated inflammation without granuloma formation. The patient was treated with vedolizumab with resolution of her symptoms. Chronic constitutional symptoms and bile duct dilation in immunosuppressed patients with CD are concerning for infection, malignancy (such as lymphoma), or primary sclerosing cholangitis. CD of the ampulla occurs in 0.5-4% of patients with ileocolonic disease and can manifest as mucosal ulcerations, erosions, or nodules. Granulomas are found on biopsies in 7-30% of cases. Patients with active ampullary CD can have upper abdominal pain, nausea, vomiting, and weight loss. There are reports of pancreatitis and biliary obstruction resulting in jaundice. Duodenal involvement of disease is rarely isolated as in our patient; 96% of patients with duodenal involvement have active disease elsewhere. Our case demonstrates a rare cause of constitutional symptoms in a patient with otherwise wellcontrolled CD.

chronic diarrhea are eventually diagnosed with MC. MC can only be confirmed with biopsy which differentiates between the two major subtypes: lymphocytic colitis (LC) and collagenous colitis (CC). Recent data suggests MC is nearly as common as classic IBD. It is typically recognized as a disease of the elderly, with an average age at diagnosis of 65 years. It is noteworthy, however, that 25% of microscopic colitis patients are younger than 45. Thirty to fifty percent of patients with MC have associated autoimmune disorders, with celiac disease being the most common. In most cases the diagnosis of the associated autoimmune disease precedes the diagnosis of MC. Microscopic colitis rarely affects children, although isolated case reports do exist. This case illustrates both the association of MC with autoimmune disorders as well as the ability of MC to occur in younger patients. With newer data suggesting a prevalence of MC higher than what was once thought, it is important to keep MC in the differential diagnosis of anyone who presents with chronic, non-bloody diarrhea, especially patients with concurrent autoimmune diseases. Furthermore, in patients with MC who fail to respond to treatment, a search for concomitant autoimmune diseases may prove helpful in reaching a diagnosis.

681 Infliximab-Associated Psoriasiform Alopecia Zenas Yiu1, Aysha Javed1, Rajani Nalluri1, David Fitzgerald1, Jimmy Limdi2, Luisa Motta1, Minal Singh1, Matthew Harries1. 1. Salford Royal NHS Foundation Trust, Manchester, United Kingdom; 2. Pennine Acute Hospitals NHS Trust, Manchester, United Kingdom. Introduction: Paradoxical psoriasiform eruptions may occur with tumour necrosis factor antagonists (anti-TNFs) treatment, but cases of anti-TNF induced alopecia where scalp psoriasiform lesions cause hair loss are less commonly reported. The nature of anti-TNF induced alopecia has not been fully determined. Method: We report two cases of infliximab-associated psoriasiform alopecia that have resolved with significant hair regrowth. Results: A 14 year old girl presented with a 4 month history of an enlarging erythematous, malodorous plaque on the vertex of the scalp. The area of alopecia extended over 12 cm in diameter and was associated with multiple small psoriasiform plaques on the trunk and limbs. She had a background of Crohn’s disease treated with azathioprine and infliximab over the preceding 12 months, with no previous history of psoriasis. Scalp biopsy showed psoriasiform changes. Infliximab was stopped, azathioprine maintained and topical clobetasol propionate initiated to good clinical effect, with evidence of hair regrowth after two months of treatment. Another patient, a 48 year old woman, presented with a 9 month history of an erythematous scaly patch on the left frontal scalp. She had a background of Crohn’s disease and had been on infliximab for 18 months, but had no previous history of psoriasis. Despite treatment with fluocinolone acetonide gel she developed alopecia in the affected area. Scalp biopsy again showed a psoriasiform changes. Treatment with topical clobetasol propionate was started and, in conjunction with the cessation of infliximab therapy, she experienced significant hair regrowth two months later. Crohn’s disease activity remained stable in both cases. Discussion: Eighteen cases of anti-TNF associated psoriasiform alopecia have been reported to date, with the majority showing non-cicatricial alopecia. Treatment strategies included additional systemic therapy (9 cases), with cessation of anti-TNF therapy or switched to another anti-TNF therapy being employed in 13 cases. Histological changes are not well defined but include psoriasiform epidermal changes and dermal inflammation; one series describes alopecia areata-like hair follicle changes. A proposed mechanism for these findings is the disruption of immune homeostasis with resulting imbalance between cutaneous inflammatory cytokines. In conclusion, we report two cases of non-cicatricial anti-TNF associated psoriasiform alopecia that responded well to potent topical steroid treatment and cessation of anti-TNF therapy.

680 Microscopic Colitis: Not Just a Disease of the Elderly Lance D. McLeroy, MD1, Jennifer Seminerio-Diehl, MD2. 1. Medical University of South Carolina, Johns Island, SC; 2. Medical University of South Carolina, Charleston, SC. Patient is an 18 y/o African American female with a past medical history significant for autoimmune lymphoproliferative disorder (ALPS) who was referred to the ER from clinic with 4-5 days of nausea, vomiting, diarrhea, crampy abdominal pain, and laboratory evidence of hypokalemia and metabolic acidosis. She stated that she had been having diarrhea for 3-4 months prior to presentation with intermittent episodes of constipation. Her diarrhea was associated with crampy abdominal pain that was relieved with defecation. She experienced nocturnal bowel movements with stool incontinence. She denied any fevers, chills, dark stools, or bright red blood per rectum. Physical exam was unremarkable. After an initial negative work-up for an infectious etiology, a colonoscopy and EGD were performed that showed normal endoscopic appearance of her stomach, duodenum, and colon. With no definitive cause for her symptoms, she was started empirically on a ten day course of Rifaximin to treat small intestinal bacterial overgrowth. Final pathologic results from colonic biopsy subsequently revealed evidence of lymphocytic colitis (LC). She was started on budesonide and experienced marked improvement of her symptoms. Microscopic colitis (MC) is a chronic inflammatory bowel disease that presents with chronic non-bloody diarrhea, crampy abdominal pain, and characteristic histopathologic features. It has emerged as a common etiology to aforementioned symptoms over the past decade. Ten to twenty percent of patients with


[681A] Figure 1.


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Abstracts


682 Psoas Abscess: A Rare Initial Manifestation of Crohn’s Disease Robin Staudinger, MD, Rupa Sharma, MD, Supriya Patel, MD. University of Illinois, Chicago, IL. A 27 year old woman was admitted with right hip pain worse with movement for 2 weeks. She also reported RLQ pain and fevers for the last 6 days. She denied diarrhea, hematochezia, nausea or vomiting. She experienced similar abdominal pain a few months prior and was referred for colonoscopy but the symptoms resolved and the colonoscopy was not scheduled. She had no other significant medical history. Vitals on admission were notable for Tmax 38.3°C and HR 105. Exam revealed moderate RLQ and suprapubic tenderness without rebound or guarding. Righ hip was fixed in a flexed position and she was unable to fully extend the hip due to pain. Labs showed WBC 11,700/L, Hgb 12.3g/dL, Plt 524x103/L, ESR 79mm/hr, CRP 20.3mg/dl, albumin 3.3g/dl. CT Abdomen and MR enterography showed inflammation and phlegmon in the RLQ with an abscess in the inflamed iliopsoas muscle. Broad-spectrum antibiotics were initiated. Colorectal surgery performed an exploratory laparoscopy which revealed an inflamed terminal ileum and cecum, fistula and adherent psoas abscess requiring laproscopic ileocecal resection. Pathology showed mucosal ulceration, chronic inflammation, chronic serositis, non-caseating granulomata and the presence of a fistula confirming the diagnosis of psoas abscess secondary to fistulizing Crohn’s disease. A psoas abscess (PA) is a rare complication of Crohn’s disease (CD) and seldom presents as the first manifestation. When treatment is delayed it can lead to significant morbidity and mortality. The iliopsoas muscle lies posterior to the ileocecal junction and adjacent to the spine, aorta and renal tract, making it a potential site of infection in the setting of intestinal diseases, osteomyelitis, infected aortic aneurysms and UTIs. PA should be suspected in any patient who presents with hip and abdominal pain. CT is the most commonly used imaging modality for diagnosis. Early antibiotic therapy, drainage and surgical consultation are critical. When CD is suspected, open surgical rather than percutaneous drainage should be considered so affected bowel can be resected if necessary. Once this is performed and the patient has recovered from surgery, treatment of fistulizing Crohn’s should be initiated. Infliximab, azathioprine and 6-mercaptopurine are most commonly used. While corticosteroids are often indicated in the treatment of CD, they should be avoided in the perioperative period as they increase the risk of postoperative complications.

[682A] Figure 1.


[682C] Figure 3.

683 Disseminated Cytomegalovirus Infection in a Patient With Crohn’s Disease on Adalimumab Therapy Nathaniel Ernstoff, MD1, Simi Singh, MD2, William Mandell, MD1. 1. Mount Sinai Beth Israel, New York, NY; 2. Mount Sinai Beth Israel, New York , NY. Disseminated Cytomegalovirus (CMV) infection can occur in both immunocompetent and immunocompromised patients. TNF inhibitor therapy increases the risk of both microbacterial and fungal infections, though it is unclear if such therapy increases the risk of viral infections. We discuss a rare case of disseminated CMV in a Crohn’s patient on adalimumab therapy. A 22 year old woman with Crohn’s disease, treated with mesalamine, 6-mercaptopurine and adalimumab, presents with 10 days of fever and weakness preceded by a rash starting 4 days prior. The patient denied cough, diarrhea, stiff neck, headache, photophobia, urinary complaints, exposures to sick persons, and sexual exposures including kissing. Admission vital signs demonstrated fever of 102F, heart rate of 130 beats per minute, and normal blood pressure and oxygen saturation. She was well appearing with a diffuse macular rash on the chest, abdomen, and back which was warm to touch. The remainder of the physical examination was within normal limits. The Hgb was 11.7 g/dL, platelet count 50,000/uL and WBC 1,500/uL with an absolute neutrophil count of 540. AST and ALT were 102 U/L and 108 U/L, respectively. Serologies for EBV, CMV, EBV, HSV6, HIV, and parvovirus were sent. The patient continued to have a fever to 105F and rash. CMV IgM was positive and the IgG was negative. CMV DNA RT PCR showed 10,428 copies/mL. Treatment was started with valganciclovir 900mg PO Q12H on hospital day 3. 5 days later the CMV PCR showed < 250 copies/ mL, a 2 log decrease. 11 days into treatment the patient defervesced. Treatment was completed after a total of 14 days. This is the first case report of a Crohn’s patient on adalimumab presenting with disseminated CMV infection. A number of cases have been reported of disseminated CMV infection in Crohn’s patients on infliximab. There are three case reports in which these patients were treated with foscarnet. This is the first case report with successful treatment using valganciclovir. Current recommendations call for valganciclovir for disseminated CMV in HIV, post-transplant, and severely immunosuppressed patients, but no recommendations exist for patients on TNF inhibitors . Our patient did not improve until starting valganciclovir and immediately responded with a 2 log decrease in viral load over 5 days. While further studies need to be performed, this case report suggests valganciclovir should be considered in patients with disseminated CMV infection on TNF therapy.


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684 Colloid Carcinoma With Signet Ring Cell Features in the Backdrop of Crohn’s Colitis: Related or Unrelated? Aftab Ahmed, MD1, Khadija Chaudrey, MD2, Tauseef Ali, MD2. 1. Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK; 2. University of Oklahoma Health Sciences Center, Oklahoma City, OK. 49 years old male with ileocolonic Crohn’s for past 7 years, on mesalamine 2.4 g/day was referred to our hospital for evaluation of pseudopolyposis and severe ulceration seen on fl exible sigmoidoscopy. His CRP was 9.6 mg/L, albumin 3.6 g/dL and Hbg 11.1 g/dL. Patient underwent colonoscopy that showed stricture in the distal ileum with scared deformity of ileocecal valve. There was a stricture in sigmoid colon and friability with nodularity in distal rectum. A rectosigmoid fistula was also noted. Multiple biopsies were taken randomly throughout the colon. Minimally to mildly active Crohn’s disease was reported on biopsies with a rectal colloid carcinoma exhibiting signet ring cell features. There were numerous fragments of colloid material containing atypical epithelial cells . A focal area of Cytokeratin positive and CD68 negative signet ring cells was identified in lamina propria, submucosal tissue was spared. Traditional dysplasia resembling tubular adenomas was not present. After expert opinion from a team of pathologist, final diagnosis of invasive colloid carcinoma with signet cell features was established. Patient underwent total proctocolectomy with perineal resection. His operative specimen was staged as T3N0 with 75% mucinous tumor component. He is currently undergoing chemotherapy. Many conventional colorectal cancers (CRCs) produce mucin. When the extracellular mucin comprises ≥50 percent of the tumor, it is classified as colloid or mucinous carcinoma. Colloid carcinoma accounts for approximately 11 to 17 percent of all CRCs. They have a predilection for the rectum and sigmoid colon. Predominant concurrence in Hereditary Non Polyposis Colon Cancer and carcinoma arising from sessile serrated adenomas points towards microsatellite instability carcinogenesis pathway. If intracellular mucin displaces tumor cell nuclei to the side and ≥50 percent of the tumor is made up of cells of this type, it is classified as a signet ring cell carcinoma. They are a rare subtype accounting for only 1 to 2 percent of all CRCs. An association between inflammatory bowel disease and signet ring cell carcinoma has been suggested, and figures of up to 14% have been reported. 30% of patients with signet-ring cell carcinoma also have ulcerative colitis. Whether these rare occurrences are sporadic in nature or related to the presence and severity of Crohn’s disease remains to be learnt further.

[684C] Figure 3.

685 A Rare Differential Diagnosis of Chronic Colitis Neha Agrawal1, Bradley Confer2, Jessica Philpott, MD, PhD2, Florian Rieder, MD1. 1. Cleveland Clinic Foundation, Cleveland, OH; 2. Cleveland Clinic, Cleveland, OH.

[684A] Figure 1.

Introduction: The differential diagnosis for chronic colitis is broad. Recognition of less common etiologies is challenging due to the significant overlap in clinical, serologic, histologic and endoscopic findings. We here present a case of a rare cause of chronic colitis. Case presentation: A 32-year-old woman presented with a two-year history of recurrent bloody diarrhea and abdominal pain. Initial evaluation at outside facilities included normal esophagogastroduodenoscopy and colonoscopy. A year later, patient was diagnosed with Crohn’s disease after detection of multiple ulcerations in the sigmoid colon. The patient was intolerant to mesalamine and oral steroids were ineffective. Two months prior to admission, she developed worsening symptoms with up to 20 bloody bowel movements per day requiring hospitalization and blood transfusions. She next developed painful oral and cutaneous ulcerations. Blisters were noted at the sites of her intravenous access, suggestive of pathergy. Physical examination revealed tender aphthous oral mucosal and multiple punched out ulcerations over the skin of extremities and torso. An ophthalmological examination was normal. Laboratory data showed anemia, leukocytosis and CRP of 23.5 mg/dl. Colonoscopy (Figure 1) revealed multiple round and geographic, deep punched out ulcers and fissures in the entire colon with normal intervening mucosa and normal terminal ileum. Colonic histopathology (Figure 2-top) showed mononuclear inflammatory cells, cryptitis and rare crypt abscesses. Skin pathology (Figure 2-bottom) revealed transmural neutrophilic ulceration with focal vasculitic changes consistent with Behcet’s disease. A plan for anti-TNF therapy was made, but the further hospital course was complicated by colonic perforation requiring exploratory laparotomy, subtotal colectomy and end ileostomy. Discussion: Behcet’s disease is a rare disorder, characterized by recurrent painful oral aphthous ulcers along with involvement of multiple organ systems, including cutaneous ulcers as well as eye, gastrointestinal, vasculitic and neurological lesions. No pathognomonic test for the diagnosis exists and the International Study Group (ISG) criteria (Table 1) remain the most widely accepted guidance. Gastrointestinal and skin involvement can mimic inflammatory bowel or rheumatologic diseases, but the combination of symptom constellation, involved organ systems, histopathology and endoscopic appearance allow a distinction with high accuracy.

[685] Criterion

Required features

Recurrent oral ulceration

Aphthous (idiopathic) ulceration, observed by physician or patient, with at least three episodes in any 12-month period

[685]

[684B] Figure 2.


Table 1. Diagnostic criteria for Behçet's syndrome

Table 2. Plus any two of the following

Recurrent genital ulceration

Aphthous ulceration or scarring, observed by physician or patient

Eye lesions

Anterior or posterior uveitis cells in vitreous in slit-lamp examination; or retinal vasculitis documented by ophthalmologist

Skin lesions

Erythema nodosum-like lesions observed by physician or patient; papulopustular skin lesions or pseudofolliculitis with characteristic acnelform nodules observed by physician

Pathergy test

Interpreted at 24 to 48 h by physician

Adapted from International Study Group for Behcet's Disease. Criteria for diagnosis of Behcet's disease. Lancet 1990;335:1078.


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Abstracts 686 Hyper-Acute Methotrexate Pneumonitis in a Patient With Crohn’s Disease Itishree Trivedi, MD1, Rishi Raj, MBBS2, Stephen B. Hanauer, MD3. 1. Division of Gastroenterology and Hepatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL; 2. Division of Pulmonology and Critical Care, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL; 3. Division of Gastroenterology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL. Case: A 64 year-old female with Crohn’s colitis presented with 2 weeks of fevers, drenching night sweats, malaise, dry cough and dyspnea. She had developed a severe flare of Crohn’s colitis 4 months earlier that was refractory to infliximab, necessitating surgical management with colectomy and diverting ileostomy. Post-operatively, she developed peristomal pyoderma gangrenosum for which she was to receive adalimumab and methotrexate(MTX) 10 mg oral every week. Two days after her first dose of MTX, she developed the presenting symptoms that worsened after her second dose. This occurred prior to initiation of adalimumab. On presentation, patient was tachycardic to 120s, hypoxic and febrile to 101°F. Rales were audible over both lung fields. Laboratory values were within ranges of normal except mild renal insufficiency. Chest CT (figure 1) showed diffuse ground glass opacities with centrilobular prominence. Non-invasive workup for infectious etiologies was negative. On bronchoscopy and bronchoalveolar lavage (BAL), antigen testing and cultures did not reveal evidence of bacterial, viral, mycobacterial or fungal infection. Elevated lymphocyte (54%) and eosinophil (11%) counts were noted on the BAL fluid cell differential. A diagnosis of MTX-induced pneumonitis (MIP) was made. She was started on 40 mg/day prednisone with tapering over 5 weeks. After 4 weeks on corticosteroids, the patient’s symptoms resolved. A follow-up chest CT (figure 2) showed resolution of radiographic abnormalities.

[685A] Figure 1.

[686A] Figure 1.

[685B] Figure 2.


[686B] Figure 2.


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Discussion: MTX is an immunosuppressive with efficacy as monotherapy in induction and remission of Crohn’s disease. Concurrent use of MTX with anti-TNFα agents can prevent anti-drug antibody formation and foster higher drug levels. MTX is associated with serious lung toxicity with MIP as the most common manifestation. MIP presents with non-specific acute or gradually progressive symptoms of cough, dyspnea, fevers and can progress to respiratory failure. MIP generally occurs after months of low-dose oral MTX therapy. Of the only two previous case reports of MTX-related pulmonary disease reported in Crohn’s disease(CD) symptom onset was at 2-18 months aft er initiation of MTX. This is the first case of hyper-acute MIP in CD with symptom onset within a few days of MTX initiation. MIP diagnosis is made based on a composite of clinical history, radiological findings and BAL results. CT chest imaging can demonstrate diffuse groundglass opacities with or without consolidation, centrilobular nodules or traction bronchiectasis. BAL fi ndings have lymphocytic and eosinophilic predominance with increase in the CD4/CD8 ratio. The treatment of MIP is MTX withdrawal. Corticosteroid therapy can be considered based on severity, duration and progression of symptoms.

687 Disseminated Histoplasmosis: A Case That Warns of Consequences of Immunosuppression in IBD Nathaniel Avila, MD1, Julie Guider, MD2, Meera Avila, MD1, Nirav Thosani, MD3, Sheila Reddy, MD2. 1. University of Texas Health Science Center, Bellaire, TX; 2. University of Texas Health Science Center, Houston, TX; 3. University of Texas, Houston, TX. A 48 year old White woman with a 8 year history of ulcerative colitis was admitted with complaints of persistent joint pain, fevers and rash. Five days prior to admission she was started on prednisone for worsening diarrhea. Over the past year, she had been treated several times with prednisone for presumed IBD flares without improvement despite being treated with infliximab and azathioprine. On admission she was taking prednisone 40 mg daily, azathioprine 150 mg daily and infliximab 5 mg/kg every 8 weeks. She was having 10-15 loose bowel movements daily with intermittent blood on admission despite steroid therapy, which the patient stated was her baseline. Notable during admission, the patient developed elevated transaminases, DIC, and was found to have hemophagocytic lymphohistiocytosis (HLH). Workup for causes with, C. Diff PCR, stool studies, and blood and urine cultures were negative. Imaging was unremarkable except for a CT abdomen/pelvis, showing mild circumferential wall thickening involving the sigmoid colon and rectum, believed to be consistent with active colitis. Gastroenterology was consulted when the patient’s hemoglobin dropped to 5.8g/dl and flexible sigmoidoscopy was performed revealing erythematous mucosa and multiple deep ulcerations from the distal sigmoid colon to rectum. Biopsies from the ulcerations revealed numerous budding yeast, consistent with histoplasmosis. Upon further investigation, Histoplasma serum and urine antigens were positive and bone marrow biopsy was positive for histoplasmosis and histoplasmosis was found to be the cause for HLH and DIC and she was found to have hepatic and CNS involvement. The patient was then treated was with amphotericin B and itraconazole for 4-6 weeks and had significant improvement in her diarrhea and other symptoms. Disseminated histoplasmosis in the setting of immunosuppression in IBD patient is a rare occurrence. However, immunosuppressive therapy is increasingly used in IBD patients, which increases the risk of potential disseminated infections. It is important to recognize atypical presentation of potentially lifethreating disseminated infections. Although rare, histoplasmosis is one such infection that can occur, particularly in the setting of chronic immunosuppression. It can present as a rapid fatal disease with diffuse reticuloendothelial involvement. Histoplasma capsulatum can be found in the GI tract in 70 – 90% of patients with disseminated histoplasmosis during autopsy, however only produces symptoms in 3 – 12% of patients. Therefore, histoplasmosis should be kept in mind in the patient with IBD on immunosuppression who presents with signs of rapid deterioration.

688 Two Cases of Hermansky-Pudlak Syndrome Highlight a Potential Biologic Explanation for Associated Crohn’s Disease M. Anthony Sofia, MD, Atsushi Sakuraba, MD, PhD, David T. Rubin, MD. University of Chicago Medicine, Chicago, IL. Introduction: Hermansky-Pudlak syndrome (HPS) is a genetic disorder associated with Crohn’s disease (CD). We report two cases of HPS with CD and propose a biologic mechanism for the association. Case 1: A 27 yo Hispanic man with HPS and CD presented with abdominal pain and hematochezia. He had oculocutaneous albinism, a tender abdomen and anal fissures. Sigmoidoscopy showed continuous ulceration and stenosis in the rectosigmoid. MR enterography demonstrated multifocal colorectal stenoses and transverse colon dilation to 11 cm. After no improvement with IV steroids and ongoing abdominal distension, he had laparoscopic loop ileostomy and medical therapy with infliximab (IFX) and azathioprine (AZA). Eight weeks later, he had rectal hemorrhage and underwent emergent proctocolectomy. Case 2: A 25 yo Hispanic man with HPS and colonic CD with perianal disease presented with rectal pain, hematochezia, urgency, and failure of IFX therapy. He had oculocutaneous albinism, a nontender abdomen and anal fissures. Sigmoidoscopy showed severe, continuous inflammation of the rectosigmoid. He achieved clinical response with tacrolimus and AZA, but this was discontinued due to rising creatinine. He is currently receiving vedolizumab and AZA. Discussion: HPS is a spectrum of diseases of lysosome related organelles manifested by oculocutaneous albinism and absent platelet dense granules. HPS type 1 is associated with Puerto Rican heritage due to a founder mutation in that population. HPS types 1 and 4 are associated with ileocolonic CD. HPS-1 and HPS-4 proteins combine to form the BLOC-3 protein. Dysfunctional BLOC-3 leads to abnormal endosome trafficking through effects on Rab proteins, especially Rab38/32. Rab38/32 dysfunction leads to classic HPS albinism and platelet function disorder. Rab32 is also thought to impart an antibacterial effect to gut epithelial lysosomes. Another endosome trafficking protein, Rab13, is responsible for tight junction maintenance in gut epithelium and is abnormally localized in CD. The relationship between BLOC-3 and Rab13 has not been investigated. We hypothesize that mutated BLOC-3 in HPS leads to the CD phenotype through abnormal endosome trafficking, dysfunctional colonic tight junctions, and


altered interactions with gut microbes. This proposed mechanism may explain resistance to anti-TNF therapy. Observations regarding this pattern of disease should lead to focused efforts to identify more precise and targeted treatment options.

689 A Case of Rare Malignancy Mimicking Crohn’s Disease Amy Doran, MD, Andrew Copland, MD, James Mann, MD, Anne Tuskey, MD, Christopher Moskaluk, MD, PhD, Brian Behm, MD. University of Virginia Health Systems, Charlottesville, VA. Introduction: Crohn’s disease (CD) is an autoimmune inflammatory disorder which may involve any portion of the GI tract. Patients typically present with diarrhea, weight loss, abdominal pain, and fever. We present a patient with a classic presentation for CD, which was actually a rare malignancy. Case Report: A 65-year-old male with medical history of hypertension presented to clinic after three months of diarrhea, abdominal pain, and unintentional weight loss. Colonoscopy at an outside hospital prior to clinic evaluation and was significant for pan-colitis and terminal ileitis, with biopsies interpreted as moderate chronic active colitis and ileitis. He subsequently developed a peri-rectal abscess that required surgical drainage. His diarrheal symptoms responded to prednisone. Upon evaluation, his clinical appearance presentation was felt to be consistent with CD. CT enterography was performed showing normal small bowel and mesenteric lymphadenopathy, favored to be reactive. He was initiated on adalimumab and a steroid taper. Initially he noted clinical improvement; however with steroids tapering he developed 6+ liters of stool daily and further weight loss. Infectious panel was negative and repeat imaging found edematous small bowel. Repeat colonoscopy revealed segmental inflammation with erythema and ulceration throughout. Upper endoscopy revealed diffuse gastritis and duodenitis. Pathology returned as Enteropathy Associated T-Cell Lymphoma (EATL). Review of prior biopsies demonstrated an abundance of T-cells, though a definitive diagnosis of EATL could not be made. Discussion: Crohn’s disease may have an increased risk of lymphoproliferative malignancies, particularly in patients on immunomodulator therapy. We were unable to find an association with CD and EATL in the literature, and EATL has not been documented as mimicking CD. EATL represents less than 5% of all GI lymphomas. Type I is associated with celiac disease. Type II EATL is not associated with celiac disease, and expresses increased CD56 and gamma-delta T cell receptors, as found with this patient. Typical presentation is refractory celiac disease, bowel obstruction, or B symptoms. EATL is an aggressive malignancy, thus early suspicion is critical. This patient had appeared to be a common presentation of a relatively common disease; this demonstrates the importance of maintaining high suspicion for rare diagnoses.

690 New Onset Multiple Sclerosis Following Treatment With Adalimumab for Crohn’s Disease Umber Ahmad, DO1, Mustafa Musleh, MD2, Sangeeta Agrawal, MD, FACG3. 1. Wright State University, Dayton, OH; 2. Wright State University, Miamisburg, OH; 3. Dayton VA Medical Center, Wright State University, Dayton, OH. Over 1.5 million patients worldwide are using TNFα inhibitors for the treatment of diseases including inflammatory bowel disease (IBD), rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and psoriasis. The first TNFα inhibitor to be approved by the FDA for the treatment of Crohn’s disease was Infliximab in 1998. Since then additional TNFα inhibitors have been approved and include Adalimumab, Certolizumab pegol and Golimumab. Side effects of these medications are infection, systemic lupus erythematous, lymphoma, congestive heart failure and demyelinating disorders. We report a case of patient who was diagnosed with Multiple Sclerosis (MS) shortly after initiating Adalimumab therapy for Crohn’s disease. A 53 year old male with history of Crohn’s and Ankylosing Spondylitis was treated with Adalimumb for Crohn’s Disease. In January 2015 he was started on Adalimumab induction then 40mg/2 weeks. In April 2015, the patient presented with symptoms of ascending numbness and paresthesia of bilateral lower extremities extending up to the hip. MRI brain showed multifocal signal changes in the supratentorial and cerebellar white matter. MRI of the thoracic spine revealed signal change in the spinal cord at T7 dorsally to T8-T9 ventrally. Analysis of CSF showed elevated IgG index and oligoclonal bands. The patient was diagnosed with MS and treated with corticosteroids. Adalimumab was discontinued and his symptoms rapidly improved. A rare adverse effect of TNFα inhibitor is demyelinating disease including MS. Most case reports regarding this adverse effect have been associated with treatment of rheumatologic diseases. With the advent of TNFα inhibitors for the treatment of IBD, demyelinating disease is to be expected in this population as well. To date, there have been only two documented cases in literature of patients developing MS while being treated with Infliximab for Crohn’s disease. The first case report was in 2004, at that time there was no strong evidence of a relationship between MS and TNFα inhibitors. The authors attributed the development of MS to a possible genetic relationship between Crohn’s and MS, supported by the higher incidence of MS in IBD patients. Patients with MS have elevated levels of TNFα in their cerebrospinal fluid. It was initially postulated that TNF alpha antagonism may be beneficial in MS. However anti-TNFα therapy have been tested in MS patient and been proven to increase MS attacks. Given the increasing use of TNFα inhibitors in inflammatory bowel disease patients, providers should be mindful of possible neurologic side effects and monitor patients closely.

691 Mesalamine-Induced Cardiogenic Shock in an Ulcerative Colitis Patient Ilnaz Salehi, MD1, Samarth Patel2, Melik Tiba, MD3, Joshua Aron2, Aaron Walfish, MD2, Raghav Bansal3. 1. Icahn School of Medicine at Mount Sinai, Elmhurst, NY; 2. Elmhurst Hospital Center, Elmhurst, NY; 3. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), Elmhurst, NY. Myocarditis is a rare complication of mesalamine therapy. Case reports describe a mild myocarditis presenting with fatigue, chest pain, or arrhythmias. We report a rare case of mesalamine induced myocarditis presenting with cardiogenic shock. A 53 years old female with ulcerative colitis (UC) presented


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Abstracts with chest pain, fever, tachycardia and hypotension. She was diagnosed with UC about 3 years prior to admission at which time she was treated with mesalamine. After 2 months she stopped her medications and remained in clinical remission. Two weeks prior to this admission, she was admitted for a UC flare and was restarted on oral mesalamine 3.6gm daily and 4gm rectally. She was also started on tapering doses of prednisone. Her UC symptoms improved however she gradually developed progressively worsening chest pain. Initial lab work revealed WBC count of 11,300/ml, elevated troponins of 15 ng/ml, ESR of 113 mm/hr and CRP of 46.7mg/dl. EKG was notable for sinus tachycardia, PR depression and low voltage. Chest radiograph revealed cardiomegaly with pulmonary congestion. An echocardiogram demonstrated diffuse hypokinesis with a left ventricular ejection fraction (LVEF) of 40%. She was admitted to the ICU where vasopressors and broad spectrum antibiotics were started. Blood and urine cultures were negative and she continued to require hemodynamic support. On hospital day 3, mesalamine was discontinued due to its association with myocarditis. Two days following the discontinuation of mesalamine therapy the patient’s condition improved. Vasopressors were discontinued, EKG findings returned to normal, and cardiac enzymes and leukocytosis trended down. Subsequent cardiac catheterization confirmed normal coronary arteries. After 2 weeks, her echocardiogram showed improvement in LVEF to 55%. Cardiac involvement is a rare extra-intestinal manifestations of inflammatory bowel disease (IBD), generally it manifests as pericarditis, pericardial effusion or pericardial tamponade. Myocarditis is even rarer in patients with IBD and it is thought to be secondary to treatment with mesalamine. In the presented case, the proximity of symptoms onset to the initiation of treatment and the resolution of myocarditis with discontinuation of mesalamine points to mesalamine as the culprit. This case is significant as it highlights the need for prompt recognition of mesalamine induced myocarditis as a life threatening condition and the need for immediate discontinuation.

692 Acute Severe Headache in Ulcerative Colitis Simranjit Singh, MD1, Vinod Kumar, MD1, Fnu Sanna, MD1, Davendra Ramkumar, MD2, Pathanjali Saravanan, MD3. 1. University of Illinois at Urbana-Champaign, Internal Medicine Residency Program, Champaign, IL; 2. Christie Clinic, Champaign, IL; 3. Christie Clinic, Urbana, IL. Introduction: Thrombosis is a well recognized but uncommon complication of Inflammatory bowel disease (IBD) and occur in 1.2-7.5% of all cases. Deep vein thrombosis and pulmonary embolism are the most common, whereas, cerebral sinus thrombosis (CST) is very rare. CST has almost double the incidence in Ulcerative colitis (UC) as compared with Crohn’s Disease (CD), and can have devastating clinical outcome. The most common manifestations are headache, paresis, seizures, dysphasia and papilledema. We present a case of CST in a young patient with UC, treated with anticoagulation. It highlights the importance of timely recognition and management of a severe disease, as headache can be the only manifestation at onset. Case: A 24-year old female with 10-month history of UC presented with 2 week history of exertional dyspnea, generalized weakness. She had peristent bloody diarrhea and abdominal pain symptoms related to UC. Exam findings were remarkable for hypotension, tachycardia and generalized abdominal tenderness. Labs revealed severe iron deficiency anemia (Hemoglobin - 4 g/dl) and thrombocytosis (681 G/l). She was treated with intavenous fluids, blood tranfusions and glucocorticoids. On the fourth day of hospitalization, she had acute onset, severe generalized headache, without any other neurological manifestation. Magnetic resonance venography (MRV) showed thrombosis of the superior sagittal sinus extending into the right transverse and sigmoid sinuses. She was started on intravenous heparin. Her symptoms including headache, bloody diarrhea continued to improve and she had no acute complication from anticoagulation during hospital course. Discussion: CST is a rare but significant thrombotic complication of IBD, given it’s high morbidity and mortality. It has variable presentation, ranging from headache to seizures and coma. Predisposing factors underlying the pro-thrombotic state are generalized inflammatory response, severe iron deficiency anemia, transient coagulation abnormalities (thrombocytosis, decreased antithrombin III & protein S, increased factor V, VIII & fibrinogen), hereditary thrombogenic mutations and acquired risk factors (steroid therapy, surgery, infections and dehydration). Role of anticoagulation is controversial, given concerns about hemorrhagic transformations of the venous infarctions. But overall, there is a strong evidence supporting anticoagulation with heparin or subcutaneous enoxaparin. Also, we successfully managed the patient with intravenous heparin without any acute cerebral or gastrointestinal complications. In conclusion, we presented a rare case of UC complicated by CST. It highlights the importance of timely diagnosis and successful management with intravenous heparin. Headache is the most frequent and can be the only manifestation.

Discussion: This case describes a novel approach to the MMR vaccination process in an IBD patient on vedolizumab with methotrexate. Although current guidelines state that MMR vaccine is contraindicated among immunocompromised IBD patients and should not be given to patients expected to start immunosuppressive agents within 6 weeks (1), these guidelines do not address organ-selective anti-integrin therapies. We believe that the gut-selective activity of vedolizumab allows for safe and effective administration of live virus vaccinations. Reference: [1]. Wasan SK, Baker SE, Skolnik PR, Farraye FA. A practical guide to vaccinating the inflammatory bowel disease patient. Am J Gastroenterol. 2010;105:1231–1238.

[693] Table 1. Summary of Measles IgG Antibody Index Before and After MMR Booster Administration

Measles IgG Antibody Index

Baseline Measles Antibodies on Vedolizumab+Methotrexate

Measles Antibodies 8 weeks After MMR Vaccination on Vedolizumab and 4 weeks after Methotrexate Restarted

0.70 (NEGATIVE)

2.06 (POSITIVE)

694 Portal Vein Thrombosis as Initial Manifestation of Ulcerative Colitis Kenneth J. Vega, MD1, Rajesh Kanagala, MD2, Zachary Smith , MD3. 1. Division of Digestive Diseases, University of Oklahoma Health Sciences Center, Oklahoma City, OK; 2. University of Oklahoma Health Sciences Center, Oklahoma City, OK; 3. University of Oklahoma Medical Center, Edmond, OK. Introduction: Although uncommon, inflammatory bowel disease (IBD) has been found to be an independent risk factor for acquired thrombosis, even rarer is portal vein thrombosis (PVT) as the presenting illness. Case Report: A 28 y/o nonsmoking female presented with 10 days of worsening abdominal pain. In addition, she reported nausea, vomiting, and bloody stools. On PE, she was alert, oriented, afebrile, mild tachycardia, normal blood pressure and generalized abdominal tenderness on deep palpation only. Routine labs indicated mild anemia, normal WBC and platelets, INR of 2.3 and elevated transaminases. Infectious stool evaluation did not reveal C. difficile, Salmonella, Shigella, Campylobacter, E. coli, or Ova/ parasitic infection. However, stool showed increased Lactoferrin. Abdominal imaging revealed acute PVT on RUQ ultrasound with Doppler and CT abdomen/pelvis suggested colitis. Hypercoagulable state assessment did not confirm Lupus anticoagulant, Factor V Leiden or prothrombin abnormalities. Colonoscopy revealed hemorrhagic, inflamed and ulcerated mucosa from the rectum to transverse colon; biopsies displayed an interstitial neutrophilic/lymphoplasmocytic infiltrate with surface ulceration, cryptitis and crypt abscesses. She was treated simultanously with intravenous methylprednisolone q8 hours and enoxaparin BID for colitis and PVT, respectively. Patient responded well to treatment, eventually transitioning to oral prednisone and mesalamine as well as warfarin with resolution of all presenting symptoms. Discussion: Fewer than 10% of IBD patients have an extra intestinal manifestation at initial presentation. These are most commonly sacroilitis, peripheral arthritis, ocular, mucocutaneous and vascular. In one study, thromboembolic complications occurred in 1.3% of IBD patients with majority having deep vein thrombosis or pulmonary embolism. In IBD patients, inpatient status and steroid therapy as well as post bowel resection are risk factors for development of porto-mesenteric venous thrombosis. However, acute PVT has not been reported as part of an IBD initial presentation previously. Conclusion: PVT is very uncommon in patients with IBD, especially at presentation. If present, complete evaluation (including hypercoagulable state assessment, medication history review, smoking status and imaging) should occur. Therapeutic options including anticoagulation or thrombolysis can be used while simultaneously treating the IBD episode.

693 Measles Vaccine Administered to a Crohn’s Disease Patient Receiving Vedolizumab Alana Wichmann, APN, Noa Krugliak Cleveland, MD, David T. Rubin, MD. University of Chicago Medicine, Chicago, IL. Introduction: Patients with IBD on immunosuppressive therapy (ISS) with thiopurines, methotrexate or anti-TNF biologics are advised against receiving live virus vaccines due to concern about infections. In addition, it is known that there is an attenuated immune response to vaccines in patients receiving immune suppression. Vedolizumab is a gut-selective α4β7 antiintegrin monoclonal antibody approved by the FDA for the treatment of moderately to severely active Crohn’s disease and ulcerative colitis. We report a case of a patient successfully vaccinated against measles virus while on vedolizumab therapy. Case Description: A 26 year old female with Crohn’s ileocolitis was receiving vedolizumab and methotrexate 15 mg PO/week. She reported having received prior measles, mumps, rubella (MMR) vaccination in childhood. Due to a nation-wide measles resurgence, we assessed her measles titers to advise her of her risk of infection. Her measles antibody index (AI) was 0.7 (negative). We instructed her to stop the methotrexate and to continue the vedolizumab. Two weeks after stopping the methotrexate, she received the MMR vaccine. The methotrexate was restarted 4 weeks later. Measles AI 8 weeks after the MMR vaccine was 2.06 (positive). In 2 months follow up after she received the vaccine, there have been no adverse sequelae.


[694A] Figure 1.


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[694B] Figure 2.

[695A] Figure 1.


695 Endoscopic Sealing of an Enterocutaneous Fistula With a Combination of Jagwire Placement and an Over-The-Scope Clip Sarina Kapoor, MD, John Nasr, MD. West Virginia University Hospital / Ruby Memorial Hospital, Morgantown, WV. Fistula formation in Crohn’s disease is a common complication that can necessitate surgical intervention. Recently, technological advancements in endoscopic treatment have led to development of an over-thescope clip (OTSC). Our case report describes an application of this clip for closure of an enterocutaneous fistula. An 85-year old male patient with a past medical history of fistulizing ileocolonic Crohn’s disease presented with recurrent subcutaneous periumbilical abscess formation due to an enterocutaneous fistula. Prior attempts at fistula closure with intravenous antibiotics and incision and drainage procedures had failed. Computed tomography of the abdomen and pelvis (Figure 2, 3) revealed an enterocutaneous fistula at the level of the open abdominal wound. Using a 0.035 inch Jagwire (Boston Scientific, Natick, MA), for fistula localization, and over-the-scope (OTSC System; Ovesco Endoscopy AG, Tubingen, Germany) system, the fistula was successfully closed. The patient presented one month later with complete healing of the fistula and cessation of drainage. When medical and biologic therapy fails, surgical management remains the mainstay of management for fistulizing Crohn’s disease. Recently, the development of new endoscopic therapeutic options has expanded the breadth of minimally invasive treatment. Our case describes a novel use of a Jagwire to localize the intestinal opening, in conjunction with an OTSC clip placement for closure of a recurrent fistula associated with active Crohn’s disease. To our knowledge, the consecutive use of endoscopic wire to aid endoscopic fistula closure has not been described elsewhere. The OTSC clip is a promising, safe,


[695C] Figure 3.


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Abstracts and effective endoscopic alternative for closure of enteric fistulas in patients who want to avoid surgical options. However, large, prospective studies are needed to compare the long term outcomes from OTSC clip repair compared to surgical intervention for fistulae.

696 Crohn’s Appendicitis Veronika Dubrovskaya, MD1, Steven Shamah, MD2, Ilan Weisberg3, Arun Swaminath, MD4. 1. SUNY Downstate Medical Center, New York, NY; 2. North Shore-LIJ Lenox Hill Hospital, New York , NY; 3. Lenox Hill North Shore-LIJ Hospital System, New York, NY; 4. Lenox Hill Hospital, New York, NY. Background: Inflammatory bowel disease (IBD) represents a spectrum of disorders characterized by chronic inflammation of the gastrointestinal luminal organs. Granulomatous appendicitis, or Crohn’s appendicitis, is another rare presentation of IBD and is usually found on a pathology specimen after the appendectomy (1). This case report presents a patient who manifested his Crohn’s colitis with acute appendicitis. The patient’s diagnosis was made based on his clinical presentation without performing appendectomy. Case: 37 yo male with h/o mild Ulcerative colitis/proctitis for one year presented with acute abdominal pain and diarrhea. Patient had a negative McBurney’s sign, yet his abdomen was tender to palpation in the peri-umbilical area. WBC 12.3 THDS/CMM, Hgb 11.8 G/DL, INR 1.6. The stool negative for any infection, including clostridium difficile. CT scan of abdomen and pelvis demonstrated a thick wall dilated appendix consistent with acute appendicitis. There was also a colonic wall thickening from rectum to trasverse colon, consistent with colitis. The diagnosis of appendicitis was entertained. Due to the fact that patient’s clinical presentation was more consistent with exacerbation of his colitis, the decision was made not to perform appendectomy. Colonoscopy was performed and demonstrated moderate to severe pancolitis. Biopsies revealed crypt abscesses and chronic inflammation. A diagnosis of Crohn’s appendicitis with Crohn’s colitis was made and the patient was started on high dose IV Methylprednisolone. Patient’s clinical condition deteriorated and he was switched to IV Infliximab. Within 12 hrs of Infliximab infusion, the patient improved and was discharged from the hospital.

[696B] Figure 3.

Discussion: Granulomatous appendicitis has been categorized as primary Crohn’s disease of the appendix based on its pathologic features (2). Appendectomy is often the surgical procedure in patients with Crohn’s disease. Few data exist on appendiceal Crohn’s disease. . This case report demonstrates the importance of correlating clinical and radiographic findings in diagnosing Crohn’s appendicitis. Medical treatment of Crohn’s appendicitis wirhout appendectomy proved to be sufficient.. References: [1]. Pal K, Granulomatous appendicitis in children: a single institutional experience, Afr J Paediatr Surg. 2014 Jan-Mar, 11(1); 26-31. [2]. Stangle PC, Crohn’s disease of the appendix, Virchows Arch, 2002 Apr; 4404); 397-403.

697 WITHDRAWN

698 [696A] Figure 1.

Crohn’s Disease, Malignant Melanoma, and Churg-Strauss Syndrome: A Treatment Dilemma Laura Pestana, DO, Darrell Pardi, MD, MS, Sahil Khanna, MBBS, MS. Mayo Clinic, Rochester, MN.

[696B] Figure 2.


A 71-year-old man with Churg-Strauss disease on low-dose prednisone (prior azathioprine use), diabetes, atrial fibrillation, and diverticular disease presented with hematochezia, pain with defecation, & increased stool frequency. He denied abdominal pain, fever, nausea, emesis, weight loss, constipation, joint pains, skin rash or eye pain. Vital signs were normal, abdomen was soft, non-tender, non-distended, and rectal examination revealed perianal irritation and significant pain without fistulae. Laboratory studies revealed elevated CRP of 92.8 mg/L (normal C. difficile, Shigella PCR and stool culture. A CT abdomen revealed 5-10 cm concentric wall thickening in the sigmoid colon with associated pericolonic mesenteric hyperemia. Colonoscopy revealed nodularity and irregularity in the rectum and an inflammatory stricture in the sigmoid colon with deep ulcerations, and pathology revealed active chronic colitis with ulceration. Of note, a colonoscopy 5 months prior was normal. Treatment with aminosalicylates was unsuccessful and due to unclear diagnosis and concern for malignancy, laparoscopic sigmoid resection with primary anastomosis was performed. Surgical pathology showed moderately active chronic colitis with creeping fat, stricture formation, transmural chronic inflammation, and granulomas consistent with Crohn’s disease. Six months later, he developed recurrent rectal bleeding and colonoscopy revealed moderately ulcerated rectal mucosa and mild inflammation of his colonic anastomosis consistent with moderately active Crohn’s disease. In the interim, he underwent excision of a mole on his back and pathology was consistent with malignant melanoma. Therefore, the decision was made to defer anti-TNF therapy and the patient was treated with vedolizumab, a gut selective antiintegrin molecule. In addition to typical dermatologic manifestations such as pyoderma gangrenosum and erythema nodosum, patients with inflammatory bowel disease (IBD) are at increased risk for non-melanoma skin cancers and malignant melanoma. A meta-analysis revealed that IBD was associated with an increased risk of malignant melanoma, independent of treatment with biologic therapy, and is increased with anti-TNF treatment and immunomodulatory medications. In contrast, since vedolizumab selectively blocks gut leucocyte trafficking, it is likely to have lower systemic immunosuppression and lower risk for melanoma.


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699 Hyperbaric Oxygen Therapy for Chronic Antibiotic-Refractory Ischemic Pouchitis Custon Nyabanga1, Bo Shen, MD, FACG2. 1. Cleveland Clinic Foundation, Cleveland, OH; 2. Digestive Disease Institute, Cleveland Clinic Foundation, Cleveland, OH. Hyperbaric oxygen therapy (HBOT) has been shown to be efficacious in treating various conditions including perianal Crohn’s disease. Here, we present a case of a 59-year-old male with a history of UC status post proctocolectomy and 2-stage J-pouch construction. He later developed chronic antibiotic-refractory pouchitis (CARP) with endoscopic signs of ischemia, believed to be secondary to vascular compromise (Figure 1). He underwent HBOT with a total 20 sessions, at 2.5-3.0 ATA, for 60-90 minutes per session. At the completion of therapy, repeat pouchoscopy showed marked improvement of the mucosal disease (Figure 2). HBOT is known to increase tissue oxygenation, reduce tissue hypoxia, alter inflammatory pathways and promote tissue healing. This case demonstrates the therapeutic role of HBOT as well as possible disease mechanism in chronic antibioticrefractory pouchitis.

received allogeneic stem cell transplant (SCT). After SCT, she developed refractory diarrhea, and was referred to our clinic. The patient had two prior episodes of Clostridium difficile infections prior to her SCT, which were treated. Despite elimination of toxin, the diarrhea continued. Routine stool studies were negative. The patient subsequently underwent endoscopic evaluation with biopsies. During her fourth colonoscopic evaluation, biopsies demonstrated a variable chronic active colitis with epithelioid cell granulomas. Acid-fast bacilli and Gomori methenamine silver (GMS) stains were negative for microorganisms. Cytomegalovirus, Epstein-Barr virus, and Adenovirus were negative on viral cultures. While the histological features could arise in the setting of graft-versus-host disease, the nature and pattern of inflammation were more characteristic of Crohn’s disease. The patient was subsequently initiated on corticosteroids and mesalamine, with improvement in her symptoms of diarrhea to her baseline. Despite reported cases of potential treatment of Crohn’s disease with SCT, here we report a case of de novo Crohn’s disease with onset that may have been influenced by SCT. Multiple factors are implicated in the pathogenesis of Crohn’s disease, including genetics, environment, infection, and immunologic factors. This case suggests that susceptibility to Crohn’s disease may be transferred during SCT. Further studies are warranted to elucidate understanding of this relationship, so that we may identify appropriate recipients and donors for SCT, given our knowledge that inflammatory bowel disease may have a multifactorial genesis.

701 Fistula Masquerading as Crohn’s Disease Yecheskel Schneider, MD1, Monica Saumoy, MD2, Nicole Panarelli, MD3, Vinita Jacob, MD3, Brian Bosworth, MD, FACG4. 1. New York Presbyterian Hospital/Weill Cornell Medical Center, Brooklyn, NY; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 3. Weill Cornell Medical College, New York, NY; 4. Division of Gastroenterology and Hepatology, Weill Cornell Medical College/ New York Presbyterian Hospital, New York, NY.

[699A] Figure 1.

Case: The patient is a 55 year old woman with a history of rheumatoid arthritis, previously on etanercept, and autoimmune hemolytic anemia requiring immunosuppression with steroids and intravenous iron infusions for the past 35 years. In 2013 she began to have increasing weight loss and a colonoscopy showed microscopic colitis for which she was treated with and maintained on budesonide. She re-presented in 2015 with a perianal abscess with bloody and purulent discharge. An MRI Enterography noted a 3.3 x 1.9 x 1.1 cm hyperintense phlegmonous abscess in the right ischioanal fossa abutting the anal sphincter and levator ani. An exam under anesthesia was performed and a seton was placed and the subcutaneous abscess cavity was curettage. It was presumed that the patient’s microscopic colitis was really an early manifestation of underlying Crohn’s disease. However, a colonoscopy was performed with no visible inflammatory changes. There was active cryptitis as well as occasional apoptotic bodies and markedly decreased plasma cells in every colonic segment. There were similarly decreased numbers of plasma cells it the terminal ileal biopsies – all suggestive of combined variable immunodeficiency (CVID). Discusssion: CVID is a heterogeneous disease that results in hypogammaglobulinemia and is the second most common immunodeficiency syndrome. Gastrointestinal manifestations are the second leading cause of morbidity in this group. CVID has been reported to mimic microscopic colitis and inflammatory bowel disease (IBD). Biopsies may report crypt distortion and granulomas, with endoscopic evidence of colitis or enteritis. Up to 10% of patients may present with an IBD-like picture. The relative paucity of plasma cells on biopsy would favor a diagnosis of CVID. To date there have been no reports of CVID-associated fistulas in the absence of concomitant IBD. It is important to distinguish between CVID and Crohn’s disease as the former is treated with intravenous immunoglobulin, and the latter is treated with immunosuppressant medications. Significance: This case highlights that physicians must have a high index of suspicion for CVID when encountering a patient with gastrointestinal findings, and is the first study to report perianal abscess and fistula in the setting of CVID without evidence of Crohn’s disease.

702 Cardiac Tamponade as a Presenting Manifestation of Infliximab-Induced Lupus in Patient Treated for Crohn’s Disease: A Case Report and Literature Review Maliha Naseer, MD1, Hussam Sabbagh, MD2, MHD Hussam Al Jandali, MD3, Zain Kulairi, MD4, Sarwan Kumar, MD4. 1. Wayne State University, Internal Medicine Department, Rochester , MI; 2. Wayne State University, Internal Medicine Department, Rochester, MI; 3. Wayne State University, Internal Medicine Department, Auburn hills, MI; 4. Wayne State University, Rochester, MI.

[699B] Figure 2.

700 de novo Crohn’s Disease After Stem Cell Transplantation Sunhee Park, MD, Stuart Seropian, MD, Ananta Gurung, MD, Dhanpat Jain, MD, Cyrus Kapadia, MD. Yale University, New Haven, CT. A 49 year-old woman with history of acute lymphocytic leukemia (ALL) underwent chemotherapy and subsequently achieved complete remission of disease. She was high-risk for relapse and subsequently


Introduction: Crohn’s disease (CD) is a chronic inflammatory bowel disease. It has been postulated that TNF-α; a proinflammatory cytokines plays a crucial role in the mucosal inflammation. Infliximab has shown to be associated with increased likelihood of achieving and maintaining remission and improving quality of life in CD. We are presenting an extremely rare case of cardiac tamponade caused by infliximab induced lupus. Case: A 30 year-old female presented to the ED with pleuritic chest pain and dyspnea. Patient denied palpitations, orthopnea, PND, fever and cough. No history of travel or sick contacts. Past medical history was significant for CD, well controlled on infliximab every 8 weeks for the past 1 year. Last dose was 2 months ago. On physical examination Temp: 98.6, HR: 120-130, RR: 41, BP: 100/60 and SaO2: 99%. Chest examination showed muffled heart sounds, raised JVD and equal breath sounds bilaterally. EKG showed sinus tachycardia. Chest X-ray, CT scan and bedside ECHO were consistent with a large pericardial effusion. Patient was taken to the OR for emergent pericardial window and chest tube insertion. Around 800 mL of pericardial fluid was removed. Pericardial fluid and biopsy were sent for further analysis. Biopsy of the pericardium showed fibrinous pericarditis. HIV screen, EBV, CMV, HSV, adenovirus, influenza A&B, Coxsackie B virus were negative. Autoimmune workup was positive for ANA, anti-dsDNA and anti-histone antibodies. A diagnosis of drug induced lupus causing pericardial effusion secondary to infliximab was made. Discussion: The risk of ANA and anti-dsDNA seroconversion with infliximab therapy has been reported to be 41%-62% and 14%-85%, respectively but only 0.2-0.8% patients develop drug induced lupus. More than 100 cases of lupus following treatment with TNF α inhibitors have been reported in literature. Common manifestations include vasculitis, lupus like syndrome and interstitial lung disease. Only few cases of infliximab induced pericarditis and cardiac tamponade has been reported. Exact underlying


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Abstracts mechanism is unknown. However, the temporal association between the use of TNFα inhibitors, the development of cardiac tamponade and the resolution of symptoms following the cessation has been a clue to the diagnosis. Conclusion: Early recognition and management of infliximab induced autoimmune complications is necessary. In conclusion, DILE should be considered as differential in cases of pericarditis with cardiac tamponade without a clear cause

703 Difficulty Distinguishing Between Crohn’s and Ulcerative Colitis: Extraintestinal Manifestations May Offer Clues to a Diagnostic Dilemma Katherine J. Hahn, MD, Shannon Morales, James Katsis, Sabeen Medvedev, Mark Mattar. MedStar Georgetown University Hospital, Washington, DC. Introduction: Extraintestinal manifestations (EIM) occur in 25-40% of inflammatory bowel disease (IBD) patients. Commonly involving the musculoskeletal, dermatologic, and hepatopancreatobiliary systems – EIM patterns differ between Crohn’s disease (CD) and ulcerative colitis (UC). Existence of specific EIM can facilitate or impede in distinguishing between the two IBD types. In this case report, we describe misdiagnosis of CD in a patient with multiple UC related EIM. Clinical Case: A 54 year-old African American woman, with past history of UC diagnosed by colonoscopy and biopsy, was admitted for non-healing lower extremity ulcers. Two months prior, the patient developed arthritis of her elbows and shoulders. The arthralgias progressed and she underwent washout of the right knee for suspected septic arthritis that resulted in large ulcers of both lower extremities. Despite procedures and continued antibiotics, the patient’s wounds worsened. On admission, physical exam revealed lower extremities with several pustular lesions and two large ulcerations on both knees and ankles. The wounds were evaluated by dermatology and were determined to be pyoderma gangrenosum (PG) with pathergy. The patient only had mild abdominal pain. Laboratory values showed white count of 39.3, creatinine of 0.63, ESR/CRP of 84/102, and alkaline phosphatase of 539. Colonoscopy showed severe colitis throughout the colon, sparing the cecum and ascending colon. Biopsies of both sides of the colon showed severe active colitis. MRI revealed multiple dilations of intrahepatic and extrahepatic biliary ducts, diagnosed as primary sclerosing cholangitis (PSC). The patient was started on mesalamine and steroid therapy, but continued to have bloody stools requiring transfusions and required a total colectomy. The surgical pathology of the removed colon revealed cobblestone appearance with transmural inflammation and focal fibrosis consistent with CD. Discussion: Distinguishing between CD and UC remains difficult. The many overlapping features of IBD make diagnosis a challenge. Specific EIM can help or hurt in diagnosis. Polyarthritis is more common in CD with colonic involvement. However, PSC and PG are common in UC. Given the concurrence of UC diagnosis on initial colonoscopy and corresponding EIM, this patient’s ultimate diagnosis of CD was unexpected. Since treatment of UC and CD widely differs and colectomy is only being curative for UC, careful diagnosis is imperative.

presence of Crohn’s disease. We present an 85 year old male with several days of worsening scrotal erythema and swelling. The patient has a remote history of colonic Crohn’s disease diagnosed in the early 1970s resulting in a partial colectomy and end-ileostomy. He had no remaining manifestations of his Crohn’s disease and was eventually lost to all follow-up. He had been having episodic flares of scrotal swelling for the past three years, often lasting 1-2 weeks. He was evaluated by multiple hospitals and specialties without a clear diagnosis. On presentation, he was afebrile. He denied symptoms of hematuria, dysuria, discharge or difficulty with urination. He had no gastrointestinal complaints. There was no known trauma or significant scrotal or penile pain. On exam his scrotum and penis were diffusely erythematous with significant edema extending onto the suprapubic region. Skin of the scrotum appeared thickened without ulcerations or nodules. There was no significant laboratory abnormalities. A CT scan of the pelvis revealed extensive scrotal edema with no discrete fluid collection or subcutaneous emphysema. A scrotal ultrasound showed diffuse scrotal wall thickening and edema. He was started on broad-spectrum antibiotics with no improvement in his symptoms. He underwent a scrotal punch biopsy which revealed lymphohistiocytic infiltrate with focal intralymphatic histiocytosis. These histological features were consistent with granulomatous lymphangitis associated with Crohn’s disease. In children, the majority of genital granulomatous lymphangitis were associated with concomitant or subsequent development of Crohn’s disease. In the older patient population, genital swelling often occurred after a long history of Crohn’s Disease and years after a colectomy. Lymphedema is thought to be the primary process and granulomatous inflammation secondary to the microflora and waste products in the dilated lymphatic vessels. Treatment with steroids, mesalamine, or metronidazole often results in partial improvement or complete remission. The rare entity of scrotal granulomatous lymphangitis in Crohn’s disease is easily missed however its accurate diagnosis has significant treatment implications.

704 Better Outcome in Hermansky Pudlak Syndrome Xiomara Cruz, Omar Perez-Jimenez, MD. Mayaguez Medical Center, Mayaguez, Puerto Rico. Hermansky-Pudlak Syndrome (HPS) is a multisystem autosomal recessive disorder characterized by oculocutaneous albinism, platelet dysfunction, and ceroid-substance tissue accumulation. Although HPS is a rare condition worldwide, a relatively high prevalence of up to 1:1800 has been reported with families of Puerto Rican heritage. Systemic complications vary greatly, and inflammatory bowel disease is a significant manifestation with up to 15% of HPS patients developing it. The IBD of HPS has generally been characterized as a granulomatous inflammation of the colon that may clinically resemble Crohn’s disease. This case series aims to document our experience and therapeutic approach with gastrointestinal tract involvement in HPS since unfortunately up to now, treatment is still not standardized. Case 1: A 22 y/o female with history of HPS presents with chronic diarrhea, abdominal pain and bloody stool. Stool studies where negative for most common infections. Colonoscopy revealed normal colonic mucosa with melanosis coli and chronic colitis non-specific on pathological exam. Patient failed 5ASA, corticosteroids, and budesonide. Treatment with anti-TNF agent adalimubab provided resolution of symptoms and weight gain. Discontinuation of biologic with eventual relapse was documented later and treatment with infliximab provided rapid resolution of symptoms.Case 2 A 25 y/o male with history of HPS presents with acute lower gastrointestinal bleeding and history of chronic diarrhea. Colonoscopy revealed focal area of colitis at cecum. Pathology revealed melanosis coli and active colitis. Treatment included budesonide, 6MP with minimal response. Infliximab was started at 5mg/kg with rapid amelioration of symptoms. Treatment was discontinued after 6 years, with no evidence of relapse after 6 months off therapy. The clinical presentation of patients with granulomatous colitis may include abdominal pain, bloody diarrhea, and mild constitutional symptoms, which are analogous to Crohn’s disease. Similar to the majority of the documented cases in the literature, neither of our patients underwent remission of disease with standard therapy. A stronger immunomodulator, in our cases infliximab, showed to be effective. These cases emphasize the importance of early diagnosis and treatment of granulomatous colitis since platelet aggregation dysfunction makes HPS patients highly prone to gastrointestinal tract bleeding and this can definitely change prognosis.

705 Skin-Deep: The Diagnosis of Scrotal Lymphangitis Associated With Crohn’s Disease Nancy Khov, MD, Klaus Helm, MD, Emmanuelle Williams, Nicholas Inverso. Penn State Hershey Medical Center, Hershey, PA. Granulomatous lymphangitis is a rare cause of genital lymphedema. The presence of scrotal swelling and granulomatous lymphangitis of the external genital is an important and often missed clue to the


[705A] Figure 1.

706 A Case of Crohn’s Disease Presenting as Enterocutaneous Fistula Srikar Mapakshi, Jonathan Chapman. Baton Rouge General - Tulane Internal Medicine Program, Baton Rouge, LA. Patients with chronic non-healing abdominal wounds or non-healing fistulas following gastrointestinal surgery, inflammatory bowel disease (IBD) should be considered in the differential diagnosis. A 67-year-old Caucasian female presents with multiple comorbidities a remote history of subtotal colectomy with elective closure of ileostomy secondary to life threatening Clostridium difficile colitis. She was noted to have later developed a complete bowel obstruction for which she underwent explorative laparotomy and lysis of adhesions. Post operatively, she developed a non-healing wound at the incision site & a low output enterocutaneousfistula(ECF) thought to be a surgical-related fistula. During recent admission she presented with high output per fistula and acute kidney injury. Given her history of delayed wound healing and ECF, general surgery and gastroenterology services were consulted. IBD was suspected & she underwent flexible enteroscopy with biopsies which were normal. Despite a lack of endoscopic or histological evidence of IBD, a diagnosis of Crohn’s Disease(CD) was made using fecalcalprotectin(FC) and a Prometheussgi® panel. Being that this patient was a poor surgical candidate and the risk benefit profile of infliximab, we decided to begin treatment with little other options available. We present a case of jejuno-cutaneous fistula which is an extremely rare presentation of CD. ECF are usually a late complicationof CD with the cumulative risk of developing a fistula being 33% and 50% percent after 10 and 20 years, respectively [1]. Our patient did not have endoscopic or histological findings of CD given her history of significant comorbidities with a complex ECF. CD diagnosis was made using the stool biomarker fecal calprotectin(FC) along with an the Prometheoussgi®, both of which were highly suggestive of CD. There has been documented evidence of the efficacy of biologics for treatment of fistulas. In a placebo-controlled trial specifically designed to evaluate healing of fistulae in CD, Infliximab was shown to be highly effective [2]. Our patient received treatment with Infliximab and FC levels were used to monitor response to treatment [3]. Her baseline FC level was around 800 through the fistula and


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258 from a rectal stool collection. Levels returned to normal with the closure of the fistula, which took 8-10 weeks. Studies also show that fistulating disease and long disease duration were associated with early relapse after treatment, which makes early disease identification essential for treatment efficacy [4]. In conclusion, our patient’s history of non healing abdominal wound with persistent fistula should prompt the physician, either internist or surgeon, to consider the diagnosis of IBD - decreasing the morbidity and economic burden of the disease. References: [1]. Management of Crohn’s disease in adults. Lichtenstein GR, Hanauer SB, Sandborn WJ, Practice Parameters Committee of American College of Gastroenterology Am J Gastroenterology. 2009;104(2):465. [2]. Long term results of infliximab treatment of fistulas in patients with Crohn’s disease in Arctic NorwayR. Heitmann R. Goll, J.R. Florholmen Journal of Crohn’s and Colitis Feb 2014, 8 (Supplement1) S241; DOI:10.1016/S1873-9946(14)60541-9. [3]. Fecal biomarkers in the diagnosis and monitoring of Crohn’s disease.Wright EK(1), De Cruz P, Gearry R, Day AS, Kamm MA. PMID: 24918319. [4]. ParsiMA, Lashner BA, Achkar JP et al. Type of fistula determines responseto infliximab in patients with fistulous Crohn’s disease . Am J Gastroenterology 2004 ; 99:445–9.

aminase levels, the patient was started on steroids with predonine prescribed to control the hepatic inflammation. Discussion: This report is the first to describe a case of DI-AIH following the use of an over-the-counter drug. In fact, DI-AIH diagnosis represents a challenge to the clinician because neither histological nor clinical pathognomonic features of AIH exist. We described a case of OTC Pabron gold®-associated liver injury, diagnosed as DI-AIH, calling for caution in the use of OTC.

709 Not a Simple Cyst: Hepatic Cyst Causing Intra-cardiac Shunting Relieved by Percutaneous Drainage Gurneet Bedi, MD1, Lisa Yoo, DO2, Simranjit Bedi, MD3, Michael Farbaniec, MD2, Thomas Riley, MD1. 1. Penn State Hershey Medical Center, Hershey, PA; 2. Penn State Milton S. Hershey Medical Center, Hershey, PA; 3. Penn State Hershey Medical Center, Hummelstown, PA. Hepatic cysts are a relatively benign and asymptomatic group of disorders, which are usually found incidentally during imaging studies. We present a case of a large hepatic cyst causing intra-cardiac

707 Co-Colitis: A Rare Case of C. difficile and CMV Coinfection in an IBD Patient Randy Chung, MD. Baylor College of Medicine, Houston, TX. Co-infection with Clostridium difficile (C. diff) and cytomegalovirus (CMV) has rarely been reported in literature but carries a high mortality rate. When present, it often poses a diagnostic challenge and can lead to a delay in treatment. A 26 year-old man with a history of ulcerative colitis (UC), currently on prednisone, was admitted for two weeks of intractable bloody diarrhea. The patient was diagnosed with UC four years ago and was started on mesalamine and azathioprine. He self-discontinued his medications one year ago when he was no longer experiencing any symptoms. Three months prior to admission, he began to have recurrence of diarrhea with occasional blood in his stool, so he was started on prednisone 40 mg daily. Two weeks prior to admission, his diarrhea continued to worsen with up to ten bloody bowel movements daily. He also had left lower quadrant abdominal pain, subjective fever, and chills. Physical examination was remarkable for mild tenderness to palpation over left lower quadrant and bright red stool on rectal exam. Laboratory studies showed normal white blood cell count, normal hemoglobin level, erythrocyte sedimentation rate (ESR) of 41 mm/h, and C-reactive protein (CRP) of 9.52 mg/L. Polymerase chain reaction assay for C. difficile in a stool sample was positive. Despite receiving oral vancomycin, the patient’s symptoms persisted. Biopsies from a colonoscopy later revealed concomitant cytomegalovirus (CMV) by immunohistochemistry. The patient was started on intravenous ganciclovir and transitioned to oral valganciclovir at discharge. Four weeks after discharge, the patient reported near resolution of his symptoms. As with this patient, most of the reported cases of co-infection with C. diff and CMV are among patients who are immunocompromised or receiving immunosuppression. CMV infection in patients with C. diff colitis is either due to a coexistent infection or secondary to disruption of the colonic mucosa following the latter infection. The diagnosis may be especially challenging in a patient with inflammatory bowel disease (IBD), as C. diff and CMV colitis often have overlapping symptomatology. As such, the identification of individual pathogen and subsequent treatment may be delayed. This case highlights the importance of working up all potential causes of diarrhea and colitis in an IBD patient receiving immunosuppression, especially when treatment for the initial diagnosis fails to resolve their symptoms.

[709A] Figure 1.

CLINICAL VIGNETTES/CASE REPORTS - LIVER

708 A Case of Over-the-Counter, Drug-Induced Autoimmune Hepatitis: Immunohistochemical and Electron Microscopic Studies Karin Takeda1, Hisako Hiramoto1, Masaya Oda2, Kumiko Tahara1, Hiroaki Yokomori1. 1. Kitasato University Medical Center, Saitama, Japan; 2. Organized Center of Clinical Medicine, International University of Health and Welfare, Tokyo, Japan. Introduction: In daily clinical practice, drug-induced liver injury(DILI) can always be a cause of liver injury in patients taking medications. Over-the-counter (OTC) drug: Pabron has been purchasing at the pharmacy in Japan, Thailand, Malaysia, and Chinese Taipei as a multi-component cold medicine. We desribed a case of DI-autoimmune hepatitis(AIH) from OTCdrug: Pabron gold®. Case description: A 64-year-old man sought treatment for common cold and was admitted for general fatigue and liver dysfunction. Blood test results included total bilirubin (T-bil), 2.4 mg/dL; direct bilirubin (D-bil), 1.4 mg/dL; AST, 1,244 IU/L; ALT 1,455 IU/L; ALP 1,242 IU/L; and γ-GTP 599, IU/L. Viral hepatitis serology was negative. Other relevant data included IgG level, 1,907 mg/dL; IgM, 95 mg/dL; ANA x80 (cut-off, < x40); ASMA x20 (cut-off, OTC, namely Pabron Gold®, prior to disease onset which was suspected as the cause of liver injury. A DI lymphocyte stimulation test for Pabron Gold® was positive, 2,447 cpm (503%) (< 179%). The liver biopsy revealed spotty necrosis and the accumulation of ceroid pigment in Kupffer cells around central vein, and piecemeal necrosis with multiple plasma cells around portal tracts. Moreover, the plasmocytic infiltration showed positive CD79a staining while negative CD20 staining. Ultrastructually, “cart-wheel” chromatin configuration in the nucleus was observed in some of plasma cells packing with a lot of rough-surfaced endoplasmic reticulum. Moreover, the characteristic granular osmiophilic materials and lipid droplet were observed in Kupffer cell. HLA typing test was HLA-DR4 positive. The score based on simplified criteria for autoimmune hepatitis diagnosis was 6, probable. With a persistent rise in aminotrans-

[709B] Figure 2.



| OCTOBER 2015

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[709C] Figure 3.

[710A] Figure 1. shunting during a workup of hypoxemia. A 68 year old male, with recently diagnosed marginal zone lymphoma of the lung, presented to the ED for dyspnea on exertion and hypoxia requiring 100% FiO2 by high-flow nasal cannula. ABG showed severe A-a gradient with PaO2 of 42 and SaO2 of 82, concerning for cardiac shunt. Transesophageal echocardiogram showed right to left inter-atrial shunt, across a patent foramen ovale (PFO), following injection of agitated saline. Further workup with CT Chest PE protocol ruled out pulmonary embolus and right-sided cardiac catheterization did not show evidence of pulmonary hypertension. Interestingly, the patient would desaturate when laying on his right side. The CT Chest and echocardiogram caught a portion of a hepatic cyst near the right atrium. A dedicated abdominal CT scan showed multiple complex cystic lesions within the liver, largest in the dome and right lobe of liver measuring 21.7x14.8 cm. The lesion in the dome of the liver caused mass effect on the right atrium. Differential of the cystic lesions were benign hepatic cysts, hydatid disease or biliary cyst adenomas. Cardiology attempted catheter-based closure of the PFO, but were unsuccessful due to the high-pressure gradient. Hepatobiliary surgery consult did not suggest resection given medical comorbidities; thus, percutaneous drainage was recommended. There was hesitation to drain the hepatic cysts percutaneously due to the possibility of echinococcus. The patient had a travel history outside of the United States and was recently exposed to farm animals. Echinococcus serum antibody IgG was tested and returned negative. Percutaneous drain was placed in the largest cyst by Interventional Radiology with 600 mL of brown serosanguinous fluid drained upon insertion. Patient had immediate symptomatic relief and oxygen requirements were weaned to room air within hours. There have been cases where large hepatic cysts caused compression of the right atrium as well as causing cardiac arrhythmias, which resolved with surgical cyst resection. There has been one other reported case of a hepatic cyst causing intra-cardiac shunting across a PFO with symptomatic relief through surgical cyst resection. We present a case in which a large hepatic cyst causing cardiopulmonary abnormalities was successfully treated with non-surgical and minimally invasive techniques.

710

[710B] Figure 2.

Cholestatic Hepatitis as the Initial Presentation of Secondary Syphilis Laura Ulmer, DO1, Rajalakshmi Iyer, MD2, Joseph Mitros, MD3. 1. Mercy Medical Center, Des Moines , IA; 2. Iowa Digestive Disease Center, Clive, IA; 3. Pathology Associates of Central Iowa, Des Moines, IA. A 50-year-old male presented to the emergency department with chest pain, weakness, right upper quadrant pain, fatigue, jaundice, clay-colored stools, and a 15-pound weight loss, which all began after a weekend alcohol binge five weeks prior. An outpatient abdominal ultrasound and viral hepatitis panel were negative. Laboratory studies showed serum alkaline phosphatase 286 IU/L (normal 30-210), serum AST 49 IU/L (normal 5-45), serum ALT 55 IU/L (normal 5-55), serum total bilirubin 4.5 mg/dL (normal 0.2-1.5), direct bilirubin 2.8 mg/dL (normal 0.0-0.3). Drug and toxicity screening were negative. MRCP showed a normal pancreas and biliary system and mild fatty infiltration of the liver. ANA, EBV, CMV, viral hepatitis panel, smooth muscle antibody, anti-mitochondrial antibody, and ceruloplasmin were all negative. A liver biopsy showed cholestatic hepatitis with an associated ductular reaction suggestive of hepatitis due to drug reaction; this specimen was sent for second pathologic review, which confirmed these findings. The patient developed scrotal and penile pain and discoloration near the glans. GC/Chlamydia and HIV testing were negative. Urology recommended symptomatic treatment. After discharge, the RPR returned positive, VDRL was positive at 1:128, and TPPA was reactive. After the clinical diagnosis of syphilis was made, the pathology specimen was re-reviewed and an immunohistochemical stain for Treponema pallidum was positive. The combination of serologic diagnosis and pathologic findings indicate that this was indeed hepatic involvement by syphilis. The patient was treated with penicillin per secondary syphilis protocol and LFTs were normalized at two-week follow-up. Discussion: Patients with symptomatic secondary syphilis usually present with generalized nontender lymphadenopathy and mucocutaneous lesions. Syphilitic hepatitis is a less common manifestation of secondary syphilis, is usually asymptomatic, varies with the stage of the disease, and is rarely the initial


presenting symptom. The purpose of this case report is to present an uncommon clinical presentation of secondary syphilis, and to serve as a reminder that it should be kept as a differential diagnosis even in immunocompetent patients. Diagnosing syphilitic hepatitis is important, as rapid resolution of this disease is seen with appropriate treatment.

711 WITHDRAWN

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713 Hyperbilirubinemia: More Than Meets the Eye Rekha Reddy, MD, Christopher Bach, MD, Prakriti Merchant, MD, Maged Bakr, MD, Justin Provost, MD, Christopher Brown, MD. Norwalk Hospital, Norwalk, CT. Bilirubin induced kidney injury is a commonly unrecognized cause of renal dysfunction in the setting of severe liver disease. Bile cast nephropathy is a type of cholemic nephrosis found in patients with severe liver disease. Here, we present a case of drug induced liver injury due to anabolic steroid use, resulting in bile cast nephropathy and acute kidney injury. The patient is a 40-year-old male who presented with two weeks of worsening jaundice and fatigue. He had no significant past medical history, and no family history of liver disease. His medications on presentation were fluticasone and ipratropium-albuterol inhalers for a recent cough; notably, he had completed a 1 month course of nandrolone, methandrostenolone, and testosterone injections six weeks prior. Labs on initial presentation were significant for ALT 636, AST 299, AlkPhos 162, total bilirubin of 11.8, and creatinine of 1.1 mg/dL. Viral hepatitis panel and markers for autoimmune disease were negative. CT Abdomen revealed a homogenous liver of normal size without bile duct dilation. Repeat labs 2 weeks later revealed a normalization of his ALT and AST levels, but an upward trend in his AlkPhos, total bilirubin, and creatinine. The INR also continued to rise to a peak of 2.5 despite Vitamin K administration. Both abdominal ultrasound and MRCP were unremarkable. The patient ultimately underwent liver biopsy, which showed severe cholestatic hepatopathy. During this period of six weeks,

the patient’s creatinine rose from a baseline of 1.1 to 2.3 mg/dL. Urine electrolytes were consistent with a pre-renal etiology, though kidney function did not improve with intravenous fluid administration. Renal ultrasound showed mildly enlarged, echogenic kidneys. The patient ultimately underwent renal biopsy, which revealed acute tubular injury with bile casts, and the diagnosis of bile cast nephropathy was made. Over the next month his bilirubin trended down and his creatinine normalized in parallel with the bilirubin trend. Although bile cast nephropathy is a well described phenomenon, it often goes unrecognized by even the most astute clinicians. Given that bile cast nephropathy occurs in those with severe liver disease, the added development of acute renal failure can dramatically affect prognosis. Recognizing this condition can lead to early treatment and better long term outcomes.

714 Fecal Microbiota Transplantation in the Management of Mild Overt Hepatic Encephalopathy: A Case Report Presidential Poster Dina Kao, MD, Brandi Roach, RN, Heekuk Park, Naomi Hotte, MSc, Karen Madsen, PhD, Vince Bain, MD, Puneeta Tandon, MD. University of Alberta, Edmonton, Alberta, Canada. Background: Hepatic encephalopathy (HE) is one of the most common complications of end stage liver cirrhosis. Although the precise pathophysiology of HE is not well defined, data suggest that ammonia (NH3) generated by the enteric bacterial flora is the critical driver of this process. The microbiota in patients with liver cirrhosis is altered compared to healthy controls, and they have more urease-producing bacteria associated with increased NH3 production. The standard of care in patients who have recurrent HE is rifaximin and/or lactulose. Although effective, many patients con-

[714] Table 1. Changes in ICT, Stroop test and serum NH3 levels over time in relation to FMT inhibitory control test (Normal 20,000 IU/L, LDH 2,190 IU/L, and fibrinogen was 154mg/dL. Diagnoses of acute hepatitis and disseminated intravascular coagulation were made. The patient had been taking amiodarone (6 mos) and simvastatin (2 yrs), which were discontinued. He was medically resuscitated in the Intensive Care Unit. Transaminases returned to near normal at post-admission day 10. Evaluation for common viral causes of acute hepatitis was negative. Consideration was given to drug-induced hepatitis, although both amiodarone and simvastatin had been well tolerated and unassociated with prior transaminase elevation. According to Naranjo’s scale for estimating the probability of adverse drug reactions, this patient’s presentation was calculated to be 4 out of 13, making amiodarone and/or simvastatin possible causes of hepatic injury. Influenza is not a hepatotropic virus. Although the mechanisms of liver injury in influenza are not fully elucidated, hepatocyte damage has been shown to be mediated by influenza-specific T-cells that interact with Kupffer cells in the absence of influenza antigen in the liver. It has been reported that during infection, influenza-specific T-cells undergo massive expansion in the lung as well as the liver, and the size of the T-cell immune response correlates with the magnitude of the hepatic inflammatory response. In experimental influenza infection in humans, transaminase elevation was not associated with fever. Given the prompt recovery of his transaminase levels and subsequent normal liver ultrasound, we believe that the acute rise in transaminases was the result of Influenza A. While it is possible that the hepatitis was secondary to amiodarone or simvastatin, it is more likely that this was an uncommon presentation for hepatitis secondary to influenza.

728 An Uncommon Cause of Concurrent Hemoperitoneum and Gastric Outlet Obstruction Tilak Baba, MD, MPH1, Charoen Mankongpaisarnrung, MD1, Mark Mattar, MD2. 1. Georgetown University Hospital, Washington, DC; 2. Georgetown University Hospital, Washington , DC.

worsening of nausea, vomiting, anorexia, abdominal discomfort and post-prandial emesis. Physical examination showed massive ascites and hepatomegaly without hepatic bruit. CT scan showed a 14 cm x 12.5 cm exophytic liver mass from inferior margin of left lobe of cirrhotic liver externally compressing the duodenum and pancreatic head and large ascites. Her hospital course was also complicated by acute anemia from hemoperitoneum. Hence, she underwent arterial embolization where branches of right and left hepatic artery as well as single branch of gastroduodenal artery (GDA) were embolized. Her bleeding continued; therefore, she underwent embolization of branches of superior mesenteric artery (SMA) that stopped the bleeding. Aft erwards, she was evaluated for duodenal stenting for palliative treatment of gastric outlet obstruction and to assume her oral nutrition in preparation for external radiotherapy (XRT) for HCC. However, upper endoscopy revealed a large obstructing mass invading the pyloric canal. The endoscope was not able to traverse the pyloric canal. She then underwent an IR-guided venting percutaneous gastrostomy tube for comfort measures after discussion about the risk of peritonitis. Due to the advanced stage of her HCC and her overall condition, no further intervention was pursued and palliative care was provided until her demise. Conclusion: Pedunculated HCC shares the similar characteristics as those with other HCCs. It usually arises from right lobe of the liver or inferior margin of the liver. It has been reported that pedunculated HCC has a better overall prognosis as compared to the others because it is usually well encapsulated and has less vascular invasion. Hence, wide-margin surgical resection is feasible. Treatment armamentarium includes radiation, transcatheter arterial chemoembolization (TACE), and surgery, which has modestly improved survival based on case series. However, despite the varied treatment modalities prognosis of patients with locally advanced HCC remains poor, early recognition is of paramount importance for prompt treatment evaluation.

729 The Efficacy of Extracorporeal Liver Support With the Molecular Adsorbent Recirculating System (MARS) in Severe Drug-Induced Liver Injury Rotimi Ayoola, MD1, Brian C. Quigley, MD2, Ram Subramanian, MD3. 1. Georgia Regents University, Augusta, GA; 2. Emory University School of Medicine, Department of Pathology and Laboratory Medicine, Atlanta, GA; 3. Emory University, Decatur, GA. A 26-year-old man who was previously healthy presented with a three week history of worsening jaundice, pruritus, clay-colored stools and dark urine. The patient started taking a bodybuilding supplement Methyl-1-Etiocholenolol-Epietiocholanolone, a pro-hormone/anabolic designer steroid, two months prior to presentation. He does not take any other medications, and does not use tobacco, illicit drugs or alcohol. Examination revealed diffuse jaundice, scleral icterus, and normal abdominal and mental status exam. Complete blood cell count, and basic metabolic panel were normal. Hepatic function panel revealed aspartate aminotransferase (AST) 67 U/L, alanine transaminase (ALT) 106 U/L, alkaline phosphatase 166 U/L, and total bilirubin 32.5 mg/dl. Hepatitis panel, coagulation labs, ferritin, f-actin antibodies, anti-mitochondrial antibodies, ammonia, ceruloplasmin, and alpha-1 antitrypsin were normal. Abdominal ultrasound revealed normal liver echogenicity without lesions, no intra- or extrahepatic biliary duct dilation or cholelithiasis. Liver biopsy showed cholestatic hepatitis with severe cholestasis, bile duct injury and inflammation, and portal and centrilobular inflammation without steatosis (Figure 1). The patient was started on molecular adsorbent recirculating system (MARS) therapy for drug induced liver injury. The patient received 4 days of MARS and total bilirbin was reduced to 20.7 mg/dl. At outpatient follow-up two months later he noted resolved jaundice, and pruritus, normal colored stools and urine. Labs at the time showed a bilirubin of 3.3 mg/dl, AST 56 U/L, and ALT 104 with nor-

Introduction: Exophytic or pedunculated hepatocellular carcinoma (HCC) is an uncommon presentation of HCC and accounts for 0.24% to 3% of all HCC cases. HCC can metastasize remotely to lung and bone; however, local invasion to GI tract is rare. We report a rare complication of exophytic HCC resulting in hemoperitoneum followed by gastric outlet obstruction (GOO) despite vascular embolization. Case Report: A 60-year-old Ethiopian female with history of decompensated hepatitis C cirrhosis and recently diagnosed HCC and failure to response to sorafenib presented with 1-week history of

[728A] Figure 1.


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[729B] Figure 2.

mal coagulation labs. MARS is an emerging option for patients with liver injury to give them additional time for the liver to regain intrinsic recovery or act as a temporizing measure until liver transplantation. MARS removes protein-bound and water-soluble toxins with albumin dialysis (Figure 2). This enables the liver cells to regenerate and reduce toxins in the plasma. The use of MARS can decrease the plasma concentrations of benzodiazepines, bilirubin, copper, creatinine, middle and short-chain fatty acids and multiple other toxins. MARS has been shown to improve hepatic encephalopathy, hemodynamic instability, renal function, pruritus and reduce portal pressures. MARS is a safe procedure that provides temporary support to organ failure. Although the mortality benefit has not been proven it may have the potential to improve the large liver transplant waitlist mortality, in the future.

730 Hydatid Cyst of the Liver Mahreema Jawairia, MD, Paul Mustacchia, MD. Nassau University Medical Center, East Meadow, NY. A 28 year old Kosovan Albanian female with no past medical history presented with abdominal pain for 2 days and weakness for 1 day. Patient had a near syncopal episode prior to coming to the emergency

[730B] Figure 2.

room (ER). Her vital signs were noted for fever of 102 deg F and tachycardia. On physical examination, she had mild right upper quadrant tenderness without rebound or guarding. Initial labs revealed lactic acidosis (lactate-11.7), hypokalemia (potassium- 2.4), mildly elevated liver tests and thrombocytopenia. Computed tomography (CT) of the abdomen with radiocontrast revealed large multiseptated cystic mass in the right hepatic lobe with areas of coarse peripheral calcification as well as several satellite cystic lesions. Echinococcus Immunoglobulin E level was found to be 72.2. Magnetic resonance imaging (MRI) of the liver with and without gadolinium showed large encapsulated hepatic mass containing multiple cystic lesions favoring infectious process such as Echinococcus. Patient was given albendazole and flagyl for superinfected cyst while awaiting enucleation of the hydatid cyst. Subsequently, she underwent enucleation of the hydatid cyst.

[730A] Figure 1.



| OCTOBER 2015

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Abstracts Listeria Monocytogenes has been recognized as a very rare pathogen. Empirical treatment with third generation cephalosporins does not provide adequate antibiotic-coverage against L. Monocytogenes. Consequently, diagnosis is often delayed because it requires confirmation via culturing Ascitic fluid. Here we describe a case of SBP caused by L. Monocytogenes in a patient with advanced alcoholic liver cirrhosis. The purpose of this case report is to alert clinicians to the atypical organism responsible for SBP, especially in patients with sub-optimal response to empiric antibiotics.

733 Nutmeg Liver: A Radiographic Manifestation of Non-cirrhotic Portal Hypertension Presenting as Chronic Abdominal Pain Carmine Catalano, MD1, Rafael A. Ching Companioni, MD2, Aaron Walfish, MD3. 1. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), East Rockaway, NY; 2. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), Elmhurst, NY; 3. Elmhurst Hospital Center, Elmhurst, NY.

[730C] Figure 3.

731

Non-cirrhotic portal hypertension (NCPH) is the presence of portal hypertension in the absence of a cirrhotic liver. Insults to the liver lead to injury to endothelial cells of portal venules causing reactive changes in the liver including nodular regenerative hyperplasia (NRH) ultimately resulting in portal hypertension. The changes in hepatic vasculature lead to hepatic venous congestion and perfusion abnormalities most prominent in the liver periphery manifesting in a nutmeg liver appearance on Computed Tomography (CT) scan. A 36 year-old female with Helicobacter pylori negative gastritis presented to clinic with post prandial epigastric pain despite twice daily dosing of a proton-pump inhibitor. Review of systems was otherwise negative. No use of alcohol, illicit drugs, hepatotoxic medications or herbal supplements. No family history of liver disease. Physical examination and blood work revealed no abnormalities. An upper endoscopy showed no esophageal varices. A gastric emptying study to evaluate for gastroparesis revealed a normal gastric emptying time. A CT scan of the abdomen and pelvis displayed a diffusely heterogeneous appearance with a mottled attenuation most pronounced in the sub capsular region of the liver. Limited enhancement was seen of the hepatic veins. The findings were consistent with congestive hepatopathy and described as a nutmeg liver. An abdominal ultrasound ruled out veno-occlusive disease. Subsequently the patient developed a minimal elevation in her aminotransaminases. A needle liver biopsy was pursued showing herniated portal vein

Serum IL-6 as a Useful Marker of Solitary Fibrous Tumor Progression: A Very Rare Case Shuhei Yoshida1, Masahiko Shimada2, Maki Tobari2, Takayoshi Nishino2. 1. Division of Gastroenterology, Yachiyo Medical Center, Tokyo Women’s Medical University, Chiba, Japan; 2. Yachiyo Medical Center, Tokyo Women’s Medical University, Chiba, Japan. Case Report: A 79-year-old man presented to our hospital with several months of right abdominal pain. CT reveled a large abdominal tumor (24 x 23 x 12 cm) involving the right hepatic lobe. HBV, HCV and HIV were all negative. Serum tumor markers, such as CEA, CA19-9, AFP, PIVKA-II, were all normal. Serum Interleukin-6 (IL-6) level elevated to 41.1 pg/mL (normal range: < 2.41). White blood cell count and differential leukocyte counts were all normal. No bacterial infection existed. Histologic examination revealed a spindle cell tumor with hyalinized change immunohistochemically stained for CD34, CD99, Bcl-2 and a negative staining against CD117 (c-kit), desmin, α-SMA, S100. Only 1% of Ki-67 positive stained area was observed. Immunohistochemical expression of IL-6 was clearly positive. A solitary fibrous tumor (SFT), arising from the retroperitoneum was diagnosed and a surgical resection was performed. This SFT partially invaded the right hepatic lobe and right kidney. The resected specimen showed a solid, encapsulated tumor with hemorrhage and weighed 4.0 kg. The tumor composed of “patternless” arrangement of spindle cells separated by dense bundles of collagen. Serum IL-6 level decreased to normal after a month of resection. Discussion: SFT is a very rare neoplasm that most frequently (80%) affects the pleura, but can also be found in many extrapleural sites (20%). SFT involving the liver is an extremely rare pathologic entity, predominantly affecting females and typically presenting in middle age. SFT is thought to have a low grade malignant potential with a slow cell proliferation. A surgical resection is thought to be a suitable therapy for SFT. However, the pathogenesis of SFT is still unclear. Furthermore, poor prognosis, such as tumor recurrences, despite of a surgical resection were reported in some cases. Interestingly, IL-6 staining in SFT was positive with a high level of serum IL-6 in our case. Immunohistochemical detection of IL-6 in SFT and elevation of serum IL-6, to our knowledge, have not been previously reported. Conclusion: The present case indicates some SFTs may contain high density of IL-6 inside and, therefore, serum IL-6 might be a useful biomarker related to progression of SFTs. Since SFT is a very rare tumor, the present case might be helpful to understand the pathogenesis of SFT. Further data accumulation, including IL-6 expression, is essential to establish the best therapeutic strategy for SFTs.

[733A] Figure 1.

732 Spontaneous Bacterial Peritonitis Caused by Listeria monocytogenes: A Rare Entity Farman Ullah. Khan, MD. Mercy Hospital, Chicago, IL. 70 YO female with PMH: HTN ,CAD s/p CABG, redo-sternomtomy and bio-prosthetic MVR, pulmonary HTN, right-sided systolic heart failure, h/o GI bleeding, liver cirrhosis, gout, CKD and hypothyroidism presented with generalized weakness and BRBPR . On examination she had bilateral leg swelling with generalized bruising. Patient required 2 units PRBC during admission. On admission, patient was also found to have acute on chronic CHF. During hospital stay, she required dobutamine assisted diuresis. One day after admission she had generalized abdominal pain and diarrhea. She was also complaining of headaches, generalized body pain. Patient also found to have spiking fever. Given history of liver cirrhosis and ascites, there was concern for SBP. WBC on admission was 6.9, increasing to 10.9. CT abdomen was negative for acute intra-abdominal changes, but showed mucosal thickening of ascending colon. Stool antigen was negative for C.difficile. Patient underwent diagnostic paracentesis. She was started on ceftriaxone. Despite antibiotics, spiking Fever persisted, necessitating antibiotic change to Vancomycin and Zosyn. Ascitic fluid PH, 8.0 Albumin, 1.9 Protein, 3.7 and Glucose was 109. WBC, 480, Neutrophils, 80 and lymphocytes were 2. Culture from ascitic fluid revealed infection with Listeria. Also found to have bacteremia with Listeria. The Listeria isolated from ascitic fluid was sensitive to ampicillin whereas the blood isolate suggested to have intermediate sensitivity only. Both were sensitive to doxycycline. She was started on a course of doxycycline. Spontaneous bacterial peritonitis (SBP) is a life-threatening complication in patients with ascites, which is caused by chronic liver disease. While Escherichia coli and Klebsiella are the common pathogens,



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structures with inflammation, sinusoidal dilatation, portal fibrosis, thickened hepatic arteriole walls, and the presence of a megakaryocyte suggestive of extra medullary hematopoiesis (see images 1 and 2). No hepatitis or infiltrative disorder seen. These finding were most consistent with NRH and concomitant obliterative portal venopathy (OPV). Both entities are precursors for NCPH. A coagulopathy work-up was unrevealing and the patient was negative for the human immunodeficiency virus. Repeat CT scan and ultrasound of the liver have since shown resolution of all changes. To date the patient has no manifestations or complications of portal hypertension and is under close monitoring. The incidence of NCPH varies worldwide and its diagnosis is subtle. The majority of cases do not present with clinical symptoms of portal hypertension or even abnormal aminotransaminases on serological studies. Perfusion abnormalities most prominent in the liver periphery on CT scan is a key finding to indicate to physicians that a more in depth work-up is necessary. Ultimately, a timely liver biopsy is needed for definitive diagnosis. The pathognomonic CT findings lead to a more prompt diagnosis and consequently early management of the complications of portal hypertension.

734 Giant Hepatic Hemangioma With Secondary Portal Hypertension Navdeep Chehl, MD, Ramakrishna Behara, DO, Bulent Arslan, MD, Edie Chan, MD, Sheila Eswaran, MD, MS, Sohrab Mobarhan, MD, Nikunj Shah, MD. Rush University Medical Center, Chicago, IL. Hepatic hemangiomas, the most common benign hepatic tumors, are typically small (< 1 cm) and asymptomatic. Giant hemangiomas measure >4 cm and can have varying clinical manifestations due to associated compression, bleeding, necrosis, thrombosis or infarction. We present a rare case of a giant hepatic hemangioma with secondary portal hypertension. A 71 year old female with past medical history of hepatic hemangioma (diagnosed 14 years prior, s/p central hepatectomy 7 years prior resulting in size decrease from 18.7 x 13.6 cm to 10.6 x 9.9 cm), transient ischemic attack (on clopidogrel), and hypertension presented with 6 months of progressively worsening epigastric pain, early satiety, nausea, and small-volume hematemesis, in addition to an unintentional 30-lb weight loss over the past year. On the present admission, vital signs were within normal limits. Physical exam was significant for right upper quadrant and epigastric tenderness to palpation, as well as hepatomegaly. Pertinent labs include alk phos 212 U/L and platelets 81,000/UL; liver function tests, autoimmune and viral hepatitis studies were normal. CT abdomen/pelvis with and without IV contrast revealed a 16.5 x 13.0 cm complex lesion in the left liver lobe occupying over 50% of the liver volume with compression of the IVC, an enlarged but patent portal vein, and splenomegaly with esophageal and splenic varices. Abdominal duplex ultrasound showed mildly elevated resistive index within the hepatic artery and patent hepatic vasculature with normal flow through the portal vein. EGD revealed two columns of small esophageal varices in the distal esophagus with no high-risk features and no evidence of recent bleeding, a small hiatal hernia, and mild gastritis. Surgery was deemed high-risk due to size of the mass and its proximity to the IVC. The patient was started on daily pantoprazole, after which her epigastric symptoms steadily improved. She followed up as planned with interventional radiology (IR) as an outpatient and successfully underwent hemangioma embolization. This is a unique case of a partially resected, recurrent giant hepatic hemangioma with mass effect on the portal vein, causing portal hypertension and subsequent development of esophageal and splenic varices with splenomegaly and platelet sequestration. The patient’s early satiety, weight loss, pain, and nausea were likely due to gastric compression by the mass. Hematemesis was attributed to gastritis in the setting of clopidogrel use. While it can be argued that most giant hepatic hemangiomas can be non-operatively managed, operative strategies should be considered for significant symptoms and complications. This patient was a poor surgical candidate, thus IR embolization of the hemangioma was deemed the optimal strategy for symptom relief.

[735A] Figure 1.

Case: An otherwise healthy and asymptomatic 53-year-old female with no significant past medical history was referred to hepatology for evaluation of persistently abnormal liver tests. There was no personal or family history of liver disease, her weight was stable, she had taken no new medications, she did not consume alcohol or herbal preparations and her viral hepatitis serologies and autoantibodies were negative. Physical examination was normal. Laboratory tests showed mild elevation of liver enzymes that had only been noted for the last year, and were previously normal, with a peak alanine aminotransferase (ALT) of 106 IU/L and peak aspartate aminotransferase (AST) of 60 IU/L. An abdominal ultrasound was obtained that showed diffuse echogenicity most likely consistent with diffuse hepatic fatty infiltration and incidentally revealed a 12 cm enhancing mass arising from the lower pole of the left kidney suspicious for RCC. She subsequently underwent successful nephrectomy with pathology demonstrating a chromophobe variant of RCC. No hepatic metastasis or main bile duct obstruction were detected by abdominal computed tomography. Her liver function test abnormalities normalized one month post-operatively. Discussion: Stauffer’s syndrome was reported in 1961 as “nephrogenic hepatomegaly” and is characterized by elevated liver function tests in the absence of metastatic disease, raised erythrocyte sedimentation rate, and occasionally jaundice. Prolongation of the prothrombin time and hepatosplenomegaly may also be seen. An important differential diagnosis is liver metastasis as an underlying etiology. Malignant diseases may cause jaundice through either main bile duct obstruction or widespread metastasis to the liver. RCC causes various paraneoplastic manifestations, which can be the main presenting symptoms. Hepatic dysfunction, in absence of liver metastases, occurs in 10 to 15% of patients with RCC, attributed to the production of cytokines from the tumor cells, including interleukin-6. Conclusion: Stauffer’s syndrome is a rare paraneoplastic manifestation of RCC. We present variant case of probable Stauffer’s syndrome with resolution of otherwise unexplained liver biochemistries after the patient underwent nephrectomy to resect a chromophobe RCC. The case also highlights the benefits of abdominal ultrasound early in the course of routine evaluation of abnormal LFTs.

736 Mixed Cryoglobulinemia in HCV Found in Association With an Atypical Guillain-Barre Syndrome Gurneet Bedi, MD, Jayakrishna Chintanaboina, MD, Thomas Riley, MD. Penn State Hershey Medical Center, Hershey, PA.

[734A] Figure 1.

735 Stauffer’s Syndrome: Renal Cell Carcinoma Presenting as Abnormal LFTs Fadi Niyazi, MD1, Syed-Mohammed Jafri, MD1, Mazen El Atrache, MD2, Stuart Gordon, MD1, Ahmed Saeed, MD1. 1. Henry Ford Hospital, Detroit, MI; 2. Henry Ford Hospital, Dearborn, MI. Stauffer’s syndrome represents a rare cause of abnormal liver biochemistries. We report a patient who presented with abnormal aminotransferase values and after a comprehensive evaluation was diagnosed with renal cell carcinoma (RCC) as the probable underlying cause.


Neurologic manifestations of mixed cryoglobulinemia in Hepatitis C patients can present with neuropathy, motor weakness or autonomic dysfunction. We present a case of mixed cryoglobulinemia secondary to Hepatitis C that masked an underlying serious neurologic disorder with atypical symptoms. A 49-yearold male with past medical history of Hepatitis C genotype 1A, treatment naive, and chronic lower back pain presented with complaints of worsening low back pain and paresthesias in his upper extremities that slowly progressed to his lower extremities. One-month prior, he underwent a liver biopsy that showed chronic hepatitis, moderate activity, consistent with chronic viral Hepatitis C. Modified histological activity index grading and staging were 4/18 and 3/6 respectively. Hepatitis C viral load was 2,852,022. Physical examination was significant for mild lumbosacral tenderness, paresthesias in hands and feet and decreased strength in upper extremities (3/5) and lower extremities (4/5). MRI of cervical, thoracic and lumbar spine showed no acute findings. Given his history of chronic viral hepatitis C (treatment naive), mixed cryoglobulinemia was suspected and was top on the differential. C3 levels were normal, however C4 and CH50 levels were low at < 8 mg/dL (14-44) and < 10 mg/dL (31-60) respectively. Cryoglobulin levels and cryofibrinogen were normal. A cryoglobulin immunofixation was sent. While waiting for these results, his symptoms continued to worsen with paresthesia in all four extremities and progressive weakness in his lower extremities. A lumbar puncture showed albuminocytologic dissociation with CSF protein of 182 mg/dL and a normal cell count, which was consistent with Guillain-Barre Syndrome (GBS). He was started on intravenous immunoglobulins. His symptoms gradually improved over the next few days. Meanwhile, the cryoglobulin immunofixation returned positive for mixed cryoglobulinemia type III. Post-discharge, he was started on ledipasvir/sofosbobir for treatment of chronic Hepatitis C. Guillain-Barre Syndrome classically presents with ascending paralysis i.e. lower extremity paresthesia and motor weakness that gradually ascends to the upper extremities. However, our patient presented with descending paralysis, which is atypical and seen in less than 10% of GBS cases. Hence, our clinical suspicion was initially high for mixed cryoglobulinemia and low for GBS as he was recently diagnosed


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Abstracts with chronic Hepatitis C one month prior to admission. Clinicians should always have a broader differential without confining to the complications of chronic Hepatitis C when a treatment naive Hepatitis C patient presents to the hospital.

737 Hepatocellular Carcinoma in a Patient With Hepatitis C and No Evidence of Cirrhosis Justin Cochrane, DO1, Jon Anderson, MD2. 1. Providence Sacred Heart Internal Medicine Residency, Spokane, WA; 2. Providence Sacred Heart, Spokane, WA. Hepatocellular carcinoma (HCC) is the sixth most common neoplasm worldwide and is the third leading cause of cancer-related mortality, responsible for 600,000 deaths annually. Risk factors associated with the development of HCC include, alcohol abuse, non-alcoholic fatty liver disease (NAFLD) or nonalcoholic steatohepatitis (NASH), hemochromatosis, chronic hepatitis B (HBV) and cirrhosis secondary to hepatitis C (HCV). We present a case of 75 year old female with development of HCC despite any evidence of cirrhosis from HCV. Case: Mrs. C a 75 year old female with history of HCV acquired secondary to blood transfusion in the mid 80’s treated with pegylated interferon with sustained virologic response (SVR) for the past 23 years. She presented to the hospital with multiple fractures secondary to mechanical fall. She was seen for perioperative clearance for repair of a left hip fracture sustained during the mechanical fall. She had experienced RUQ pain several months earlier and evaluation by her primary care physician several weeks before admission demonstrated elevated liver enzymes and a liver mass by ultrasound (Figure 1). Physical exam demonstrated normal vital signs, pain to palpation in the RUQ with no Murphy’s sign or rebounding/guarding, and no scleral icterus, ascites, hepatomegaly, or findings of cirrhosis. Liver enzymes ALT 112 IU/L, AST 255 IU/L, and Alkaline Phosphatase 98

[737C] Figure 3.

IU/L. Liver function INR 1.0, and total bilirubin of 0.6 mg/dL. HCV antibody positive, PCR RNA undetectable, and alpha fetoprotein 392,535 ng/mL. CBC and BMP within normal limits. Contrast CT abdomen/pelvis demonstrated a 12 cm infiltrative mass within the right lobe of the liver with portal vein thrombus and marked gallbladder distension with no characteristic findings of cirrhosis noted (Figure 2). MRI obtained demonstrated T1 hypointense lesion involving a majority of the right hepatic lobe measuring 10.3 x 11.4 x 11.8 cm concerning for HCC or cholangiocarcinoma with no evidence of cirrhosis noted (Figure 3). CT guided biopsy identified a high grade hepatocellular carcinoma with no evidence of cirrhosis. She was placed on palliative therapy with Sorafenib and ultimately succumbed to her cancer. HCC can develop in patients without evidence of cirrhosis and with the predicted decrease in level of cirrhosis secondary to new HCV treatment options, should patients receive screening regardless of evidence of cirrhosis as is current guidelines.

[737A] Figure 1.

738 HSV Hepatitis in an Immunocompetent Female: Do the Nonfulminant Cases Go Undiagnosed? Asad Jehangir, MD1, Anthony Donato, MD, MPHE1, Supriya Kuruvilla, MD1, Nirav Shah, MD2. 1. Reading Health System, West Reading, PA; 2. Digestive Disease Associates, Wyomissing, PA.

[737B] Figure 2.


Elevated transaminases are commonly encountered in clinical practice, and have a broad differential that includes viral illnesses. While HSV-2 is a ubiquitous virus that is known to cause fulminant hepatic presentations in the immunocompromised, it is not commonly reported as a cause of mild symptomatic transaminitis in the immunocompetent host. A 32-year-old female without significant medical history presented to the emergency department with one day of nausea, vomiting and moderately severe right upper quadrant abdominal pain which worsened with fatty food intake. On examination she did not have any mucocutaneous lesions and a benign abdomen except for a tender liver edge. Laboratory tests revealed AST of 54 IU/L ALT of 110 IU/L with a normal alkaline phosphatase, bilirubin, albumin, PT/INR and leukocyte count. An abdominal ultrasound and computerized tomography of the abdomen/pelvis were unremarkable. An esophagogastroduodenoscopy was performed which was unrevealing. Hepatobiliary iminodiacetic acid scan showed delayed visualization of tracer in the small bowel, prompting laparoscopic cholecystectomy for suspected biliary dyskinesia. During laparoscopy, extensive miliary lesions of the right and left lobes of the liver were visualized on gross inspection of the liver, varying in size from a few millimeters to about a centimeter (figure 1). The biopsy showed patchy areas of hepatocyte necrosis, microabscesses, with a mixed inflammatory infiltrate. Several hepatocytes within areas of necrosis revealed characteristic intranuclear ground glass inclusions (figure 2) that stained strongly positive with confirmatory HSV immunostains (figure 3). The patient’s serology was positive for IgG against HSV 2, but negative against HSV. She and her husband denied any prior history of symptomatic oral or genital herpes. A Pap smear was negative for any evidence of genital herpes infection. HIV screening was negative. She was treated with valacyclovir for 2 months after which she underwent a laparoscopic tubal ligation which incidentally noted significantly improved liver surface. On her follow-up visit after 4 months, she reported improvement of the abdominal pain with normalization of her hepatic panel. While HSV Hepatitis is often reported as a fulminant hepatic failure in the immunocompromised host with high mortality, this case demonstrates that there may be milder cases that go undiagnosed in immunocompetent individuals. In light of the very high prevalence of exposure of this virus, physicians should consider HSV as a potential cause of acute, symptomatic transaminitis, even in those without classic immunosuppressive risks (steroid use, pregnancy, transplant recipients).


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739 Non-cirrhotic Portal Hypertension: An Unusual Side Effect of Azathioprine Alexander Mensah, MD1, Pallavi Arora, MD, MPH2. 1. Department of Medicine, Rochester General Hospital, Webster , NY; 2. Department of Medicine, Rochester General Hospital, Rochester , NY.

[738A] Figure 1.

Hepatic toxicity is a recognized side effect of azathioprine; a thiopurine commonly used as an immunomodulatory agent. The most common presentation is usually a mild elevation of liver enzymes, which normalizes on discontinuation of the drug. Hypersensitivity reactions, idiosyncratic cholestatic reactions, veno-occlusive disease, perisinusoidal fibrosis and nodular regenerative hyperplasia have also been described. Non cirrhotic portal hypertension has been rarely reported with azathioprine. An 80-year-old man with myasthenia gravis presented with several months of progressive abdominal distension. He had no history of alcohol or intravenous drug use and did not have any other risk factors for chronic liver disease. His medications included azathioprine 50 mg and pyridostigmine 60 mg which he had been taking daily for more than 5 years. Examination revealed a distended abdomen with a fluid wave, shifting dullness, and splenomegaly. Other signs of chronic liver disease such as jaundice, spider angiomata, gynecomastia, palmar erythema, digital clubbing, and asterixis were absent. Laboratory investigation showed normal liver enzymes, platelets, albumin and INR. Work-up for other causes of chronic liver disease including viral hepatitis panel, antinuclear antibody, anti-mitochondrial antibody, anti-smooth muscle antibody, iron studies, α-1 antitrypsin phenotype, and, ceruloplasmin were all negative. Abdominal ultrasound showed ascites, normal sized liver and splenomegaly. Doppler revealed patent portal and hepatic veins with elevated portal venous pressure gradient of 16 mmHg. Abdominal paracentesis showed straw colored ascetic fluid with a protein level of 1.1 g/dl and serum-ascites albumin gradient of 2.5 g/dl and negative cytology for malignancy.Transjugular liver biopsy showed hepatocellular unrest with inflammatory infiltrate in the portal areas with no evidence of bridging fibrosis or collapse. Within the lobule were scattered lymphocytes and occasional eosinophils. The presence of eosinophils, in particular, raised the possibility of drug related hepatic injury. Azathioprine was discontinued and he was started on diuresis with furosemide and spironolactone. Transjugular intrahepatic portosystemic shunt was eventually required due to ascites that was refractory to diuretics.





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Abstracts This case illustrates the potential of azathioprine to cause non-cirrhotic portal hypertension (NCPH). The frequency of this complication is rare, but likely underestimated due to its non-specific and prolonged preclinical course. Further studies are needed to establish monitoring guidelines for early detection of NCPH in patients on azathioprine, as routine liver function tests are usually normal and the development of portal hypertension signals irreversibility.

740 Endovascular Reconstruction of a Chronic Non-cirrhotic Extra-hepatic Portal Vein Thrombosis by “Neo-Porta” System: A Case Report José A. Velasco-Zamora, MD1, Jorge M. Antolinez-Mota, MD2, Manuel Guerrero-Hernández, MD1, Aldo Torre, MD, MSc1. 1. Instituto Nacional de Ciencias Médicas y Nutrición “ Salvador Zubirán”, Mexico D.F., Mexico; 2. Instituto Nacional de Ciencias Médicas y Nutrición “ Salvador Zubirán”, Mexico D.F., Mexico. Introduction: Chronic portal thrombosis can present itself with symptoms that fail to respond to conventional treatments, in this scenario management with transjugular intrahepatic portosystemic shunt (TIPS) might be an option. Nevertheless in presence of portal cavernoma this procedure is generally thought to be contraindicated due to technical difficulties. We describe the case of a symptomatic patient with noncirrhotic chronic portal thrombosis in which with porto-mesenteric stent and TIPS placement portal axis reconstruction was achieved. Case Report: 57 year-old white man was refer to our center with chronic portal thrombosis secondary to abdominal surgery. He received medical treatment however he kept complaining of post-prandial severe abdominal pain. Abdominal tenderness was remarkable and all laboratory data was normal. CT scan showed permeability of right intra-hepatic portal vein (IHPV) and its segmental branches, cavernous transformation of the extra-hepatic portal vein (EHPV) and the ending of the native EHPV forming a fibrous cord until its communication with the superior mesenteric vein. Considering these findings we decided to perform an endovascular approach in order to re-establish portal flow. A percutaneous micropuncture aiming for the right IHPV was done followed by native EHVP canalization all the way to the superior mesenteric vein restoring in this manner portal permeability (Figure 1, A-E). Once the porto-mesenteric stent was placed, flow redistribution from the cavernoma was achieved (Figure 2) therefore portal pressure was reduce and patient symptomatology was resolved. Three months later the patient developed ascites due to hyperdynamic flow on the right IHPV. A TIPS was placed using the “neo porta” system with successful resolution of portal hypertension, patient improvement and discharge (Figure 1, G, H). Discussion: In this case, as in many others, cavernous transformation reduces treatment options; based on the patient clinical and radiological findings we propose this endovascular approach hypothesizing that reconstruction of the portal axis with porto-mesenteric stent and TIPS could be successful. In selected patients with chronic thrombosis of the portal axis this approach can be considered as therapeutical option. Conclusion: Endovascular treatment in this particular scenario should not be considered contraindicated with adequate patient selection this approach can be successful with improvement of patient’s life quality.

741 de novo Autoimmune Hepatitis in a Patient Treated for Recurrent Hepatitis C After Liver Transplantation With Non-interferon-Based Therapy: A Case Report Aishwarya Kuchipudi, MD1, Yakir Muszkat, MD2, Yousuf A. Siddiqui, MD3, Keith Mullins, MD2, Mark Blumenkehl, MD4, Dilip Moonka, MD2, Kimberly Brown, MD2, Syed-Mohammed Jafri, MD2. 1. Henry Ford Hospital, Internal Medicine, Detroit, MI; 2. Henry Ford Hospital, Detroit, MI; 3. Henry Ford Hospital, Sterling Heights, MI; 4. Henry Ford Medical Group, Detroit, MI. Introduction: The pathogenesis of de-novo autoimmune hepatitis (AIH) after therapy for hepatitis C virus (HCV) is not well understood, although various mechanisms have been implicated including the role of interferon-based therapy. Interferon has been shown to have potent immunomodulatory properties resulting in a broad-range of immune-related disorders including de-novo AIH. Most of the reported cases of de-novo AIH in this population have been in patients treated with interferon-based therapy. We describe a patient treated for hepatitis C with all-oral therapy who develops de-novo AIH. Case: A 56-year old male underwent orthotopic liver transplantation (OLT) for cirrhosis secondary to genotype 1b hepatitis C. Prior to transplant, he underwent two attempts at HCV antiviral therapy, which were unsuccessful due to cytopenias from interferon monotherapy and pegylated interferon and ribavirin. Pre-transplant native liver biopsies were all consistent with chronic hepatitis C with no evidence of autoimmune hepatitis. Two years post-OLT, the patient underwent liver biopsy showing recurrent hepatitis C. with fibrous expansion of the portal tracts and Ishak stage III fibrosis. A decision was made to treat the patient for recurrent hepatitis C with all-oral antiviral therapy. The patient was initiated on Sofosbuvir and Daclatasvir for a period of 24 weeks. Viral load was undetectable within 3 weeks of treatment and remained undetectable. Approximately 8 weeks after treatment completion, the patient’s transaminases were noted to be elevated with AST: 104, ALT: 120. As HCV RNA remained undetectable, liver biopsy was performed with pathology showing de-novo autoimmune hepatitis with Ishak

[740B] Figure 2.

[740A] Figure 1.



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stage 4 fibrosis. He was immediately started on 3 days of high dose corticosteroids with increase in Prograf and Cellcept doses. Patient’s transaminases trended down to normal ranges. The patient was subsequently started on a prednisone taper and continues to have normal transaminases with a negative HCV RNA. We demonstrate a case of de-novo autoimmune hepatitis occurring after HCV therapy even in the absence of interferon. Further studies are required to understand the potential for immune dysfunction after hepatitis C viral suppression in the post-liver transplant setting.

742

tiocytic and neutrophilic lobular inflammation was also present. Since atorvastatin had been stopped several weeks earlier, diltiazem was the most likely etiology. Contacting the patient’s outpatient pharmacy elucidated that just prior to original presentation his diltiazem was switched to a generic without his knowledge. The diltiazem was stopped and over four months his LTs trended downward with clinical improvement. In limited previous case reports diltiazem was associated with an acute hepatocelullar reaction. We observed a mixed hepatocellular and cholestatic injury with marked hyperbilirubinemia that has not been previously reported. Also, identifying the switch to generic diltiazem was a challenge and the most likely etiology of this presentation. Diltiazem should be considered as a cause of elevated LT in both a hepatocellular and cholestatic patterns.

Diltiazem-Induced Mixed Hepatocelluar and Cholestatic Hepatitis Muhammad S. Mansoor, MD1, Paul Feuerstadt, MD, FACG2. 1. Department of Medicine, Yale-New Haven Hospital, Yale University School of Medicine, Hamden, CT; 2. Division of Gastroenterology, YaleNew Haven Hospital, Yale University School of Medicine, Milford, CT. A 79 year old man with GERD, CAD, HTN, CABG and hyperlipidemia presented with chest pain, underwent a cardiac catheterization with patent coronary vessels. Despite being previously normal, his LT’s were: AST 565 U/L, ALT 552 U/L, alkaline phosphatase (ALP) 312 U/L, total bilirubin (Tb) 4.53 mg/dl and direct bilirubin (Db) of 3.07 mg/dl. The patient’s daily medications included omeprazole 20 mg, ASA 81mg, diltiazem 120 mg and atorvastatin 20 mg. Initial workup showed a normal RUQ sonogram and negative infectious hepatitis serology. The LT changes were attributed to atorvastatin and it was stopped. Three weeks later the patient presented with jaundice, generalized weakness, weight loss and early satiety. LTs were AST 420 U/L, ALT 329 U/L, ALP 238 U/L, Tb 18.5 mg/dl and Db 15.3 mg/dl with preserved synthetic function. RUQ sonogram and CT showed mild cholelithiasis without acute cholecystitis; MRCP indicated an ill-defined 1.2 cm hypointense, hypovascular lesion in the pancreatic head without biliary or pancreatic duct dilation. EUS-FNA showed an 8 x 10 mm lesion with benign glandular cells. Comprehensive infectious, metabolic and autoimmune serology was unrevealing. Tb and Db continued to rise with AST 345 U/L, ALT 220 U/L, ALP 282 U/L, Tb 33.2 mg/dl and Db 25.47 mg/dl. Liver biopsy was performed revealing portal, periportal and bridging fibrosis, severe mixed acute and chronic inflammatory cell infiltrates with scattered plasma cells, as well as bile ductular reaction (Images 1-2). There was marked interface hepatitis and hepatocytes showed cytoplasmic cholestasis associated with feathery degeneration. Patchy lymphohis-

743 Liver With Small Cells: Big Problem Scott McShane, DO1, Ruth Franks-Snedecor, MD2. 1. Banner - University Medical Center, Mesa, AZ; 2. Banner - University Medical Center, Internal Medicine Program, Phoenix, AZ. Introduction: Small Cell Carcinoma (SCC) typically occurs as a primary malignancy of the lung. A primary liver SCC is a rare finding, we present a case of rapid progression of a primary SCC in the liver leading fulminant hepatic failure. Case presentation: A 78 year-old man brought to the emergency department for concern of altered mental status. In the previous month he had developed lower extremity swelling, somnolence, confusion, and loss of appetite. In the past 24 hours these symptoms had worsened and he developed jaundice. The patient was seen by his primary physician one month prior to presentation, at which time his LFT’s were normal. His last drink of alcohol was 30 years ago and he had no risk factors for or history of viral hepatitis. He was in good health with well controlled chronic conditions. On admission his LFT’s were elevated: AST 537 U/L, ALT 545 U/L, and ALP 415 U/L. Total bilirubin was 25.5 mg/dL and INR was 1.4. RUQ Ultrasound showed no stone or ductal dilation and patent blood vessels. CT scan of the abdomen showed ascites and a nodular appearing liver without evidence of biliary dilation. Paracentesis confirmed portal hypertension without infection. Tylenol level was nor-

[743A] Figure 1.

[742A] Figure 1.


[743B] Figure 2.


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Abstracts the mechanism of injury involves ischemia as well as an unknown toxic metabolite. This presents a serious risk as hypoxic hepatitis has been shown to increase intensive care unit mortality rates by 4 fold. Case reports describing synthetic methamphetamine (Crystal Meth) induced hepatitis have not been previously reported. We present a 39 year old female who had a two week history of respiratory distress, nausea and severe abdominal pain. Past medical history included type I diabetes mellitus, end stage renal disease on hemodialysis, and ischemic cardiomyopathy. Review of medications was not suspicious for hepatotoxic drugs. There was no history to suggest a recent clinical illness or episode that could lead to hypotension or systemic hypoperfusion. At the time of presentation, she denied illicit drug use including cocaine. On exam she was agitated, had abdominal tenderness localizing to the epigastrium, and had no jaundice. Laboratory tests were significant for abnormal liver panel (AST 6122 IU/L, ALT 3809 IU/L, LDH 7979 IU/L, albumin 4.1 g/dL, total bilirubin 2.3 mg/dL and INR 2.41). Testing for other causes of hepatic injury was negative including viral hepatitis, autoimmune hepatitis and serum acetaminophen level. Abdominal ultrasound and cholescintigraphy were negative. Doppler sonography of the abdomen showed patent hepatic, portal and mesenteric veins. Empiric treatment was begun with N-acetylcysteine, intravenous fluids and pain control. After further questioning, the patient admitted to use of Crystal Meth for the first time in her life two weeks prior to her presentation. The patient left against medical advice on day 3 with some improvement of her symptoms and improving liver function panel (AST 3963 IU/L, ALT 1865 IU/L, LDH 6626 IU/L, total bilirubin 0.8 mg/dL and INR 1.56). This is a rare case of synthetic methamphetamine-induced hepatitis. Conservative management with close monitoring improved the status of our patient without the need for liver transplantation. It is imperative to raise awareness regarding this complication associated with use of Crystal Meth among the general population and healthcare professionals.

746 [743C] Figure 3.

mal. Despite this, N-Acetylcysteine treatment was initiated and the patient was transferred to the ICU in severe shock. He did not respond to supportive care provided in the ICU. Additional imaging was obtained that showed no other abnormalities in his chest, abdomen or pelvis. Within 48 hours of admission, the patient died from fulminant hepatic failure. An autopsy was performed to determine the cause of death. The liver was grossly nodular and histological evaluation of the liver revealed anaplastic SCC. No other primary site was discovered on extensive autopsy. Discussion: The most common primary site of SCC is the lung. Having metastatic spread to other organs is common. Non-lung primary sites occur, including the larynx, stomach, and gastrointestinal tract. Liver primary SCC is rare, the first case reported in 1934. Since then approximately 20 cases have been described in the literature. The majority are associated with liver cysts, teratoma, biliary disease, or cirrhosis of the liver. In this case we see SCC of the liver without chronic injury, cyst, or biliary pathology. SCC of the liver carries a high mortality and this case shows that it can rapidly cause fulminant hepatic failure.

744 Solifenacin-Induced Hepatitis: A Rare Case Wajihuddin Syed, MBBS, Maria Fariduddin, MBBS, Shalin Kothari, MBBS, Arunpreet Kahlon, MBBS, Brian Changlai, MD. SUNY Upstate Medical University, Syracuse, NY. Introduction: Solifenacin is a drug commonly used for urge incontinence. We report a case of an elderly female who presented with Solifenacin induced hepatitis. Case: An 84 y/o female presented to the hospital with abdominal pain, nausea and bilious vomiting for 24 hours. At admission, her labs suggested acute hepatitis with AST: 567, ALT: 939, Alkaline phosphatase: 171, with rest of the work up including bilirubin, total protein, platelet count and PT, PTT and INR being within normal limits. A right upper quadrant ultrasound of the abdomen showed small amount of hyperechoic shadows in the gallbladder without any thickening of the wall or biliary ductal dilation. An extrahepatic obstruction was unlikely with the hepatocellular pattern of liver injury with a disproportionate elevation in Alkaline phosphatase and a normal bilirubin. Other causes of hepatocellular injury with marked aminotransferases elevation such as acute viral hepatitis, acetaminophen toxicity, autoimmune hepatitis, alcoholic hepatitis, malignant infiltration, and sepsis were excluded by patient’s presentation and lab work. It was noted that the patient was started on solifenacin two weeks earlier for urge incontinence. The medication was stopped during the hospitalization and the patient improved remarkably. Her ALT and AST trended down to normal within 48 hours. The temporal relationship between the onset of drug intake, the clinical presentation, the rapid clinical recovery and laboratory normalization after the solifenacin was discontinued, is highly suggestive of a solifenacin induced liver injury in this patient. Discussion: Solifenacin is a commonly used antimuscarinic drug which reduces the frequency of micturition in patients with urgency and incontinence by reducing the smooth muscle tone in the bladder. Studies show that there are no clinically relevant differences in safety of use of solifenacin in patients with impaired liver function. However there is no literature to suggest that solifenacin causes liver injury. Drug-induced liver injury (DILI) has an estimated annual incidence of 1 in 10,000 to 100,000 persons exposed to prescription medications. DILI may not be detected prior to drug approval, because most of the new drugs are tested in fewer than 3000 people in clinical trials. It has been estimated that for any drug that is tested clinically, out of every 10 cases of alanine aminotransferase elevation (more than 10 times the upper limit of normal) there will be one case of severe liver injury once the drug becomes widely available. Solifenacin appears to have joined this arsenal of agents that can cause hepatotoxicity, making it important to recognize the possibility of drug induced liver injury in patients on solifenacin with elevated transaminases and thus, avoid potentially fulminant hepatotoxicity.

745 First Reported Case of Crystal Meth-Induced Ischemic Hepatitis Omar Mousa, MD, Rushikesh Shah, MBBS, Matthew Basciotta, Savio John, MD. SUNY Upstate Medical University, Syracuse, NY. Amphetamine use has been previously associated with acute liver injury. Clinical courses described are similar to those observed in ischemic and hyperthermia induced liver injury. It has been proposed that


A Case of Budd-Chiari Syndrome: An Unusual Cause of a Rare Disease Shaina M. Lynch, DO1, Imad Ahmad, MD2, Swales Colin, MD3. 1. University of Connecticut Health Center, West Hartford, CT; 2. University of Connecticut Health Center, Farmington, CT; 3. Connecticut GI, PC, Hartford, CT. Budd-Chiari Syndrome is a clinical disorder caused by occlusion of the hepatic venous outflow with resulting abdominal pain, hepatomegaly, and ascites. Renal cell carcinoma is associated with invasion into the inferior vena cava (IVC) in about 4-10% of cases, but extension into the hepatic veins causing hepatic venous outflow obstruction and Budd-Chiari Syndrome is rare. This is a case of a 70 year old male with no past medical history who presented as a transfer from an outside hospital with a chief complaint of abdominal distention and lower extremity swelling for two weeks. He reported having symptoms of weight loss, anorexia, and jaundice for the 5 months prior that had progressively been getting worse. A CT of his abdomen showed a large amount of abdominal ascites, mild hepatosplenomegaly, and retroperitoneal lymphadenopathy, along with multiple small cysts of both kidneys. Abdominal ultrasound was significant for an expanding thrombus in the inferior vena cava (IVC) as well as the ostia of the hepatic veins. Gastroenterology was consulted and due to the progressive symptoms of weight loss, anorexia, and jaundice, and endoscopic ultrasound was performed with concern for underlying malignancy. The procedure identified a mass with invasion into the hepatic veins and IVC, and Fine needle aspiration (FNA) was performed and sent for cytology. While in the hospital the patient continued to have worsening renal function, poor oral intake, and increasing abdominal girth, and before the final results of the pathology were available, the patient rapidly decompensated. Due to the patient’s rapid deterioration and overall poor prognosis, the patient was made comfortable and died within 48 hours. The final result of FNA cytology was most consistent with a renal cell carcinoma, although no evidence of a renal mass was seen on initial CT scan. Budd-Chiari Syndrome is a rare disorder that is the result of hepatic venous outflow tract obstruction, and when the occlusion in the hepatic veins is the result of material not originating from the venous system, it is considered a secondary cause. Renal cell carcinoma is an unusual cause of Budd-Chiari Syndrome and results from extension of an IVC thrombus into the hepatic veins. As shown in a review of 12 patients with this condition by Kume et al., aggressive surgical treatment with thrombectomy and nephrectomy can prevent liver failure and death in patients with Budd-Chiari syndrome due to renal cell carcinoma. Unfortunately for our patient, Budd-Chiari Syndrome and liver failure were the first major manifestations of his renal cell carcinoma, although he did have indications of an underlying process in the preceding months with his symptoms of weight loss, anorexia, and jaundice.

747 Liver Failure Secondary to Amyloid Light-Chain Amyloidosis Michael Loudin, Ryan Childers, MD, Adam Zivony, MD, Christian Lanciault, MD, PhD, Michael F. Chang, MD, MSc, Joseph Ahn, MD, MS, FACG. Oregon Health & Science University, Portland, OR. Presentation: A 61 year-old African-American male previously in good health presented with subacute onset of swelling in his abdomen and lower extremities over 2 months. Physical exam was significant for bilateral lower extremity edema, tense ascites, and jugular venous distention. Labs were significant for albumin 2.1 g/dL, alkaline phosphatase (AP) 718 IU/L, AST 158 IU/L, ALT 119 IU/L, total bilirubin (TB) 0.5 mg/dL, INR 1.07, creatinine of 0.9 mg/dL and nephrotic range proteinuria. A viral hepatitis panel, anti-nuclear antibody, anti-smooth muscle antibody, anti-mitochondrial antibody, ferritin, SPEP, and ceruloplasmin were normal. An abdominal CT showed ascites with a possibly nodular liver and no hepatosplenomegaly. Paracentesis revealed a serum albumin ascites gradient > 1.1, and was negative for infection; cytology was negative for malignancy. Transthoracic echocardiogram showed left ventricular hypertrophy concerning for an infiltrative process. A sigmoid biopsy was positive for amyloid and mass spectroscopy performed on the biopsy showed a peptide profile consistent with primary (AL) amyloidosis. The patient was discharged, and was readmitted approximately 1 month later with worsening ascites and new onset jaundice. TB had increased to 21.6 mg/dL, AP to 1317 IU/L, AST to 260 and ALT to 104 IU/L. A transjugular liver biopsy confirmed amyloidosis without significant inflammation or granulomas. No fibrosis or malignancy were identified. The patient’s MELD score increased from 14 to 29, and his renal function worsened. Liver transplant was considered, but his multi-organ involvement with amyloid precluded the patient from being listed. He was transitioned to comfort care and died 1 week after discharge in hospice. Discussion: Systemic primary (AL) amyloidosis involves the liver in 60-90% of cases and is commonly clinically silent, characterized by mild abnormalities in liver function with hepatomegaly. However, a subset of patients with AL amyloidosis present with severe cholestatic liver failure. Once jaundice is present,


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the median survival is 3 months, compared to 2 years in AL amyloidosis patients with liver involvement without jaundice. Liver failure also limits treatment options as potential therapies such as bortezomib and melphalan are metabolized by the liver. Although AL amyloidosis rarely presents with liver failure, this universally fatal entity should be considered by clinicians, and evaluation should be initiated promptly.

748 Pushing the Margin: Advancing Toward an Interferon-Free Strategy in Marginal Zone Lymphoma in Patients With Underlying HCV Kevin Piro, MD, Adam Zivony, MD, Joseph Ahn, MD, MS, FACG. Oregon Health & Science University, Portland, OR. A 55 year old man with recently diagnosed stage IV-B nodal marginal zone lymphoma (NMZL) based on bone marrow biopsy presented for evaluation of a painful rash of his lower extremities. The patient had a history of HCV genotype 1a with previous non-response to interferon (IFN) and ribavirin and was referred for potential retreatment of HCV. Physical exam was notable for lower extremities with tender purpuric rash with central ulceration and oozing of serosanguinous fluid. Laboratory testing revealed a WBC of 3.06 K/mm3, Hb of 8.7 gm/dL, and platelets of 627 K/mm3. Basic metabolic panel and hepatic panel were normal. HCV PCR was 140,000 IU/mL. Serum was positive for cryoglobulins. CT imaging showed right supraclavicular, mediastinal, and bilateral inguinal lymphadenopathy, as well as splenomegaly. Given the previously reported association between NMZL and HCV cryoglobulinemia, the patient was begun on treatment with ledipasvir 90 mg and sofosbuvir 400 mg without ribavirin for an anticipated 12 week course of therapy. Four weeks into his therapy his HCV PCR was undetectable and he was started on weekly infusions with rituximab for treatment of his NMZL. Eight weeks after starting his HCV therapy, a restaging CT imaging showed resolved adenopathy and unchanged splenomegaly. During treatment, his liver tests remained normal, and his anemia (11.1 gm/dL) and lower extremity lesions improved. He tolerated 12 weeks of ledipasvir/sofosbuvir without complications and achieved sustained virological response. He has no signs of recurrent disease NMZL or HCV at 6 months. Marginal Zone Lymphomas (MZL) are clonal proliferations of B-cells arising from the marginal zone of the secondary lymphoid follicle. MZL has been well associated with chronic infection, including hepatitis C with and without associated cryoglublinemia. There have been several case series demonstrating that eradicating the underlying hepatitis C viremia with IFN and ribavirin can induce MZL (splenic and nodal subtypes) remission. Patients with hepatitis C are now being treated with IFN free, directly acting antiviral therapies (DAA) which have more tolerable side effect profiles and increased efficacy. This case is one of the first reports of the use of DAA therapy for treatment of HCV associated NMZL, with or without adjunct chemotherapy with rituximab. Our case demonstrates that the treatment of HCV with an IFN-free DAA regimen can induce remission in patients with concurrent MZL and is an easier to tolerate alternative to IFN and ribavirin based regimens.

extremity swelling, yellowing of the skin, 20 pound weight loss, and generalized malaise. On initial presentation, patient was afebrile with otherwise normal vitals. Physical exam was notable for jaundice, distended abdomen with positive fluid wave and shifting dullness. There was significant pitting edema of bilateral extremities extending to his hips and scrotum. CBC was notable for hemoglobin, hematocrit, and red cell distribution were 12.1, 36.3, and 16.6 respectively. CMP showed albumin of 1.9, total bilirubin 3.7, elevated alk phosphate 175, AST 276, ALT 48, INR 1.5 and PT of 15.2. Ascites fluid was suggestive of portal hypertension without signs of spontaneous bacterial peritonitis. MRI of abdomen and pelvis showed Hepatic cirrhosis, splenomegaly, ascites, and multiple hepatic masses throughout both lobes of the liver. This was consistent with multifocal hepatocellular carcinoma with hemorrhage. Additionally, imaging revealed tumor thrombus expanding to the right portal vein and suprahepatic IVC at the junction with right atrium. Viral hepatitis C antibody was positive with hepatitis C RNA viral load of 11, 500. Within days, patient developed fulminant liver failure with encephalopathy and hepatorenal syndrome. Unfortunately, due to poor prognosis, patient elected to be placed hospice. Discussion: Hepatocellular carcinoma is the fourth leading cause of death in both men and women worldwide. Majority of HCC are diagnosed at late stage once patients develop obstructive jaundice, ascites, hepatic encephalopathy, and portal vein tumor thrombosis. One of the most common causes of HCC is hepatitis C infection (1). To date, there is an estimate of 180 million individuals with hepatitis C in the world (2). Of those, an estimated 45-85% do not know their status. Individuals with chronic hepatitis C infection have 15-40% risk of developing HCC or Cirrhosis (4). Therefore, routine screening of high risk patients is key an improving prognosis. Once patients with known risk factors for HCC including chronic hepatitis B, C, and cirrhosis are identified, they should undergo surveillance for hepatocellular carcinoma with ultrasound and alpha fetoprotein every six months. Early tumor detection has proved to reduce mortality of HCC by 70% (6). Patient with extrahepatic HCC with Child Purg score of A or B and performance status of 1 or 2 can be managed with chemoembolization and sorafenib as a palliative measure (7). Patient to Child-Purg grade of C or performance status score of 3 or 4 are usually not a candidate for treatment and discussion of comfort care should be initiated (7).

749 Systemic Amyloidosis Presenting as Rapidly Progressive Liver Failure Artemio Santiago, MD, MPH1, Rocio Feliu, MD2, Wilnelya Morales, MD2, Ivan Antunez, MD2, Irene S. Villamil, MD2, Keila Rivera, MD2. 1. University of Puerto Rico, Carolina, Puerto Rico; 2. University of Puerto Rico, San Juan, Puerto Rico. Systemic Amyloidosis is a rare condition associated with multiple inherited and inflammatory disorders in which extracellular deposits of fibrillar proteins are responsible for tissue damage and functional compromise. Depending on the type, amount and location they can result in a wide range of clinical manifestations. Hepatic involvement is usually mild, consisting of gradual onset of symptoms including hepatomegaly and elevated Alkaline Phosphatase. We present an unusual and fatal case of Systemic Amyloidosis causing acute hepatic failure. A 54-year-old Hispanic female with history of Hypothyroidism presented to the ER with complaints of general malaise, dry cough, pedal edema and jaundice of 3 weeks duration. Physical exam revealed an obese woman with scleral icterus and hepatomegaly. Laboratory evaluation showed Direct Hyperbilirubinemia (8.03 mg/dL), Coagulopathy and an Acute Kidney Injury. Liver function tests also revealed elevated Alkaline Phosphatase (1,018 U/L). Urinalysis showed marked proteinuria. She underwent multiple imaging studies including Liver Ultrasound with Doppler, Abdominopelvic CT Scan and MRCP that showed mild hepatomegaly, a small amount of ascites and no evidence of hepatic biliary or pancreatic ductal dilation. Toxins, infectious etiologies and cardiovascular compromise where ruled out; Additionally, normal levels of Alpha Fetoprotein, Smooth Muscle Antibody, Liver-Kidney Microsomal Antibodies, Alpha1-Antitrypsin, Serum Iron, Immunoglobulin G, Anti-Mitochondrial Antibody and Ceruloplasmin where found. She developed altered mental status and rapid hepatic decompensation, with an increase in total bilirubin to 18.2 mg/dL just 5 days after initial presentation. Given the clinical picture an infiltrative disorder was suspected; however, due to rapid deterioration the patient died before biopsy could be done. Amyloidosis involving the Liver, Heart, Lung and Kidneys was confirmed with Congo Red Stain on autopsy. This case represents the importance of including infiltrative disorders in the differential diagnosis of any patient who presents with cholestatic injury along with absence of obstruction by imaging. Another clue to aid in the diagnostic process includes signs of multi organ involvement, such as proteinuria. Although Amyloidosis carries a grave prognosis, Liver involvement is usually mild and gradual; early diagnosis offers time for prompt evaluation and classification, for which chemotherapy or transplant can be offered.

[750A] Figure 1.

750 Fatal Initial Presentation of Hepatocellular Carcinoma Invading IVC to Right Atrium, Missed Opportunity for Cure Lediya Cheru, MD. Albany Medical College/Albany Medical Center, Albany, NY. A 63 year old Caucasian male with known history of unsterile tattoo who never received hepatitis screening by primary physician presented with three week history of abdominal fullness, bilateral lower


[750B] Figure 2.


| OCTOBER 2015

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Abstracts

751 Newly Diagnosed Liver Abscess: Colonoscopy Required Manan Jhaveri, MD1, Priyanka Makkar, MD2, Kinesh Changela, MD3, Raquel Olivo, MD2, Sofia Nigar, MD4, Kimberly Lam, MD2, Andrea Culliford, MD1, Jay P. Babich, MD5. 1. St. Barnabas Hospital, SBH Health System, New York, NY; 2. St. Barnabas Hospital, SBH Health System, Bronx, NY; 3. The Brooklyn Hospital Center, Brooklyn, NY; 4. The Brooklyn Hospital Center, Yonkers , NY; 5. St. Barnabas Hospital, SBH Health System, Teaneck, NJ. Introduction: Liver abscesses occur as the result of pyogenic or amoebic infection and are more commonly found in immunodeficient patients. Their occurrence is very rare and only accounts for 0.02% of all hospital admissions. Klebsiella pneumonia and Pseudomonas aeruginosa are the most common causes of liver abscesses especially in Eastern Asian countries. We report a case of a liver abscess mimicking metastasis in a newly diagnosed diabetic patient who was later discovered to have an occult sigmoid colon cancer. Case report: A 45-year-old male from Senegal presented to our institution with a three-day complaint of abdominal discomfort refractory to antacids, fevers, malaise and weight loss. Initial laboratory data was significant for mild leukocytosis (WBC: 11,800 / μL) and moderate transaminitis (AST/ALT: 67/105 IU/L). CT scan of the abdomen/pelvis demonstrated a 7.5 cm x 7.0 cm mass in the left hepatic lobe with areas of central necrosis. The sigmoid wall thickening with focal irregularity raised suspicion for a mass lesion (Figure 1). Tumor markers were negative. A colonoscopy showed a 5 cm pedunculated polyp in the sigmoid colon, which was removed with hot snare polypectomy (Figure 2). The polyp was a moderately differenti-

[751C] Figure 3.

ated invasive adenocarcinoma without lymph or vascular invasion and clear margins (Figure 3). A liver biopsy was performed due to persistent temperature spikes and was consistent with a hepatic abscess. Cultures were positive for Klebisella Pneumoniae. The plan was to treat the abscess with antibiotic followed by surgical resection. CT scan of the abdomen/pelvis was obtained on the 21st day after initiation of antibiotics and it demonstrated almost complete resolution of liver lesion. Patient successfully underwent laparoscopic lower anterior resection of the sigmoid colon. Pathology demonstrates residual tubular adenoma with unremarkable margins and lymph nodes. Discussion: Various etiologies of liver abscess have been proposed. More recently, especially in the eastern countries, studies have reported liver abscesses as a silent manifestation of colon cancer and may represent the initial manifestation of the disease. This type of pyogenic liver abscess has now been reported worldwide and is regarded as a herald sign of colorectal cancers. Other common associations include the diagnosis of diabetes mellitus type II. The sigmoid colon is the most common site of tumor, and Klebsiella Pneumoniae is the most common pathogen isolated in the Eastern Asian countries. The proposed pathogenesis for the above is the destruction of the mucosal barrier and repeated bacterial translocation. Conclusion: In patients with cryptogenic liver abscess, colonoscopy should be performed to rule out an occult colonic lesion.

[751A] Figure 1.

752 Sorafenib Use in High-Risk Post-Transplant Patients With Hepatocellular Carcinoma Leybelis Padilla1, Mark Russo, MD, MPH2, Philippe Zamor, MD2. 1. Carolinas Healthcare System, Charlotte, NC; 2. Carolinas Medical Center, Charlotte, NC. Introduction: Very little data exists supporting the use of adjuvant chemotherapy in the post liver transplant setting for hepatocellular carcinoma (HCC). Tumor characteristics such as size, number of lesions, grade of differentiation and lymphovascular invasion are predictors of recurrence of HCC post liver transplantation. There are no large randomized studies investigating this subject matter. Smaller studies have described the use of targeted chemotherapy in the post-transplant period and have been shown to possibly increase survival. Given the limited data, we sought to describe our transplant center’s experience in providing sorafenib as adjuvant therapy in patients considered high-risk for HCC recurrence in liver transplant patients. Methods: We retrospectively reviewed our transplant database to identify patients whose explant revealed HCC that exceeded Milan criteria and/or evidence of lymphovascular invasion and were treated with sorafenib post-transplant. Results: Five patients were identified and 3 of those patients had tumor size beyond Milan criteria and lymphovascular invasion. Patients were followed an average of 21 months post-transplant with the longest followup period of 36 months. Table 1 outlines patient demographics, etiology of cirrhosis, tumor characteristics, sorafenib dose and duration, and baseline immunosuppression. Surveillance imaging was performed routinely posttransplant at 3, 6 and 12 months. None of our patients had recurrence of HCC. Sorafenib was discontinued after 12 months of therapy. Discussion: Our experience with the empiric use of sorafenib in patients whom demonstrated high risk of HCC recurrence had 100% disease free survival. More studies with larger number of patients are needed to further define the role of sorafenib in the posttransplant setting.

[751B] Figure 2.



S329

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[752]

Table 1. Summary of Patient and Explant Characteristics

Underlying liver disease

Year of transplant

Explant characteristics

Immunosuppression

Length of followup

Duration of therapy

Cryptogenic cirrhosis, HCC

2011

Macrovascular invasion, 2.2 cm

Tacrolimus

34 months

9 months

Cryptogenic cirrhosis, HCV, HCC

2012

Microvascular and macrovascular invasion; multiple nodules (>3), 0.9–4 cm

Sirolimus

25 months

12 months

HCV

2013

No lymphovascular invasion; 8 tumors (0.8–2.8 cm) not seen previously

Tacrolimus

21 months

12 months

HCV, HCC

2013

Microvascular and macrovascular invasion; 3 lesions, 3.2–5.5 cm

Tacrolimus

19 months

12 months; dose decreased to 200 mg BID due to hand/foot swelling and pain

NASH

2013

Microvascular invasion; HCC and cholangiocarcinoma, 0.6–3.5 cm not seen previously

Tacrolimus

6 months

5 months

Abbreviations: HCV hepatitis C; NASH Nonalcoholic steatohepatitis; HCC hepatocellular carcinoma.

753 Acute Hepatocellular Injury With Autoimmune Features Associated With Move Free® Dietary Supplement Hannah Do, MD1, Vic Navarro, MD2, David E. Kleiner, MD3, Huiman Barnhart, PHD4, Andrew Stolz, MD5. 1. University of Southern California, Los Angeles, CA, 2. Albert Einstein Medical Center, Philadelphia, PA, 3. National Cancer Institute, Bethesda, MD, 4. Duke University, Durham, NC, 5. Division of Gastrointestinal and Liver Diseases, University of Southern California, Los Angeles, CA. Introduction: Move Free® is an herbal and dietary supplement (HDS) advertised to improve osteoarthritis composed of glucosamine, chondroitin, hyaluronic acid, methylsulfonylmethane, vitamin D and a proprietary anti-oxidant blend of herbs including Chinese skullcap root (Scutellaria baicalensis) and black Catechu wood (Acacia catechu). This abstract describes 4 cases of acute hepatitis that developed in previously healthy subjects after Move Free® use. Method: The DILIN database of adjudicated cases enrolled from 2004 to March 2015 (1499 cases) were reviewed for Move Free® implicated DILI as described (Gastroenterology 135:1924). Results: Four cases of liver injury attributed to Move Free® were enrolled between 2010 and 2014; 1 scored as very likely and 2 as probable with one awaiting adjudication. All 4 were adult female who rapidly developed acute hepatitis with autoantibodies after relatively short exposure (< 4 weeks) in 3 out of the 4 cases (Table). Liver biopsies done in 3 subjects revealed changes consistent with immune mediated injury with inflammatory infiltrates of lymphocytic and plasma cells. Conclusions: DILI associated with Move Free® presented with rapid development of acute hepatitis with autoantibodies and inflammatory cells on liver biopsy strongly suggests immune mediated liver injury possibly in predisposed autoimmune hepatitis (AIH) individuals. The ingredient in Move Free responsible for liver injury is unknown, but may be skullcap. Additional analysis of the Move Free®’s components may help to define the mechanisms of immune mediated liver injury in herbal related liver injury or possible activation of AIH in at risk individuals.

to have some issues with hypokalemia, even despite oral supplementation (peak low of 2.3 mmol/L), and a normal anion gap metabolic acidosis that even required an inpatient hospitalization. Her serum creatinine peaked at 1.22 mg/dL during this time, and during her hospitalization, her urinalysis noted glycosuria (despite a normal serum glucose). At subsequent follow up appointments, she has reported a marked improvement in her symptoms with subsequent normalization of her serum potassium and bicarbonate. Discussion: Our patient’s clinical presentation and lab abnormalities are most consistent with a Tenofovir induced Fanconi syndrome. Fanconi syndrome is an uncommon condition that causes proximal renal tubule dysfunction leading to impaired re-absorption of amino acids, uric acid, bicarbonate, glucose and phosphate with associated increased urinary excretion of these solutes. Acquired Fanconi syndrome is often a drug induced side effect with Tenofovir being identified as a known cause, however, there are only limited case reports in the literature regarding this phenomenon. Prior case reports are similar to our patient’s presentation with subsequent resolution of lab abnormalities following cessation of Tenofovir therapy. Although this syndrome is rare, this case presentation highlights the importance of periodic electrolyte and renal function lab monitoring for patients starting Tenofovir.

755 Glycogenosis: A Rare Etiology of Transaminitis Avantika Mishra, MD1, Mohammed Albugeaey, MD2, Rohit S. Satoskar, MD3. 1. MedStar Georgetown University Hospital, Department of Internal Medicine, Washington, DC; 2. MedStar Georgetown University Hospital, Department of Gastroenterology, Washington, DC; 3. MedStar Georgetown University Hospital, Department of Hepatology, Washington, DC. Hepatic glycogenosis is a rare etiology of elevated hepatic transaminases reported in the literature. Glycogenosis is associated with uncontrolled diabetes and can be confused with other forms of acute liver injury. This disease can be diagnosed via liver biopsy and reversed by ensuring tight glycemic control. Given this diagnosis is unrecognized but curable, we highlight a case of hepatic glycogenosis in a patient treated at our institution. Patient is a 24 year-old female with past medical history of depression and uncontrolled Diabetes Mellitus Type 1 with recurrent hospital admissions for Diabetic Ketoacidosis (DKA). She presented to the hospital with one day of nausea and vomiting; she was subsequently diagnosed with DKA, and admitted to the intensive care unit for further clinical care. The patient was initiated on fluids and insulin drip for DKA treatment and continued on her home regimen of duloxetine for depression management. Several days into her admission, the patient developed increases in aspartate transaminase (AST) and alanine transaminase (ALT), with initially normal then elevated alkaline phosphatase. Bilirubin and INR remained with normal limits. Over 10 days, lab values peaked with AST of 535, AST of 465, and alkaline phosphatase of 194. Initial serology including HBs Ag, HBc Ab, HCV Ab, CMV, EBV, HIV, ANA, AMA, antiSMA, and ferritin were negative. Given that there was no history of herbal intake or new hepatotoxic medications initiated, suspicion for drug induced liver injury was low, albeit remained on the differential. There were no episodes of hypotension or active infection throughout the admission. A right-upperquadrant ultrasound was performed with unremarkable findings. During previous admissions for DKA, there were similar acute instances of elevated liver-associated enzymes (Figure 1). Given concern of this recurrent transaminitis, a liver biopsy was pursued. Hematoxylin & eosin (H&E) staining revealed glycogen deposits with no hepatitis or fibrosis, convincing for a diagnosis of hepatic glycogenosis (Figure 2).

[753A] Figure 1.

754 Tenofovir-Induced Fanconi Syndrome Alexandria Hatch1, Anthony Michaels, MD2. 1. The Ohio State University Medical School, Columbus, OH; 2. Section of Hepatology, Division of Gastroenterology, Hepatology, & Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH. Introduction: Tenofovir is a nucleotide reverse transcriptase inhibitor that is considered a first line therapy for a hepatitis B infection. Although generally well tolerated, Tenofovir can potentially have adverse side effects including significant renal and electrolyte abnormalities. Case Presentation: A 67 year old female with a history of decompensated cirrhosis secondary to hepatitis B was started on Tenofovir at an outside office. At that time the patient’s serum potassium, bicarbonate, and creatinine were normal. At subsequent follow up appointments a few months after starting Tenofovir, she began to complain of progressively worsening nausea, decreased appetite, weight loss and ended up having multiple visits to her local Emergency Department with labs significant for hypokalemia and a normal anion gap metabolic acidosis. The patient denied any of these issues prior to initiating Tenofovir. The patient’s Tenofovir was discontinued. Shortly after stopping her Tenofovir, she continued


[755A] Figure 1.


| OCTOBER 2015

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Abstracts

[755B] Figure 2.

Hepatic glycogenosis should be suspected in the appropriate clinical situation after other etiologies are ruled out. It is easily treatable with strict glycemic control. Given the reversibility of liver injury in these patients, raising awareness about an underreported and unrecognized disease is undoubtedly clinically significant in medical practice.

providers. Her initial infectious work-up was negative; however, a CT examination revealed cirrhosis and features of portal hypertension. Due to ongoing, unexplained fevers she was admitted to our hospital. Vital signs revealed tachycardia and a temperature of 102°F. Physical exam was notable for a distended, non-tender abdomen, with fluid wave and lower extremity edema. Cardiopulmonary, lymph node, skin, and joint exams were unremarkable. Labs were notable for albumin 2.7, AST 55, ALT 22, alkaline phosphatase 220, INR 1.4, WBC 13.6 (81% neutrophils), hemoglobin 10, and platelets 254. Blood, sputum, urine, stool, and ascites cultures were obtained. Tspot, quantiferon gold, stool and sputum TB PCR, Q fever Ab, brucella Ab, coccidiomycosis Ab, blastomycosis Ab, urine histoplasmosis Ag, HIV Ab, RPR Ab, and a viral hepatitis panel were sent. An echocardiogram was unremarkable. The patient was started on broad antibiotics including levofloxacin and defervesced. A liver biopsy was completed and sent for culture and universal PCR. Pathology showed necrotizing granulomas within a background of cirrhosis and steatohepatitis. The patient did not have a history of alcohol use. All serologies and cultures completed prior to the liver biopsy returned negative. Universal PCR, fungal, AFB, and bacterial cultures completed on the liver biopsy samples also returned negative. Fever of unknown origin has a broad differential including infectious, rheumatologic, and hematologic/oncologic considerations which can be narrowed in the setting of necrotizing granulomatous liver disease. Considerations include sarcoidosis, granulomatous hepatitis, primary biliary cirrhosis, fungal diseases, Q fever, brucellosis, and tuberculosis. In a physician who is on anti-TNFa therapy and working with refugees, disseminated TB is at the top of the differential. Necrotizing granulomatous liver disease occurs in 70% of patients with extra-pulmonary TB. Our patient improved on initial antibiosis due to the partial coverage of TB by levofloxacin. She remains afebrile on empiric TB treatment today.

757 Another Round? Liver Biopsy Determined the Diagnosis and Management in Patients With Alcohol Recidivism and Recurrent Acute Jaundice

756 Fever of Unknown Origin in a Patient With Newly Diagnosed Cirrhosis Emilie H. Regner, MD1, Marilyn E. Levi, MD2, Kiran M. Bambha, MD, MSc2. 1. University of Colorado, Denver, CO; 2. University of Colorado, Aurora, CO. We present an unusual case of cyclic fevers and newly diagnosed cirrhosis in a 56 year-old woman working as a pediatrician serving Indian refugees. Her past medical history is significant for metabolic syndrome and rheumatoid arthritis that was recently treated with adalimumab. Three months prior to admission she developed fevers of unclear etiology for which she was evaluated by multiple

Nitzan C. Roth, MD, PhD1, Jared Macklin, MD2, Gary C. Kanel, MD3, Behnam Saberi, MD4, Andrew Stolz, MD5, Neil Kaplowitz, MD5, John A. Donovan, MD5. 1. Division of Gastrointestinal and Liver Diseases, University of Southern California, Pasadena, CA; 2. Department of Internal Medicine, University of Southern California, Los Angeles, CA; 3. Department of Pathology, University of Southern California, Los Angeles, CA; 4. Division of Gastroenterology and Hepatology, The Johns Hopkins University, Baltimore, MD; 5. Division of Gastrointestinal and Liver Diseases, University of Southern California, Los Angeles, CA. Background: Reports of recurrent severe alcoholic hepatitis (AH) do not include confirmation by liver biopsy. We describe the clinical and histologic features of three patients with recurrent episodes of jaundice and suspected acute liver injury due to alcoholic recidivism.

[757] Table 1. Clinical and histologic features of three patients with alcohol recidivism and recurrent episodes of acute jaundice due to alcoholic hepatitis (AH) or alcoholic fatty liver with cholestasis (AFLC) Patient #1 Episode 1 (AH) Interval between episodes (months)

Patient #2

Episode 2 (AH)

Episode 1 (AFLC)

12

Patient #3

Episode 2 (AFLC)

Episode 1 (AFLC)

27

Episode 2 (AH) 68

Preceding abstinence (weeks)

3

3

4

1

16

3

Duration of jaundice (weeks)

2

2

4

4

4

3

Bilirubin (mg/dl)

23.1

16.6

9.3

36.8

20.1

10.0

International normalized ratio

1.3

1.7

1.3

1.3

1.5

1.6

Albumin (g/dl)

2.9

2.2

3.1

3.6

3.5

2.3

Alkaline phosphatase (U/l)

244

219

686

510

87

260

AST (U/l)

226

109

218

232

407

131

ALT (U/l)

46

47

28

46

157

26

Leukocyte count (×109/l)

12.9

15.9

5.2

8.5

10.7

18.1

Creatinine (mg/dl)

Clinical parameters at admission:

0.8

0.9

0.6

0.5

1.2

0.9

Ascites

+

+

−

+

+

+

Hepatic encephalopathy

−

−

−

−

−

+

Discriminant function

35

47

30

50

44

37

MELD

21

23

18

23

24

21

Severity scores:

Histologic parameters: Portal fibrosis

F4

F4

F1

F1

F2

F3

Fatty change

3+

1+

4+

4+

4+

3+

Cholestasis

+

+

+

+

+

+

Hepatocyte ballooning

+

+

−

−

−

+

Mallory-Denk bodies Lobular inflammation (predominant cell types)

Treated with corticosteroids Outcome

+

+

−

−

−

+

+ (neutrophils/ lymphocytes)


+/− (lymphocytes)

+/− (lymphocytes)

+/− (lymphocytes/ monocytes)


+

+

−

−

−

+

Jaundice resolved within 3 months

Alive at 1.5 months, remained jaundiced, follow-up ongoing


Alive at 3 weeks, remained jaundiced, lost to follow-up


Alive at 32 months, jaundice resolved within 2 months but recurred



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Abstracts

Methods: Evaluation of 120 patients with acute alcoholic liver injury included two with distinct hospitalizations between 2005 and 2012 for the recent onset of jaundice and a suspicion for severe alcoholic hepatitis (AH) defined by a discriminant function (DF) >32 or a MELD score of >18. A third patient later identified is included. Particular to these cases, a liver biopsy was performed during the index and a subsequent episode. Results: The clinical and histologic features for the first and subsequent episodes of acute alcoholic liver injury are presented in Table 1. Each patient had resolution of jaundice within 2-5 months after the first presentation. Recurrent jaundice in the context of alcohol recidivism occurred at an interval of 1-6 years. Patient #1 had cirrhosis and two episodes of biopsy-proven AH with histologic features of hepatocyte ballooning, Mallory-Denk bodies, and neutrophilic lobular inflammation. Treatment with corticosteroids for 7 days on both occasions resulted in partial responses with calculated Lille scores of 0.23 and 0.38, respectively. Patient #2 had two episodes of acute alcoholic fatty liver with cholestasis (AFLC), without histologic evidence of AH. Cholestasis, prominent macrovesicular fat, mild portal fibrosis, and mild lymphocytic lobular inflammation were present. Treatment was supportive. Patient #3 had an initial episode of self-limited jaundice due to AFLC followed by periods of recidivism and three recurrent episodes of jaundice over a period of >6 years. During the second recurrence, a liver biopsy showed AH. A calculated Lille score after 7 days of corticosteroids was 0.21, and 28-day treatment resulted in complete resolution of jaundice. Conclusions: After a first episode of acute alcoholic liver injury, jaundice may recur in patients with alcohol recidivism. The histologic pattern of recurrent liver injury is not always the same. Liver biopsy remains important in evaluating recurrent episodes in order to distinguish between recurrence of the first injury, including AH, or other alcoholic liver diseases, like AFLC, that can have similar clinical presentations.

[758B] Figure 2.

758 Hepatic Actinomycosis Five Years After Abdominal Surgery Chuong Tran, MD, Shanaz Sikder, MD, Lory Wiviott, MD. California Pacific Medical Center, San Francisco, CA. Introduction: Actinomycosis is a rare chronic infection by Actinomyces spp., Gram-positive anaerobic bacteria normally seen in the human oropharyngeal, gut, and genitourinary flora. The disease most commonly affects the cervicofacial region (up to 70%), and abdominal disease has been seen in less than 20% of reported cases. Primary hepatic actinomycosis accounts for about 5% of all cases. On imaging, it is often indistinguishable from malignancy, tuberculosis, or abscesses from more common pathogens. We report a case of hepatic actinomycosis in a 65 year-old man with remote abdominal surgery. Case: A 65 year-old man with no known liver disease presented in January 2014 with a few weeks of vague right upper abdominal pain. His surgical history was significant for hemicolectomy for diverticular disease and lysis of adhesion for small bowel obstruction, 12 and 5 years prior to presentation. Physical examination and blood tests were unremarkable. Ultrasound revealed a 21x18 mm low-density cystic lesion in the inferior right hepatic lobe. Liver biopsy showed nonspecific inflammatory cells, and surveillance was recommended. On MRI 1 year later, the lesion had evolved into a 7.2x4.8 cm, thickwalled, peripherally enhancing mass. CBC, CMP, viral hepatitis panel, HIV, and tumor markers (CA 19-9, CEA, AFP) were all negative. The mass was surgically removed. Specimen staining showed branching Gram-positive rods, and Actinomyces israelii was subsequently identified by anaerobic culture. The patient received 6 weeks of parenteral penicillin G followed by oral ampicillin for up to 6 months. Discussion: The above patient presented initially with a simple cystic liver lesion that evolved into a complex appearing mass. The patient did not have significant risk factors other than remote abdominal surgeries. Percutaneous liver biopsy has not been reported to cause hepatic actinomycosis. He also did not exhibit commonly reported manifestations such as fever, weight loss, leukocytosis, and anemia. This case illustrates the challenge in diagnosing hepatic actinomycosis, as lesions can initially appear benign or can mimic malignancy or tuberculosis. Percutaneous liver biopsy may not be helpful, and surgical resection is often necessary for definitive diagnosis. Actinomycosis should be considered in any liver lesion without obvious cause, regardless of symptomatology. Finally, the importance of ongoing surveillance of seemingly benign liver lesions should also be emphasized.

[758A] Figure 1.


759 Life-Threatening Variceal Bleed Caused by Secondary Portal Hypertension Controlled by Emergent Splenopneumopexy Kevin Patel, MD1, Daniel Berger, MD2, Sheila Eswaran, MD, MS1. 1. Rush University Medical Center, Chicago, IL; 2. Rush University Medical Center, Riverwoods, IL. Introduction:Variceal bleeding is a common and feared complication of portal hypertension. In cases of recurrent bleeding despite pharmacologic therapy and endoscopic variceal ligation, portal decompressive therapy is often pursued. We present a case of a life-threatening variceal bleed caused by portal hypertension secondary to extensive pre-sinusoidal thrombosis as a result of schistosomiasis. The patient’s bleeding was managed with emergent splenopneumopexy, a procedure that created a portopulmonary shunt via anastomosis of the splenic veins and pulmonary veins. Case Description: A 49-year-old male with past medical history of schistosomiasis initially presented to a community hospital with hematemesis and hematochezia. An EGD revealed multiple grade 3 esophageal varices that were banded with resolution of bleeding. Three weeks later, the patient had recurrent hematemesis requiring hospitalization. CT of the abdomen/pelvis revealed occlusion of portal, splenic, and superior mesenteric veins. An EGD was repeated but no targets for band ligation were identified due bleeding and presence of clots. A TIPS procedure was attempted but was unsuccessful due to completely occluded vasculature. The patient experienced ongoing hematemesis and hematochezia with hypotension requiring resuscitation. He was stabilized and transferred to our hospital for higher level of care. Upon arrival, he was intubated for airway protection. A Blakemore tube was placed for balloon tamponade and he was taken to the OR for emergent surgery. The patient underwent splenopneumopexy for creation of a portopulmonary shunt as well as transection of the esophagus with primary esophageal anastomosis. The patient did well post-operatively, remaining hemodynamically stable and did not

[759A] Figure 1.


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Abstracts 761 Severe Myositis With the Use of Sofosbuvir/Ledipasvir for Hepatitis C Infection: A Case of Unexpected Interactions Shyam Patel, MD1, Sushrut Trakroo, MD2, Sirish Sanaka, MD2, Kamran Qureshi, MD3. 1. Temple University Hospital, Philadelphia, NJ; 2. Temple University Hospital, Philadelphia, PA; 3. Temple University School of Medicine, Philadelphia, PA.

[759B] Figure 2.

have any further bleeding. The etiology of his pre-sinusoidal thrombosis was thought to be secondary to schistosomiasis given prior history of infection. A hypercoagulable workup was unremarkable and liver biopsy revealed normal hepatic parenchyma. The patient received empiric treatment for schistosomiasis and was discharged 14 days post operatively. Six months after discharge, the patient had not had any further bleeding. Discussion: Splenopneumopexy was first developed in Japan in the 1960s for treatment of portal hypertension in patients with Budd-Chiari Syndrome. The operation induces a portopulmonary shunt via anastomosis of the superior pole of the spleen and exposed pulmonary veins in the left lower lobe. In our patient’s case, extensive pre-sinusoidal thrombosis from schistosomiasis precluded successful TIPS procedure and in the setting of refractory variceal bleeding, the patient’s life was ultimately saved by emergency decompressive surgery with splenopneumopexy.

Case Report: This 66-year-old female presented to emergency room with one week of nausea, nonbloody vomiting, weakness and diarrhea. Her medical history was significant for compensated Hepatitis C (HCV) associated liver cirrhosis, prior treatment failure chronic HCV infection, stage III chronic kidney disease, coronary artery disease, and gout. She had started Ledipasvir/Sofosbuvir combination drug along with renally dosed Ribavirin a month prior to this admission. In addition she was on Atorvastatin and Colchicine for prior several months without any side effects. On admission, her HCV RNA was undetectable, creatine kinase (CK) was of 9055 U/L, ALT 166 U/L, AST 362 U/L, GFR 30 mL/min/1.73 m2, and a urinalysis was notable for large amount of blood but no RBCs, suggesting rhabdomyolysis. Atorvastatin was stopped on the day of admission and she was aggressively fluid resuscitated. Patient complained of profound weakness and myalgia. Initial workup was unremarkable, with normal aldolase, C3 and C4 complement, TSH, and serum protein electrophoresis. EMG showed diffuse muscle irritability suggesting inflammatory myopathy. The conclusion reached was that this patient’s myositis was drug induced, possibly from interaction between Ledipasvir/Sofosbuvir, Atorvastatin and Colchicine. Colchicine was subsequently stopped. The rhabdomyolysis resolved and she had normal CK levels and although her myalgias improved, she was discharged home with persistent muscle weakness which subsequently improved over next 4 weeks as she continued her HCV treatment. Discussion: Ledipasvir/Sofosbuvir is a new Direct Acting Antiviral combination that was introduced in 2014 to treat chronic HCV genotype 1 infection in adults. Sofosbuvir’s metabolite is renally excreted and patient’s stage III CKD could have played a critical role in increasing the chance of unanticipated toxicity. Ledipasvir/Sofosbuvir is known to increase the blood concentration of Rosuvastatin, but Atorvastatin interaction has not been specifically studied, indicating that Ledipasvir/Sofosbuvir could interact with statins as a class. Based on the Naranjo probability scale (score of 6) this patient’s adverse event correlates to an adverse drug reaction caused by interaction between Ledipasvir/Sofosbuvir, Atorvastatin, and Colchicine. Conclusion: It is important for physicians’ prescribing Ledipasvir/Sofosbuvir to be aware of the potential drug interaction with all statins as a class and with Colchicine, in the setting of CKD so that appropriate medication changes can be made to avoid myositis and rhabdomyolysis.

762 A Case of Hepatosplenic Gamma-delta T Cell Lymphoma with Intravascular Lymphoma Like Features in a Young Male With Autoimmune Hepatitis Matthew Miles, MD1, Sudeep Shivakumar, MD2. 1. Dalhousie University Internal Medicine, Halifax, NS, Canada; 2. Dalhousie University Department of Medicine, Halifax, NS, Canada.

760 Chylous Ascites Ten Years After Liver Transplant: A Rare Diagnosis Kamran Qureshi, MD1, Dan Liu, MD2, Hicham Khallafi, MD3. 1. Temple University School of Medicine, Philadelphia, PA; 2. Florida Hospital, Orlando, FL; 3. University of Central Florida, Orlando, FL.

Hepatosplenic gamma delta T-cell lymphoma (HSGDTL) is a rare and aggressive hematologic malignancy that has been associated with long term use of immunosuppressive agents. Here we report a 22-year-old male on azathioprine and prednisone for autoimmune hepatitis who presented to hospital with abdominal pain, night sweats and 20lbs of weight loss. On exam he had hepatomegaly and splenomegaly but no lymphadenopathy. His initial lab tests were WBC 5.39 x 109/L, Hb 70 g/L, platelets 25 x 109/L, total bilirubin 74 μmol/L, AST 151 U/L, ALT 55 U/L and LDH 5932 U/L. He had marked

Body Cavity Lymphomas (BCLs), or Primary Effusion Lymphoma (PEL), are rare, primary nonHodgkin’s lymphomas that proliferate within the serous body cavities and result in recurrent effusions. Hisorically BCL is seen in patients with AIDS. Rarely, BCL occurrs in the settings of solid organ transplantation. It is viewed as an uncommom presentation of posttransplantation lymphoproliferative disease (PTLD), one of the leading causes of late death. We describe a case of a 54 year-old male who underwent Orthotopic Liver Transplantation for decompensated Hepatitis C related Liver cirrhosis 10 years prior to his presentation with new onset ascites. His initial posttransplant course was complicated with an episode of acute cellular rejection as well as biliary stricture for which he underwent multiple ERCP interventions. Later he was maintained on low dose tacrolimus and mycophenolate for immunosuppresion. He underwent paracentensis and 4 liters of milky acites fuid was removed. Acites fluid analysis revealed 354 leukocytes with 84% monocyte, 2,000 erythrocytes, a triglyceride of 2,323, protein of 2.7 g/dL, amalyse of 24, lipase of 91 and LDH of 69 IU/L. Bacterial, TB and fungus cultures were negtive. Initial cytology did not find atypical lymphocytes or other maligant cells. He developed recurrent ascites which needed multiple paracentesis and was reforactory to diuresis. The patients did not have any recent abdominal surgery or trauma. Hemogram revealed a WBC count 3,400, cells/ mm3 with 25% lymphcyte, hemoglobin of 13 g/dL, and platelet count of 181000/microl. Chemistry showed mildly eleveted liver funtion test, lactate dehydrogenase (LDH) at 126U/L and lipase at 94; serum triglyceride was 190; CRP was 5.2; Hepatitis C viral (HCV ) quantity was 367,080, indicating recurrence of HCV infection. He underwent liver biopsy with the finding of chronic, grade 2, stage 2, HCV infection. Repeated paracentesis again revealed chylous acites with triglyceride of 181,425. Subsequent ascitic fluid cytology revealed atypical lymphocytes expressing CD19, CD38, CD79a, and CD20, suggesting high grade B cell lymphoma. Bone marrow biopsy, CT imaging as well as PET scan were then performed which did not reveal any evidence of solid lymphoma. The patient was subsequently diagnosed with the rare form of PTLD and BCL. Notebly, furhter workups including serum PCR for HHV8, HIV, EBV as well as immunostaining for HHV8 and EBV antigen in acites were negative. The patient was started on R-CHOP Chemotherapy. Atypical lymphocytes were undetectable after first cycle of chemotherapy. We are currently closely moitor this patient during his chemotherapy. His PTLD remains localized to the peritoneal cavities with no formation of solid tumor masses up to date. Recurrent chylous acites with unknown eltilogy in posttransplation patient should raise suspisions to rule out BCL.

[762A] Figure 1.



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hepatosplenomegaly without lymphadenopathy on abdominal CT scan. Bone marrow and liver biopsies confirmed the presence of HSGDTL. Unfortunately he did not respond to multiple cycles of chemotherapy and passed away. On autopsy he had multiorgan involvement of an intravascular lymphoma like (IVLL) T-cell population. There are no definitive risk factors for HSGDTL but an association with immunosuppressive agents has been well documented in renal transplant recipients and patients with inflammatory bowel disease (IBD). Specifically, the use of thiopurines for at least two years in young males with IBD has been linked to an increased risk of developing HSGDTL. To our knowledge, however, previous cases of HSGDTL in autoimmune hepatitis patients have been minimally reported in the literature. Unique to our case was the finding of an intravascular lymphoma like component on autopsy that was present in tissue samples from the patient’s lungs, kidneys, heart, thyroid and testicles. As far as we know, a widespread multi-organ intravascular lymphoma in a HSGDTL patient is exceedingly rare. In fact we found only one other case in the literature. Therefore, it is difficult to assess the impact of this finding. It is possible the presence of intravascular lymphoma represents a subtype of HSGDTL and may provide insight into the aggressive nature of this disease. We must also consider an association between autoimmune hepatitis and HSGDTL with IVLL component independent of immunosuppressive therapy. However, future research into this little known and seldom reported malignancy will be required to fully appreciate these findings. Overall, we hope our case report will contribute to better understanding the association between T-cell lymphoma and long term use of immunosuppressive agents as well as identify new populations, specifically autoimmune hepatitis patients, who may be at risk of developing this deadly disease.

763 Disseminated Blastomycosis Dermatitidis Causing Hepatitis in an Immunocompromised Patient Douglas Mills, DO, Hina Omar, MD, Timothy Laurie, DO. Advocate Lutheran General Hospital, Park Ridge, IL. We present a case of disseminated blastomycosis causing acute hepatitis in an immunocompromised patient. A 46 year-old female with Crohn’s disease on adalimumab and methotrexate presented with chest pain, shortness of breath and fevers for one week. Physical examination revealed anicteric sclera, normal heart, lung, and abdominal examinations. Labs on admission showed a total serum bilirubin of 0.7 mg/dl, alkaline phosphatase (ALP) of 313units/L, and a serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) of 655units/L and 961units/L, respectively. Computer tomography scan of the chest, abdomen and pelvis revealed mild fatty liver and diffuse gallbladder wall thickening, but also a right lower lobe infiltrate and mild effusion. A hepatobiliary iminodiacetic acid scan was normal. Autoimmune liver and viral hepatitis panels were negative. Urine histoplasma antigen was positive. The patient had a bronchoscopy with bronchoalveolar lavage with cultures sent. She was started on liposomal amphotericin B. Adalimumab and methotrexate were not continued. Her AST, ALT and conjugated bilirubin continued to increase to 1361, 914 and 7.5 respectively. She clinically improved despite the increasing transaminases. Blastomyces dermatitidis antigen was positive and cultures eventually grew blastomyces dermatitidis. Amphotericin B was changed to oral itraconazole. She was discharged home with improved transaminases. Our patient presented with mild flu like symptoms, which is a common presentation for blastomycosis, but she also had markedly elevated transaminases. The most common extra-pulmonary sites of blastomyces in humans are skin, skeleton, male genitourinary system, and central nervous system. Liver involvement is rare. A far more common infectious source of both lung and liver is histoplasmosis, however this was not the cause in our patient. A false positive histoplasma urine antigen can occur secondary to cross reactivity with blastomyces. The initial treatment for disseminated blastomycosis is IV amphotericin B.

Two other cases of patients presenting with acute blastomycosis pneumonia and elevated transaminases are reported, however the transaminase elevation was not attributed to the infection. The first is a case of a 44 year-old white female who presented with fever, cough and alcoholic hepatitis and ultimately died of delirium tremens. Her transaminase elevation was attributed to the alcoholic hepatitis. The second case involves a seventeen-year-old male who presented with cough, hemoptysis, weight loss, and skin lesions and developed elevated transaminases following treatment with amphotericin B. To our knowledge, this is the first reported case of acute hepatitis caused by disseminated blastomycosis.

764 Herpes Hepatitis in a Patient With Crohn’s Disease: A Case Report Robin Zachariah, MD1, Jeffry Katz, MD1, Deepak Venkat, MD2. 1. University Hospitals Case Medical Center, Cleveland, OH; 2. University Hospitals Case Western Reserve University, Cleveland, OH. Background: Herpes Simplex (HSV) is an extremely rare cause of hepatitis. Mortality can be as high as 90% in untreated patients and in treated cases, roughly 50% will progress to death or liver transplant. Early initiation of acyclovir can drastically reduce mortality. As a result, clinicians should maintain a high index of suspicion for herpes hepatitis especially in the immunocompromised. Crohn’s disease patients are often treated with immunosuppressive agents increasing their risk of such rare infections. Case Report: A twenty-three year old male with severe fistulizing Crohn’s disease, requiring extensive immunosuppressive therapy and recent development of oral/genital lesions, was admitted to the hospital with abdominal pain. Symptoms included severe right upper quadrant abdominal pain associated with fever, tachycardia, and increased non-bloody bowel movements. Notably, he had been on a prednisone taper and received vedoluzimab the day before admission. Initial lab findings revealed a white blood count of 2.8 X10E9/L, platelet count of 130 X10E9/L, INR of 1.2, ALT of 1195 U/L, AST of 2046 U/L, and a lactate of 2.71 mmol/L. Imaging was negative for acute pathology and ultrasound did not reveal thrombosis. He was started broad spectrum antibiotics, acyclovir and N-acetylcysteine. Extensive serologic testing for the cause of his acute hepatitis was performed; most of which were negative. He had a positive HSV-2 IgM, positive genital/oral cultures for HSV-2 and HSV-2 PCR Quant greater than 10E8 copies/mL. The patient improved with acyclovir and immunosuppression reduction, however his course was further complicated by a recurrent Crohn’s flare. He was eventually discharged on high dose oral acyclovir, budesonide and prednisone with follow-up. As his viral count had drastically decreased, he was restarted on outpatient vedolizumab infusions. He was continued on lifelong acyclovir for viral suppression due to his immunosuppression. Discussion: Herpes hepatitis should be considered in immunosuppressed patients presenting with acute liver injury. While biopsy remains the gold standard, diagnosis can also be made by serologic testing in the appropriate clinical setting, as seen in the current case. Additionally, given that he improved after initiation of acyclovir, the diagnosis of herpes hepatitis was further supported. Since he received a vedolizumab infusion only one day before his presentation, it is unlikely to have caused his herpes hepatitis.

765 Acute Liver Injury Related to Intermittent Intravenous Ketamine for the Treatment of Migraines Christina Tofani, MD, Kunjal Gandhi, MD, Dina Halegoua-DeMarzio, MD. Thomas Jefferson University Hospital, Philadelphia, PA. A 58 yo female was admitted to the neurology ward for inpatient management of migraines. On admission, the patient had normal labs, including liver function tests (LFTs) (total bilirubin 0.2 mg/dL, AST

[765A] Figure 1.



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Abstracts 20 IU/L, ALT 17 IU/L, alkaline phosphatase 111 IU/L). On day 2, the patient was started on a ketamine infusion. On day 3, one day after starting the ketamine infusion, the patient had abnormal LFTs (total bilirubin 0.5 mg/dL, direct bilirubin < 0.2mg/dL, AST 224 IU/L, ALT 186 IU/L, alkaline phosphatase 141 IU/L). The LFTs were trended daily and peaked on day 4 (total bilirubin 1.0 mg/dL, direct bilirubin 0.4 mg/dL, AST 721 IU/L, ALT 1034 IU/L, alkaline phosphatase 289 IU/L). An abdominal ultrasound demonstrated gallstones without gallbladder wall thickening, mild common bile duct dilation (9mm) without choledocholithiasis and mild hepatic steatosis. The LFT abnormalities were felt to be related to the ketamine infusion. The ketamine infusion was held. The next day, the LFTs improved (total bilirubin 0.4 mg/dL, direct bilirubin 0.2 mg/dL, AST 385 IU/L, ALT 806 IU/L, 282 IU/L). The patient was discharged the following day, as her LFTs continued to trend down. Unfortunately, she was lost to follow up. The patient had 3 prior admissions for ketamine infusion for chronic migraines. During the initial admission, over 2 years prior, LFTs were normal on admission but never rechecked. During the following 2 admissions, the patient had normal LFTs on admission but was found to have LFT abnormalities after the initiation of a ketamine infusion. The LFTs peaked on day 4 of the 2nd admission (total bilirubin 0.7 mg/dL, direct bilirubin 0.5 mg/dL, AST 220 IU/L, ALT 373 IU/L, alkaline phosphatase 353 IU/L) and on day 2 of the 3rdadmission (total bilirubin 0.8 mg/dL, direct bilirubin 0.6 mg/dL, AST 507 IU/L, ALT 611 IU/L, alkaline phosphatase 234 IU/L). On both admissions, the LFTs improved shortly after cessation of the ketamine infusion. Discussion: Hepatotoxicity is recognized among ketamine abusers. Ketamine abusers have been found to have bile duct dilation, bile duct injury and liver fibrosis. The mechanism of these findings is unclear. Our patient had common bile duct dilation on ultrasound. An abdominal MRCP was recommended but was not obtained, for unknown reasons. Due to lost follow up, a repeat ultrasound was not obtained after cessation of intravenous ketamine and normalization of LFTs. To our knowledge, this is the first reported case of abnormal LFTs related to intermittent intravenous ketamine for the management of migraines. Hepatotoxicity is well-described in abusers of ketamine. However, there is limited literature describing liver abnormalities in patients receiving intravenous ketamine in the treatment of chronic pain syndromes.

766

liver biopsy and splenectomy was performed. Pathology revealed diffuse non-necrotizing granulomatous inflammation consistent with sarcoidosis of both the liver and spleen, and a diagnosis of extrapulmonary sarcoidosis was made. Resected spleen weighed 2,022 g easily meeting criteria for massive splenomegaly by weight. Pathology also revealed stage 2-3 fibrosis of the liver, iron staining and AFB staining was negative for mycobacteria in both organs. Pt never had any pulmonary symptoms and multiple chest x-rays failed to demonstrate the hallmark hilar lymphadenopathy and reticular opacities of pulmonary sarcoidosis. Sarcoidosis is a disease of unknown origin, characterized by noncaseating granulomas in involved organs with pulmonary involvement in 90% of cases. Isolated extrapulmonary disease is rare, occuring in only 10% of cases. This patient’s presentation with symptomatic massive splenomegaly and pancytopenia in the setting of isolated hepatic and splenic sarcoidosis is very rare. After nearly a month long hospitalization, he was discharged on ursodiol. On follow up, he was then transitioned to prednisone and later to methotrexate with the discontinuation of prednisone due to an elevation in his LFTs. As a result of his treatment, the patient gained back some weight, his liver enzymes decreased to AST of 97 and ALT of 89, alkaline phosphatase decreased to 305, and his pancytopenia completely resolved.

767 An Unusual Cause of Hepatic Rupture Minni Meka, MD, Dhara Chaudhari, MD, James Swenson, MD. East Tennessee State University, Johnson City, TN. Introduction: The Liver is a highly vascular organ that is vulnerable to traumatic injury because of its size and fixed position in the right hypochondrium. We present a unique case of a patient who presented with hepatic rupture following vigorous coughing. Case description: An 83 year-old female with history of chronic obstructive pulmonary disease presented with epigastric pain, nausea and vomiting following an episode of vigorous cough on exposure to dust. She denied hematemesis, melena or fever. Physical examination: heart rate 102/min, and blood pressure 109/56 mm Hg, decreased breath sounds with bilateral wheezing, diffusely tender, distended

Isolated Extrapulmonary Hepatic and Splenic Sarcoidosis With Hepatomegaly and Symptomatic Massive Splenomegaly Brandee Albert, DO, MS1, Khusbu Patel, DO2. 1. Carolinas Health System - Blue Ridge, Morganton, NC; 2. Carolinas Health System - Blue Ridge, Hickory, NC. A 28-year-old white male with a history of chronic abdominal pain, GERD and IV drug abuse presented to the Emergency Department complaining of fatigue, abdominal pain, nausea and vomiting for 3-4 months, and rapid weight loss of 90 lbs. CT scan of his abdomen revealed hepatosplenomegaly, portal hypertension and portacaval lymphadenopathy. Initial labs were remarkable for pancytopenia, elevated serum creatinine of 2.9, elevated serum calcium of 12.7, elevated AST of 69 and ALT of 65, and alkaline phosphatase of 506. Hepatitis C antibody was positive with a negative viral load. Due to the concern for underlying malignant process, he underwent endoscopic ultrasound with periportal lymph node biopsy which was nondiagnostic. SPEP was unremarkable, alpha-1 antitrypsin was normal, ferritin was mildly elevated, ceruloplasmin was elevated, ANA was negative, antimitochondrial antibodies weakly positive, ANCA negative, anti-smooth muscle antibody moderately to strongly positive, light chains elevated, the CMV and EBV viral load were negative, HIV was negative, and ACE level was elevated. Pt then underwent bone marrow biopsy, no evidence of a lymphoproliferative disorder was found. Subsequently, a

[767A] Figure 1.

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[767B] Figure 2.


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[768A] Figure 1.

[767C] Figure 3.

abdomen with guarding but no rigidity. Laboratory data: Total bilirubin 4.5 mg/l, Aspartate transaminase 43 IU/l, Alanine transaminase 99 IU/l, Alkaline phosphatase 136 IU/l, Serum lipase 51 U/l, negative hepatitis panel. Chest X-ray showed no rib fractures. Computed tomography (CT) revealed large fluid collection posterior to the stomach, no bowel perforation or cholecystitis. CT guided drainage showed bilious fluid. She was initially managed conservatively with the drain in place but failed to improve. Endoscopic retrograde cholangiopancreatography (ERCP) showed an obvious leak of contrast from the left lobe of the liver flowing and draining through the drain. Sphincterotomy and stent placement were done during ERCP with significant improvement in her condition. Hepatobiliary (HIDA) scan after 4 weeks showed no bile leak and stent was removed. Discussion: Hepatic laceration is often a fatal complication of trauma, pregnancy, anticoagulant therapy, connective tissue disorders, liver infiltrative diseases, hepatocellular carcinomas, and rarely cough as in our case. Patients present with severe right upper quadrant pain, abdominal distention, anemia or hypotension. Suspicion of injury is raised from presentation, physical examination and laboratory findings. CT abdomen usually confirms the injury and defines injury grade. Biliary tree disruption is a frequent complication of non-operative management; diagnosis and evaluation of the leak site may be made by ERCP and HIDA scan. Drainage of the bile collection followed by close observation serves as definitive therapy, but some patients have persistent bilious drainage that can be managed by ERCP with sphincterotomy and/or biliary stent placement. Conclusion: Hepatic laceration, though life-threatening, is not a well-described complication of cough. This report provides a detailed account of such a complication along with an unlikely site of bile collection occurring secondary to vigorous coughing.

768 Non-metastatic Fibrolamellar Hepatocellular Carcinoma Presenting With Hyperammonemia: A Case Report

[768B] Figure 2.

Ahmad Nakshabandi, MD1, Angel Alsina, MD1, Edson Franco, MD2, Nyingi Kemmer, MD, MPH, MSc1. 1. Tampa General Medical Group, Tampa, FL; 2. Tampa General Hospital, Tampa, FL. A 23 year old female presented with a 2 week history of nausea, vomiting, generalized weakness, and intermittent right upper quadrant pain. Following admission, computerized tomography of abdomen revealed a large hepatic mass measuring 13 x 9 cm (figure), without evidence of metastasis. Multiple internal enhancing vessels and altered vascular architecture were visualized. Liver function tests included AST (47 U/l), ALT (41 U/l), total bilirubin (2.2 mg/dl) and INR (1.5). Patient began to show signs of altered mentation, as ammonia levels began to peak at 437 mcg/dl. A core needle biopsy confirmed Fibrolamellar hepatocellular carcinoma (FL-HCC), while pathology report revealed a 16 cm well differentiated FL-HCC without lymphovascular invasion. After the tumor was deemed unresectable the patient was listed for transplantation. The patient was placed on immunosuppression post transplantation, which included corticosteroids, mycophenolate mofetil and tacrolimus. At 1 year follow-up, the patient continues to live without recurrent disease while on sorafenib adjuvant therapy. FL-HCC is a rare hepatocellular tumor arising in non-infected, non-cirrhotic livers, accounting for 0.3% of all HCC cases. It is more frequent in young adults with no sex preponderance. Only two cases


of FL-HCC accompanied by hyperammonemia due to intrahepatic shunting have been published, none of which were successfully treated. We present a rare case of FL-HCC in a patient who was comatosed from hyperammonemia and was successfully transplanted later. This case illustrates various aspects of complex management decision that includes: treatment of a patient with features of acute liver failure, management of encephalopathy, and determination of tumor resection or transplantation (LTx). The liver transplant literature on these tumors is outdated and historically, not favorable. However, systemic therapies and immunosuppressants with anti-cancer activities are now available. This patient with advanced encephalopathy was deemed unresectable and was urgently transplanted. Outcomes reported for LTx in FL-HCC are poor as the data is outdated (from 1990’s). The 5-year survival rate ranged from 29% to 55%. Only two cases have been reported of FL-HCC presenting with hyperammonemia, one from the United States of America, and another from Argentina. Young patients with unresectable FL-HCC co-existing with hyperammonemia but without evidence of metastatic disease should be considered for LTx.


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Abstracts 769 An Extremely Rare Primary Osteosarcoma of the Liver: Case Report and Review Jack Husney, MD1, Kevin Tin, MD, MBA1, Robert Kalter, MD1, Swan Thung, MD2, Rabin Rahmani, MD, FACG1. 1. Maimonides Medical Center, Brooklyn, NY; 2. Icahn School of Medicine at Mount Sinai, New York, NY. Primary extra skeletal osteosarcoma is a rare entity. It is often reported in the soft tissue of the limbs, and more rarely found in the organs such as heart, kidney, uterus, thyroid and liver. Thus far, there have only been ten cases of primary osteosarcoma of the liver documented in the literature. A 54 year old male with a past medical history of hepatitis C, presented with worsening right intermittent epigastric pain. Physical examination was positive for abdominal distention, with epigastric tenderness and hepatomegaly. Laboratory results revealed elevated LFTs and Alpha feto-protein level, while CEA and CA19-9 levels were normal. For further evaluation a CT scan was performed which revealed a 4.8 x 4.2 x 5.9 cm low attenuated lesion with peripheral sepatations and rim enhancement within the right hepatic lobe. The differential included a liver mass, likely HCC and a liver abscess. CT guided biopsy was completed and revealed few cores of tumor compromised of fibroblastic malignant cells producing lacelike osteoid matrix. There were also rare osteoclast-like giant cells and mitotic figures. The spindle tumor cells were negative for HepPar1, AE1, AE2, and strongly reactive for vimentin on immunostains, which were consistent with osteosarcoma. Further work-up for metastasis including a PET scan, was negative. The patient’s condition continued to deteriorate with new onset cirrhosis and he was not a candidate for resection of the liver mass and subsequently expired. Primary osteosarcoma of the liver is a very rare neoplasm of the liver. The other sarcomas that have been identified include fibrosarcoma, leiomyosarcoma, liposarcoma, rhabdomyosarcoma and angiosarcoma. From the cases, to date, the ages range from the 19- 73. Of those patients, nine cases, including ours, have been in male patients while only one known case report identified the patient as a known carrier of Hepatitis C. While there are many theories for the etiology of primary liver osteosarcoma, there has

[769C] Figure 3.

been no definitive causality. Some hypotheses have included DNA alteration or damage secondary to hepatitis virus, genetic predisposition, chemotherapy, or ischemic stress. The effect of hepatitis on the osteosarcoma is still not clear, as so far only three of the eleven cases have had hepatitis. At the same time, five cases have been documented as cirrhotic, prior to the diagnosis of the liver osteosarcoma, which can stimulate oncogensis in these patients. Our case was unique for the rare diagnosis of primary hepatic osteosarcoma with a history of hepatitis C. This diagnosis should be contemplated in liver masses with calcification. Pathological identification and exploration of other causes must be completed in order to make such a diagnosis.

770 Intractable Hypoglycemia: A Paraneoplastic Complication of Hepatocellular Carcinoma Ofor Ewelukwa, MD, MSc, Roniel Cabrera, MD, MS. University of Florida, Division of Gastroenterology, Department of Internal Medicine, Gainesville, FL.

[769A] Figure 1.

Introduction: We present a case of intractable hypoglycemia (IH) as a rare paraneoplastic complication of advanced hepatocellular cancer (HCC) during the terminal stages of the disease. Case: A 54 year-old male with HCV related cirrhosis and advanced HCC with portal vein (PV) invasion was admitted for symptomatic IH after taking a bowel preparation for endoscopies and fasting. Low Insulin and C-peptide suggested a non-islet cell etiology. Surreptitious insulin use was excluded with regular monitoring. Implicating medications were stopped and adrenal insufficiency was ruled out with cortisol stimulation test. Patient was treated with dextrose infusion, Prednisolone, Octreotide and Frequent High Complex Carbohydrates (Carbs) but nocturnal IH persisted. Insulin-like growth factor 2 (IGF-2) level was low indicating a non-IGF2 mediated process. Surgical and cyto-reductive therapies were unable to be done due to the tumor size and PV infiltration. Patient deteriorated on supportive comfort care, was unable to be discharged and died in the hospital. Discussion: IH occurs in about 4-27% of HCC patients during its late stages. Two types have been described. Type A has high tumor utilization of glucose in a malnourished patient with depleted glycogen stores and defective gluconeogenesis. This type is seen during the late stages of HCC when tumor growth is increased and mortality can occur within 2 weeks. In type B, there is increased secretion of IGF-2, not metabolized due to defective hepatocytes in cirrhosis. Our patient’s IGF-2 level was low making it more likely due to type A. Steroids are a commonly used therapy. Prednisolone is believed to decrease pre IGF2 levels and stimulate gluconeogenesis though this would be difficult in cirrhosis. Octreotide and Carbs are often used but failed in our patient. Surgical reduction, systemic chemotherapy and ethanol injection to reduce the tumor size are the most effective treatments. Surgery and trans-arterial therapies could not be performed due to the large tumor size and PV infiltration. Dextrose infusion is often used but is believed to induce endogenous Islet cell insulin production, which further worsens the condition. Most patients deteriorate and die soon after. Conclusion: IH as a paraneoplastic complication of HCC usually occurs during the terminal stages of the disease and signifies increased mortality despite several treatment modalities.

771 Hepatocellular Carcinoma Presenting With Spinal Cord Compression Vincent Petros, DO1, Matthew Maslonka, MD2, Leah Low2, Habeeb Salameh, MD, CMQ3. 1. University of Texas Medical Branch, Texas City, TX; 2. University of Texas Medical Branch, Galvetson, TX; 3. University of Texas Medical Branch, Galveston, TX.

[769B] Figure 2.


We present a 55-year-old female with chronic HCV cirrhosis and morbid obesity who had presented with complaints of new bilateral lower extremity weakness and was admitted with flaccid paralysis and paraplegia. Over the prior month she had an additional 4 ER visits and 2 clinic visits all for non specific abdominal, chest, and back pain without conclusive diagnosis despite extensive investigations. MRIs of the thoracic and lumbar spine revealed intradural mildly enhancing mass surrounding the thoracic spinal cord suspicious for malignancy or infection. Core biopsies of the thoracic mass were positive for


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dropout consistent with DILI without any massive hepatocellular necrosis, interface hepatitis, macrovesicular steatosis, lymphoid aggregate, features of cholangitis or fibrosis. He was counseled to avoid supplements. Cholestyramine and ursodiol were initiated, with prednisolone 40 mg daily added 1 month later, as he continued to show cholestatic injury with rising bilirubin. With a 4 week taper of prednisolone, LFTs improved (AST 44 U/L, ALT 27 U/L, total bilirubin 38 mg/dL, and alkaline phosphatase 178 U/L). DILI is the leading cause of drug withdrawal from the United States market. The severity of liver injury due to androgenic or anabolic steroids ranges from minor transient serum enzyme elevations to profound prolonged cholestasis. Early recognition allows for prompt discontinuation of the inciting agent and treatment allowing for a successful recovery. Merely decreasing the dose of the offending agent or switching to another formulation is not appropriate and should be discouraged. Healthcare providers should be aware of the potential for liver injury due to supplements.

773 No Medication Is Benign: Fulminant Hepatic Failure and Autoimmune Hemolytic Anemia After Trimethoprim / Sulfamethoxazole Use Jessica McKee, DO1, Sara West, DO2, Robert Smith, MD2, Nina Ahuja, MD2, Michael Komar, MD, FACG3, Nihar Shah, MD2. 1. Geisinger Medical Center, Selinsgrove, PA; 2. Geisinger Medical Center, Danville, PA; 3. Geisinger Health System, Danville, PA.

[771A] Figure 1.

metastatic clear cell hepatocellular carcinoma. AFP was elevated at 101 compared to 59 from one-month prior. She received palliative radiation therapy for pain control, and was discharged to home hospice. Discussion: Extra-hepatic spread of HCC occurs commonly to the lungs (37%-70%) and regional lymph nodes (23%-45%). Spine metastasis is an occurrence in approximately 5% of HCC cases. SCC is a rare event in the natural course of metastatic HCC. HCC spine metastasis presumably happens due to the hematological spread of neoplastic cells thru the portal and vertebral vein plexuses due to portal hypertension. Approximately one quarter of these patients have symptoms secondary to metastasis, corresponding to location of lesion, including pain, neuropathy, paralysis, and pathologic fracture from bone involvement. Our patient did have back pain, with the addition of atypical chest and epigastric pain, which confounded reaching a correct diagnosis until a spine MRI was performed. The patient had CT abdomen/pelvis with contrast before this presentation but it missed the primary and metastatic lesions, which is not uncommon, as sensitivity is only slightly above 70%, missing 20 of 71 bony lesions in one study. AFP typically correlates well with HCC tumor stage and progression and is one of the most sensitive markers for early HCC, but did not in our patient, with levels mildly elevated at 59 one month prior to diagnosis. However, AFP levels may be normal in over 10% of patients with HCC. This case illustrates a rare clinical manifestation of newly diagnosed extrahepatic HCC, that even with the aid of in-depth radiological and biochemical testing, had gone undiagnosed by numerous healthcare professionals because of its atypical presentation of non specific chest, abdominal, and back pain, combined with surprisingly low AFP levels although metastatic.

772 Drug-Induced Liver Injury With Warzone: A War Against Drug Supplements? Jessica McKee, DO1, Sara West, DO2, Nina Ahuja, MD2, Nishal Ravindran, MD3, Harshit S. Khara, MD2, Michael Komar, MD, FACG4, Nihar Shah, MD2. 1. Geisinger Medical Center, Selinsgrove, PA; 2. Geisinger Medical Center, Danville, PA; 3. Geisinger Medical Center, Danville , PA; 4. Geisinger Health System, Danville, PA. Drug induced liver injury (DILI) is an important cause of hepatic injury and is a growing challenge given the increasing number of drugs. We describe a rare case of severe liver injury after the use of Warzone and Protex. A 29-year-old man with a history of depression and GERD presented with 2 weeks of progressive jaundice, pruritus and nausea after 3 weeks of initiating a body building supplement - Warzone (Trenavar, DMZ, Carbopol, Methystem, and Halodrol). Upon becoming jaundiced, Protex (milk thistle, n-acetyl cysteine, alpha lipoic acid and selenium) was self-initiated to support hepatic function. No family history of liver disease, recent travel or sick contacts. No alcohol use, illicit drug use, body piercing or tattoos. On exam, he was afebrile, hemodynamically stable, well appearing but icteric. No hepatosplenomegaly, encephalopathy or asterixis noted. Laboratory studies showed AST 183 U/L, ALT 524 U/L, total bilirubin 8.8 mg/dL (peaking at 52 mg/dL 4 weeks later), alkaline phosphatase 73 U/L and INR of 0.94. Hemogram, renal function, tests for autoimmune hepatitis, viral hepatitis, Wilson’s disease, alpha 1 antitrypsin deficiency and hemochromatosis were unremarkable. Abdominal US and CT showed unremarkable liver and bile ducts, without stones or sludge. Liver biopsy showed marked cholestasis, moderate chronic inflammation with hepatocellular


Drug induced liver injury (DILI) is an important cause of hepatic injury and ranges in severity. We describe a case of fulminant hepatic failure and autoimmune hemolytic anemia after Trimethoprim/ Sulfamethoxazole (TMP/SMX) resulting in death. A 69-year-old male with hypertension, hypothyroidism, and hyperlipidemia presented with prostatitis and was prescribed TMP/SMX. On day 2 he began to feel fatigued, dyspneic with abdominal pain preceding jaundice. He discontinued TMP/SMX after 5 days and represented. Chronic medications included HCTZ, synthroid, simvastatin. He consumed 1 alcoholic beverage daily. No family history of liver disease. Vitals were stable. WBC 24 K/uL, hemoglobin of 3.6 g/dL, platelets 267 K/uL, differential with spherocytes and 12 bands. Reticulocytes and lactate dehydrogenase elevated, haptoglobin under 20 mg/dL, AST 408 U/L(peaking at 1615 U/L), ALT 297 U/L(peaking at 651 U/L), total bilirubin 12.2 mg/ dL(peaking at 73 mg/dL), direct 4.9 mg/dL, alkaline phosphatase 324 U/L. Antibody identification positive for IgG and weakly positive C3 confirmed warm autoimmune hemolytic anemia. Ultrasound showed hepatic steatosis and CBD 3.8 mm. Corticosteroids, rituximab, IVIG and plasmapheresis improved his anemia. Transaminases also improved, however a direct hyperbilirubinemia persisted. Autoimmune and viral hepatitis, wilson’s disease, alpha 1 antitrypsin deficiency and hemochromatosis were negative. Liver biopsy showed pericholangitis, cholestasis, minute foci of hepatocellular necrosis, mild iron deposition in kupffer cells and hepatocytes, periportal fibrosis with focal perivenular and perisinusoidal fibrosis consistent with DILI confounded by systemic injury. He declined developing enterobacter bacteremia, was transitioned to comfort measures and expired. TMP/SMX induced liver injury varies in severity from mild elevations, to symptomatic hepatitis, to prolonged cholestasis, and acute liver failure. Most cases resolve rapidly with drug discontinuation, fully recovering by 8 weeks. Severe cholestatic injury may be prolonged and rare cases of chronic liver injury have been reported. Mechanism of injury may be a drug-allergy or hypersensitivity, perhaps through metabolism to a toxic, reactive or antigenic metabolite. Sulfonamides have also been implicated to elicit immune reactions resulting in acquired autoimmune hemolytic anemia. Early recognition of DILI allows prompt drug discontinuation and full recovery in the majority of cases.

774 The Proof Is in the Rash Donald Tsynman, MD1, Li Zhang, R-PAC2, Poline Yiu, R-PAC2, Anthony J. Ng, MD1. 1. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 2. Ng Medical, New York, NY. Case Report: A 36 year old Chinese-American male with a history of unilateral uveitis and a BMI of 36 was referred to our outpatient practice in downtown Manhattan. One month prior, the patient was diagnosed with “eczema” by a dermatologist. The patient had a long-standing history of abnormal LFTs (manifested as an elevated ALT with upward limit of 150). During annual examination, ALT remained elevated. An US was completed with findings concerning for cirrhosis. Subsequently a CT confirmed cirrhotic morphology of the liver, fatty infiltration, numerous too-small-to-characterize hypodensities of the liver and spleen, intrahepatic biliary ductal dilation, and paraaortic lymphadenopathy with associated bilateral hilar lymphadenopathy. He had no symptoms of chronic liver disease. Serologies were negative for any viral or chronic etiology of liver disease, PPD was negative, and aside from obesity, the patient did not have any risk factors. Subsequent liver biopsy noted steatosis as well as noncaseating, sclerotic granulomas. Discussion: Sarcoidosis is a systemic granulomatous disease first described in 1877 by the English doctor Jonathan Hurtchinson as a skin disease causing red, raised lesions. Incidence is highest in individuals younger than 40 and peaks in patients from 20 to 29. Sarcoidosis occurs worldwide with an average incidence of 16.5/100,000 in men and 19/100,000 in women. It is most common in Northern Europe. The disease is rare in the Chinese population. In the US, sarcoidosis is more common in people of African descent than in Caucasians, with annual incidence reported as 35.5 and 10.9 per 100,000. Hepatic involvement was described in 11.5% of 736 patients enrolled in the ACCESS study. Lab abnormalities include hypergammaglobulinemia and increases in serum alk phos activity. Liver sarcoid is characterized by epithelioid, noncaseating granulomas generally scattered widely. In rare instances, liver sarcoidosis is complicated by portal hypertension or chronic cholestasis. A minority of patients progress to chronic cholestatic disease, portal hypertension, and cirrhosis that may require liver transplantation. Treatment should be reserved for patients who manifest this spectrum of disease. Glucocorticoids are first-line therapy for hepatic sarcoidosis, improving symptoms and abnormal laboratory values but generally having no effect on progression of disease. Additionally, azathioprine, methotrexate, hydroxychloroquine, and infliximab have been used with some positive effects on symptoms, LFTs, and hepatomegaly. However, none have shown to prevent progression of disease. Ultimately, in cases of overt liver failure, liver transplant is the definitive treatment. Overall, treatment for hepatic sarcoidosis is targeted toward alleviation of symptoms but has no curative potential at this time.


| OCTOBER 2015

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Abstracts 775 Y90 Treatment in Pregnant Woman With Fibrolamellar Hepatocellular Carcinoma Pedro A. Manibusan, Jr., DO, MBA1, Emuejevoke Okoh, MD2, Raul Palacios, MD1. 1. Brooke Army Medical Center, Ft. Sam Houston, TX; 2. SAUSHEC Department of Gastroenterology, San Antonio, TX. Introduction: Fibrolamellar hepatocellular carcinoma (FLHCC) is a rare primary malignancy of the liver. There are only case reports of FLHCC occurring in pregnancy. This case report describes management of FLHCC patient to include treatment of FLHCC during pregnancy with yttrium-90 microspheres (Y90). Case Report: 23y/o female at 17 weeks gestation presented for evaluation of upper abdominal pain, elevated liver associated enzymes, and thrombocytopenia found to have multiple intrahepatic lesions and enlarged spleen on ultrasound of the abdomen. Non-contrast MRI revealed multiple hepatic lesions with largest measuring 8.3x10.9cm in the left hepatic lobe with extension into portal vein. EGD revealed grade II esophageal varices and portal hypertensive gastropathy. FNA of hepatic lesions was performed during EUS revealed fibrolamellar hepatocellular carcinoma. Perigastric, splenic, esophageal and pancreatic varices was noted during EUS and patient was placed on beta blocker therapy. Serum AFP was 30. Multidisciplinary tumor meeting held and decision for interventional radiology (IR) consultation for treatment of FLHCC with Y90. Surgery determined patient not a surgical candidate given involvement of hepatic vasculature. Patient received two doses of Y90 to both hepatic lobes during her pregnancy and tolerated without significant issues. Subsequent imaging did not reveal significant change to tumor burden and plan was for possible repeat Y90 nine months after last dose. Management of baby was performed by OB services and was taken to emergent cesarean at 32 weeks gestation of healthy child. Post-delivery patient discussion regarding Sorafenib for treatment of FLHCC however patient declined in order to breast feed which she was did for 3 weeks. Patient agreed to trial with Sorafenib however stopped due to side effects

[775C] Figure 3.

after only doses. Decision was made for patient to move closer to family and her husband was relocated to duty station near family. Discussion: Care of this young patient involved difficult decisions much of which has no formal guidelines. Portal hypertension secondary to large hepatic tumor burden was managed expectantly; however treatment of her FLHCC in the setting of pregnancy with Y90 was a novel approach. Throughout, patient ultimately made decisions to ensure the safety and well-being of her child over her own survivability. Conclusion: FLHCC in pregnancy have no formal guidelines for treatment. Treatment of FLHCC with Y90 during pregnancy can led to viable child delivery and prolonged maternal survival. However, limited data in this setting exist.

776 Hitting Two Liver Diagnoses With One Needle Justin Rheem1, Kathy Pan, MD1, Paulette Balasan, NP1, James Yeh, MD1, Daniel Eshtiaghpour2. 1. HarborUCLA Medical Center, Torrance, CA; 2. UCLA, Marina del Rey, CA.

[775A] Figure 1.

Introduction: In hepatic amyloidosis, excess deposition of misfolded proteins into liver tissues may lead to liver dysfunction, portal hypertension, liver failure, and even death. Hepatic amyloidosis is most commonly attributed to systemic light chain amyloidosis; however, other subtypes of amyloid are increasingly recognized. We present a case of rare and novel amyloid subtype, previously described mostly in cases in renal amyloidosis. Case Description: A 54-year-old Hispanic woman with history of diabetes mellitus and chronic kidney disease stage 4 presented with two months of abdominal pain. The pain was not associated with any fever, chills, night sweats, weight loss, or hematemesis. On exam, she was afebrile and noted to have RUQ tenderness without Murphy’s sign, jaundice or ascites. White blood cell count and hemoglobin level were 14,600/mm3 and 11.3 g/dL, respectively. Liver panel was unremarkable except elevated alkaline phosphatase level of 137 U/L. Abdominal ultrasound showed a smooth-surfaced liver with a 6.7 x 5.4 x 5.3 cm irregularly shaped heterogeneous lesion within the right hepatic lobe, and a 0.9cm hyperechoic lesion in the anterior left hepatic lobe. Further imaging studies, including CT and MRI, confirmed the ultrasound findings. Technetium-Labeled Red Blood Cell Bleeding scan showed liver lesions with characteristics not definitive for hemangioma. Patient underwent an ultrasound-guided liver biopsy, which showed a globular amyloidosis and a capillary hemagioma. Further pathology staining showed negative kappa and lambda stains; the results of patient’s serum protein electrophoresis, serum light chain assays, and quantitative immunoglobulins were not compatible with AL amyloidosis. On mass spectrometry (MS), the liver specimen was shown to have an Alect-2 (Leukocyte Chemotactic factor-associated Amyloidosis) amyloid. Discussion: ALect-2 amyloidosis is a rare type of systemic amyloidosis that primarily involves the kidneys, spleen, and liver. Although there are limited numbers of cases reported in the literature, most patients appear to be of Hispanic ethnicity, and show a globular pattern of amyloid deposition on biopsy. Subtyping hepatic amyloid deposits by an accurate analytic method such as MS is required for optimal diagnosis of hepatic amyloidosis patients and avoiding incorrect and unnecessarily toxic therapies. To date, no specific therapy for ALect-2 has been reported.

777 Dyspnea and Dysuria: Compressive Symptoms of a Massive Hepatic Abscess Nizar H. Senussi, MD, Olalekan Akanbi, MD, Binod Khatiwada , MD. Presence Saint Joseph Hospital, Chicago, IL

[775B] Figure 2.


Pyogenic hepatic abscesses usually present with predominantly gastrointestinal symptom which include nausea, vomiting, abdominal pain and abdominal distention. Although rare, massive abscesses can cause


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Entamoeba Histolytica antibodies were negative. He improved clinically with antibiotics as pig tail drainage progressively reduced. He was discharged home in stable condition, after a 10 day hospital stay, on a 1 week course of oral cephalexin & metronidazole. Repeat CT scan of the abdomen showed complete resolution and drainage of the abscess

778 Autoimmune Hepatitis With Primary Sclerosing Cholangitis and Co-Existent Necrotizing Myopathy: A Rare Association Anusha Shirwaikar Thomas, MD1, Viviane Bunin, MD, PhD2, Suzanne Powell, MD2. 1. Houston Methodist Hospital, Pearland, TX; 2. Houston Methodist Hospital, Houston, TX.

[777b] Figure 2.

more global symptoms by directly compressing nearby anatomy. Direct compression of the diaphragm and secondary pleural effusions can cause symptoms of dyspnea with respiratary compromise. Direct mass compression of the urinary bladder can present with urinary symptoms like dysuria and retention. The diagnosis is easily confirmed by radiographic imaging like ultrasound or computed tomography. Treatment involves aspiration and percutaneous catheter drainage with Initiation of empiric antibiotics pending culture and susceptibility result. In this case report, we would like to illustrate the potential compressive symptoms that can exhibit secondary to a massive hepatic abscess. A 55 year old male presented with a 3 month history of progressive abdominal swelling and pain with new onset dyspnea and dysuria. Initial vitals showed tachycardia and tachypnea. Physical exam revealed an acutely ill appearing man in respiratory distress with scleral icterus. His abdomen was markedly distended with RUQ/suprapubic tenderness. Rt lower extremity pitting edema was noted. Chest auscultation revealed decreased air entry with coarse crackles at the Rt base. Labs were remarkable for an AST 100, ALT 70, ALP 311, T. Bil. 3.1, Lactate 2.1. CXR showed a Rt sided pleural effusion with Rt diaphragmatic elevation. CT scan abdomen showed a massive cystic structure associated with the liver extending against a distended bladder causing considerable mass effect upon the organs & bowel. He was admitted to ICU for management of severe sepsis with a probable hepatic focus. IR guided drainage of the hepatic collection produced 5L of green pus and a percutaneous drain was retained and left to suction IV antibiotics, Flagyl & Ceftriaxone, were initiated per sensitivity results after drain cultures grew E coli. Pancultures were unremarkable. CEA, AFP, CA 19-9, Echinococcus &


A forty six year old black woman with a fifteen year history of autoimmune (AI) hepatitis with primary sclerosing cholangitis (PSC) intermittently treated with Azathioprine and steroids (in remission till approximately ten months ago) presents with worsening abdominal distention for three days. Pertinent findings on examination include a cachectic woman with supraclavicular hollowing, facial wasting, intense scleral icterus, severe conjunctival injection, scratch marks on legs, healed acne scars on back, thick plaque like discoloration of skin overlying bilateral metacarpophalangeal joints, ejection systolic murmur at sternal border, diffusely tender distended abdomen with fluid thrill and umbilical hernia, decreased proximal muscle strength in bilateral upper extremities with limited passive and active range of motion of both shoulders and pitting pedal edema bilaterally extending to the knees. Pertinent laboratory values were as follows: Sodium 126, potassium 5.2, albumin 1.6, lactate 2.4, alkaline phosphatase 148, alanine transferase 332, aspartate transferase 883, direct bilirubin(BR) 9.2, total BR 12.4, INR 2.5, creatinine phosphokinase 15415, ANA titre 1:320, anti-smooth antibody 1:320, CA 19-9 56, CA-125 417, total Immunoglobulin G(IgG) 1844 with subclass IgG4 43. Abdominal imaging studies and colonoscopy were consistent with liver cirrhosis, ascites and negative for malignancy respectively. A muscle biopsy revealed necrotizing myopathy, extensive myofibre regeneration and increased lipid droplets on Oil Red O stain. The patient was treated with high dose steroids for a flare of underlying AI hepatitis and AI myositis with moderate improvement in muscle strength. While awaiting a liver transplant, she unfortunately passed away after a cardiac arrest. Necrotizing myopathy (NM) may be immune mediated (IM) and nonimmune mediated (NIM). IMNM is associated with anti-signal recognition particle antibodies, vasculitis, cancer, statin exposure and infections (HIV, Hepatitis C). NIMNM is linked to toxin exposure. Clinically, patients have proximal muscle weakness with varied severity. Pathologically, this myopathy demonstrates necrosis of muscle fibers in the absence of lymphocytic inflammatory infiltrates. Although there are no controlled trials to guide therapy, treatment of IMNM is immunosuppression while that of NIMNM is removal of toxin exposure. To our knowledge, this is the first reported case of co-existent AI hepatitis with PSC and necrotizing myopathy.

779 Ruptured Hepatic Adenoma Associated With an Ectopic Pregnancy Anjana Sathyamurthy, MD, Ghassan Hammoud, MD, MPH. University of Missouri, Columbia, MO Introduction: Hepatic adenomas are benign epithelial liver tumors that uncommonly occur in otherwise normal liver. They occur more commonly in childbearing women and are mostly associated with contraceptive use. We present a case of rupture hepatic adenoma associated with an ectopic pregnancy.


| OCTOBER 2015

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Abstracts 780 Cryoglobulinemia: A Potential Mimicker of Autoimmune Hepatitis Ozdemir Kanar, MD1, Andrew C. Berry, DO2, Rahman Nakshabendi, MD1, Robert Krieger, BS3, Wally Plante, MD4, Jeffrey Winder, DO5. 1. University of Florida Health College of Medicine, Jacksonville, FL; 2. Department of Medicine, University of South Alabama, Muskego, WI; 3. Kansas City University of Medicine and Biosciences, Kansas City, MO; 4. University of Florida College of Medicine, Jacksonville, FL; 5. Department of Medicine, University of Florida College of Medicine, Jacksonville, FL. A 50-year-old male with a history of vertebral osteomyelitis, alcohol abuse, and hepatitis C antibody presented with bilateral lower extremity non-blanching rash and foot pain. Initial labs consistent with acute liver injury, transaminitis >15x upper limit of normal (AST 1117, ALT 1080), alkaline phosphatase 170 and hyperbilirubinemia (total bilirubin 2.3, direct 1.4). Hepatitis panel was positive for hepatitis C antibody, but HCV RNA was undetectable. Pertinent positives included elevated ESR (121), CRP (12.2), LDH (302), decreased C3 (83.1) and C4 (4.2) complement proteins, elevated IgG (3531) and IgM (315), positive ANA 1:1280 (homogenous pattern) and positive anti-smooth muscle antibody. Initial impression was cryoglobulinemia secondary to positive hepatitis C antibody given the vasculitic rash, however, cryoglobulins were negative. Abdominal ultrasound was remarkable for adenomyomatosis of gallbladder and echogenic changes in the liver suggestive of hepatocellular disease and cirrhosis. Biopsy was taken of the vasculitic rash, showing nonspecific dermal inflammation (Figure 1). Liver biopsy confirmed autoimmune hepatitis (Figure 2, Figure 3). Over the course of his stay, liver injury improved, and enzymes continually trended down. Vasculitic rash and foot pain had completely resolved by day 3-4 of admission. Given the extent of liver injury, the patient was instructed to stop taking any NSAIDs, including his celebrex. Prednisone/azathioprine was recommended, but the patient refused prednisone given prior side effects while taking it, so the patient was discharged on a tapering dose of budesonide and told to follow-up in 2 weeks.

[779A] Figure 1.

[779B] Figure 2.

[780A] Figure 1.

Report of a case: A 34-year-old Caucasian female with no significant past medical history presented initially to the hospital with right lower quadrant (RLQ) pain. Her initial evaluation with pelvic ultrasound revealed evidence of ruptured right ectopic pregnancy for which she underwent laparoscopic total salpingectomy. Post discharge she continued to have severe RLQ pain however radiating to right shoulder. Laboratory data revealed mildly elevated liver transaminases (AST 81 U/L, ALT 69 U/L, ALP 63 U/L) with normal platelets ( 209x 10 (9)/L) and normal serum glucose (110 mg/dL). She had no evidence of preeclampsia and her vital signs were stable. A Computed Tomography (CT) of the abdomen and pelvis was obtained for further evaluation which revealed a large hepatic hematoma in the right lobe of the liver secondary to ruptured hepatic adenoma (Figure 1). She was managed conservatively and discharged thereafter with no need for percutaneous drainage. Follow-up Magnetic Resonance Imaging (MRI) of the abdomen revealed evidence of small other hepatic adenomas in the right and left lobes of the liver along with decrease in the size of previously diagnosed subcapsular hematoma (Figure 2). She was followed up in the clinic where the discussion of future pregnancy was done. She was informed that monitoring of the size of hepatic adenomas during future pregnancy may be warranted. Discussion:Several cases of ruptured hepatic adenoma during gestation have been described in literature. The association may be related to the increase in endogenous levels of steroid hormones. Prognosis may vary from a benign course to maternal and/or fetal mortality. Mortality may be related to delay in diagnosis due to low suspicion or confusing clinical picture. Conclusion: Ruptured hepatic adenoma in the setting of ectopic pregnancy is a rare association. Healthcare providers may need to be aware of this rare coincidental entity and include it in the differential diagnosis of abdominal pain in child-bearing women.

[780B] Figure 2.



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782 Splenic Artery Steal Syndrome Post Liver Transplant Causing Ischemic Biliary Stricture Nina Ahuja, MD1, Nihar Shah1, Mustafa Huseini2, Hamdani Syed1, Jessica McKee, DO3, Waseem Butt, MD1, Chuan L. Miao, MD, MPH1, Marie Le1, Anil Kotru1, Harshit S. Khara, MD1, Amitpal Johal1, Aalpen Patel1, Chintalapati Varma1, Michael Komar, MD, FACG4, Robert Smith, MD1. 1. Geisinger Medical Center, Danville, PA; 2. Geisinger Medical Center, Danville , PA; 3. Geisinger Medical Center, Selinsgrove, PA; 4. Geisinger Health System, Danville, PA.

[780C] Figure 3.

Cryoglobulinemia (type II and III) is usually associated with infection by hepatitis C virus. Symptoms such as arthralgias and myalgias are common in type II and III. Skin manifestations, particularly the lower extremities, include erythematous macules and purpuric papules (90-95% occurrence), as well as ulcerations (10-25% occurrence). This case presentation is unique due to its atypical presentation of a bilateral painful non-blanching rash on the lower extremities. Prior labs showed hepatitis C antibody positivity and abnormal C3 and C4, suggesting cryoglobinemia. However, skin biopsy was negative for this. It was later found that the patient was positive for autoimmune antibodies and presented with a case of autoimmune hepatitis confirmed by liver biopsy.

Introduction: Splenic artery steal syndrome post liver transplant is rare. If present, there can be significant graft dysfunction and potential graft loss. We present a case of a patient with decompensated cirrhosis secondary to Wilson’s disease who underwent orthotopic liver transplant complicated by splenic artery steal syndrome. Case: A 47 yo male was diagnosed with Wilson’s disease as a teenager. Thirty years later, he presented with ascites, upper GI bleed, MELD of 40, and transferred to our Transplant Center. He underwent orthotopic liver transplant from a 49 yo healthy O +, Hbcab Igm + donor. Cold ischemic time was 8 hours and 50 minutes and warm ischemic time was 55 minutes. He was given HbIg intraoperatively, started on empiric Entecavir, and given additional HbIg during the first week post-transplant. Liver function tests (LFT’s) were noted to be elevated with an ALT 365, AST 576, Total Bilirubin (TB) 21, and INR 2.46 on POD#3. Abdominal doppler showed diminished hepatic arterial flow with a resistive index (RI) of 1.0. Coil embolization of the gastroduodenal artery was done on POD#3 to help improve hepatic perfusion. Post embolization, he was noted to have continued bilirubin elevation (TB 18-20) through POD#6. Repeat abdominal ultrasound showed decreased diastolic flow in the main hepatic artery (RI of 0.79). Diagnostic ERCP showed an anastomotic biliary stricture treated with biliary stenting. His bilirubin trended downward from 18 to 14. Hepatic artery angiogram then showed a large diameter splenic artery with diversion of blood away from the liver. Splenic artery coil embolization was done on POD#9. His LFT’s continued to trend downward thereafter: ALT 132, AST 80, TB 6, INR 1.02. Repeat ERCP at 6 weeks showed an improved anastomotic stricture. Abdominal ultrasound 7 weeks post initial transplant showed adequate hepatic arterial flow (RI of 0.59) with normalization of LFT’s. Discussion: Within the first week post-transplant, survival of the liver graft is dependent on adequate arterial oxygen supply. This patient showed signs of splenic arterial steal syndrome, manifested by his elevated liver enzymes. Arterial hypoperfusion of the graft as a result of shift in blood flow into the splenic or gastroduodenal arteries causes hepatic hypoperfusion and potential allograft dysfunction. Timely diagnosis and management with ERCP and IR embolization helped prevent postoperative morbidity and graft loss.

783 Dyspnea in a Cirrhotic: Don’t Forget About Hepatopulmonary Syndrome

781 Azithromycin-Induced Liver Injury Ranya Selim, MD1, Monica Saumoy, MD2, Ira M. Jacobsen3, David W. Wan, MD2. 1. Department of Internal Medicine, Henry Ford Health Systems, Detroit, MI; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 3. Mount Sinai Beth Israel, New York , NY. A 19 year-old woman presented with jaundice for 1 week. 1 month prior to presentation, she complained of a persistent cough that lasted for several weeks. 1 week prior to developing jaundice, she was prescribed a 5-day course of azithromycin. 3 days after completing it, she noticed yellowing of her eyes and skin, clay colored stools and dark urine. She initially presented to an outside hospital; on admission her vitals were stable, and on exam she had jaundice with a normal mental status. Her initial labs revealed an AST 912, ALT 795, total bilirubin 11.9, ALP 616, albumin 3.7, WBCs 9.5 and lipase 95. She was negative for ANA and anti-mitochondrial antibodies. Hepatitis, CMV, EBV, and HIV serologies were all negative. Abdominal sonogram and CT showed gallbladder thickening with no stones, borderline dilation of the CBD, and splenomegaly. CT also revealed fatty infi ltration of the liver. A HIDA scan showed hepatocellular dysfunction, no biliary ductal dilatation, and poor visualization of the gallbladder. She was started on a prednisone taper for her cough, which was associated with a decrease in her LFTs, but rose again after discontinuation of steroids. The patient was transferred to New York Presbyterian Hospital for further management, and underwent an MRCP, which showed hepatomegaly with periportal edema, normal intrahepatic and extrahepatic biliary ducts, patent hepatic and portal vessels, and no masses. Liver biopsy showed many ballooned hepatocytes and apoptotic cells within lobules, as well as inflammatory cell infiltrates composed of lymphocytes, histiocytes, neutrophils, eosinophils and few plasma cells. Some interlobular bile ducts showed lymphocytic ductitis. There was no portal fibrosis, or iron or copper deposits. This inflammatory pattern was suspected to be due to azithromycin-toxicity. The patient was restarted on steroids, and her LFTs downtrended until discharge. Azithromycin has been reported to cause DILI. Patients typically present within 1 to 3 weeks after initiation of the antibiotic. The damage is primarily hepatocellular, and can be accompanied by cutaneous reactions, chronic liver injury, and other serious complications potentially leading to death or requiring transplantation. Management of DILI involves halting the offending agent. There is minimal evidence to support the use of steroids, but appeared to help in this case. Further studies are required to determine other preventative or therapeutic measures for DILI. Reference: Martinez MA, Vuppalanchi R, Fontana RJ, Stolz A, Kleiner DE, Hayashi PH, Gu J, Hoofnagle JH, Chalasani N. Clinical and histologic features of azithromycin-induced liver injury. Clin Gastroenterol Hepatol. 2015 Feb;13(2):369-376.e3. doi: 10.1016/j.cgh.2014.07.054. Epub 2014 Aug 9.

Jason D. Jones, MD1, Lee Sigmon, MD2, Joel Bruggen, MD2. 1. Wake Forest School of Medicine, Department of Internal Medicine, Winston-Salem, NC; 2. Wake Forest School of Medicine, Department of Gastroenterology, Winston-Salem, NC. Case Report: A 44 year old Caucasian female with a history of alcohol induced cirrhosis, esophageal varices, hepatic encephalopathy, and COPD presented to the emergency department with a chief complaint of nausea, emesis, and flank pain. The patient was admitted with pyelonephritis, however, she endorsed concomitant shortness of breath, dyspnea on exertion, and platypnea. On physical examination, the patient was found to have fixed splitting of the second heart sound and significant clubbing present on all four extremities. A transthoracic echocardiogram with bubble study was performed which demonstrated a pulmonary shunt and arterial blood gas analysis showed a calculated alveolar-arterial gradient of 22. The aforementioned historical, physical examination, and laboratory findings including portal hypertension, pulmonary shunt, and elevated A-a gradient culminated in a diagnosis of hepatopulmonary syndrome. Discussion: Chronic liver disease has been shown to lead to the development of several pathologic processes throughout the body. Hepatopulmonary syndrome represents the most common pulmonary complication, with a prevalence of 5-30% in cirrhotics.In HPS, pulmonary pre-capillary and capillary dilatation leads to arterial hypoxemia via a ventilation-perfusion mismatch, impaired diffusion, and shunting. This typically manifests as dyspnea, platypnea, orthodeoxia, and clubbing.Platypnea and orthodeoxia are defined as an increase in dyspnea(platypnea) or a decrease in the arterial partial pressure of oxygen(orthodeoxia) with positional change from supine to upright. These physical exam findings should be recognized by the astute bedside physician and are manifestations of the ventilation-perfusion mismatch seen in HPS. The presence of platypnea and/or orthodeoxia should prompt further evaluation of any cirrhotic patient reporting dyspnea. Diagnosis is made by observation of the following: Liver disease, Alveolar-arterial gradient ≥15 mmHg or ≥20 mmHg in patients > 64 years of age, and the presence of intrapulmonary shunting.It is important to note that portal hypertension is not a prerequisite for the diagnosis of HPS.Intrapulmonary shunting is demonstrated with the use of either contrast-enhanced echocardiography demonstrating the rapid appearance of microbubbles in the left atrium after intravenous injection or macroaggregated albumin radioactive lung perfusion scan showing the presence of radiolabeled particles in the brain, spleen, or kidneys.Definitive treatment for HPS is liver transplantation and patients with HPS are given MELD exception points. Oxygen is typically utilized for symptomatic relief but HPS is associated with an increased mortality when compared to unaffected patients with liver disease.

784 Rapid Resolution of Cholangitic Abscess in a Liver Transplant Recipient With Hepatic Artery Stenting: A Case Report Dhruvan Patel, MD1, Sushrut Trakroo, MD2, Antonio Di Carlo, MD2, Kamran Qureshi, MD3. 1. Mercy Catholic Medical Center, Philadelphia, PA; 2. Temple University Hospital, Philadelphia, PA; 3. Temple University School of Medicine, Philadelphia, PA. Introduction: Incidence of hepatic artery stenosis (HAS) post liver transplant (LT) is 4 to 10%. Hepatic artery (HA) circulation consitutes the only blood supply to biliary system of transplant liver. Presentation



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Abstracts

[784A] Figure 1.

of delayed HAS, thus underperfusion, is less clear and may range from asymptomatic to biliary localized infection and sepsis. Studies have shown decreased incidence of biliary necrosis with early intervention for HAS. We present a case of rapid resolution of cholangitic abscess with stenting for HAS post LT. Case report: A 60-year old male presented with 3 days of high-grade fever, tachycardia and hypotension. He underwent LT for cryptogenic cirrhosis 3 years back which was complicated by delayed onset anastomotic biliary stricture. He underwent ERCP stent exchange a week prior to current presentation. CT abdomen suggested liver abscess and Liver Doppler showed HAS. He was admitted to ICU for septic shock secondary to ascending cholangitis requiring broad-spectrum antibiotic, pressor support, reduction in immunosuppression and hemodialysis. Blood culture grew extended spectrum beta lactamase producing (ESBL) Klebsiella pneumoniae and antibiotic coverage was accordingly modified. Despite percutaneous abscess drainage that grew ESBL Klebsiella, he remained febrile and bacteremic. Repeat CT showed persistent liver abscess for which dual carbapenem coverage was instituted. Despite aggressive medical management for 3 weeks, he remained bacteremic. HAS was subsequently treated on day 21 with IR guided endovascular stent placement in a effort to revascularize the affected biliary ducts and improving access of antibiotics. He showed dramatic clinical improvement over the next 24 hours with sterile cultures and was discharged 3 days post stenting. Follow up CT showed resolved of liver abscess and ERCP done 3 months later, showed a remodeled stricture that did not require stenting. Discussion: The HA is paramount in preserving biliary integrity. Delayed presentation of HAS after LT is rare and can potentially lead to graft loss and mortality. Pathophysiology of delayed HAS include transplant-associated arteriosclerosis, vascular intimal thickening, medial attenuation, and vasoconstriction. Early recognition and treatment is vital in preventing hepatic artery thrombosis, biliary strictures, biliary necrosis, intrahepatic biloma, sepsis, everting graft loss and death. Our patient’s clinical condition deteriorated despite maximal medical management and percutaneous abscess drainage. Appopriate recognition and stenting of HAS led to dramatic clinical improvement with return to baseline graft function with healed stricture requiring no stenting on follow up ERCP.

785 Hepatic Fibrosis as a Consequence of Iron Overload in Pyruvate Kinase Deficiency Nayna Riyat, MD1, Jinping Lai, MD, PhD2, Bruce Bacon, MD3. 1. Saint Louis University School of Medicine, Department of Internal Medicine, Saint Louis, MO; 2. Saint Louis University School of Medicine, Department of Pathology, Saint Louis, MO; 3. Saint Louis University School of Medicine, Division of Gastroenterology and Hepatology, Saint Louis, MO. Pyruvate kinase deficiency, which results in a non-spherocytic hemolytic anemia, can be associated with secondary hepatic iron overload and fibrosis (1). We describe a patient with pyruvate kinase deficiency heterozygous for the H63D mutation in HFE who developed hepatic iron overload with advanced fibrosis. A 21-year-old female presented with abdominal pain, scleral icterus, and jaundice. She was diagnosed with pyruvate kinase deficiency at birth, received multiple blood transfusions, and had a splenectomy at age 5. Current laboratory studies revealed a hemoglobin of 6.8 g/dL, a ferritin of 5101 ng/mL, and a transferrin saturation of 100%. Liver enzymes, bilirubin, and LDH were also elevated (Table 1). Tests for


[785] Table 1. Hemoglobin, Ferritin, Transferrin Saturation, Liver Enzymes, Total Bilirubin, and LDH at Baseline and 24 Months Post-Deferoxamine Therapy Basline Prior to Deferoxamine Hemoglobin (g/dl) Ferritin (ng/ml)

24 Months Post-Deferoxamine Therapy

6.8

8.3

5101

1492

Transferrin Saturation (%)

100

89

Alkaline Phosphatase (units/l)

110

100

ALT (units/l)

183

31

AST (units/l)

151

23

Total Bilirubin (mg/dl)

12.2

3.0

LDH (units/l)

312

247

viral hepatitis, alpha 1 antitrypsin, ceruloplasmin, AMA, and ANA were negative. A CT of the abdomen showed a homogeneous liver. Liver biopsy revealed massive iron overload and bridging fibrosis (Figure 1). Chelation therapy with deferoxamine was initiated to reduce hepatic iron stores, hoping to prevent progression to cirrhosis. Chelation resulted in improvement in ferritin, liver enzymes, bilirubin, and LDH levels at 24 months (Table 1). Iron overload is commonly described in thalassemia, but less frequently in pyruvate kinase deficiency. Salem et al. described a patient with iron overload and cirrhosis in pyruvate kinase deficiency (2). Liver iron concentrations above a critical threshold of 350-400 mumoles/g can cause hepatocellular damage (3). Chelation has been shown to reduce iron overload in pyruvate kinase deficiency (4). Alternative therapies are important for non-responders to chelation who have not progressed to cirrhosis. One group reported successful bone marrow transplantation in a child with pyruvate kinase deficiency (5). Gene targeting and liver transplant may be options in secondary iron overload, and warrant further investigation. References: [1]. Zanella A,Fermo E,Bianchi P,Roberto Chiarelli L,Valentini G. Pyruvate kinase deficiency: the genotype-phenotype association. Blood Reviews. 2007,21:217-231. [2] .Salem HH,Van Der Weyden MB,Firkin BG. Iron overload in congenital erythrocyte pyruvate kinase deficiency. Med J Aust. 1980 May31;1(11):531-2. [3]. Bassett ML,Halliday JW,Powell LW. Value of hepatic iron measurements in early hemochromatosis and determination of the critical iron level associated with fibrosis. Hepatology. 1986,6:24-39. [4]. Hilgard P,Gerken G. Liver cirrhosis as a consequence of iron overload caused by hereditary nonspherocytic hemolytic anemia. World J Gastroenterol. 2005;11(8):1241-1244. [5]. Tanphaichitr VS, et al. Successful bone marrow transplantation in a child with red blood cell pyruvate kinase deficiency. Bone Marrow Transplant. 2000 Sep;26(6):689-90.


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[785A] Figure 1.

786 Novel ABCB11 Missense Mutation Associated With Benign Recurrent Intrahepatic Cholestasis 1

2

1

Jennifer Phan, MD , Guy A. Weiss, MD , Francisco Durazo, MD . 1. University of California Los Angeles, Los Angeles, CA; 2. UCLA, Los Angeles, CA. Background: Familial intrahepatic cholestasis is a group of genetically heterogenous disorders which includes benign recurrent intrahepatic cholestasis (BRIC). BRIC type 2 is a rare autosomal recessive disorder characterized by intermittent episodes of cholestasis leading to often severe symptoms of jaundice and pruritus.1 This inherited disease is associated with a mutation in ABCB11 gene on chromosome 2q24. We present a case of BRIC in a 32 year-old female with a novel missense mutation in the ABCB11 gene. Results: Our case involves a 32 year-old female who was referred to hepatology clinic with worsening diffuse pruritus and unintentional forty pound weight loss within four months. She initially developed jaundice and pruritus ten years ago, with total bilirubin that peaked to 26 mg/dl. She was closely followed with resolution of symptoms and normalization of total bilirubin to 0.5mg/dl over the next few years. Our patient has no family history of hepatic disorders. Laboratory results were normal except for elevated total bilirubin of 3.5mg/dl. Magnetic resonance imaging of the abdomen showed a normal sized liver without intrahepatic bile duct dilatation or enhancing masses. Hepatic biopsy revealed bile duct injury and marked cholestasis with mild focal pericentral fibrosis. Genetic testing showed a missense variant in allele 1 of the ABCB11 gene causing a substitution of tyrosine for cysteine at amino acid 129 (C129Y). Comment: This mutation is a previously unreported mutation, with mutation software predicting “deleterious” functional effect. In light of our patient’s negative family history, this may be a de-novo mutation causing BRIC 2. She was controlled with rifampin and genetic testing was encouraged for family members.

[787]

Table 1. Serum Ammonia Level (umol/l) During Hospitalization

Days of Hospitalization

Day 1

Day 2

Day 3

Day 4

Day 5

Day 6

Day 7

Day 8

Ammonia Level (umol/l)

72

66

89

116

85

31

30

22

787 Non-Hepatic Hyperammonemic Encephalopathy After Gastric Bypass Surgery Ahmed Elhassan, MD, Adnan Ahmed , MD, Nkem Iroegbu, MD, MPH. Department of Internal Medicine, Presence Saint Joseph Hospital, Chicago, IL. The rise in obesity has led to an increase in gastric bypass surgery in the United States, which as a procedure leads to metabolic abnormalities and nutritional deficiencies. Gastric bypass surgery has been described as a rare cause of encephalopathy at times fatal. We present a clinical vignette of a 47 year old female with past medical history of hypertension, obesity status post Roux-En-Y gastric bypass surgery in 2006, who presented to our institution with altered mental status, abdominal pain, distention, nausea and vomiting. Detailed physical exam revealed asterixis, distended, and non tender abdomen with hypoactive bowel sounds.


[787A] Figure 1.


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[788]

Table 1. Improvement in liver function tests with time Alkaline Phosphatase

Total Bilirubin

AST

ALT

Presentation

1020

12.8

363

295

5 days of UDCA

944

9.8

159

126

1 month of UDCA

921

2.1

103

123

has anti-inflammatory, anti-apoptotic, and immuno-modulatory effects. In addition, UDCA acts to alter the bile acid pool by rendering it less hydrophobic and likely displaces the hepatotoxic biliary components. While the use of UDCA has been studied in chronic cholestatic conditions and neonatal CMV, it has been seldom studied in the management of acute viral hepatitis. We propose that UDCA may have a role in the treatment of acute viral hepatitis as it improves cholestatic indices, theoretically decreases hydrophobic bile acids consequently protecting hepatocytes from apoptosis and necrosis, and provides symptomatic relief for patients. Further randomized-controlled trials would be helpful in establishing the utility of UDCA in acute viral hepatitis induced cholestasis.

789 Macro-AST: A Normal Explanation for Abnormal Liver Function Tests Omar K. Jilani, MD, MBA1, Jeffrey A. Shrensel, MD, MS2, Vijay Kanakadandi, MD3, Jawad Ahmad, MD4. 1. Mount Sinai Beth Israel Hospital, New York, NY; 2. Mount Sinai Beth Israel, New York, NY; 3. University of Kansas, Kansas City, KS; 4. Mount Sinai Hospital, New York, NY.

[787B] Figure 2.

Her initial labs showed anemia, normal electrolytes, coagulation profile and a mildly elevated liver enzymes with elevated ammonia level. A CT scan of abdomen was normal. Hepatitis panel, HIV test, Urine toxicology screen, serum ceruloplasmin, serum copper, autoimmune hepatitis panel, Alpha 1 Antitrypsin, and serum acetaminophen level were all normal. Further testing showed a decreased thiamine, zinc, carnitine levels and screening for urea cycle disorders was negative. Liver Biopsy showed mild cholestasis, with mild portal fibrosis. The patient was started on lactulose, rifaxmin, alongside with pyridoxine, thiamine and zinc supplementation after which she showed marked improvement in mental status after which she was discharged home. Disorders commonly associated with increased serum ammonia levels include hepatic failure, urea cycle defects, organic acidemias, Reye’s syndrome, and gastrointestinal bacterial overgrowth. Iatrogenic etiologies include transjugular intrahepatic portosystemic shunting (TIPS), total parenteral nutrition, and adverse drug effects. Encephalopathy is a rare complication of gastric bypass surgery, and has been attributed to deficiencies of thiamine, zinc, carnitine and other nutrients. In this clinical vignette, our patient with prior surgical history gastric bypass was found to have hyperammonemic encephalopathy in the absence of acute or chronic liver disease. The patient clinically improved with antibiotic therapy and micronutrient supplementation so her hyperammonemia was presumed to be secondary to malnutrition and micronutrient deficiency and bacterial over growth post gastric bypass surgery. We think it is important to make clinicians aware of this association so that it can be recognized early, to implement therapy that might prevent the fatal outcome.

Elevated levels of AST can be seen in patients with liver, cardiac and skeletal muscle disease. Isolated elevation of AST suggests a diagnosis of macro-aspartate aminotransferase (macro-AST). Macro-AST complexes are formed from self-polymerization or binding to immunoglobulins, leading to decreased renal clearance and a false positive elevation of AST. We describe a case of macro-AST in a healthy adult resulting in a diagnostic dilemma. A 38-year-old Caucasian man presented for a routine physical for life insurance. He denied any complaints. He admitted to social alcohol use but denied other toxic habits. He was only taking supplements including fish oil 1g BID, vitamin E 400 IU in the morning and 200 IU in evening, folic acid 1 mg BID and “Super Green”, a powder containing anti-oxidant extracts from several vegetable sources. He denied drug allergies. His physical examination was unremarkable. Laboratory evaluation was significant only for an elevated serum AST of 314 IU/L (normal: 20 IU/L). As the remainder of the lab-work was normal, the patient was asked to stop taking dietary supplements. A repeat follow-up AST level remained elevated. He tested negative for viral hepatitis, muscle disorders, and metabolic and autoimmune liver diseases. Imaging was unrevealing. He was referred to the hepatology clinic for a second opinion. With no evidence of underlying liver disease and only AST elevation on repeated testing, the patient was evaluated for the presence of macro-AST using polyethylene glycol (PEG) precipitation. PEG precipitation revealed 88.2% precipitable activity with a post-PEG precipitation AST level of 16 IU/L, confirming the presence of macro-AST. Persistently elevated AST with an otherwise negative work-up led to the consideration of macro-AST. Macroenzymes are serum enzymes that have self-polymerized with each other or with larger protein molecules such as immunoglobulins (IgG and IgA). With decreased clearance compared to normal enzymes and increased molecular weight, the macro-enzymes accumulate in the blood, causing erroneously elevated AST levels on routine laboratory assays. A literature review indicates most individuals are asymptomatic and do not require further work up. The diagnostic tests for macro-AST are only available in a few laboratories, which may further delay diagnosis and expose patients to undue stress. For example, our patient was initially denied life insurance as the elevated AST:ALT ratio was attributed to alcohol abuse.

790 788 Ursodeoxycholic Acid (UDCA) Therapy in Acute Cytomegalovirus (CMV) Hepatitis Associated Cholestasis Sheeva K. Parbhu, MD1, Abdul Haseeb, MD, MPH 1, Juan F. Gallegos-Orozco , MD2. 1. University of Utah & Affiliated Hospitals, Department of Internal Medicine, Salt Lake City, UT; 2. University of Utah & Affiliated Hospitals, Division of Gastroenterology, Salt Lake City, UT. Introduction: Cytomegalovirus (CMV) infection can be associated with sporadic cases of acute viral hepatitis with cholestasis, especially in the immunocompromised population. Ursodeoxycholic acid (UDCA) therapy is frequently used for chronic cholestatic syndromes, but has not been widely studied in acute hepatitis associated cholestasis. We present a case of acute CMV hepatitis associated cholestasis treated with UDCA. Case Report: A 48 year-old Caucasian female with a history of AIDS, noncompliant with antiretroviral therapy, presented with a week of rapidly progressing jaundice, pruritus, and diarrhea. Her pertinent labs at the time of presentation included a CD4 T-cell count < 50, total bilirubin of 12.8 mg/dL and alkaline phosphatase of 1020 U/L. She underwent a complete infectious workup, which revealed disseminated Mycobacterium Avium Intracellulare infection and an elevated CMV titer of > 2,000,000 IU/ mL. Although she was started on IV ganciclovir, she continued to have worsening pruritus and a persistent cholestatic lab pattern. Subsequent Magnetic resonance cholangiopancreatography (MRCP) showed severe peri-portal edema. A liver biopsy was not performed due to severe thrombocytopenia despite the suspicion for AIDS cholangiopathy versus a vanishing bile duct syndrome. After a week into her hospitalization, she was started on UDCA 300 mg three times daily. The patient’s pruritus and liver function tests significantly improved after five days of therapy (Table 1). Discussion: Acute viral hepatitis is associated with significant morbidity and mortality. CMV is a known cause of acute viral hepatitis and associated cholestasis. While UDCA has no effect on viral clearance, it


An Unexpected Pulmonary Complication Following TACE With Low-Dose Doxorubicin-Eluting Beads and Small-Volume Lipiodol for a Small HCC Quan Nhu, MD, PhD1, Harry Knowles, MD2, Paul Pockros, MD2, Catherine Frenette, MD2. 1. Scripps Clinic / Scripps Green Hospital, La Jolla, CA; 2. Scripps Clinic, La Jolla, CA. Background: Transarterial chemoembolization (TACE) is a widely accepted palliative intervention for hepatocellular carcinoma (HCC). We report an unexpected pulmonary complication in a patient who underwent low-dose doxyrubicin-eluting bead (DEB)-TACE followed by small-volume lipiodol for a small HCC. Case Presentation: A 62-year-old male with HCV cirrhosis, complicated by a new HCC and portopulmonary hypertension, underwent a DEB-TACE for a 3.9-cm right hepatic lobe HCC without complications resulting in tumor size reduction. He had a second DEB-TACE seven months later for a small recurrent HCC with Doxorubicin (40 mg/5ml)-eluting 100-300 μm LC beads, followed by only 1 ml Lipiodol. The patient developed hypoxemia (SpO2 88%) immediately after the procedure. Chest CTA was negative for PE, but showed multiple bilateral areas of ground-glass opacities. TTE showed mild RV enlargement, worsened pulmonary hypertension with worsened tricuspid regurgitation. Patient was transferred to the ICU on hospital day 3 for worsening respiratory distress, and was treated empirically with broad-spectrum antibiotics initially. Work up for infectious causes of acute hypoxemic respiratory failure was negative. SoluMedrol was initiated on hospital day 7 for post-TACE acute lung injury (ALI). Hypoxemia resolved two days later. The patient subsequently underwent a successful liver transplant. His respiratory function has completely normalized, but he continues to have significant pulmonary hypertension requiring medical therapy. Discussion: Post-TACE pulmonary complications, e.g., ALI, ARDS, are rare events. The injected ethiodized oil or chemotherapeutic agent is thought to migrate to the lung vasculature via arteriovenous (AV) shunts within the hypervascular HCC tumors, causing chemical injury. In rabbits, lipiodol infusion causes severe hypoxemia and lung inflammation. Perfusion of foxhound lungs with doxorubicin causes


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dose-dependent tissue damage. In humans, doxorubicin is associated with capillary leak syndrome and bronchiolitis obliterans organizing pneumonia. The acute hypoxemic respiratory failure following TACE in our patient may have resulted from pulmonary embolism with doxorubicin-eluting beads and/or lipiodol. The known risk factors for post-TACE pulmonary complications – e.g., large hypervascular HCC, AV shunts, large-volume lipiodol, and trans-inferior phrenic artery embolization – were all absent in our patient, making the post-TACE ALI in our patient an unexpected event.

791 Coadministration of a Kampo Drug, Saireito, enabled Withdrawal from Corticosteroid in Elderly Female with Autoimmune Hepatitis Shinya Fukunishi, MD, PhD1, Akira Asai, MD, PhD1, Yasuhiro Tsuda1, Kazuhide Higuchi, MD, PhD2. 1. 2nd Department of Internal Medicine, Osaka Medical College, Osaka, Japan; 2. The Second Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan. Introduction: Autoimmune hepatitis (AIH) is a common disease among middle-aged to elderly females. Because AIH follows the course of chronic liver disease, many patients take corticosteroids (CS) orally for long periods. However, elderly female patients occasionally suffer serious adverse reactions to CS. In patients with AIH who are placed on low-dose oral CS and whose pathological conditions are relatively stabilized, how long oral administration should continue is a frequently discussed problem. Case Report: An 82-year-old female,who had left partial mastectomy at the age of 79 due to cancer of the left breast and had no remarkable individual or family history, first visited our department in 2010 because she suffered from liver dysfunction. At that time, she was diagnosed with cirrhosis due to AIH and treated on an outpatient basis. The drug treatment started with PSL at a dose of 20mg. The transaminase levels decreased immediately after initiation of PSL therapy. During PSL maintenance therapy, lumber vertebral compression fracture from osteoporosis happened. Then, the transaminase levels gradually increased (AST 79 IU/l, ALT 106 IU/l) about one year initiation of oral administration of PSL at a maintenance dose of 5 mg, the patient was hospitalized to receive medical treatment. The results of various examinations suggested that exacerbation of AIH might elevate the transaminase levels. Then, the dose of PSL was increased to 20 mg and further treatment was initiated of administration of PSL at the increased dose of 20 mg, the transaminase levels started to decrease although they did not decrease to the levels within normal ranges. as rapidly as they did after initial PSL administration. The patient was placed on long-term PSL therapy and experienced adverse effects of PSL was reduced to 10 mg and concomitant oral administration of Saireito at a dose of 9.0 g was initiated. Two weeks after initiation of this combination therapy, the transaminase levels were promptly normalized (AST 29 IU/l, ALT 19 IU/l). Then the dose of PSL was further reduced and its oral administration was discontinued eight weeks after co-administration of Saireto. Since then, the transaminase levels have been maintained at the levels within the normal range, and the patient has experienced no exacerbations and has made favorable progress for about three years. Conclusion; In the treatment of AIH, a Kampo drug, Saireito, is an effective drug that may serve for reducing the dose of a steroid hormone preparation and can be used in maintenance therapy after achievement of remission. More cases will need to be accumulated before our finding become clear.

[793A] Figure 1.

792 A Puzzling Case of Spontaneous Spleenorenal Shunt and Large Isolated Gastric Varices, Not Accompanied with Liver Cirrhosis or Encephalopathy Rukevwe Ehwarieme, MD, Amina Chaudhary, MD, Neha Jain, MD, Ali Shagufta, MD. McLaren Flint, Flint, MI. Porto-caval shunts are usually secondary to hypertension in the portal venous system. Warren’s operation is one of the procedures used for decompression of the portal pressure by creating a spleno-renal shunt. Spontaneous splenorenal shunts are very rare and reported case have been associated with patients who had advanced liver cirrhosis. We present the case of a 53 y/o AAF with no known medical condition or surgical history, who presented with a hemoglobin of 2.7, ferritin of < 0.4, MCV of 50.1, found to have multiple large gastric varices on upper endoscopy and hemorrhoids on colonoscopy. Computed tomography of the abdomen revealed a large spleenorenal shunt, portal vein recanalization, fatty liver, normal sized spleen, multiple dilated vessels in the gastric and retroperitoneal space, and patent splenic and mesenteric vessels. Further work up for hypercoagulability state was negative. On further investigation, she denied history of heavy alcohol consumption. Hepatitis panel, and autoimmune hepatitis screen were negative. Hepatic ultrasound revealed a fatty liver with absence of a mass or cirrhotic features. She was subsequently started on beta blockers for the varices and sent for a fibro scan, a gastroenterology follow up, and liver biopsy. Unfortunately, she was lost to follow up. Cases of spontaneous spleenorenal shunt have often been attributed to patients with advanced hepatic cirrhosis. Unlike other reported cases, our patient had no features or evidence of advanced liver cirrhosis, no thrombosis or occlusion was noted in the spleenic vessels and hypercoagulability work up was negative.

[793B] Figure 2.

793 An Interesting Case of Painless Jaundice: Primary Hepatic Lymphoma Jason Rubinov, MD, Jonathan D. Weinberger, MD, Franklin Kasmin, Neil Theise, MD. Mount Sinai Beth Israel, New York, NY. A 77-year-old male with a history of a resolved hepatitis B infection, HTN, depression and a distant history of EtOH abuse presented with jaundice and an acute change in mental status. The patient also noted decreased appetite, weight loss and fatigue over the prior four weeks. He denied any abdominal pain, nausea, vomiting or change in bowel movements. Physical exam was notable for jaundice, hepatomegaly and mild abdominal distention without any tenderness to palpation. There was no palpable superficial lymphadenopathy. Laboratory findings showed deteriorated liver function, elevated lactate dehydrogenase (LDH), hypercalcemia and elevated blood lipid levels (Table 1). Serologic tests for hepatitis A and C


[793C] Figure 3.

and for HIV were negative. Serologic testing for hepatitis B showed evidence of a past infection. Tumor markers including serum α-fetoprotein and carcinoembryonic antigen were negative. CT of the abdomen and pelvis showed an enlarged and nodular liver without discrete parenchymal liver lesions. The pancreas, spleen and biliary tract were unremarkable. There was no evidence of abdominal lymphadenopa-


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Abstracts thy. Core liver biopsy showed heavy infiltration of small, round cells with a high nuclear to cytoplasmic ratio, prominent nucleoli (Image 1) and which were strongly positive for CD20 and CD45, but negative for CD3. These indicated a large B-cell lymphoma. Given no signs of extra-hepatic involvement, a diagnosis of primary hepatic non-Hodgkin’s lymphoma was made. Rituximab and prednisone were initiated with the intention of starting additional systemic chemotherapy agents upon signs of clinical improvement. Despite all attempts at therapy, the patient’s liver failure progressed with rapidly worsening MELD scores (Table 2). The patient ultimately expired on hospital day twenty-one. Primary hepatic lymphoma (PHL) is a rare form of lymphoma, comprising < 1% of all extra-nodal lymphomas. It is most commonly found in middle-aged men and with varying presentations. HCV infection has been found in approximately 40% of patients with PHL. Presenting symptoms may vary and can be non-specific. Abdominal pain and nausea are most common, in addition to weight loss, fevers, B-symptoms and, less commonly, jaundice. 40% of PHL patients are found to have hypercalcemia for unknown reasons. Liver imaging is variable and can range from numerous, sometimes confluent lesions to a solitary mass. Biopsy showing lymphoma, and disease confinement to the liver is necessary for diagnosis. Treatment typically consists of combination chemotherapy, specifically R-CHOP. Our case presents a rare malignancy represented in literature mostly by way of case reports and case series.

[794B] Figure 2.

794 A Case of Hepatitis B Reactivation in an Inactive Carrier During Breast Cancer Therapy Akihiko Ikura1, Yukishige Okamura1, Seiichiro Fukuhara2, Yuu Aoki1, Ken Teramoto1, Naofumi Kamioka1, Toshihiko Higashizawa1, Takahisa Shiraishi1. 1. Sano Kousei General Hospital, Gastroenterology and Hepatology, Sano, Japan; 2. Sano Kousei General Hospital, Gastroenterology and Hepatology, Tochigi, Japan.

795 Endoscopic Findings of Portal Hypertension Throughout the Gastrointestinal Tract

Recent advancements in medical care and the increase in the number of cancer patients due to an aging society have led to chemotherapy being performed more frequently and the use of more powerful drugs. As a result, reactivation of hepatitis B virus (HBV) infection due to chemotherapy is becoming more common. Reactivation of hepatitis presents with serious symptoms, as well as high rates of fulminance and mortality. In addition, hepatitis reactivation has recently drawn attention owing to the involvement of not only gastrointestinal medicine but also several other branches of medicine. A 65-year-old woman presented with the chief complaint of general malaise. She had been visiting a gastroenterology department to receive care for her inactive hepatitis B carrier status. After undergoing partial mastectomy for stage I right breast cancer at the breast surgery department, she underwent 4 courses of adriamycin + cyclophosphamide therapy as postoperative adjuvant chemotherapy over the course of 2 months. During that time, she maintained an ALT level < 30 IU/L and an HBV-DNA level < 4 log copies/mL. At a subsequent outpatient visit to the breast surgery department, she was diagnosed with acute hepatic disorder due to HBV reactivation on the basis of her blood work (Bil 5.26 mg/dL, AST 5850 IU/L, ALT 2085 IU/L, PT% 51.0%, Plt 88000 /mm3, HBsAg 17789.84 IU/mL, HBV-DNA 7.8 log copies/mL, and she was admitted to our hospital on an emergency basis. She began treatment with 1mg/kg/day prednisolone, 6 million units/day IFN-β, and 0.5 mg/day entecavir. At one month after the beginning of treatment, the HBV-DNA decreased to 3.1 log copies/mL, PT% was 131%, Bil was 1.21 mg/dL, and ALT decreased to 20 IU/L. The yellow discoloration of the bulbar conjunctiva and malaise had also improved, and the patient was subsequently discharged. She continues to receive entecavir and shows undetectable HBV-DNA levels. Japanese guidelines recommend that entecavir be administered prophylactically to all HBsAg-positive patients who undergo chemotherapy. The frequency of HBV reactivation in HBsAg-positive patients who undergo chemotherapy has been reported to be 24–53%. In addition, the frequency of HBV reactivation in HBsAg-positive breast cancer patients who undergo chemotherapy including adriamycin and cyclophosphamide is reported to be 20.7–41.0%. Unlike most other cancers, breast cancer (including stage I breast cancer, such as the present case) involves postoperative chemotherapy based on pathologic diagnosis, and thus requires greater caution. When initiating chemotherapy for patients already infected with HBV or for HBV carriers, it is important to collaborate closely with medical departments involved in cancer treatment and to exercise meticulous caution.

Melinda Wayde, MD1, Nyla Hazratjee, MD1, Salma Akram, MD1, Sangeeta Agrawal, MD, FACG2. 1. Wright State University, Dayton, OH; 2. Dayton VA Medical Center, Wright State University, Dayton, OH.

[794A] Figure 1.

[795A] Figure 1.


Introduction: Portal hypertension is an important sequel of liver cirrhosis that can cause characteristic endoscopic changes throughout the gastrointestinal (GI) tract. We present a case of portal hypertension that illustrates the diffuse reach of this entity and a less common etiology of portal hypertensive hemorrhage. Case Description:A 62-year-old Caucasian male with a long history of alcohol dependence and irondeficiency anemia was admitted to the hospital for hypovolemic shock, new-onset ascites, and severe symptomatic anemia with hemoglobin of 3.6 g/dl, MCV: 65.8. The patient denied melena, hematochezia, hematemesis, and hematuria. He was transfused a total of 5 units of packed red blood cells. Fluid obtained from paracentesis was consistent with ascites from portal hypertension. After stabilization, the patient underwent upper and lower endoscopy. The esophagogastroduodenoscopy (EGD) demonstrated 4 columns of grade 1-2 esophageal varices in addition to gastropathy and duodenopathy with friable mucosa prone to bleeding on contact. The colonoscopy revealed diffuse colitis from rectum to cecum with congested, friable hyperemic mucosa, 2 columns of grade 1-2 rectal varices, and multiple ulcerations, the largest of which measured 5 cm and had a large overlying clot. The patient was started on diuretics, antibiotic prophylaxis for bacterial peritonitis, a proton pump inhibitor, and advised to abstain from alcohol. Discussion: Our patient’s endoscopic findings are consistent with many classic features of portal hypertension seen throughout the GI tract. Esophagogastric varices, the most common complication of portal hypertension and the most frequent cause of hemorrhage, were not our patient’s major source of bleeding given their low grade and lack of stigmata of recent bleed. The major source of bleeding was likely the colon given the large ulcers and presence of overlying clots, though a much less common cause of hemorrhage. Varices found outside the esophagogastric region account for only 1-5% of variceal bleeds. It is important to remember that the effects of portal hypertension can be found throughout the GI tract and all of them are possible sources of the major complication of portal hypertension: hemorrhage. Our patient’s findings demonstrate the importance of a complete endoscopic evaluation in the setting of a GI bleed in a patient with portal hypertension.


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796 A Case of Acute Liver Failure Following Initiation of Valproic Acid Shannon J. Morales, MD1, Katherine J. Hahn, MD1, Ryan M. Kwok, MD1, Mohammed Albugeaey, MD2, Mrigender S. Virk, MD1, Amol S. Rangnekar, MD3, Rohit S. Satoskar, MD3. 1. MedStar Georgetown University Hospital, Washington, DC; 2. MedStar Georgetown University Hospital, Department of Gastroenterology, Washington, DC; 3. MedStar Georgetown University Hospital, Department of Hepatology, Washington, DC. Introduction: Valproic acid (VPA), an anticonvulsant used in the treatment of seizure disorders, migraines, and bipolar disorder, has been shown to cause drug-induced liver injury (DILI) in 5-10% of individuals. Effects can range from subclinical transaminase elevations to acute liver failure and death. Herein, we report a case of acute liver failure 18 days following initiation of VPA. Case Report: A 39 year-old woman with a history of a seizure disorder and schizophrenia treated with olanzapine presented to an outside hospital with breakthrough seizures. She was successfully treated with an anti-epileptic regimen including phenytoin, levetiracetam, VPA and lacosamide and discharged. Two days later she was readmitted to our institution with altered mental status and

incontinence. Physical exam revealed orientation only to self, flat affect, and icteric sclera. Labs were significant for pH 7.1, lactate 7.1, AST 282, ALT 343, total bilirubin 2.2 and INR 1.1. A non-contrast head CT was normal. She was treated with IV fluids and IV bicarbonate, and was admitted to the medical ICU. By hospital day 5, her labs revealed AST 2129, ALT 1625 and INR 2.4. Initial serologic testing, including levels for acetaminophen, salicylates, alcohol and carbamazepine, a viral hepatitis panel, toxicology screen, anti-mitochondrial antibody, anti-smooth muscle antibody, HIV, CMV, EBV, HSV, RPR, VZV, and AFP, was negative. A transjugular liver biopsy (Figure) was consistent with VPA induced hepatotoxicity. Despite discontinuing all anti-epileptic medications and initiating IV carnitine, the patient developed ventilator-dependent respiratory failure and acute kidney injury requiring hemodialysis and was listed for liver transplantation. Several weeks following the termination of VPA, the patient’s liver associated enzymes and renal function normalized. The patient experienced a recurrent seizure and was restarted on levetiracetam prior to being discharged on hospital day 83. Discussion: The absence of other risk factors, the livery biopsy histology, and the timing of liver injury and recovery are all consistent with VPA-induced acute liver failure. A Roussel Uclaf Causality Assessment Method score of 8 was calculated. The mechanism of toxicity is thought to be due to impairment of liver mitochondrial function. Treatment with VPA requires a high index of suspicion for DILI and early discontinuation of this medication may spare patients from liver transplantation or death.

797 Unusual Cause of Acute Pulmonary Embolism: Giant Hepatic Hemangioma Supannee Rassameehiran, MD1, Hatice D. Baser2, Srisung Weeraporn 2, Mamoun Bashir2, Tinsay Woreta2. 1. Texas Tech University Health Sciences Center, Lubbock, TX; 2. Texas Tech University Health Sciences Center School of Medicine, Internal Medicine Department, Lubbock, TX.

[796A] Figure 1.

Introduction: Giant hepatic hemangioma, characterized as cavernous hemangiomas larger than 4 cm in diameter, may cause various symptoms or complications depending on the size, location and the degree of compression on adjacent structures. Pulmonary emboli (PE) may occasionally arise from deep vein thrombosis (DVT) in less common locations including inferior vena cava (IVC). IVC thrombosis is a rare entity, and may result from external compression of IVC by giant hepatic hemangioma. Case Presentation: A 53-year-old African American man presented with a 3-day history of worsening shortness of breath, pleuritic chest pain and hemoptysis. On admission, the patient was hemodynamically stable. Physical examination revealed diffuse abdominal tenderness and hepatomegaly. Past medical history was remarkable for hypertension. He drank alcohol daily and reported recreational drug abuse. He reported no recent surgery or immobilization, prior venous thromboembolic event, or family history of hypercoagulability. Computed tomography (CT)angiogram of the chest showed bilateral segmental PE in the upper lobes, right middle lobe, and lower lobes. Contrast-enhanced CT scanning of the abdomen revealed two large low density lesions in the liver, one in segment IV measuring approximately

[797A] Figure 1.



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[797B] Figure 3.

15.3 x 13 cm in size and another in segment VIII measuring 9 x 13.8 cm in size. There was peripheral nodular puddling with enhancement slowly filling in towards the center, becoming increasingly isodense at the periphery on the delayed scan, suggestive of giant cavernous hemangioma. The diagnosis was confirmed with magnetic resonance imaging. Hepatic Doppler ultrasound (US) revealed a filling defect in the center of the retrohepatic IVC with high blood velocities adjacent to the region. Color Doppler US of the lower extremities did not reveal DVT. Surgical resection and enucleation was not possible in this case due to large and multiple lesions that occupied nearly all the liver. Anticoagulation with warfarin was initiated due to bilateral PE and IVC thrombus. Discussion: Selective compression of IVC by giant hepatic hemangioma may have caused thrombosis in the IVC leading to pulmonary embolism. Another possible mechanism is the migration of thrombi from the hemangioma itself to the hepatic veins and IVC. This case highlights the importance of detailed abdomen work-up in acute pulmonary emboli, particularly in patients with PE without evidence of DVT of lower extremity.

[798B] Figure 2.

798 Glycogenic Hepatopathy: A Case of Acute and Episodic Elevations in Liver Transaminases Sharon E. Kim, MD, Rayhan Lal, MD, John Donovan, MD. Los Angeles County + USC Medical Center, Los Angeles, CA. Background: Mauriac (in 1930) described the syndrome of growth retardation, cushingoid features, delayed puberty and hepatomegaly in children. In this syndrome, hepatomegaly is caused by excessive glycogen accumulation and is associated with abnormal liver enzyme tests. Several terms has been used to describe this phenomenon: glycogen hepatopathy, hepatic glycogenosis, and DM-associated glycogen storage hepatomegaly. We present a case of recurrent glycogenic hepatopathy causing episodic AST and ALT “flares” (figures 1 and 2) in a patient during multiple admissions for uncontrolled diabetes including diabetic ketoacidosis (DKA) and non-DKA admissions. Case presentation: A 24 year old Hispanic man with type I DM and prior admissions for DKA presented to the emergency room with 2 days of general malaise, nausea, and non-bloody emesis. Social history was unremarkable. Physical examination: notable only for a palpable, nontender liver 4cm below the costal margin. Laboratory Results: At admission: sodium 133 mmol/L (N: 135-145), chloride 91 mmol/L (N: 100-110), carbon dioxide 26 mmol/L (N: 20-30), creatinine 0.48 mg/dL (N: 0.50-1.30), glucose 334 mg/dL (N: 65-99), alkaline phosphatase 216 U/L (N: 40-130), AST 1464 U/L (N: 10-40), ALT 713 U/L (N: 10-55), albumin 4.2 g/dL (N: 3.5-5.0), total protein 6.9 g/dL (N: 6.0-8.0), WBC 5.9 K/cumm (N: 3.7-10.3), hemoglobin 14.8 g/dL (N: 13.8-16.9), platelet 326 K/cumm (N: 150-350), and hemoglobin a1c of 11.5% (N: 4-6). Markers for viral hepatitis and autoimmune hepatitis were negative. Ultrasound imaging: Fatty liver and hepatomegaly. Liver Biopsy: Glycogen hepatopathy manifested by diffuse hydropic change with minimal focal lobular inflammation and scanty to 1+ fatty change, normal portal tracts and absence of steatohepatitis (Figure 3). Conclusion: This report describes a patient with episodic and acute AST and ALT elevations associated with biopsy proven glycogenic hepatopathy. Liver enzyme elevations were associated with hyperglycemia with and without DKA. Glycogenic hepatopathy can occur unpredictably and indicates the important need to consider this condition when evaluating the hyperglycemic patient with hepatomegaly and acute or episodic AST and ALT elevations.


[798C] Figure 3.

799 An Avoidable Case of Acute Hepatitis B Infection Jason Rubinov, MD, Alfred Burger, MD. Mount Sinai Beth Israel, New York, NY. A 33-year-old man with no past medical history was referred to our institution for an acute elevation of his liver function tests. The patient had one-week of generalized malaise, loose bowel movements, mild epigastric discomfort and dark appearing urine. Laboratory testing showed severe hepatocellular injury (Table 1). An acute viral hepatitis panel was positive for hepatitis B surface antigen and hepatitis B core IgM antibody, indicative of an acute viral hepatitis B infection. At hospital admission a more detailed history was obtained. The patient had recent sexual activity with multiple male partners, and admitted to instances of unsafe sexual practice. He denied any history of intravenous drug use, tattoos, past blood transfusions or healthcare related employment. He was born in the Philippines and moved to the United States as a child. He was not aware of ever receiving a Hepatitis B vaccine series in the past. He followed with a pediatrician as an adolescent and later visited several different physicians on a sporadic basis, during which time he does not recall his hepatitis B vaccine status ever being addressed. During the hospitalization, he was treated supportively and his liver function tests improved. He was discharged with plans for outpatient follow up to monitor for resolution of this infection. Worldwide, an estimated 500,000 to 1.2 million infected individuals will die from cirrhosis and hepatocellular carcinoma related to hepatitis B virus infection each year. Effective vaccines have been available in the U.S. since 1982. Current guidelines recommend universal vaccination of infants and routine vaccination of previously unvaccinated children and adolescents. For adults not already immune or infected, both the CDC and the American Association for the Study of Liver Disease (AASLD) recommend screening high risk patient groups. Our patient fell into two of the deemed high risk groups: men who have sex with men and those born in high or intermediate endemic areas. Unfortunately, despite these guidelines and many prior physician encounters, our patient’s lack of hepatitis B immunity was not clearly established nor acted upon if known. As a result, he acquired an acute hepatitis B infection that could have been prevented. Our findings demonstrate an example of poor adherence to current AASLD guidelines. A recent study published in The American Journal of Gastroenterology in June of 2014 simi-


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[799A] Figure 1.

larly reported poor adherence to current AASLD recommendations in regards to hepatitis B infection, although their focus was primarily on management and treatment. In regards to screening for hepatitis B infection, it is likely that many physicians are not well informed of current guidelines. Greater efforts must be taken to increase physician awareness.

[801A] Figure 1.

800 Bactrim-Induced Hepatotoxicity: A Rare Occurrence Umair Sohail, MD1, Ashraf Almashhrawi, MD1, Rubayat Rahman, MD, MPH1, Imran Ashraf, MD1, Douglas Nguyen, MD2, Matthew Bechtold, MD, FACG1. 1. University of Missouri, Columbia, MO; 2. University of California Irvine, Anaheim Hills, CA. Introduction: Bactrim is a synthetic antibacterial combination of a sulfonamide and a methoprime. It is widely used to treat infections such as urinary tract and upper respiratory infections as well as prophylactic purposes in immuno-compromised patients. Bactrim is known for its potential to cause idiosyncratic liver injury that has features of drug-allergy or hypersensitivity. The pattern of injury is typically cholestatic or mixed and can be prolonged. This case represents a rare occurrence of Bactriminduced hepatotoxicity. Case:52-year-old white female presented with right upper quadrant pain and abnormal liver tests. Earlier in the week, she developed leg cellulitis for which she was treated with one dose of vancomycin and discharged home on Bactrim DS. Few days after discharge, she started having RUQ pain, nausea, and vomiting. She had no confusion and did not notice any jaundice. She did not take Tylenol, herbs, or over-the-counter medications. Physical examination was unremarkable except for a temperature of 38.2 degrees, palpable and severely tender liver with jaundice. Blood pressure and heart rate were within normal range. AST >7000 units/L, ALT 3973 units/L, alkaline phosphatase 300 units/L, total bilirubin 3.5 mg/dl, albumin 2.8g/dl, INR 1.7, lactate dehydrogenase >2500 units/L, and acetaminophen. Discussion: It is very imperative for health-care providers to be aware of the potential risks of drug induced liver injury that can be caused by Bactrim. Immediate discontinuation of the medicine and close monitoring of the liver enzymes and function should be done.

801 Isolated Gastric Varices: Use of Balloon-Occlusive Retrograde Transvenous Obliteration Thomas R. McCarty, MD1, Mena Bakhit, MD2, Tarun Rustagi, MD3. 1. Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, Yemen; 2. Department of Internal Medicine, Yale University School of Medicine, New Haven, CT; 3. Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT. Clinical Vignette: A 51-year-old man with alcoholic cirrhosis decompensated by hepatic encephalopathy (HE) presented with a 2-week history of hematemesis and melena. Initial labs were notable for hemoglobin of 3.1 gm/dL. Esophagogastroduodenoscopy showed isolated, large fundic varices, and minimal portal gastropathy without esophageal varices (Image A). Further evaluation with abdominal computed tomography demonstrated a patent splenic vein and extensive, large gastric varices. Interventional radiology was consulted for potential transjugular intrahepatic portosystemic shunt (TIPS); however, a decision was made to perform balloon-occlusive retrograde transvenous obliteration (BRTO) for the management of isolated gastric varices. The procedure involved occlusion of the outflow veins of the portosystemic shunt using an occlusion balloon with subsequent injection of a sclerosing agent directly into the varix endovascularly. Fluoroscopy with contrast dye was injected to illustrate the varices prior to embolization with 25 mL of sodium tetradecyl sulfate in foam solution and 24-hour balloon placement to prevent loss of the sclerosant. The patient tolerated the procedure well and follow-up venography demonstrated complete obliteration of the gastric varices (Image B). He was discharged the next day with no further episodes of bleeding; however, repeat endoscopy one-month post-procedure showed the emergence of 3 columns of grade I esophageal varices. Discussion: Isolated gastric variceal bleeding is far less common than esophageal variceal hemorrhage. Although less prevalent and less likely to bleed than esophageal varices, gastric varices tend to require


[801B] Figure 2.

more blood transfusions and have higher mortality when bleeding occurs. While treatment options for gastric varices include medical, surgical, endoscopic, and endovascular approaches, procedural approaches center around two methodologies: 1) indirect decompression of the portal system (i.e. TIPS) and 2) direct exclusion from the portosystemic system (i.e. BRTO). Although decreasing portal pressure is an effective strategy in reducing esophageal variceal hemorrhage, it is inconsistently effective for gastric varices, which tend to occur and bleed at even lower portal pressures. A direct approach with BRTO as used in this patient is a frequently utilized procedure in Japan where the incidence of isolated gastric varices is much higher. The main advantage of BRTO is the preservation of hepatic flow with significantly reduced risk of HE – a major limitation and concern with TIPS. One complication of BRTO includes transient worsening of portal pressures due to a reduction in the vascular space via sclerosis. This is known to cause aggravation of esophageal varices as seen in this patient and may also increase the risk of developing ascites.


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Abstracts 802 A Rare Cause of Lower Gastrointestinal Bleed in a Cirrhotic Patient Caroline R. Jouhourian, MD1, Gabriela Kuftinec2, Scott Sequeira, MD3, Manish Tandon, MD4. 1. Tufts Medical Center, Boston, MA; 2. Tufts School of Medicine, Sacramento , CA; 3. Tufts University School of Medicine/ St. Elizabeth’s Medical Center, Brighton, MA; 4. St. Elizabeth’s Medical Center, Brighton, MA. Background: Bleeding varices are a known complication among cirrhotic patients, leading to increased morbidity and mortality. The most common type are gastroesophageal varices, however ectopic varices have been described in the literature. Ectopic varices are those not involving the gastroesophageal mucosa, but rather the rectum, and small and large bowel. They are most often found in the duodenum and rectum, making colonic varices an even rarer entity. Furthermore, ectopic varices are a rare cause of bleeding in cirrhotic patients. The reported incidence of colonic varices regardless of their etiology is about 0.07%. Our current literature is limited to less than 100 case reports among cirrhotics with portal hypertension. The varices are often incidentally found on imaging or endoscopy during an acute bleed. Accurate diagnosis of these varices is quite difficult with colonoscopy alone as the findings are often misinterpreted as exophytic lesions or obscured by bleeding. Due to the paucity of literature and ability to accurately diagnose these lesion, optimal management and treatment of bleeding colonic varices remains unclear. We describe a case of bleeding cecal varices and our management approach. Case: A 59 year-old male with alcoholic cirrhosis and known esophageal varices, presented with an obscure, overt lower gastrointestinal (GI) bleed necessitating intensive care. Over 10 units of packed red blood cells were needed to maintain a hemoglobin of 7 G/dL. Upper and lower endoscopies failed to reveal the source of his anemia. Blood clots were noted in the right colon. A tagged red blood cell scan

showed tracer leakage localized to the right lower quadrant (superior mesenteric artery). A diagnosis of right sided colonic varices was subsequently made on CT-angiogram (picture 1). The patient underwent a transjugular intrahepatic portosystemic shunt placement with initial clinical stabilization. The bleeding recommenced and the patient required angiography with coiling of the large mesocaval shunt (picture 2). Conclusion: Lower GI bleeding from colonic varices is rare and associated with severe complications. Our case emphasizes a unique presentation of a lower GI bleed in a cirrhotic patient and the importance of a proper diagnosis due to the associated lethality. We provide a means of diagnosis via tagged red cell scan and CT-angiogram and highlight subsequent treatment options with eventual selective embolization of the bleeding varix.

803 Symptomatic Disseminated Histoplasmosis Acquired by Liver Transplantation Fadi Niyazi, MD, Ahmed Saeed, MD, Kimberly Tosch, Keith Mullins, MD, Syed-Mohammed Jafri, MD. Henry Ford Hospital, Detroit, MI. Background: The infection caused by the dimorphic fungus Histoplasma Capsulatum among solid organ transplantation recipients could occur via primary infection or reactivation of previous latent infection. There are no documented cases of demonstrated transmission from a liver donor allograft. Case: A 61-year-old Caucasian male with cirrhosis associated with non-alcoholic steatohepatitis who received an orthotopic liver transplant. The donor’s spleen was noted to have granulomatous inflammation and appearance consistent with histoplasmosis on autopsy. Donor blood histoplasmosis antigen was negative. The recipient also had a negative antigen testing. The recipient was started on itraconazole prophylactically based on the the donor’s autopsy results. The patient stopped the treatment against medical advice due to headaches. His immunosuppressive regimen included prednisone taper, tacrolimus and Mycophenolate Mofetil. Five months post transplant, he was admitted to the hospital for evaluation of fever, pancytopenia and abdominal pain. Standard infectious workup including chest x-ray, blood and urine cultures was negative. Abdominal imaging was only consistent with splenomegaly seen prior to the transplant and prominent appendix with no inflammatory changes. The fever resolved and he was discharged home. He was re-admitted after several days for persistent fever and continued headaches. He did not have any respiratory or urinary symptoms. Physical examination revealed a soft abdomen with mild right lower quadrant tenderness. Skin and respiratory exams was normal. Standard blood, urine and serologic workup was repeated and remained negative. He had mild elevation in his tranaminases and alkaline phosphatase. A CT scan of the chest revealed a pulmonary nodule. CT guided biopsy of lung nodule showed chronically inflamed lung tissue with fungal yeast forms consistent with Histoplasma species. The urine histoplasma antigen was also positive. The patient was restarted on Itraconazole with resolution of fever and abdominal pain. His headaches improved over the next month. He had no recurrence of symptoms after restarting therapy. Discussion: Histoplasmosis is an intracellular mycotic infection of the reticuloendothelial system. In the field of solid organ transplant, immunosuppression is a strong risk factor for dissemination of Histoplasmosis. Patients with disseminated infection often present with pancytopenia, hepatosplenomegaly and hepatic enzyme elevation. The diagnosis is made with a combination of imaging, serologic and histologic testing. Our case shows that transmission through liver transplantation from infected donor is possible and highlights the importance of prophylaxis in this setting.

804 Cholestatic Liver Injury as a Feature of Hemophagocytic Lymphohistiocytosis

[802A] Figure 1.

[802B] Figure 2. © 2015 by the American College of Gastroenterology

David W. Wan, MD1, Numa Rahman2, Fouad Otaki3. 1. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 2. New York Medical College, New York, NY; 3. Weill Cornell Medical College, New York, NY. We present the case of a 29-year-old male with Crohn’s disease on 5-ASA/6MP therapy who was admitted for 11 days of worsening fevers, cough, chest pain and malaise. He had no recent travel or sick contacts and had recently tested negative for HIV. On admission, he was taking levofloxacin per his PCP for suspected pneumonia, but noted that his symptoms had not improved at all. His admission labs revealed pancytopenia and he continued to spike fevers up to 40°C. His AST/ALT/ALP/Total bilirubin were 125/58/131/1.2, and an abdominal ultrasound on admission showed a distended gallbladder wall and pericholecystic fluid with no evidence of calculi, suggestive of acalculous cholecystitis. He was started on vancomycin, aztreonam and metronidazole while awaiting blood culture results and further workup. His blood cultures came back negative, but his LFTs progressively increased to 213/67/251/5.7 to reveal a cholestatic picture. A subsequent HIDA was negative and a CT of the abdomen and pelvis showed only hepatosplenomegaly. His serologies confirmed immunity to Hepatitis B virus and non-exposure to Hepatitis A and C viruses, and he had no evidence of cirrhosis on history or physical exam. He was found to have CMV/ EBV viremia, which normally causes hepatocellular injury, so the reason for his cholestatic injury still remained mysterious at this point. A bone marrow biopsy performed to elucidate the cause of his pancytopenia revealed marked hemophagocytosis. Further testing revealed a significantly elevated ferritin level at 11700 ng/ml (normal < 336 ng/ml). His sCD25, a marker of immune system activation and inflammation, was grossly elevated as well. The patient was eventually diagnosed with hemophagocytic lymphohistiocytosis (HLH) on the basis of his fevers ≥38.5°C, splenomegaly, peripheral blood cytopenias, hyperbilirubinemia, hemophagocytosis in the bone marrow, ferritin > 3000 ng/ml, and elevated sCD25. He was started on treatment with etoposide and dexamethasone, with eventual resolution of his cholestatic liver injury. He is now awaiting results of a genetic panel to screen for HLH-causing mutations. HLH is a rare syndrome that occurs due to immune system dysregulation, often triggered by infection in susceptible individuals. In HLH, NK cells and cytotoxic lymphocytes fail to downregulate activated macrophages, resulting in a cytokine storm. High levels of IFN-γ and other cytokines cause severe tissue damage and organ failure, necessitating prompt management.


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805 Rocky Mountain Spotted Fever: An Unusual Cause of Elevated Liver Function Tests Nicole Shen, MD, Monica Saumoy, MD, David W. Wan, MD. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY. 26 year old male bodybuilder using anabolic steroids presented with three weeks of a constellation of symptoms including headache, blurry vision, worsening bilateral lower extremity weakness, numbness, tingling, abdominal pain, urinary retention, constipation, and arthralgias. On admission, his vital signs were unremarkable and on exam he had bilateral lower extremity weakness without sensory deficits and a firm mildly distended abdomen without skin rash. He was empirically started on acyclovir, ceftriaxone, vancomycin and doxycycline. Initial lumbar puncture was remarkable for lymphocytosis and imaging showed pons colliculitis with possible transverse myelitis. His motor function and paresthesias worsened, so the patient was started on steroids and IVIG. His laboratory work-up was notable for elevated WBC of 17.5 with neutrophil predominance, mild thrombocytopenia 130, mild hyponatremia 130, abnormal liver enzymes with AST of 88, ALT of 125, ALP of 27, and normal bilirubin and INR. Abdominal ultrasound showed hepatomegaly and splenomegaly. Hepatitis serologies were consistent with clearance of prior hepatitis B exposure and negative for hepatitis A and C. Other viral PCRs were negative. Other pertinent results included toxicology screen positive for benzodiazepines, elevated aldolase, negative autoimmune serologies, and positive Rocky Mountain Spotted Fever (RMSF) IgM (1:128). All medications were stopped with exception of doxycycline. His aminotransferases up-trended to a peak AST of 216 and ALT of 380 with a discharge AST of 106 and ALT of 198. He clinically improved and was discharged home. The differential for his hepatomegaly and elevated liver enzymes was drug induced liver injury (DILI) secondary to testosterone supplementation or medications started in the hospital versus RMSF. DILI seemed less likely as this typically causes liver enzyme elevations that peak and normalize while using the inciting drug. It was concluded RMSF was the cause of his transient transaminitis, which typically manifests as abdominal pain, splenomegaly, hepatomegaly, and elevated liver enzymes.1 On pathology rickettsia have been observed in the portal triads with inflammation and sinusoidal eryhtrophagocytosis.2 It is important to recognize the hepatic manifestations of RMSF in patients who present with neurological changes as well as gastrointestinal changes. References: [1]. Middleton DB. Rocky Mountain spotted fever: gastrointestinal and laboratory manifestations. South Med J 1978;71:629-32. [2]. Adams JS, Walker DH. The liver in Rocky Mountain spotted fever. Am J Clin Pathol 1981;75:156-61.

[806B] Figure 2.

806 Systemic Mastocytosis as an Unconventional Cause of Variceal Bleeding: Think Outside the Box Mayurathan Kesavan, MD1, Moiz Ahmed, MD2, Hafiz M. Khan3, Sherif Andrawes, MD3, Frank Gress, MD4, Liliane Deeb , MD5. 1. Staten Island University Hospital, Staten Island , NY; 2. Siuh, Staten Island, NY; 3. Staten Island University Hospital, Staten Island, NY; 4. New York Presbyterian Hospital/Columbia University Medical Center, New York, NY; 5. Staten Island University Hospital/NorthShore LIJ Health System, Staten Island, NY. Systemic mastocytosis is a rare infiltrative disease caused by excessive mast cell proliferation and accumulation in various organs including skin, bone marrow, digestive system, liver and spleen. Common gastrointestinal symptoms include abdominal pain, diarrhea, nausea and vomiting. Gastrointestinal bleeding is seldom reported in mastocytosis and is predominantly caused by peptic ulcer disease secondary to excessive histamine secretion by mast cells resulting in hyperacidemia. Though exceptionally rare, non cirrhotic portal hypertension is peculiar in mastocytosis and is caused by perisinusoidal mast cell infiltration and fibrosis. Those patients typically present with variceal bleeding in the setting of preserved liver function. Herein we report a rare case of systemic mastocytosis that was disclosed after a massive variceal bleeding. 59 year old male with atrial fibrillation on coumadin, congestive heart failure and smoldering multiple myeloma presents with hematemesis and melena of 1 day duration. At presentation, he was hemodynamically unstable with severe blood loss (Hb:5.2g/dl) and supratherapeutic INR of >15. His liver profile was unremarkable except for albumin of 2.3. After resuscitation and reversal of anticoagulation, EGD reveals large gastroesophageal varices (Fig1) with red whale signs. Band ligation was performed and control of bleeding achieved. He denied any history of liver diseases, hepatitis or alcohol abuse. Abdominal sonogram revealed normal liver parenchyma and patent hepatic and portal veins without any evidence of cirrhosis. Serologic tests for hepatitis A, B, C, HIV, markers of autoimmune hepatitis (AMA, ASMA, LKM antibodies), ceruloplasmin, iron indices and tumor markers were all unrevealing. Liver biopsy revealed severe perisinusoidal fibrosis with focal nodule formation (Fig2). CD117 (c-kit) immunostain disclosed abundant mast cells in portal tracts (Fig3). Serum tryptase level was elevated: 104 ng/ml (refer-

[806C] Figure 3.

ence: 2 to 10) and bone marrow biopsy revealed hypercellular marrow infiltrated predominantly by mast cells, establishing the diagnosis of systemic mastocytosis. This unique report highlights an out of the ordinary reason of variceal bleeding due to non cirrhotic portal hypertension in a patient with systemic mastocytosis. In this rare myeloproliferative disease, mast cell derived factors (tryptase, TNF α, PDGF and chymase) induce excessive collagen formation and fibrosis deposition in the hepatic sinusoids which lead to compression of portal veins and increased portal pressures. Typically liver function is preserved, which serves as an important clue for the diagnosis. Bone marrow biopsy is essential for diagnosis. Heightened awareness of this unique and rare presentation of mastocytosis is advised, to improve early recognition and avoid unnecessary investigation.

807 AIH Meets PSC: A Rare Twist in Hepatobiliary Disease Punita Shroff, DO1, Simi Singh, MD2, Rouchelle dela Cruz, MD1, Neil Theise, MD1, Jahnavi Naik, MD1. 1. Mount Sinai Beth Israel, New York, NY; 2. Mount Sinai Beth Israel, New York , NY.

[806A] Figure 1.


18% of patients with autoimmune hepatitis (AIH) present with a second auto-immune disease, which is termed “overlap syndrome.” Unlike AIH-primary biliary cirrhosis overlap syndrome, autoimmune hepatitis-primary sclerosing cholangitis (AIH-PSC) overlap syndrome is usually diagnosed in childhood. Limited data exist regarding adult diagnosis and treatment given the small number of cases in literature. Here we report a case of a young adult initially diagnosed with AIH. An otherwise healthy 24 year old male presented with right upper quadrant pain to our clinic. He denied jaundice, pruritis, fatigue, arthritis, prescription or OTC medications, dietary supplements and recent alcohol use. There was no known family history of liver or autoimmune disease. Serum tests were normal except for AST=319, AST=439, and ALP=794. ANA and ASMA titers found to be both positive at 1:160 and 1:40, respectively. An abdominal ultrasound showed a thickened gallbladder wall


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Abstracts and sludge. Endoscopic ultrasound showed a normal common bile duct without gallstones. Steroid treatment was initiated for autoimmune hepatitis and his pain improved. However, with ALP’s five fold elevation from normal, ursodiol was started and a cholangiogram was performed. Pathology showed small duct sclerosing cholangitis without plasma cells. Colonoscopy was negative for ulcerative colitis.

Liver enzymes initially improved on steroids, but worsened with steroid taper. Given his high ANA titer, steroid-responsiveness and cholangiogram findings, our patient was diagnosed with AIH-PSC. Treatment with ursodiol, azithioprine and steroids resulted in improved symptoms and biochemical response. The pathogenesis of AIH-PSC overlap syndrome is poorly understood, but may be due to a shared genetic background. HLA-B8 and DR-3 have been reported in AIH-PSC. AIH-PSC also more commonly occurs in the presence of IBD, which our patient did not have. As in this case, patients with significant biochemical cholestasis should raise suspicion of AIH-PSC and prompt further investigation with a cholangiogram. The best indicators for differentiating PSC and AIH-PSC are IgG, gammaglobulins and the presence of ANA and ASMA. No standard of treatment has been established, but immunosuppression to decrease hepatic inflammation and cholestatic therapy may be beneficial. Half of adult patients can develop cirrhosis within only a few years of an AIH-PSC diagnosis, which indicates the need for early management. Further studies are necessary to help guide clinicians in their diagnosis and management.

808 The First Case Report of Hepatitis B Virus (HBV) Reactivation in an Inactive Carrier of Chronic HBV After the Initiation of Treatment for Tuberculosis Ahmed Al-Khazraji, MD1, Carmine Catalano, MD2, Rafael A. Ching Companioni, MD1, Ilnaz Salehi, MD3, Melik Tiba, MD1, Nnaemeka Anyadike, MD1. 1. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), Elmhurst, NY; 2. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), East Rockaway, NY; 3. Icahn School of Medicine at Mount Sinai, Elmhurst, NY.

[807A] Figure 1.

Introduction: The HBV is a DNA virus that causes inflammation of the liver whether the infection is acute or chronic. After the initial phase of acute infection with HBV, resolution occurs in about 15% of patients, while chronic HBV infection is seen in about 85% of patients. Despite serological recovery, HBV DNA persists in the hepatocyte through integration into the host genome; therefore clinicians need to be aware of the risk of HBV reactivation in patients receiving chemotherapy and other immunosuppressive medications. Case Presentation: A 32-year-old female with a history of chronic HBV in the inactive carrier state and tuberculous lymphadenitis presented to the emergency department with generalized weakness, nausea, vomiting and jaundice for two weeks. She had recently been started on Ethambutol, Levofloxacin and Capreomycin by her private medical doctor for tuberculosis treatment. She denied use of any other medications or herbal supplements. She denied alcohol or illicit drug use. Her family history was unremarkable for liver disease. Physical examination was notable for scleral icterus but otherwise unremarkable. HIV test was negative. Her hepatic function tests returned as follows; aspartate transaminase 1397 U/L, alanine transaminase 1234 U/L, gamma-glutamyl transpeptidase 107 IU/L, total bilirubin 2.3 mg/dL, and direct bilirubin 0.6 mg/dL. Liver enzymes were normal four months prior to admission. Due to concern for drug-induced liver injury her anti-tuberculosis medications were discontinued. An abdominal ultrasound revealed mild increased liver echogenicity. Hepatitis C Virus antibody was non-reactive. HBsAg was reactive, anti-HBs was non-reactive, and anti-HBc was reactive and IgM anti-HBc nonreactive. HBV DNA level was greater than 1,000,000,000 IU/mLconsistent with a diagnosis of reactivation of HBV. The patient was started on tenofovir 300 mg PO daily. Ultimately the patient was discharged home. Follow up one month later revealed normalizing liver enzymes and an HBV DNA level of 471 IU/mL. Conclusion: Reactivation of HBV after starting chemotherapy or immunosuppressive medications is well described. Our case report is the first to describe HBV reactivation after starting anti-tuberculosis medications. Screening for HBV infection should be considered prior to initiating anti-tuberculosis therapy due to concern for reactivation of HBV, which can be severe and potentially fatal.

809 [807B] Figure 2.

Herpes Simplex Hepatitis: Is Mickie Mouse Infectious? George Cholankeril, MD1, Adam C. Lessne, MD2, William Bivin, MD3, Qiang Liu, MD2, Harmit Kalia, DO2. 1. Roger Williams Medical Center, Providence, RI; 2. Montefiore Medical Center, Bronx, NY; 3. Montefiore Medical Center, Bronk, NY.

[807C] Figure 3.


Background: Herpes simplex virus (HSV) hepatitis is a rare complication of HSV infection, but it can often lead to acute liver failure (ALF). It is predominantly seen in immunocompromised patients and pregnant women. However, up to 25% of reported cases occurred in immunocompetent patients. It is unclear why immunocompetent patients are at risk. One theory is that a high inoculation of HSV viremia at initial infection may overcome a competent immune system. Case Report: A 23 year old male with no medical history was admitted with fevers, diffuse abdominal pain, diarrhea, non-bloody emesis, and a centripetal malar rash on his lower extremities. One week prior to admission, he traveled to an amusement park in Florida on a family vacation. Shortly afterwards, he became symptomatic and arrived to our hospital 4 days after presentation. Upon initial evaluation he was found to be pancytopenic (WBC 2.9, Hgb 10.9, Plt 55,000) with hepatocellular LFT abnormalities (AST 273, ALT 236, ALP 71, INR 1.1). He was treated empirically with doxycycline for tick borne illnesses and piperacillin/tazobactam for possible aspiration pneumonia seen on CT. His clinical status deteriorated with persistent fevers, lethargy, and increasing hepatocellular liver tests (AST peaked at 3733, ALT peaked at 2564, INR peaked at 1.4). He was empirically started on acyclovir with hepatitis serology, EBV, CMV, HSV, and HIV PCR pending. A liver biopsy was performed and serum PCR was positive for HSV 1. Over the next few days, the patient improved clinically with normalization of his laboratory values. Patient was discharged on a 3-week course of acyclovir. Discussion: Common features of HSV hepatitis on presentation include fever, leukopenia, thrombocytopenia, encephalopathy, elevated aminotransferases, and coagulopathy. Interestingly, oral and/or genital lesions are seen in only 44 % of patients. Unfortunately, HSV hepatitis is frequently diagnosed post mortem due to its non-specific clinical presentation with high morbidity and mortality. HSV patients who were promptly treated with acyclovir had a much lower progression to death or liver transplantation than untreated patients; 55.1% to 81%. Therefore empiric treatment with acyclovir should be initiated early in a toxic patient prior to confirmation of HSV.


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of multiple myeloma involvement in the liver is often noted upon autopsy, very few patients ever had clinical or laboratory evidence of this.5 To our knowledge, there have been only three other cases of biopsy proven plasma cell infiltration of the liver leading to cholestatic jaundice.1,2,5

[809A] Figure 1.

[810A] Figure 1.

[809B] Figure 2.

810 A Rare Case of Obstructive Jaundice Secondary to Multiple Myeloma Hannah Jones, DO, MBA1, Erin Smith, BS2, Scott Swendsen, MD1, Thomas Sing, DO1, Vu Nguyen, MD1. 1. Baylor Scott & White, Temple, TX; 2. Texas A&M Health Science Center, Temple, TX. An 83 year old Caucasian female presented to the Gastroenterology clinic for evaluation of abnormal liver laboratory tests and painless jaundice. Physical exam demonstrated scleral icterus and jaundice. Laboratory testing demonstrated an obstructive and even infiltrative pattern with alkaline phosphatase 986 IU/L, aspartate aminotransferase 277 IU/L, alanine aminotransferase 274 IU/L and bilirubin 8.6 mg/dL. An abdominal ultrasound demonstrated intrahepatic biliary ductal dilatation and multiple hepatic masses concerning for metastatic disease. Subsequently, an endoscopic retrograde cholangiopancreatogram (ERCP) was performed and a stricture in the right hepatic duct and a filling defect in the distal duct were found. A sphincterotomy was performed and a small amount of biliary sludge was removed. The right hepatic stricture was dilated after brushings were obtained. A 10 French by 15cm stent was placed beyond the stricture. At the time of ERCP, an esophagogastroduodenoscopy (EGD) was performed which revealed multiple gastric ulcers. Cytology from the ductal brushings revealed atypical plasmacytoid cells consistent with multiple myeloma. Gastric ulcer biopsies revealed lambda restricted neoplastic plasma cells, also supportive of multiple myeloma involvement. Liver enzymes and bilirubin trended downward after stent placement. However, complications related to metastatic multiple myeloma persisted despite treatment, and she developed sepsis secondary to E.coli. She was admitted to the ICU for aggressive treatment. Approximately two weeks after presenting to the GI clinic, she passed as a result of complications related to sepsis and multiple myeloma. Multiple myeloma rarely involves the gastrointestinal system and the liver and presents with extraosseous manifestations in less than 5% of patients.2,3,5 Several cases of cholestatic jaundice have been reported secondary to abdominal plasmacytomas leading to biliary obstruction.5 However, liver dysfunction does not correlate with the classic presentation of multiple myeloma. Such cases are most commonly due to hepatic amyloid deposition or plasma cell infiltration of the pancreatic head.1,5 While evidence


[810B] Figure 2.

811 Elmiron-induced Hepatotoxicity: A Rare Case Ashraf Almashhrawi, MD1, Umair Sohail, MD1, Rubayat Rahman, MD, MPH1, Imran Ashraf, MD1, Jared Coberly, MD1, Douglas Nguyen, MD2, Matthew Bechtold, MD, FACG1. 1. University of Missouri, Columbia, MO; 2. University of California Irvine, Anaheim Hills, CA. Introduction: Pentosan polysulfate sodium (Elmiron) was approved in 1996 for the treatment of interstitial cystitis. A rare complication is elevation in liver function tests which are not associated with jaundice or other clinical signs or symptoms. We report a rare case of Elmiron-induced hepatotoxicity. Case: 32 year-old female with past medical history of interstitial cystitis, idiopathic thrombocytopenia, and chronic joint pain presented for evaluation of abnormal liver tests. She has no previously reported abnormal liver tests. She has been placed on Elmiron for her urinary symptoms. She had no jaundice or skin rash. Other GI symptoms were diarrhea, abdominal cramps, and hematochezia. She denies the use of herbs, alcohol, cigarettes, or use illicit drugs. Physical exam was unremarkable except for nonspecific mild abdominal tenderness. AST 47 units/L, ALT 173 units/L, alkaline phosphatase 114 units/L, total bilirubin 0.9 mg/dl, albumin 4.8 g/dl, INR 0.9, platelets 135 x109/L, hemo-


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Abstracts globin 13.3 g/dl, WBC 9.9 x103/mcl. Anti-nuclear antibodies, anti-smooth muscle antibodies, total immunoglobulin, anti-mitochondrial antibodies, alpha 1 anti-trypsin, ceruloplasmin, viral hepatitis panel, and celiac disease panel were all unremarkable. MRI abdomen/ MRCP showed normal liver with no intra or extrahepatic biliary ducts dilation. Liver biopsy showed focal minimal lobular inflammation. A periodic acid–Schiff with diastase digestion revealed no alpha-1-antitrypsin globules. An iron stain was negative. Trichrome stain showed no fibrosis. Abnormal liver tests were attributed to drug-induced liver injury (DILI) and Elmiron was discontinued. Liver enzymes showed nice trend downward and eventually normalized. Discussion: Elmiron-induced hepatotoxicity has been rarely reported. This case indicates that hepatotoxicity could very well occur when routine dosages are used. Providers should be aware of the association to timely manage Elmiron-induced liver injury.

812 A Case of Spontaneous Liver Rupture as a Cause of Hemoperitoneum Elliot Coburn1, Amit Desai2, David W. Wan, MD1, Sonal Kumar, MD, MPH3. 1. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, New York City, NY; 3. Weill Cornell Medical College, New York, NY. A 51 y/o Chinese male hepatitis B carrier, presented with dull RUQ pain and abdominal distention. Vitals were T 37.8, HR 100, BP 117/60. Exam notable for soft and distended abdomen, shifting dullness, periumbilical bruise, but no stigmata of cirrhosis. Labs were H/H 7.2/22.3, WBC 7.1, Plt 179, BUN/Cr 34/2.1, INR 1.5, Alb 3.1, AST 176, ALT 133, Alk Phos 530, T bili 0.8, Lactate 4.4, ABG 7.42/32/64. CT revealed moderate hemorrhagic ascites, hepatomegaly with steatosis, and prominent perigastric lymph nodes. Paracentesis revealed bloody fluid, RBC 2,420,000, HCT 19%, WBC 260 (75% PMN), Alb 1.7

(SAAG 1.4). Cultures were negative (including AFB). Cytology revealed reactive mesothelial cells but no malignancy. LDH was > 2000 raising suspicion for lymphoma with liver infiltrative disease. CT angiogram was performed (see Figure 1). Liver biopsy was planned, however the patient became unstable. Hgb was 6, lactate 21, and arterial pH 6.9. Hemorrhagic shock was suspected. Massive transfusion protocol was initiated. Patient went for exlap where 3L bloody ascites was evacuated. Intraoperatively, the liver appeared nodular, swollen, with multiple briskly bleeding cracks in parenchyma. The liver was packed with pads. Patient then underwent hepatic artery embolization. He soon went into acute liver failure and expired. Autopsy was not performed. Etiology of liver disease suspected to be an infiltrative process (i.e. amyloid secondary to a hematologic malignancy or lymphoma itself). SH is rare but life-threatening. It can be the result of non-traumatic intra-abdominal organ rupture or abdominal vasculature pathology. Surgery and/or angioembolization are the mainstays of treatment.1 Liver etiologies of SH include HCC rupture, hemangioma rupture, adenoma rupture, HELLP syndrome, infiltrative disease (i.e. amyloid), and peliosis hepatis2,3,4,5. Diagnosis relies on imaging such as ultrasound or CT.5 Early surgical intervention is critical in this highly morbid disease. References: [1] Kasotakis G. Spontaneous hemoperitoneum. Surg Clin North Am. 2014 Feb;94(1):65-9. [2] Lugito NP, et al. Hemoperitoneum caused by spontaneous rupture of hepatocellular carcinoma. Acta Med Indones. 2015 Jan;47(1):56-60.3) [3] De Beul P, et al. Spontaneous rupture: a rare complication of hepatic hemangiomas. JBR-BTR. 2014 Sep-Oct;97(5):287-8. [4] Mascarenhas R, et al. Spontaneous hepatic rupture: a report of five cases. HPB : The Official Journal of the International Hepato Pancreato Biliary Association. 2002;4(4):167-170. [5] Pan W, et al. Surgical treatment of a patient with peliosis hepatis: A case report. World Journal of Gastroenterology : WJG. 2013;19(16):2578-2582.

813 Completely Reversed: A Rare Case of Colon Cancer With Hepatic Metastasis in a Patient With Situs Inversus Totalis Youran Gao1, Gregory M. Grimaldi, MD2, Tai-Ping Lee, MD2. 1. Long Island Jewish Medical Center, North Shore-LIJ Health System, Glen Oaks, NY; 2. Long Island Jewish Medical Center, North Shore-LIJ Health System, Manhasset, NY. Introduction: Situs inversus totalisis a rare condition characterized by inverted positioning of part or all the thoracic and abdominal viscera creating a mirror image. It occurs in about 1 in 8000-10000 cases. Patients with situs inversus totalis have similar life expectancies as the general population. Many times these patients will be diagnosed incidentally on radiological imaging. Diagnosis and treatment are often delayed due to unawareness of the possibility of situs inversus. Herein, we report a patient with situs inversus totalis having colon cancer with metastasis to the liver and urinary bladder. Case Report: A 72 year-old man with history of DM, hypertension, sleep apnea, achalasia, status post sigmoid colon resection for diverticulitis, and situs inversus totalis was referred to our institution for management of a colon mass and liver lesion. He developed rectal bleeding. A colonoscopy one year ago showed umbilicated, near circumferential mass at 20cm above anal verge and large 1cm polyp in descending colon. Biopsy report showed moderately differentiated invasive adenocarcinoma with high grade dysplasia and tubular adenoma respectively. Computed Tomography (CT) of abdomen showed complete situs inversus with no biliary or vascular anomaly (Image 1). He subsequently underwent a low anterior resection of sigmoid colon mass and excision of perivesicular mass. The surgical resection showed a 6.0cm infiltrative high grade adenocarcinoma of intestinal phenotype, pT4bpN1c. Post-operative course was complicated by small bowel obstruction requiring exploratory laparotomy and lysis of adhesions followed by adjuvant chemotherapy. An indeterminate lesion of 2 cm in the liver was seen on a CT of the abdomen (Image 2) prior to surgery. Follow up MRI demonstrated interval increase to 4cm despite chemotherapy for 3 months. An exploratory hepatectomy of segments 6 and 7 with cholecystectomy was successfully performed. The patient continued on chemotherapy postoperatively. Discussion: Although our case of situs inversus totalis with colon cancer and liver metastasis did not demonstrate any vascular or multiple hepatobiliary anomalies, many of these patients may have variations in anatomy. It is important to thoroughly review radiological imaging of vasculature and organs prior to procedures or surgeries to decrease complications.

[812A] Figure 1.

[813A] Figure 1.



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816 Anorexia Nervosa-Induced Hepatocyte Autophagy Resulting in Severe Acute Mixed Cholestatic and Hepatocellular Liver Injury Parit Mekaroonkamol, MD, James Spivey, MD. Emory University, Atlanta, GA.

[813B] Figure 2.

814 Dengue Infection With Severe Acute Hepatitis and Acalculus Cholecystitis: A Diagnostic Challenge Teong Jin. Tee, MD. Nilai Medical Centre, Kuala Lumpur , Malaysia. Introduction: Dengue is one disease entity with different clinical presentations and often with unpredictable clinical evolution and outcome.It is the most frequent arbovirus disease in the world and the most important one in terms of morbidity and mortality.With rising disease burden atypical manifestations have increased as well which are missed most often due to lack of awareness. We present one atypical dengue infection with severe acute hepatitis, acalculus cholecystitis and normal platelet count. Case Report: A 19 year-old Bangladeshi student without any past history was admitted to ward due to fever, nausea ,vomiting ,jaundice and epigastralgia for 1 week.Patient denied of any drug or alcohol history .Generally he is jaundice and lethargy. His blood test AST 2502 U/L,ALT 2331 U/L,Bil(T) 242.6 umol/L, Bil(D) 216.4 umol/L, AlK-P 195 U/L,Albumin 38 g/L,INR 1.89,PT 20.3 S,APTT 33 S,Platelet 181000 ul,Hepatitis marker HBsAg (-),Anti HCV (-),Anti HAV(-) leptospirosis IgM(-),Abdomen Ultrasound was done with acalculus cholecystitis and bilateral pleural effusion. During hospitalization Blood investigation of ANA ,C-ANCA and P-ANCA ,Anti Mitochondrial antibodies,Anti HIV ,blood film for malarial antigen all are negative. Day 3 of admission ,dengue blood tests were taken Dengue NS-1 Ag (-) ,Dengue IgM(+),Dengue IgG (-).Adequate Intravenous Normal saline hydration fluids replacement ,prophylactic antibiotics were given .He was hospitalized for 13 days and discharged .One week later ,he follow up in clinic ,his blood test results AST 57 U/L,ALT 138 U/L, Bil(T) 45.7umol/L, Bil(D) 35.8 umol/L,INR 1.23,PT 14.7S,APTT 31S ,Platelet 452000 ul.This patient had recovered uneventfully with great improvement. Discussion: Most common dengue fever symptoms are fever ,myalgia, headache, rash, arthralgia and epigastralgia.Rare manifestation are severe hepatitis, hepatic failure ,dengue encephalitis ,renal failure, acalculous cholecystitis. The exact pathogenesis of dengue hepatitis is unknown .It could be either virus direct cytotoxicity to hepatocytes or its immue mediated injury led to stimulating apoptosis and microvesicular steatosis leading to severe dengue hepatitis.The elevation in the level of AST enzyme is normally greater than the elevation in the level of ALT in dengue patients during the first week of infection, and this is an uncommon phenomenon in patients with hepatitis A, B, or C. Dengue related acalculous cholecystitis resolves spontaneously with supportive care in majority of cases. Conclusion: Clinical doctors should be alert to detect and manage the atypical manifestations of dengue fever.Clinical vigilance about these presentations is vital for dengue early treatment.

815

Anorexia nervosa is a debilitating psychosomatic disease with prevalence ranging from 0.3-4%. Although mild AST/ALT elevation can occur in malnourished patients, severe acute liver injury is rare and can pose a diagnostic dilemma in this population whose iron and copper metabolism are deranged. Here, we report a case of an anorexic patient who developed starvation-induced, severe, acute, cholestatic and hepatocellular liver injury. A 22-year-old female with anorexia nervosa presented with failure to thrive. Her body mass index was 9.1 kg/m2. Initial liver function tests were normal except for mildly elevated ALT of 51 unit/L. During her hospitalization, she refused to eat anything but liquid diet. Despite intravenous fluid support and some oral intake, she could not reach her caloric goal. After 4 weeks of conservative treatment, she developed right upper quadrant abdominal pain and jaundice. Laboratory tests revealed elevation of liver biochemical tests including AST of 5416 unit/L, ALT of 4227 unit/L, ALP of 700 unit/L, and total bilirubin of 4.7 mg/dL. MRCP was unremarkable with patent vessels. The INR increased to 1.7. Ammonia level was 103 mcmol/L but with intact mental status. Her electrolytes and creatinine remained normal except for hypophosphatemia of 1.6 mg/dL and hypokalemia of 3.0 mg/dL. She was well hydrated with no hypotension. Viral hepatitis panel and autoimmune hepatitis markers were negative. No new medications had been initiated. Other evaluation included low ceruloplasmin of 11 mg/dL and immeasurably high transferrin saturation (ferritin of 4297 ng/mL, TIBC of 116 mcg/dL, serum iron of >500 mcg/dL). Parenteral nutrition support was promptly started. She slowly regained her weight with an inverse decline of her liver enzymes. All liver function tests returned to baseline after 14 days of parenteral nutrition. This case underscores starvation as a principle cause of severe acute liver injury. The lack of other precipitators, together with gradual recovery after parenteral nutrition led us to believe that hepatocyte autophagy played an important role. Similar cases have been reported when BMI is less than 13 kg/ m2. The degree of liver injury has been shown to inversely correlate with BMI as demonstrated in our case. Elevation of transferrin saturation and ceruloplasmin level should be interpreted with caution as they can be misleading in malnourished patients. Aggressive nutritional repletion is the cornerstone of treatment.

[816A] Figure 1.

A Case of Sickle Hepatopathy Secondary to Influenza A Brett Van Leer-Greenberg, MD1, Barra Neary, MD1, Sagar Shroff, MD2, Sonali Sakaria, MD3. 1. Emory University School of Medicine, J. Willis Hurst Internal Medicine Residency Program, Atlanta, GA; 2. Emory University, Atlanta, GA; 3. Emory University Division of Digestive Diseases, Atlanta, GA. Sickle Cell Intrapheatic Cholestasis (SCIC) is a rare and potentially fatal complication of sickle cell disease characterized by abdominal pain, hepatomegaly, and hyperbilirubinemia with variable transminase levels. Its clinical course ranges from benign lab abnormalities to acute liver failure carrying a mortality rate of greater than 50%. We present an unusual case of SCIC precipitated by Influenza A infection. A 41 year-old African-American male with a history of HbS-Beta Thalassemia presented with one week of diffuse myalgias and fevers. On admission, the patient was febrile to 38.6°C with SaO2 96% on room air. He had diffuse jaundice, normal lung exam, and tender hepatomegaly. His laboratory studies were significant for WBC count 13.8x103/μL, hemoglobin 8.5 g/dL, platelets 297x103/μL, total bilirubin 12.5 mg/dL (direct 7.0 mg/dL), AST 733 U/L, ALT 738 U/L, AP 238 U/L, INR 1.4, and HbS index of 35%. Infectious work-up was negative for blood cultures, hepatitis and viral serologies, but Influenza A titer was positive at 1:16. The patient was initially managed for Influenza A and Sickle Cell Crisis with intravenous fluids, analgesia, and oseltamavir. Hematology consultation deferred Exchange Blood Transfusion (EBT) because the HbS index downtrended from 35% to 15% with traditional blood transfusions; however, his clinical course worsened, marked by increasing abdominal pain and encephalopathy. While transaminases normalized, his total bilirubin and INR continued to rise to 60 mg/dl and 11.6 respectively over ten days. A diagnosis of acute liver failure due to SCIC was reached based on laboratory and clinical assessment. He experienced multiple complications of acute liver failure and died. Just over 50 cases of SCIC have been reported in the adult and pediatric literature to date. SCIC is caused by diffuse sickling within the hepatic sinusoids that leads to hypoxic hepatic damage and acute hepatic failure. Infection is thought to trigger SCIC in some cases, but Influenza A has not previously been reported as a precipitant of SCIC. The only known effective intervention is Exchange Blood Transfusion to decrease Hbs to below 30% in order to remove sickle cells from participating in vaso-occlusive events, reduce hemolytic complications, and provide added oxygen carrying capacity. If EBT is ineffective, liver transplantation remains an option although the literature suggests poor outcomes in this patient population.


817 Ascites as a Manifestation of Constrictive Pericarditis Jacqueline Rampy, MD, Sumeet Asrani, MD, MSc, L. August Clark, MD. Baylor University Medical Center, Dallas, TX. In the United States, ascites is most often due to portal hypertension related to liver cirrhosis. We describe a case of constrictive pericarditis presenting with abnormal liver function tests, anasarca, and ascites. A 50-year-old Caucasian man presented with anasarca. Two years prior to presentation, he experienced dyspnea, lower extremity swelling extending to the scrotum, and a 40 pound weight gain. One year later, he started developing ascites. On physical exam, he was found to have jugular venous distention, marked hepatomegaly, dullness in flanks, and anasarca. Laboratory tests revealed mildly elevated alkaline phosphatase, INR, and indirect bilirubin. Workup for chronic liver disease was unrevealing and ultrasound of the liver showed ascites and hepatosplenomegaly without evidence of cirrhosis, portal vein, or hepatic vein thrombosis. Paracentesis revealed an elevated serum-ascites albumin gradient (SAAG) and increased total protein in the ascites fluid. Computed tomography of the chest showed pericardial thickening and moderate ascites. A right heart catheterization showed a positive Kussmaul sign with markedly elevated and equal filling pressures in the heart consistent with constrictive pericarditis. The patient subsequently underwent a full pericardial resection with resolution of his symptoms and normalization of his liver tests. A cardiac cause of ascites can be easily mistaken for primary hepatic cirrhosis when a patient presents with ascites, elevated liver function tests, and peripheral edema. A SAAG of greater than or equal to 1.1 g/dL and an ascites fluid total protein level of greater than 2.5 g/dL suggest constrictive pericarditis. In cirrhosis, the SAAG is much greater than 1.1 g/dL while the ascites fluid total protein level is less than 2.5 g/dL. A right heart catheterization showing elevation and equalization of the right atrial pressure, pulmonary capillary wedge pressure, mean pulmonary arterial pressure, right ventricular diastolic pressure, and left ventricular diastolic pressure can support the diagnosis of constrictive peri-


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Abstracts of liver disease. On initial physical exam, she was noted to be anicteric without evidence of chronic liver disease. On admission her alkaline phosphatase was 363 U/L, aspartate transaminase 99 U/L, alanine transaminase 224 U/L, lactate dehydrogenase 304 U/L, total bilirubin 2.9 mg/dL, direct bilirubin 2.4 mg/dL, and ESR 70 mm/hr. Two months prior, her liver function tests were normal. Hepatitis A, B, and C serologies were negative. Immunoglobulin G, anti-mitochondrial antibody, and antinuclear antibody were negative. Anti-smooth muscle antibody was positive with a titer of 1:20. Right upper quadrant ultrasound was normal and MRCP was negative for AIDS Cholangiopathy. Liver biopsy showed moderate eosinophils with active hepatitis consistent with either drug-induced liver injury (DILI) or autoimmune hepatitis. Her HAART medications were stopped and liver function tests were monitored because of possible DILI. Five months later her liver function tests worsened despite being off HAART; ALP 2236, AST 460 ALT 405, LDH 337, total bilirubin 1.9, and direct bilirubin 1.3. She was then placed on a trial of prednisone 40 mg daily for suspected autoimmune hepatitis. Three days later she had notable improvement in her labs; ALP was 972, ALT 124, AST 192, LDH 308, total bilirubin 0.8, and direct bilirubin 0.5. Discussion: The patient’s autoimmune hepatitis score was 19; a score >15 indicates definite autoimmune hepatitis. This patient had characteristic histologic findings of AIH and a prompt improvement in liver function tests after initiation of corticosteroid therapy. For clinicians who care for patients with HIV and are initiated on HAART, abnormal LFT’s may be secondary to autoimmune hepatitis from IRIS.

820 Masquerading Myositis: An Important Cause of Elevated LFTs Jeffrey Dueker, MD, MPH1, Joseph Ahn, MD, MS, FACG1, Willscott Naugler, MD1, Atif Zaman, MD, MPH1, Sarah Diamond, MD2. 1. Oregon Health & Science University, Portland, OR; 2. Portland, OR.

[817A] Figure 1.

carditis. In cases of constrictive pericarditis, diagnosis and treatment in a timely manner is important, as most patients have resolution of symptoms with pericardiectomy.

818 Intrahepatic Lithiasis in a Westerner Drew Triplett, DO1, Nyla Hazratjee, MD2, Christopher Barde, MD2. 1. Wright State University Boonshoft School of Medicine, Dayton, OH; 2. Wright State University, Dayton, OH. Intrahepatic lithiasis, defined as calculi proximal to the confluence of the right and left hepatic ducts is a common entity in Asian populations, but rare in Americans, that can be challenging to diagnose in western populations. A 40 year old Caucasian male presented to medical attention multiple times over a period of greater than ten years for recurrent abdominal pain. He initially underwent cholecystectomy at the age of 20 for symptomatic cholelithiasis. A few years later he presented with recurrent abdominal pain mimicking his prior symptoms before cholecystectomy and underwent ERCP which showed common bile duct dilatation and intrahepatic duct dilatation. Endoscopic stone removal and biliary duct stenting were preformed leading to symptom improvement. He subsequently represented with abdominal pain, nausea and vomiting. Repeat ERCP showed common bile duct dilatation and a large obstructing stone of the left hepatic duct. After electrohydraulic lithotripsy dozens of non-faceted, pearly white stones were released from the left lobe of the liver. After representing with similar symptoms, he was treated by ERCP with a fully covered metal stent placed in the common bile duct to allow unimpeded passage of the stones. The patient continues to have occasional episodes of cholangitis from stent occlusion where only a few stones have been observed. But a large number of stones are still visible intrahepatically and a future treatment to be considered is a hepatic resection. Often intrahepatic lithiasis is an asymptomatic process, with some patients becoming symptomatic over a period of years. The most common symptoms of presentation are cholangitis, abdominal pain, or jaundice. The etiology of these stones is most often pigmented stones, and it is theorized that most stones in Western persons are of gall bladder etiology, while parasitical or bacterial infections are most commonly found in Asian patients. A genetic link to an acidic glycoprotein, osteopontin, seems to be involved with hepatolithiasis, but more studies are needed to classify the exact link. Biliary sepsis, intrahepatic abscess and cholangiocarcinoma are all potential complications. Conservative treatment options in mild cases are reasonable, more severe cases may require endoscopic or surgical intervention. This case highlights intrahepatic lithiasis as a rare cause of biliary stones and cholangitis like symptoms in a western person.

819 Immune Reconstitution Inflammatory Syndrome Causing Autoimmune Hepatitis in an HIVinfected Patient Started on Highly Active Antiretroviral Therapy Brian T. Moy, DO1, Houman Rezaizadeh, MD2. 1. Department of Medicine, University of Connecticut Health Center, Hartford, CT; 2. Division of Gastroenterology and Hepatology, University of Connecticut Health Center, Farmington, CT. Introduction: Immune Reconstitution Inflammatory Syndrome (IRIS) is seen in patients with human immunodeficiency virus who begin Highly Active Antiretroviral Therapy (HAART). Patients with IRIS can experience a hyperactive immune system from reconstitution leading to antibody formation to autoantigens. Here we report the rare case of autoimmune hepatitis caused by IRIS. Case Report: A 33-year-old African American female with HIV/AIDS (CD4 count of 17) was recently started on cobicistat, elvitegravir, emtricitabine, and tenofovir (HAART) 1 week prior to admission. She presented to the hospital complaining of fever, chills, and muscle aches. Her infectious workup was unrevealing and she was subsequently diagnosed with IRIS. She consumes less than 25 grams of alcohol daily, denies the use of over the counter or herbal supplements, and denies a preexisting or family history


Clinical Presentation: A 42 yo Native American man with hepatitis C virus (HCV) and alcoholic cirrhosis (Child B) presented with lower abdominal pain and elevated liver function tests (LFTs) after an uneventful colonoscopy four days prior to admission. Labs at presentation were AST 658 U/L, ALT 179 U/L, and total bilirubin (TB) 1.5 mg/dL. Baseline labs 6 weeks prior were AST 59, ALT 38, and TB 1.8. Urine drug and blood alcohol screens were negative on admission. Diagnostic paracentesis was negative for spontaneous bacterial peritonitis. An ultrasound showed a cirrhotic liver with moderate ascites and without portal vein thrombosis. A transjugular liver biopsy was planned for further evaluation, but was aborted when creatinine kinase (CK) returned at 6700 U/L (normal range 49-397 U/L). Further history revealed proximal upper extremity weakness, and additional testing revealed positive antinuclear antibodies (ANA) at a titer of 1:1280 in a speckled pattern. An MRI of the pelvis/thighs showed features consistent with myositis within the lower anterior abdominal and pelvic walls. A sartorius muscle biopsy demonstrated severe necrotizing myopathy with mild inflammation. The differential diagnosis included both necrotizing and inflammatory myopathies, and the possibility of an HCV-related myopathy was raised. The patient was started on immunosuppressive therapy for the possibility of inflammatory myopathy. Three months later, although CK levels declined to 835 U/L, the patient’s muscle weakness and dysphagia had progressed, requiring feeding tube placement. Treatment of the patient’s HCV is being planned. Discussion: Necrotizing myopathies can be due to immune-mediated causes, including connective tissue diseases, malignancies, and HCV. Non-immune mediated causes of necrotizing myopathies include drugs, such as statins, as well as alcohol and cocaine. An important learning point is that an elevated AST can result from non-liver sources, usually muscle, as seen in this case. In addition, nearly every abnormality in blood tests used to assess hepatic infl ammation, injury, or function, can all arise from non-hepatic sources, and awareness of these scenarios is helpful in arriving at the correct diagnosis, as well as avoiding unnecessary procedures like liver biopsy. This is especially true for patients with pre-existing liver disease, where attention can be inadvertently focused solely on the liver.

821 Hepatogastric Fistula Presenting as Melena Rucha Mehta, MD, Vishal Desai, MD, Shubha Singh, MD, Rana Abraham, MD, Sohrab Mobarhan, MD. Rush University Medical Center, Chicago, IL. A 63-year-old female with non-small cell lung cancer with metastasis to the brain, liver, and stomach presented with abdominal pain, melena, and acute blood loss anemia with a hemoglobin of 4.4 g/dL. She recently underwent radioembolization of her liver metastatic disease and was doing well until her presentation with a GI bleed. EGD revealed a large ulcer on the anterior wall of the duodenum with pathology consistent with poorly differentiated carcinoma presumed to be metastatic disease. However, abdominal imaging revealed a large mass extending from the liver to the duodenum with an associated hepatogastric fistula with debris concerning for food debris. GI was reconsulted for management of rebleeding but deferred endoscopic intervention given need for embolization, performed by IR. Bleeding resolved after direct embolization of the gastroduodenal artery, superior mesenteric artery, and branches of the right hepatic artery. Metastatic disease to the liver is more common than primary liver cancer (1). Lung, breast, and colon cancer are the three most common culprits of metastatic disease to the liver (1). Cases have been described of hepatogastric fistulas as complications of cholangiocarcinoma, hepatocellular carcinomas, transarterial chemoembolization procedures, and pyogenic liver abscesses, but this is a a rare case of metastatic non-small cell lung cancer with development of melena, which led to the detection of a hepatogastric fistula (2,3,4,5). As such, this case is relevant to the literature, and GI fistulizing disease should be considered in the setting of hepatic metastatic disease in non-small cell lung cancer. . References: [1]. Ananthakrishnan, Ashwin, Veena Gogineni, and Kia Saeian. “Epidemiology of Primary and Secondary Liver Cancers.” Semin Intervent Radiol Seminars in Interventional Radiology 23.1 (2006): 047-63. [2]. Brown, Cortlyn, Charlie Chen, and Charles Cha. “Gastrohepatic Fistula as a Complication of Laparoscopic Radiofrequency Liver Ablation in a Patient With Intrahepatic Cholangiocarcinoma.” Journal of Clinical Gastroenterology (2014): 1. [3]. Naymagon, Steven, et al. “Gastroduodenal Ulceration Associated with Radioembolization for the Treatment of Hepatic Tumors: An Institutional Experience and Review of the Literature.” Dig Dis Sci 55.9 (2010): 2450-458. [4]. Sayana, Hari, Osama Yousef, and Wendell K. Clarkston. “Massive Upper Gastrointestinal Hemorrhage Due to Invasive Hepatocellular Carcinoma and Hepato-gastric Fistula.” WJG World Journal of Gastroenterology 19.42 (2013): 7472. [5].


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[822]

Table 1. Time Course of Events

Date

Event

April 2013

Pneumoperitoneum, likely from perforated ulcer Placed on SBP prophylaxis

May 2013

First episode of C. Difficile Infection

May 2013–July 2014

4 episodes of C. Difficile Infection despite vancomycin tapers

July 2014

Discontinuation of SBP prophylaxis Fecal microbiota transplantation

Present

No recurrence of C. Difficile Infection

Gandham, V. S., B. Pottakkat, L. C. Panicker, and R. V. Hari. “Hepatogastric Fistula: A Rare Complication of Pyogenic Liver Abscess.” Case Reports 2014.Jul17 1 (2014).

was discharged on ciprofloxacin (750 mg weekly) for SBP prophylaxis. One month later, the patient developed CDI and was treated with vancomycin due to renal insufficiency. Following this, the patient had four more episodes of CDI despite prolonged vancomycin tapers. SBP prophylaxis was discontinued due to recurrent CDI and no ascites on an abdominal ultrasound. He underwent FMT with clearance of Clostridium difficile toxin, cessation of diarrhea, improvement in nutritional status, and no recurrence of ascites or hepatic encephalopathy. Discussion: While there is clear efficacy for FMT in the treatment of recurrent CDI, there is no data on its safety in patients with liver cirrhosis. The ramifications of altering the number and composition of colonic bacteria in this patient subgroup with high mortality from infections due to bacterial translocation are unknown. Changes in the gut microbiota may affect the permeability of the small bowel, alter the mucosal and systemic immunity, and contribute to hepatic inflammation. Most data on the role of altered gut microbiota in the development of complications from liver cirrhosis are based on animal studies. The above case illustrates the successful use of FMT in a patient with liver cirrhosis without ascites. Evidence for the efficacy and safety of FMT in patients with cirrhosis remains quite limited. Subgroup analysis of FMT in patients with liver cirrhosis, particularly decompensated or with ascites, warrants additional study.

822

823

Fecal Microbiota Transplantation in a Patient With Liver Cirrhosis: Changing the Intestinal Microbiota in a High-Risk Group

Cholestatic Hepatitis in a Patient With Eosinophilic Granulomatosis and Polyangiitis

[821A] Figure 1.

Kelly Pitts, MD, Neeral Shah, MD, Dushant Uppal, R. Ann Hays, MD. University of Virginia, Charlottesville, VA. Introduction: Liver cirrhosis is associated with immune dysfunction and a high rate of mortality due to infections, with the most common source being gut microbes. Antibiotic prophylaxis is often used to limit translocation of enteric organisms although likely increases the risk of Clostridium difficile infection (CDI). In this case, we present a patient with cirrhosis and bacterial peritonitis who was started on antibiotic prophylaxis and developed recurrent CDI requiring fecal microbiota transplantation (FMT). Case: A 79-year-old man with alcoholic cirrhosis, hepatic encephalopathy, and gastric varices was admitted for abdominal pain and was found to have pneumoperitoneum likely due to a contained gastric ulcer perforation. Despite conservative management with IV fluids, metronidazole, ciprofloxacin, and decompression with a nasogastric tube, he developed worsening ascites. A paracentesis demonstrated WBC of 11,129 with 91% polymorphonuclear leukocytes. The patient improved with antibiotics and

Sean Doran1, Khalil Abuamr2, Fadi Hamid, MD3. 1. University of Missouri, Kansas City, MO; 2. University of Missouri, Kansas City, Overland Park, KS; 3. St. Luke’s Hospital of Kansas City, Leawood, KS. Introduction: Eosinophilic Granulomatosis with Polyangiitis (EGPA) is a multisystem disorder, commonly treated with chronic steroid therapy, characterized by asthma, chronic rhinosinusitis, and

[823]

Table 1. Liver Function Tests Before and After Treatment Course Total Bilirubin

AST

ALT

Alkaline Phosphatase

Pre-Treatment Value

6.9

185

212

365

Post-Treatment Value

0.8

37

49

155

[823A] Figure 1.



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Abstracts prominent eosinophilia. EGPA can involve any organ system, lungs being most common. Eosinophilic gastroenteritis is the most common gastrointestinal involvement, typically presenting with abdominal pain and diarrhea. Liver/biliary involvement in EGPA is reported but rare. The case below is a patient with EGPA who has had a several year history of RUQ abdominal pain, intermittent elevated LFTs, and jaundice and further evaluation revealed EGPA-related cholestatic hepatitis by liver biopsy. Case Description: The patient is a 57 y/o male with a history of EGPA on chronic steroids, GERD, and gallstone pancreatitis that has had several admissions since 2009 for chronic RUQ pain, nausea, elevated LFTs and jaundice. He underwent cholecystectomy in 2009 with liver biopsy at that time which revealed portal and periportal hepatitis as well as centrilobular cholestasis. On his most recent presentation, it was thought he had choledocholithiasis and possible cholangitis. His bilirubin remained elevated despite an ERCP that was done with extraction of small stones and sludge. He underwent a second ERCP with sludge extraction and common bile duct stent placement but his bilirubin remained elevated. Chronic liver disease markers were negative. Given his previous biopsy results, another liver biopsy was obtained and demonstrated liver parenchyma with cholestasis, predominantly in pericentral zones and accompanying mild to moderate mixed acute and chronic lobular inflammation with evidence of hepatocyte damage. This is consistent with a cholestatic hepatitis seen in patients with Churg-Strauss Syndrome/EGPA. His steroids were increased to 60mg daily for 1 month. Weekly labs were obtained and his liver chemistries normalized over two months. His prednisone was tapered down to his original dose of 20mg daily. Discussion: Liver involvement in EGPA is rare but should be considered in patients with a history of EGPA who present with cholestasis. Better control of EGPA with immunosuppression has shown significant improvement in these cases.

[824B] Figure 2.

824 Intestinal Tuberculosis After Liver Transplantation: Are Current Pre-transplant Latent TB Screening Tests Adequate? Arvind R. Murali, MD1, Sanjeev Patil, MD2, Jose Gonzales Zamora , MD3, Sarah Hoehnen, MD4. 1. University of Iowa Hospitals and Clinics, Iowa City, IA; 2. University of Iowa Hospitals and Clinics, Coralville, IA; 3. Georgia Regents University, Augusta, GA; 4. Rush University Medical Center, Chicago, IL. 52 year old gentleman with hepatitis B received Liver Transplantation (LT) for decompensated cirrhosis. He had negative Tuberculin skin test (TST) and normal chest Xray on pre-LT screening. No known tuberculosis(TB) contacts. 2 years post-LT he presented with 8 weeks of abdominal pain, intermittent hematochezia and weight loss. He was on tacrolimus, cellcept and adefovir. Stool studies were negative. Serum CMV PCR was negative. CT scan showed thickening of ascending colon, cecum, appendix and terminal ileum(TI) with mesenteric stranding. Colonoscopy showed 50% circumferential ulcerated, polypoid mass at the junction of the cecum and ileocecal valve. Biopsy revealed fragments of inflammatorytype polyp with ulceration without dysplasia or malignancy. The cause of ulceration was histologically indeterminant. Immunostains for CMV, HSV and AFB were negative. Due to concern for lymphoproliferative disease, a right hemicolectomy was performed during which hard white studding throughout the distal small bowel, induration, and mass like conglomeration of the TI and the cecum were noted. Frozen section revealed granulomas. Histopathology revealed extensive transmural enterocolitis and necrotizing granulomas in the ileum, colon, appendix and several regional lymph nodes. Stains for AFB and fungi were negative. CT chest showed few small calcified perivascular and left hilar lymph nodes reflecting prior granulomatous disease. He was started on 4 drug anti-TB regimen. Two weeks later, tissue cultures grew acid fast bacilli that were identified as mycobacterium tuberculosis with DNA probe. At 3 month follow up, patient reported complete resolution of symptoms. LT recipients are screened for latent TB prior to LT with TST, interferon-γ release assays and chest X ray. TST has poor sensitivity due to anergy in cirrhotics. A number of patients with advanced cirrhosis have indeterminate test results with Quantiferon gold. History of prior exposure to TB, though important, has low sensitivity. One study showed improved detection of latent TB infection using chest CT scan. CT scan may not be feasible or cost-effective in all patients, but it could be considered in patients at high risk for latent TB (endemic regions, incarceration). Diagnosing TB reactivation post-LT is challenging. Quantiferon gold test requires adequate activation of T cells by TB antigens, which may be diminished post-LT. Hence, a high index of suspicion is needed to identify TB reactivation post-LT.

825 An Unexpected Interaction Between Simeprevir and Sirolimus: A Case Report Kamran Qureshi, MD1, Sushrut Trakroo, MD2, David Johnson, PharmD, BCPS2. 1. Temple University School of Medicine, Philadelphia, PA; 2. Temple University Hospital, Philadelphia, PA. Case report: 58 year old male was started on combination regimen of Sofosbuvir 400 mg daily and Simeprevir 150 mg daily for recurrent Hepatitis C infection (HCV), 3 years after liver transplant (LT) which was performed for HCV genotype 1a related decompensated liver cirrhosis. He was on stable dose of Sirolimus 2 mg daily for immunosuppression because of stage 3 chronic kidney disease due to calcineurin inhibitors induced nephrotoxicity. He showed rapid virologic response with undetectable viral load by week 2, but we also noticed a sudden rise in Sirolimus trough levels from a steady baseline state (Figure 1). Sirolimus dose was reduced to half then further to one-fourth of the pre HCV treatment dose by week 4. Ultimately Sirolimus had to be held because of continued rise in its levels. At that time he showed significantly worse proteinuria indicating Sirolimus related nephrotoxicity. With holding Sirolimus, its levels trended towards a baseline of 6-7 mcg/ L, and then it was reinitiated at the dose of 1 mg every other day at 9 weeks of HCV therapy and was maintained at that level till 12 weeks treatment completion. 4 weeks after the completion of HCV treatment, Sirolimus levels began to drop and dose was increased to 1 mg daily. At 8 weeks post treatment Sirolimus levels remained sub-therapeutic and it was increased to a pretreatment dose of 2 mg daily. He showed a steady therapeutic range Sirolimus levels at week 12 post treatment completion and continued to be on a 2 mg daily dose of sirolimus and achieved Sustained Virologic Response. Discussion: Cytochrome-P450 (CYP3A4) in enterocytes and hepatocytes and P-glycoprotein (P-gP) on enterocytes play a major role in sirolimus metabolism lowering its bioavailability to 14%. Drugs acting on CYP3A4 and P-gP affecting sirolimus levels are well described. Sofosbuvir does not affect CYP 3A4 or P-pg and although simeprevir is a substrate for CYP3A4 metabolism, >90 % is excreted unchanged. Simeprevir inhibits gut CYP 3A4 and organic anion transporting polypeptide (OATP). These inhibitions are not clinically relevant in interaction studies with tacrolimus and cyclosporine. However, the pharmacokinetics of simeprevir has not been studied with sirolimus. Simeprevir could potentially increase sirolimus levels by 2 mechanisms: increase absorption by inhibiting gut CYP3A4 and decrease clearance from blood by inhibiting P-gP. These pathways are likely routes for the elevated blood levels of sirolimus seen in our patient. Conclusion: Direct Acting Antivirals for HCV medications are relatively new and have limited real world experience. Physicians prescribing them should be wary of unpredicted and untested drug interactions and therefore frequent monitoring is warranted.




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826 A Rare Cause of Abnormal Liver Enzymes in an HIV-Infected Patient Hao Chi Zhang, MD, Nabil Mansour, MD, Maya Balakrishnan, MD, MPH. Baylor College of Medicine, Houston, TX. Introduction: Abnormal liver enzymes are frequent among HIV-infected individuals, commonly attributed to co-infection with viral hepatitis, alcohol, or medications. Consequently, autoimmune liver disease may be missed and requires a high level of suspicion. Case presentation: A 52-year-old woman presented with jaundice. She had HIV infection, acquired ten years prior, treated with a stable anti-retroviral regimen, Graves disease, and remote alcohol use. For three years, she experienced fatigue, periodic abdominal discomfort, and fluctuating transaminases. She had a negative HCV antibody and isolated positive HBV IgM with an undetectable viral load. For concern of drug injury, she stopped methimazole and underwent thyroid ablation for treatment of Graves disease. The liver enzymes continued to worsen in a mixed hepatocellular and cholestatic pattern. Her physical exam revealed jaundice without hepatomegaly or stigmata of advanced liver disease. Admission labs revealed: ALT 571 U/L, AST 908 U/L, alkaline phosphatase 377 U/L, total bilirubin 6.2 mg/dL, CD4 count 540 (undetectable viral load), ANA titer 1:640, and positive anti-smooth muscle and anti-mitochondrial antibodies. Transjugular liver biopsy with pressure measurements was performed. Liver histology was characterized by plasmacytic infiltrates, interface hepatitis, bile duct proliferation, and stage 4 fibrosis. Hepatic venous pressure gradient was 10 mm Hg. Autoimmune hepatitis/primary biliary cirrhosis (AIH/PBC) overlap syndrome with progression to cirrhosis was diagnosed. Oral prednisone and ursodiol were started, with improvement in jaundice and liver enzymes. Discussion: We report a rare case of AIH/PBC overlap syndrome in an HIV-positive woman. Recognizing this diagnosis is challenging as confounding clinical factors may obscure aggressive evaluation of liver enzymes. Interestingly, this patient had two autoimmune conditions diagnosed after acquiring HIV: Graves disease and AIH/PBC overlap syndrome. Proposed mechanisms for autoimmunity specific to HIV include the direct role of viral particles, molecular mimicry, and potential immune restoration consequent to antiretroviral therapy. Recognizing the potential link between HIV infection and autoimmune disease is important. While viral hepatitis, alcohol, and drug toxicity account for the preponderance of abnormal liver enzymes cases, the possibility of autoimmune liver disease ought to be considered to avoid missing this treatable condition.

[827A] Figure 1.

827 Advanced Combined Hepatocellular Carcinoma and Cholangiocarcinoma (cHCC-CC) in a Patient With Alcoholism and Chronic Hepatitis C Youran Gao1, Tai-Ping Lee, MD2, Cathy Fan3. 1. Long Island Jewish Medical Center, North Shore-LIJ Health System, Glen Oaks, NY; 2. Long Island Jewish Medical Center, North Shore-LIJ Health System, Manhasset, NY; 3. North Shore-LIJ Manhasset, Department of Pathology, Manhasset, NY. Introduction: A combined hepatocellular and cholangiocarcinoma (cHCC-CC) is rare subtype of primary liver cancer accounting for 0.87% of primary liver tumors. It is a distinct type of primary liver cancer with aggressive behavior, which is morphologically and phenotypically intermediate between HCC and CC. Although few studies have shown the increased occurrence of cHCC-CC in chronic hepatitis B patients, there is a lack of association with chronic hepatitis reported in US studies. We present a patient with advanced cHCC-CC and history of alcoholism and chronic hepatitis C(CHC). Case: A 64-year-old man with history of alcohol abuse and CHC, treatment naïve, was referred to hepatology for jaundice for 2 weeks (blood work in table 1). Ultrasound of the abdomen showed a 6.6cm mass in left hepatic lobe extending to the hilum causing intrahepatic ductal dilatation(IHD), a 5.5cm mass in right hepatic lobe and scattered small liver lesions. MRI of the abdomen with Eovist revealed an 8.6cm mass in segment 4 extending to the hilum resulting in right(RT) and left(LT) IHD dilation and a 6cm mass in posterior right hepatic lobe. There were also smaller satellite nodules in both lobes, occlusion of the main portal vein with extensive cavernous transformation, and thrombus within the RT and LT intrahepatic portal veins. Liver was non-nodular while enhancement suggested CC. Liver biopsy showed CK7 positive, poorly differentiated CC with rare glandular architecture(Image 1). It also showed poorly differentiated HCC with giant cell features consistent with cHCC-CC (Image 2,3). Jaundice worsened and total bilirubin(TB) trended up to 30. A biliary drain was placed and TB decreased to 18. After the drain was capped 5 days later, he developed acute renal failure, leukocytosis and encephalopathy. Antibiotics, rifaximin, and albumin were given and his renal function and mental status improved. Palliative care was consulted for advanced cHCC-CC and the patient was discharged to home hospice. Conclusion: The diagnosis and treatment of cHCC-CC can be challenging due to clinical, imaging and histological features that overlap with pure HCC and CC. Our patient, although did not have ascites, had advanced stage disease with satellite lesions, multiple tumors, biliary, vascular and regional lymph node involvement. Further studies are needed to evaluate the risk of CHC in development of cHCC-CC. This may ultimately help us to screen for early disease and to improve prognosis.

[827]

Table 1. Labs

Labs

[827C] Figure 3. 4/8/15

4/24/15

5/15/15

WBC

12.2

30

18

AST

80 u/l

100

45

ALT

88 u/l

69

59

5.7 mg/dl

30

18

Total Bilirubin AFP

22,449 ng/ml

CA 19-9

609 U/ml

CEA

609 U/ml

HCV Genotype HCV Viral Load by PCR

[827B] Figure 2.

1a 366,938 IU/ml


828 Transient Elastography and Serum Mac-2 Binding Protein (M2BPGi) May Reflect Amyloid Deposition in AL Hepatic Amyloidosis: A Rare and Curious Case Shuhei Yoshida1, Masahiko Shimada2, Maki Tobari2, Takayoshi Nishino2. 1. Division of Gastroenterology, Yachiyo Medical Center, Tokyo Women’s Medical University, Chiba, Japan; 2. Yachiyo Medical Center, Tokyo Women’s Medical University, Chiba, Japan. Case Report: A 67-year-old woman presented to our hospital with edema and severe liver dysfunction. Biochemical examination showed AST: 67, ALT: 35, ALP: 2056, GGTP: 124, T-BIL: 1.5, ALB: 2.5, ChE: 90, HPT: 50, PLT: 27.5x104, NH3: 236. HBV and HCV were negative. IgM elevated to 4094 (normal: 60-250). IgG and


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Abstracts IgA were normal. HLA-DR4 was positive. Antinuclear antibody and antimitochondrial M2 antibody were negative. CT reveled hepatomegaly with low density on arterial phase imaging. Splenomegaly and collateral blood flow were not observed. Progressive biliary fibrosis, such as PBC or PSC, was suspected. However, ERCP showed no evidence of PSC. Sinusoidal amyloid-depositions with positive Congo Red staining and strong atrophy of hepatocytes were diffusely observed in liver histology. Fibrotic changes, such as an enlargement of portal region or bridging fibrosis, were not found. Cardiac and renal dysfunctions did not exist. Brain MRI showed no abnormal findings. AL hepatic amyloidosis, which demonstrated severe hepatic dysfunction, was diagnosed. Serum IgM-kappa was detected. Kappa free light chain elevated to 168.00 (normal: 2.42-18.92). Serum IL-6, IL-8 levels elevated to 36.9, 69.1 (normal: < 2.41, < 8.0, respectively). Serum markers related to liver fibrosis, P-III-P and type IV-collagen 7S, were normal levels (0.6, 3.2, respectively). However, Mac2binding protein (M2BPGi), a novel biomarker of liver fibrosis, elevated to 6.35 (normal: < 1.00). Transient elastography (TE) revealed transcended 75.0 kPa of liver stiffness (E), which is a maximum level (normal: < 6.0). Discussion: Amyloid deposition in the liver directly impairs hepatic metabolism. Mechanism of liver damage caused of hepatic amyloid deposition is completely different from process of liver fibrogenesis. TE is a very useful device for liver stiffness measurements. However, to our knowledge, its usefulness for amyloid deposition in the liver has never been reported. Interestingly, TE showed transcended maximum E level despite absence of liver fibrosis. Of note, an elevated serum M2BPGi was found despite normal levels of P-III-P and type IV-collagen 7S. Conclusion: Our present case indicates TE and serum M2BPGi may be novel useful tools to predict hepatic amyloid deposition in AL amyloidosis patients. Further data accumulation, including transient elastography and serum M2BPGi in AL amyloidosis patients, is essential to understand the pathogenesis of AL hepatic amyloidosis.

829 Vanishing Bile Duct Syndrome Leading to Biliary Cirrhosis in a Patient With Remote History of Non-Hodgkin Lymphoma Christopher J. Kim, MD, Eric Swanson, MD, Bita Naini, MD. UCLA, Los Angeles, CA. We present a case of a 60-year-old man with a remote history of non-Hodgkin Lymphoma (NHL) who developed cirrhosis during the course of his lymphoma. Investigation into the underlying cause of cirrhosis was negative including viral and autoimmune serologic markers and imaging studies of biliary tree. He had no history of alcohol abuse. While his NHL was eventually successfully treated with chemotherapy, he developed multiple sequelae of end stage liver disease including variceal bandings, spontaneous bacterial peritonitis, and acute coagulopathic episodes before successful liver transplantation nearly two decades after his diagnosis of NHL. Histologic exam of the explanted liver showed a biliary pattern of cirrhosis with near total loss of interlobular bile ducts. Chronic biliary injury and cholestasis was confirmed by the presence of excess copper deposition and copper binding protein by copper and Victoria blue stains, respectively. There were no features of primary sclerosing cholangitis or primary biliary cirrhosis. There was no steatosis, no evidence of alpha-1-antitrypsin disease, hemochromatosis, or veno-occlusive disease. There was no evidence of lymphomatous involvement. It was determined that the patient had likely developed VBDS and biliary cirrhosis in association with his NHL. Vanishing bile duct syndrome (VBDS) refers to a clinicopathologic group of conditions resulting from progressive destruction and disappearance of intrahepatic bile ducts. It can be seen in a variety of conditions including primary liver disorders or manifestations of systemic illnesses. VBDS has also been reported in association with many drugs. VBDS is an uncommon but potentially fatal complication of Hodgkin lymphoma, and in exceptionally rare cases, NHL. The exact mechanism is unknown but is thought to be a paraneoplastic phenomenon, or possible sequelae of drug induced/chemotherapy injury. There are only 3 prior published cases of VBDS in association with NHL. In 2 of the cases the patients died, one of acute liver failure and the other of multiple organ failure secondary to his underlying lymphoma. The third case demonstrated reversibility of the VBDS with near normalization of total bilirubin levels 6 weeks after onset of chemotherapy. To our knowledge, our case is the first to demonstrate a prolonged course of VBDS in association with NHL, eventually leading to chronic end stage liver disease and biliary cirrhosis, despite complete remission of NHL.

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Acute HIV infection is associated with transaminitis in 21% of patients though the elevation of AST and ALT is generally mild. There have only been two reported cases of acute HIV with significant transminitis. The degree of transminitis in these cases varied significantly with one case reporting AST 347 U/L and ALT 554 U/L while the second case reported AST 4410 U/L and ALT 4450 U/L. HIV induces liver injury by apoptosis of hepatocytes through interaction of HIV envelope glycoprotein gp120 with CXCR4 on hepatocytes via G protein signaling.

831 Solitary Extra-hepatic Recurrence of Hepatocellular Carcinoma in Sternum After Liver Transplantation Chitharanjan Duvoor, MBBS, MD, Jagpal Singh Klair, MD, Mohit Girotra, Farshad Aduli. University of Arkansas for Medical Sciences, Little Rock, AR. Background: Incidence of recurrent hepatocellular carcinoma (HCC) following liver transplantation (LT) is between 6-56%, and common sites of recurrence include liver graft, lungs, abdominal lymph nodes, bones, adrenal glands and peritoneum. While post-LT metastasis to bones is described, recurrence in sternum as initial presentation is not yet reported in literature. Case: A 70 year-old caucasian man with non-alcoholic steatohepatitis (NASH) cirrhosis and HCC status post LT 1-year ago, was seen in transplant clinic for routine follow-up. The explanted liver histopathology showed a viable tumour with vascular invasion into the right lobe measuring 3.5x3.0x2.8 cm, which put him at risk for recurrence. He was stable on current tacrolimus and everolimus based immunosuppression, and his blood work was unremarkable. On physical exam, he was discovered to have a 3-cm soft, palpable, non-tender, immobile lesion on his chest wall. A computed tomography (CT) scan revealed 3.4x4.1 cm destructive soft tissue lesion involving the inferior portion of sternum just above xyphoid region. CT guided biopsy of the lesion confirmed HCC. In lieu of his metastatic disease, he was started on Sorafenib 400 mg BID and referred to radiation oncology for radiotherapy. Discussion: Patients with explant tumor characteristics within the currently acknowledged criteria for transplantation are reported to have a recurrence rate of about 8%. The time range from LT to recurrence varies greatly, with one study reporting mean of 12.3 months. The size of primary tumor and number of nodules are strong determinants of recurrece risk after LT. It is believed that metastasis to the bones occurs via portal vein-vertebral vein plexuses (due to either portal thrombus and/or portal hypertension which allows it to bypass through plexus), thus elucidating the more frequent cranio-spinal metastases. Therefore, presence of vascular invasion, especially of the portal system, is one of the major factors related to relapse. Metastatic spread to the bones occurs in 13 to 16% of HCC, however, it infrequently appears as the first manifestation of recurrence. The most common sites of skeletal involvement, in descending order, are vertebrae, pelvis, ribs, skull, and long bones.Radiation therapy is utilized for recurrent unresectable HCC. Molecular targeted therapy with Sorafenib has been demonstrated in two independent phase-3 trials, to prolong survival in patients with advanced or metastatic HCC.

832 Pneumocystis jirovecii Infection of the Liver Presenting With Acutely Elevated Liver Functions Tests Bilal Gondal, MD, MRCSI1, Emma Whitcomb, MD2, John Hart, MD1, Anouar Teriaky, MD3, Andrew Aronsohn, MD1. 1. University of Chicago Medicine, Chicago, IL; 2. University of Chicago, Chicago, IL; 3. University of Chicago Medicine, Chicago, IL, Canada. Introduction: AIDS related Pneumocystis Jirovecii [PJ] typically presents as a pulmonary infection. Liver involvement is thought to be rare and has previously been described in a case of hepatic and splenic infiltration of PJ1 and after discovery on antemortem liver biopsy.2 We report a rare case of acute hepatocellular injury with cholestasis in a patient with PJ infiltration seen on liver biopsy. Early diagnosis and treatment led to rapid recovery in this case. Case Presentation: A 38 year old African American man presented with nausea, vomiting and dry cough of 1 week duration. He had a past medical history of untreated HIV. He had a prior hospitalization 3 days ago with similar symptoms, and due to concern for pneumonia he was started on levofloxacin and Bactrim. He denied recent travel history and had no localizing findings on physical examination. His HIV RNA viral load was 79593 copies/ml and CD4 count was 12. CXR and CT

Acute HIV-Induced Transaminitis Muhammad S. Mansoor, MD1, Robert Frankel, MD2. 1. Department of Medicine, Yale-New Haven Hospital, Yale University School of Medicine, Hamden, CT; 2. Division of Gastroenterology, Department of Medicine, Yale-New Haven Hospital Yale University School of Medicine, New Haven, CT. A 23 year old man with no significant past medical history presented with RUQ abdominal pain, nausea, vomiting and anorexia. Four days prior to admission he reported multiple episodes of emesis with streaks of blood following heavy alcohol consumption. Low dose acetaminophen was unable to relieve the symptoms. He was not taking any prescribed or over the counter medications. Surgical and family history was unremarkable. Social history was significant for a half pack per day smoking and alcohol binge drinking twice a month. He was in a monogomous relationship with a male partner for 18 months though he did report an unprotected sexual encounter with another male four months ago following which he was diagnosed with chlamydia but tested negative for HIV. He reported occasional use of condoms and was the receptive partner during sexual intercourse. His vitals on presentation were normal except for a temperature of 100.8oF. His physical examination was remarkable only for moderate RUQ and epigastric tenderness. His laboratory tests were remarkable for AST of 1440 U/L and ALT of 1690 U/L, total bilirubin of 2.07 mg/dl, ferritin of 14,100 ng/ml but were otherwise normal including an INR of 1.0. Comprehensive infectious, metabolic and autoimmune serologies performed were unrevealing, including testing for hep A, B, C and E, HSV, CMV, EBV, VDRL, iron saturation, ceruloplasmin, acetaminophen level, ANA and ASMA. Abdominal USG was normal with patent vasculature. HIV Ag/Ab screen was positive, though refl ex HIV-1 and HIV-2 antibodies were negative. HIV PCR revealed a viral load >10,000,000 copies/ ml while the CD4 count was 633 /ul. These studies were consistent with an acute HIV infection. A liver biopsy was deferred due to patient’s preference. In addition to supportive care the patient was started on HAART. His AST and ALT checked 11 days later on follow-up decreased to 30 U/L and 66 U/L respectively.


[832A] Figure 1.


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[832B] Figure 2.

revealed bilateral upper lobe ground glass opacities and cystic changes suspicious for pneumocystis pneumonia. Liver function tests were normal on admission however during this hospitalization, became increasingly abnormal with an alkaline phosphatase of 260, while AST and ALT increased to 1506 and 859. Total bilirubin remained normal. Initially this was presumed to be due to drug related liver injury possibly from Bactrim and Fluconazole, however after all potentially offending agents were discontinued, his liver function tests continued to worsen. Liver biopsy was performed which showed patchy areas of hepatocellular necrosis Fig1 and stained positive for PJ Fig2. Due to concern for Bactrim related liver injury, the patient was treated with alternative medications: Primaquine and Clindamycin. His liver enzymes improved and patient was discharged to complete a total of 21 days course of PJ directed antimicrobial therapy. Patient was also started back on HIV retroviral therapy Raltegravir and Emtricitabin-Tenofovir. Discussion: PJ is notorious for causing severe atypical pneumonia in AIDS. Our case highlights an important fact that disseminated PJ, although rare, should be considered as a possible cause of acutely worsening liver function tests in immune compromised patients. Early diagnosis and treatment is crucial and can lead to dramatic clinical improvement and decrease overall morbidity and mortality. References: [1]. Fishman EK1, et al. J Comput Assist Tomogr. 1990;14(1):146-8. [2]. Merkel IS, et al. J Clinical Gastroenterology 1992;15(1):55-8.

[834A] Figure 1.

833 Potential Treatment of Marginal B-Cell Lymphoma With Antiviral Therapy Fadi Niyazi, MD, Ahmed Saeed, MD, Dilip Moonka, MD. Henry Ford Hospital, Detroit, MI. Background: The association between hepatitis C (HCV) and subtypes of B-cell lymphomas was initially described in epidemiological studies. These subtypes mainly are marginal zone lymphomas (MZLs) and lymphoplasmacytic lymphomas, both of which are indolent lymphomas. Hence there is a reported association - there is a potential role for antiviral strategies to influence the clinical course of these lymphomas. Case: We present a 39-year-old female patient with past medical history of hepatitis C with cirrhosis who underwent orthotropic liver transplantation. She was found to have periportal lymphadenopathy intraoperatively which were sampled. Pathology revealed marginal zone B-cell lymphoma. An MRI obtained one month postoperatively which showed persistent periportal, portocaval and gastrohepatic lymphadenopathy. She was asymptomatic without symptoms of night sweats, fever or weight loss. A subsequent bone marrow biopsy revealed small atypical lymphoid infiltrates suggestive of minimal bone marrow involvement. Given it was a low-grade B-cell lymphoma; patient was followed up and no treatment was initiated. One month later - she was noticed to have jaundice and worsening transaminases. Subsequently, she underwent liver biopsy, which showed changes consistent with severe recurrent hepatitis C. After thorough evaluation, she was started on Sofosbuvir and Ribavirin. The patient completed 24 weeks of therapy and achieved sustained viral response. Subsequently she had a PET scan, which showed no abnormal FDG uptake in the neck, chest, abdomen and pelvis or osseous structures. She remained in remission through her last follow up. Discussion: We report here the response to antiviral treatment of a liver transplant patient with low grade B-cell lymphoma associated with HCV infection. This further supports the potential link between some sub-types of B-cell lymphoma and HCV infection, and supports the use of antiviral treatment in this setting.

834 Sepsis of Unknown Origin Secondary to Liver Abscess Caused by Fish Bone Migration Armando Peixoto1, Regina Gonçalves1, Marco Silva2, Guilherme Macedo3. 1. Centro Hospitalar de São João, Porto, Portugal; 2. Gastroenterology Department - Centro Hospitalar São João, Porto, Portugal; 3. Centro Hospitalar São João, Porto, Portugal. The authors present the case of a woman of 80 years of age, without relevant medical history, which presented to the emergency department for fever (38-39ºC), chills, nausea and vomiting, and persistent pain in the right hypochondrium lasting for two days. Initial clinical assessment revealed hypotension,


[834B] Figure 2.

hypoxemia (pO2 < 70mmHg), slight leukocytosis, CRP 176mg/L and increased lactates (3.0mmol) and the imaging studies (chest X-ray and abdominal CT) showed no change. Then the patient was hospitalized in intermediate care unit where she was started on antibiotics with a diagnosis of sepsis of unknown origin. Two days after, the patient was clinically better but maintained abdominal complaints and so it was performed a new abdominal CT scan where we were able to identify a linear foreign body with approximately 30mm perforating the intestinal wall at the level of the pylorus, contacting with the hepatic parenchyma where a multiloculated abscess with 44mm was seen (figure 1 [arrow]). After further conversation with the patient, it was found to be of a fishbone ingested days before. Consequently, an upper endoscopy was performed where it was found a swollen area in the antero-superior duodenal bulb wall with a central fistulous opening (figure 2). After discussion with the surgical team it was decided to maintain a conservative strategy (antibiotics plus imaging surveillance). Once there was gradual improvement of the clinical picture, the patient was transferred to the surgery ward and then discharged to outpatient consultation.


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Abstracts A myriad of ingested sharp-pointed objects have been described and not always the patients are aware of foreign body ingestion, and in these cases the diagnosis is only made on the occurrence of complications, such as in the reported case. Cases of hepatic abscess due to ﬁsh bone penetration are very rare and may be fatal. Since the first reported case, treatments usually include drainage of the abscess, removal of the foreign body, and administration of appropriate antibiotics. Surgery is considered the treatment of choice in current clinical practice, but when the diagnosis is not initially suspected, and if the patient shows clinically improvement, a conservative approach can be attempted. In this case, once the patient was better under empirical antibiotics we preferred not to submit the patient to a surgical procedure. So we suggest that medical approaches could be attempted ﬁrst in such cases.

835 Urinary Ascites Raj Shah1, Beenish Ahmed2, Khalil M. Abuamr3, Osama Yousef, MD4. 1. University of Missouri, Kansas City, MO; 2. University of Missouri, Kansas City, Kansas City, MO; 3. University of Missouri, Kansas City, Overland Park, KS; 4. University of Missouri/Truman Medical Center, Kasas City, MO. Introduction: Atraumatic bladder rupture is a rare occurrence and therefore not considered highly on the differential for a patient who presents with new onset ascites. We present this case to show the complexity of diagnosing and managing ascites secondary to bladder rupture. Case Report: A 43 year-old female with untreated multiple sclerosis (MS) presented with abdominal pain beginning immediately after voiding. Initial labs revealed mild leukocytosis with normal liver function, creatinine and lipase. Contrast tomography (CT) abdomen/pelvis showed large ascites with normal appearing liver. Pelvic ultrasound demonstrated a small left paraovarian cyst. General surgery and gynecology ruled out acute abdomen, thought the presentation was due to ruptured ovarian cyst and recommended conservative management. Paracentesis fluid was concerning for secondary bacterial peritonitis with labs showing serum albumin-ascites gradient of > 1.1, white blood cell count of 3610, polymorphonuclears of 88%, total protein of 1.3, glucose of 36, and creatinine of 8.27. Five days later, the patient started to have worsening abdominal pain, leukocytosis and renal function. Repeat CT of the abdomen/pelvis showed a marked increase in abdominal ascites as well as an abnormality of the bladder wall that likely represented a bladder diverticulum, but a bladder wall rupture or diverticular rupture could not be excluded. Cystogram confirmed bladder rupture which was thought to be from obstructive uropathy secondary to neurogenic bladder from her untreated MS. She failed conservative management with increased abdominal pain and ileus and subsequently underwent a cystoscopy, cystorrhaphy, and diverticulectomy with drain placement. Discussion: While traumatic rupture of the bladder is a more common occurrence, ascites secondary to a spontaneous bladder rupture is a rare occurrence, documented sparsely in case reports. Due to the delay in diagnosis, patients have poorer outcomes and a high mortality rate. A PubMed search found two other cases of bladder rupture in MS patients, but unlike our patient they presented with signs of acute abdomen. Conclusion: Perforated urinary bladder should be considered in the differential diagnoses in patients presenting with new onset ascites and acute kidney injury without any evidence of chronic liver or heart disease or any other common causes of ascites. Early diagnosis can greatly improve the patient’s hospital course and overall outcome.

[836A] Figure 1.

836 Clostridium perfringens Liver Abscess Complicated With Bacteremia Charles Rives, MD1, Dhara Chaudhari2, Pranav Patel3, James Swenson1, Chakradhar Reddy1, Mark Young1. 1. East Tennessee State University, Johnson City , TN; 2. East Tennessee State University, Johnson City, TN; 3. East Tennessee State Univeristy, Johnson City, TN. Liver abscess (LA) due to Clostridium perfringens (CP) is a rare and often fatal event that requires a high degree of suspicion and immediate treatment with drainage and antibiotics. We present a case of Clostridium pefringens liver abscess and sepsis that was successfully treated with antibiotics and drainage. Case report: 63 year old male with history of stage III colon cancer status post resection and chemotherapy with resolution of liver metastasis with palliative chemotherapy admitted with weight loss and obstructive jaundice with intra-extra hepatic biliary dilation due to extrinsic compression of the biliary tree at the porta hepatis. Endoscopic retrograde cholangiography with placement of a fully covered metal stent in the common bile duct and right hepatic duct was performed and the patient was discharged from the hospital with down trending bilirubin. Ten days later the patient was re-admitted with dyspnea, abdominal pain and fever 100.1F. Physical exam: left chest pain at lower costals, mild epigastric tenderness. Laboratory test: WBC 21.3 u/mcl, bilirubin 7.6 mg/dL with alkaline phosphatase 212 U/L , blood cultures were positive for CP. CT abdomen showed a new 2.9 x 3.1 cm gas containing fluid collection in the left lobe of the liver. The patient was successfully treated with intravenous piperacillin-tazobactum, abscess drainage and metal stent removal. Discussion: CP is a rapidly growing (doubling time 7 minutes), spore forming anerobic, gram positive bacilli that produces 5 types of toxins and is often found in the human bowel but rarely causes LA and sepsis. To the best of our knowledge there have only been approximately 22 reported cases of CP LA septicemia, many of which were fatal. CP infection has a mortality of 70-100%, often infects immunosuppressed patients and can present with fever, abdominal pain, gas forming abscess and massive hemolysis. CP LA is most often diagnosed with blood cultures, radiographic evidence of LA or autopsy. It is most commonly treated with drainage and antibiotics based on sensitivities, most often, high dose penicillin and clindamycin. CP LA is a rare, often fatal infection, in which, one must have a high suspension for when presented with radiographic evidence of gas-filled liver abscess and must begin aggressive treatment immediately.


[836B] Figure 2.

837 Cryoglobulinemia in Hepatitis C Presenting With Diffuse Alveolar Hemorrhage Gaurang Vaidya, MBBS, Aiga Rakhesh, MBBS, Jalaluddin Umar, MBBS, Savio John, MD. SUNY Upstate Medical University, Syracuse, NY. Introduction: Cryoglobulinemic vasculitis(CV) is characterized by vascular deposition of circulating antibodies commonly produced by stimulation of B-cells by Hepatitis C virus(HCV), usually affecting skin and kidneys. We describe an unusual presentation of mixed cryoglobulinemia(MC) with altered mental status, purpura and renal failure masquerading as thrombotic thrombocytopenic purpura(TTP), with subsequent progression to respiratory failure from diffuse alveolar hemorrhage(DAH). Case: 63 year old male with untreated chronic HCV infection presented with fever, cough and body rash for 2 weeks, without hemoptysis. He was febrile & had palpable purpura on thighs. His platelet count was 52000/μl(past value 84000/μl), INR 1.04, normal ammonia, HCV RNA >400K, chronic elevation of transaminases and creatinine 2.1(previously normal). The initial suspicion of TTP was ruled out based on normal peripheral smear, haptoglobin and LDH. Urinalysis was consistent with pre-renal picture. Two days later, his respiratory status deteriorated with worsening mental status requiring intubation. Blood gas showed respiratory alkalosis with hypoxia. Chest Xray showed bilateral fluffy infiltrates, pulmonary embolism was ruled out via CTA thorax which showed diffuse airspace disease. Diagnostic


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[837A] Figure 1.

bronchoscopy revealed DAH. Simultaneously, serum cryoglobulin came positive with positive ANA homogeneous pattern and elevated histone antibody. Complement C3, C4 levels were low and rheumatoid factor was positive. Serum protein electrophoresis showed IgM kappa paraproteins with monoclonal band. Blood cultures were negative. He was started on pulsed dose methylprednisolone followed later by rituximab 1gm twice over 2 weeks. There was significant improvement in his condition after initiation of steroid therapy with improved mentation and resolving skin lesions. He was successfully extubated and discharged on prednisone taper. Plasmapheresis was deferred due to patient’s refusal and subsequent improvement. Discussion: Early bronchoscopy is necessary for diagnosis. No treatment protocols have been defined but our patient improved with early immunosuppression with steroids without sequelae. Rituximab inhibits cryoglobulin producing B-cells and is more efficacious than steroids or plasmapheresis. Keypoints: -DAH in MC is rare but mortality can be upto 95% without early treatment. -Anti-HCV therapy should be initiated early, but in severe vasculitis, Rituximab should be considered prior to antivirals.

[839A] Figure 1.

838 Blame It on the Kava? Dimitrova Maya, MD1, Yecheskel Schneider, MD2, David W. Wan, MD3. 1. Weill Cornell Medical College, New York, NY; 2. New York Presbyterian Hospital/Weill Cornell Medical Center, Brooklyn, NY; 3. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY. A 58 year old woman with hypertension, severe aortic insufficiency and type A aortic aneurysm status post repair (2003) presented to the hospital for a repeat operation of her aortic arch conduit. Pre-operative labs revealed an transaminitis in the 2000s, an alkaline phosphatase of 463 and a hyperbilirubinemia to 3.7 (mostly direct); INR was normal. An ultrasound showed no biliary dilatation. A history revealed one month of epigastric pain and one week of jaundice. She initially denied any new medications, herbal supplements or acetaminophen use, but later remembered that six weeks prior she began to drink Kava tea two times per day. Hepatitis serologies revealed a positive Hepatitis C antibody, with viral load greater than 100,000 units (she denied known risk factors). A liver biopsy showed lobular inflammation, acidophil bodies and cholestasis with a diagnosis made of drug induced liver injury. Her transaminases peaked after four days, quickly downtrended, and she was soon discharged. Her acute liver injury was attributed to Kava and the FDA was alerted. Notably, her repeat Hepatitis C PCR obtained several weeks later was non-detectable. Herbal induced liver injury is a diagnostic challenge; the use of herbal/dietary supplements in the United States is unregulated and there is often uncertainty as to the contents of a particular supplement. Kava has been used as an anxiolytic in Polynesia for over 2000 years. It can exist in three formulations, all of which are now thought to be responsible for hepatotoxicity.Diagnosis of herbal liver injury can be difficult; a positive re-exposure test can help establish causality. Clinically, one may present with high serum transaminases compared to alkaline phosphatase; liver biopsy may reveal liver necrosis. In 2002 the FDA issued a warning regarding kava use. In this case, Kava was initially thought to be the cause of her liver injury. When her Hepatitis C viral load was repeated and found to be undetectable, the possibility of acute Hepatitis C was raised. Review of the liver pathology revealed it to be consistent with either a drug-induced, or acute Hepatitis induced liver injury. Ultimately, acute hepatitis C was thought to be the cause of her liver injury. This case highlights the importance of taking a detailed history for herbal and tea supplements, as well as a reminder that drug-induced liver injury is a diagnosis of exclusion, and other possibilities must be sought before making a diagnosis.

[839B] Figure 2.

839 Spontaneous Bacterial Peritonitis and Henoch-Schönlein Purpura in a Patient With Liver Cirrhosis Neil Gupta, MD1, Alexander Perelman, DO, MS1, Basile Njei, MD, MPH2. 1. Yale University School of Medicine, New Haven, CT; 2. Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT. Henoch-Schönlein purpura (HSP), a small vessel systemic vasculitis predominantly affecting children, is characterized by a tetrad of palpable purpura, arthralgia, abdominal pain, and renal disease. HSP in adults is rare, and no case has been described of HSP in liver cirrhosis with spontaneous



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Abstracts bacterial peritonitis (SBP). Our patient is a 58-year-old male with past medical history of type 2 diabetes, depression, HTN, and chronic alcohol abuse, who presented to our hospital with worsening left-lower quadrant abdominal pain over three weeks and painless hematuria for five days with no known history of liver or kidney disease. After labs and imaging showed newly diagnosed liver cirrhosis, paracentesis was performed, consistent with SBP and portal HTN (corrected PMN 917, SAAG 2.1). Four days after admission, he had diarrhea, and thirteen days later, he developed new purpuric macules and papules, about 0.3–1.5 cm in size, most prominent on his elbows. Skin biopsy showed fibrin, neutrophils, and neutrophil fragments near vessels with mixed cellular infiltrate and extravasated erythrocytes. Direct immunofluorescence (DIF) studies showed deposition of IgA and C3 in vessel walls, supporting HSP. Due to worsening renal function with creatinine rising to 4.9, renal biopsy was performed revealing mesangial proliferative glomerulonephritis with crescents and IgA, also consistent with HSP. He ultimately required emergent hemodialysis and then became acutely hypotensive, with a sudden hemoglobin drop to 4.8. After two units of transfusion to hemoglobin of 8.8, he coded one day later with profuse hematemesis after an episode of bright red blood per rectum and died. In our patient, the diagnosis of HSP was demonstrated clinically by his palpable purpura, diarrhea, hematuria, and abdominal pain and confirmed pathologically by his renal and skin biopsies demonstrating leukocytoclastic vasculitis and IgA complexes. While HSP is predominantly a pediatric disorder, its existence in adults is rare and its association with liver cirrhosis is even more scant. There are only a few case reports describing the association between liver cirrhosis and HSP. We believe that this is an example of altered IgA processing in cirrhosis leading to the development of IgA immune complexes and ultimately HSP. The patient additionally had SBP, which may have increased his risk for developing HSP given antigen processing by mucosa-associated lymphoid tissues leading to immune complex deposition, which may not have been effectively cleared due to his liver disease. SBP has not been previously reported in case reports of patients with combined HSP and liver cirrhosis. The patient unfortunately died of gastrointestinal hemorrhage, unclear to be due to his underlying cirrhosis or a gastrointestinal manifestation of HSP itself.

840 Hepatitis C Virus Window Period Causing a False Negative Screening Result Despite Sensitive Screening Methods Charles Rives, MD1, Minni Meka1, Parag Brahmbhatt2, Chakradhar Reddy1. 1. East Tennessee State University, Johnson City , TN; 2. Department of Gastroenterology, East Tennessee State University, Johnson City, TN. Hepatitis C virus (HCV) is very accurately detected by screening an individual’s blood with a generation three enzyme-linked immunosorbent assay (ELISA). We report a case in which a patient had a negative ELISA screening test but a positive polymerase chain reaction (PCR). Case Report: A 45 year old white male with a history of poly substance abuse presented with nausea, vomiting, watery diarrhea and right upper quadrant discomfort for 10 days. The patient denied recent drug use, blood transfusions and tattoos. On admission, the patient had a normal liver function tests (LFTs) which trended up within 2 days. HCV screening results were negative. LFTs trended down on day 3 and were normal at discharge. Despite a negative HCV screening test a high suspicion for acute Hepatitis C remained due to fluctuating LFTs. HCV PCR was performed and positive with >20,000,000 IU/ml, confirming the diagnosis of HCV. Discussion: Hepatitis C virus (HCV) is a blood transmitted enveloped RNA virus that has infected approximately three percent of the world’s population and is major cause of liver disease. HCV infects liver cells where it undergoes replication, eventually leading to cell necrosis and chronic hepatitis in up to 80% of those infected. It is most commonly transmitted by sharing needles with infected people while engaging in intravenous drug use, blood transfusions and medical procedure errors. HCV is most often diagnosed by screening blood of individuals with risk factors with a generation three ELISA. However, individuals screened within 8 weeks of infection have a higher false negative rate of approximately 6% due to being in a window period, in which, the infected individual has not made antibodies to the HCV. Individuals with risk factors, signs of HCV infection, such as, increased or fluctuating liver function test, nausea, jaundice, right upper quadrant pain and or immunodeficiency should undergo HCV RNA detection with PCR. PCR can detect HCV RNA within one week of exposure and has a sensitivity and specificity approaching 99%. In conclusion, one must consider confirming any negative HCV screening test results with PCR when patients have risk factors for HCV and may be in the window period.

841 Surviving a Wilsonian Crisis Without Liver Transplantation Lindsay S. Mohrhardt, DO1, Kathryn Wisser, DO2. 1. Michigan State University, East Lansing, MI; 2. Michigan Gastroenterology Institute, East Lansing, MI. Introduction: Wilson’s Disease (WD), a disorder of copper excretion, is a rare but important indication for urgent liver transplantation. Chelation therapy is ineffective in acute Wilsonian crisis, necessitating liver transplantation as the treatment of choice. Case Report: A 19 year old female presented to the ED after feeling weak, fatigued, complaining of RUQ abdominal pain and hematuria for 5 days. She experienced increasing weakness over the last 4 months, loss of singing voice, and had symptoms of biliary colic with fatty foods. She recently started on birth control, but had no other past medical history. On admission she was jaundiced with total bilirubin 10.8, direct bilirubin 3.1, AST 177, ALT 11, Alkaline Phosphatase 8, Albumin 3.4, INR 1.6, hemoglobin 6.6, MCV 112, white blood cell 18.0, platelets 195, Creatinine 1.47, bilirubinuria, and bilateral pleural effusions. Abdominal ultrasound revealed ascites, dilated common bile duct, and biliary sludge. She was admitted to the PICU. She had a coombs-negative hemolytic anemia, requiring seven units of blood in seven days. She had a paracentesis on day two with a SAAG consistent with portal hypertension. The patient underwent an extensive workup while hospitalized with no answers


and on day three she was empirically started on steroids. Her ceruloplasmin was 21, which is low normal. She underwent a liver biopsy during cholecystectomy for persistent RUQ pain, showing cirrhosis and swollen glycogen rich hepatocytes, suggestive of glycogen storage disease; this returned after her discharge. She recovered from the hemolytic anemia and was sent home on day fourteen with steroids. She followed up with GI and 24 hour urine copper was ordered finding 144μg of copper. Prompt ophthalmology referral revealed Kayser-Fleisher rings. She was diagnosed with WD and started on Trientine. Follow up labs revealed decreasing urinary copper, gene mutation of ATP7B, and improvement of her singing voice and fatigue. This case represents an often fatal presentation of WD without transplant. This patient survived without transplantation and I question if steroids played a role in her improvement without transplant. It also serves as a reminder of the complexity of recognizing WD in the acute setting.

842 Granulomatous Hepatitis Due to Etanercept Therapy Armando Peixoto1, João Santos-Antunes1, Pedro Pereira1, Joanne Lopes2, Guilherme Macedo2. 1. Centro Hospitalar de São João, Porto, Portugal; 2. Centro Hospitalar São João, Porto, Portugal. The authors report the case of a 76 year-old man with rheumatoid arthritis diagnosed in 1994 and previously treated with methotrexate and infliximab, and since 2006 with etanercept. Daily chronic medication included prednisolone 7.5 mg, simvastatin 10 mg, and etanercept 50 mg every two weeks. The patient was hospitalized for marked asthenia and persistent changes in liver tests lasting for six months, with a citocolestatic pattern (AST 251 U/L; ALT 650 U/L; GGT 552 U/L; AP 132 U/L; bilirubin, albumin and coagulation were normal), even after simvastatin suspension. The patient denied intake of new drugs or dietary/herbal supplements. Imaging studies, including ultrasound and computed tomography (CT) showed hepatic steatosis. Consequent additional study for chronic liver diseases only revealed positivity for anti-nuclear antibodies (title 1/320, nuclear pattern), with the remainder being normal or negative. Given the absence of an evident causative factor for the changes in liver tests, we opted to perform a percutaneous liver biopsy. The histopathological evaluation revealed moderate portal fibrosis without fibrous septation of the parenchyma, noncaseating granulomas in some portal spaces, and focal macrovesicular steatosis. Search of amyloid substance and acid-fast bacilli was negative. Consequently, we performed an etiologic study of granulomatous diseases that was negative, including: angiotensin-converting enzyme, chest CT, screening for Mycobacterium tuberculosis (MT) latent infection, Wright’s reaction, anti-Coxiella Burnetti antibodies and cryptococcal antigen. The molecular analysis for the presence of MT’s, Bartonella’s and Coxiella’s DNA in the liver tissue was negative. Due to persistence of the liver tests abnormalities, it was decided to suspend etanercept, with a subsequent gradual improvement on analytical parameters that normalized three months later. Recently there have been published paradoxical reports of new sarcoidosis-like diseases in patients receiving anti-TNF agents, mainly etanercept, affecting one or more organs. To date, only one case of granulomatous liver disease associated with an anti-TNF agent was described in the literature. This case also raises the question whether the development of granulomatous processes associated with anti-TNF agents, including etanercept, has been underdiagnosed due to the presence of other concomitant immunosuppressant therapies, mainly steroids.

843 Docetaxel Induced Sclerosing Cholangitis Jennifer L. Horsley-Silva, MD1, Christine O. Menias, MD1, Maxwell Smith2, Estrella Carballido2, Keith Lindor, MD3, Hugo Vargas4. 1. Mayo Clinic, Phoenix, AZ; 2. Mayo Clinic, Scottsdale, AZ; 3. Arizona State University, Phoenix, AZ; 4. Mayo Clinic Arizona, Phoenix, AZ. A 78 year-old man with history of high-grade metastatic prostate cancer was referred to hepatology for abnormal liver function tests. Prior to evaluation, tumor had been surgically removed, he was started on dual androgen deprivation therapy with leuprolide and bicalutamide, and underwent 43 fractions of palliative radiation. Then single agent docetaxel treatment was initiated. Labs drawn with second dosing of the agent, a month after first dose, demonstrated elevated liver injury tests (LITs): alkaline phosphatase 859 u/l, alanine aminotransferase 87 u/l, aspartate aminotransferase 121 u/l, total bilirubin 1.1 mg/dL, which had never been abnormal previously. Patient was asymptomatic, and CT of the abdomen and pelvis prior to initial docetaxel dosing when LFTs were normal, demonstrated normal liver appearance. After abnormal LITs repeat CT demonstrated new diffuse intrahepatic biliary dilatation with periductal enhancement suggestive of a diffuse cholangitis picture. Docetaxel was held, and patient was followed for two additional months without resolution of abnormal LITs, which prompted magnetic resonance imaging (MRI). MRI demonstrated continued multifocal narrowing and dilatation of intrahepatic bile ducts, including peripheral bile ducts, with the appearance of sclerosing cholangitis. IgG4 level was normal. Patient underwent liver biopsy two months later when LITs continued to be abnormal. Biopsy revealed subacute bile duct obstruction and stricturing with moderate hepatocanalicular cholestasis, and reactive changes as evidenced by numerous eosinophils. There was biliary-type bridging fibrosis with no architectural distortion or regenerative nodules and Batts-Ludwig fibrosis stage 2/4, consistent with drug-induced inflammation and sclerosing cholangitis. Additional staining with CK7 and copper stain also supported the diagnosis. Docetaxel is an anti-mitotic agent with extensive liver metabolism. Known adverse effects can include hepatotoxicity in the form of elevated LITs, which was the initial presentation of this patient. However, to our knowledge, it has never been associated with inducing secondary sclerosing cholangitis. Given the correlation of timing and direct comparison imaging showing the distinct changes of bile ducts associated with drug administration and LIT changes, without other cause being identified, it appears this patient’s sclerosing cholangitis is secondary and likely caused by docetaxel.


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and radiation to the tumor bed was completed. One month later, she was admitted for nausea, vomiting and abdominal distension. CT scan showed no disease recurrence but noted new ascites. Ultrasound showed hepatomegaly with fatty/fibrotic infiltration and doppler revealed a portal vein thrombus. Liver biopsy showed extensive steatosis, bridging fibrosis with severe micro and macrovesicular steatohepatitis involving 80% of the parenchyma, concerning for chemotherapy associated steatohepatitis, with no evidence of bile duct injury or cholestasis, interface hepatitis, sinusoidal congestion or dysplasia. The patient had no history of liver disease and was not taking medications known to cause liver injury. She subsequently had GI bleeding from portal hypertensive gastropathy and grade II esophageal varices. She was continued on nadolol, lasix and spirinolactone. TIPS procedure was considered as a secondary measure to prevent bleeding. Conclusion: Gemcitabine and capecitabine are pyrimidine analogues used in solid tumor chemotherapy. Mild to moderate aminotransferase elevations with gemcitabine therapy occur frequently due to direct hepatic toxicity but dose modification is rarely necessary. Direct hepatotoxicity from capecitabine is rare and generally mild. The mechanism of CASH is believed to be due to production of reactive oxygen species intended to cause tumor cell apoptosis. It is important for clinicians to recognize and treat CASH appropriately to prevent progression of liver disease.

845 A Rare Case of Epithelioid Hemangioendothelioma of Liver Saurabh Rana, MD, Pratik Naik, MD, Michael Goldberg, DO. William Beaumont Army Medical Center, El Paso, TX.

[843A] Figure 1.

Introduction: Epithelioid hemangioendothelioma (EHE) is a rare aggressive neoplasm of vascular origin that is most commonly found in the liver, lungs, and other vascular organs. The exact etiology of EHE is unknown. It usually affects adult females. We present a case of EHE with initial symptoms of jaundice, abdominal pain, and hemoptysis. Case presentation: A 39 year old white male presented to our facility with chief complaint of abdominal pain, jaundice, and hemoptysis for three weeks. Patient also endorsed dyspnea and early satiety. He had no significant past medical history and denied smoking and alcohol use. A computed tomography (CT) of the chest, abdomen, and pelvis was remarkable for multiple hepatic and lung lesions with pathologic para-aortic lymphadenopathy. Right upper quadrant abdominal ultrasound showed no intra-extrahepatic ductal dilation but was remarkable for ascites. Complete blood count was remarkable for thrombocytopenia of 70 (150-440 K/uL) and macrocytic anemia. Direct bilirubin was elevated to 18.5 (0.3-1.2 mg/dL), which was due to intrahepatic cholestasis from tumor burden. Hemoptysis was attributed to tumor burden in the lungs. Esophagogastroduodenoscopy (EGD) was preformed to further assess early satiety, which was significant for portal hypertensive gastropathy, esophageal varices, as well as extrinsic compression of the lesser curvature from the enlarged liver. Liver biopsy was obtained. Histopathology and immunochemistry of the tumor was consistent with a diagnosis of EHE. Patient was started on Sunitinib, which is a tyrosine kinase inhibitor. Discussion: Most common EHE presentations are liver alone (21%), liver plus lung (18%) and lung alone (12%). This is a rare malignancy thought to be a low to intermediate grade angiosarcoma-like malignancy ranging from benign to aggressive tumor with metastatic potential. Most patients are asymptomatic but liver EHE can resemble the clinical presentation of decompensated cirrhosis. Primary liver EHE with lung involvement has poor prognosis with 5 year survival rate of 24%. There have been case reports utilizing tyrosine kinase inhibitors, such as sunitinib and sorafenib, in this disease. Three case reports utilizing sunitinib demonstrated prolonged survival and/or objective response. In patients presenting with nodular liver masses and painful jaundice, EHE should be considered.

846 Transarterial Chemoembolization (TACE) Leading to Gastric Ulceration After Hepatic Artery Infusion Neel Malhotra, MD, Kareem Qumosani, MD. Western University, London, ON, Canada.

[843B] Figure 2.

844 An Unintended Consequence: Chemotherapy Associated Steatohepatitis Sara West, DO1, Clark Gunnerson, DO1, Michael Komar, MD, FACG2, Nihar Shah, MD1. 1. Geisinger Medical Center, Danville, PA; 2. Geisinger Health System, Danville, PA. Introduction: Steatohepatitis may occur following exposure to overnutrition (non-alcoholic), ethanol consumption, chemotherapy, or industrial toxins. The NAFLD epidemic demonstrates that steatohepatitis may lead to decompensated cirrhosis, hepatoma, liver transplant, cardiovascular events and even death. Chemotherapy associated steatohepatitis (CASH) may result in similar outcomes. We report a rare case of CASH in pancreatic cancer. Case: A 57 year old woman with nephrolithiasis was incidentally found to have a complex mass in the junction of the body and tail of the pancreas on CT scan. EUS was performed and FNA showed cytologically bland glandular cells, histiocytes and inflammatory cells suggestive of a mucin-producing tumor. She underwent distal pancreatectomy and splenectomy with pathology showing moderately differentiated ductal adenocarcinoma, perineural invasion and 1/14 lymph nodes positive for metastatic adenocarcinoma. Adjuvant chemotherapy with gemcitabine for 6 cycles followed by 6 weeks of capecitabine


Commonly experienced symptoms post transarterial chemoembolization include abdominal pain, nausea, fever and ileus. There are case reports of non-target embolization. The goal is to describe a unique case of suspected chemotherapy induced gastric ulcers after hepatic artery infusion. A 72-year-old man with hepatitis C-related cirrhosis presented to our tertiary care center for transarterial chemoembolization (TACE) of a known hepatocellular carcinoma (HCC). The patient had initially been treated with the first dose of loco-regional therapy using 50 milligrams (mg) of doxorubicin in DC Bead™. There were no noted complications from this procedure. Six months later, he was brought to IR for consideration for repeat TACE as a treatment as well as a possible bridge to surgical intervention. During transarterial chemoembolization, a 5-French catheter was advanced to identify the ostium of the celiac artery. An angiogram was performed, demonstrating adequate catheter position. A microcatheter was then advanced into the left hepatic artery. The catheter could not be advanced distally due to the presence of spasm despite giving nitroglycerin. An additional angiogram was performed, which demonstrated the known HCC in the left lobe. Chemoembolization was performed with approximately 70 mg of doxorubicin in DC Bead™. There was no evidence of nontarget embolization of any adjacent organs including the gastric cardia. The patient experienced persistent nausea and vomiting that prompted admission for two days post-procedure. It was treated conservatively with pharmacologic 5-HT3 receptor antagonists as needed. The symptoms were attributed to the doxorubicin and resolved at time of discharge. 72 hours later, the patient presented to hospital with acute onset hematemesis and suspected upper gastrointestinal bleeding. He was stabilized with blood products and vasopressor therapy. Urgent gastroscopy revealed multiple irregular ulcers. There was a Forrest class 1b ulcer on the lesser curvature and a Forrest class 2c ulcer noted on the incisura. Treatment was applied with both epinephrine and clips with good hemostatic response. Biopsies were taken from the edge of the ulcer. Biopsy samples were reviewed to rule out possible malignancy. The histologic findings included basophilic microspheres on the background of purulent exudate and necrotic debris. The findings were most consistent with gastric ulcers secondary to drug eluting beads. Repeat gastroscopy showed that the previous ulcerations had coalesced to encompass a large portion of the lesser curvature of the stomach. There


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[847A] Figure 1.

[846A] Figure 1.

Initial hepatitis panel was unremarkable: HAV IgM(-), HBV surface Ab/Ag(-), HBV DNA(-), HCV Ab and RNA(-), autoimmune panel and ceruloplasmin normal. Abdominal ultrasound and subsequent Magnetic Resonance Cholangiopancreatography demonstrated cholelithiasis, with no evidence of cholecystitis, and no intra or extra hepatic biliary dilation. Patient liver function continued deteriorating, with total/direct bilirubin peaking at 81.4/50.8 mg/dl. Therefore he underwent liver biopsy which showed marked canalicular and intracellular cholestasis, suggestive of cholestatic hepatitis. Eventually, further serologic work-up resulted positive for HEV (IgG and IgM positive). Patient was managed with ursodeoxycholic acid, bilirubin started to trend down 2 weeks after presentation and patient improved clinically until complete recovery. Worldwide HEV infection causes significant morbidity and mortality. High risk groups as pregnant women have increased risks for fulminant hepatic failure. Hepatitis E also occurs in industrialized countries mostly as zoonotic transmission. There are 3 vaccines in development, however the benefit of its use as a generalized preventive measure worldwide is yet to be determined. Overall, It is important to be aware of this entity when approaching patients with suspected viral hepatitis and negative serology for Hepatitis A and B viruses in industrialized countries given this is a condition that can potentially have a poor outcome if present in specific high risk groups of patients and therefore the benefit of a prompt diagnosis is unquestionable.

848 Sofosbuvir and Ribavirin: Successful Treatment of Chronic Hepatitis C Virus Infection in a Renal Transplant Recipient With Concomitant Chronic Kidney Disease Hussein Abidali, DO1, Yousef Usta, MD1, Ali Abidali, DO1, Andrew C. Berry, DO2, Geetha Kolli, MD1. 1. Department of Medicine, Banner-Good Samaritan Medical Center, Phoenix, AZ; 2. Department of Medicine, University of South Alabama, Muskego, WI.

[846B] Figure 2.

was no evidence of active bleeding. Subsequently, the patient was treated conservatively and observed until discharge from hospital.

847 The Forgotten Virus: An Atypical Presentation of Acute Hepatitis E Infection Alan Urbina, MD1, Tarek Almouradi, MD1, Gijo Vettiankal, MD1, Bashar M. Attar, MD, PhD, FACG2. 1. John H. Stroger Jr. Hospital of Cook County, Chicago, IL; 2. John H. Stroger Jr. Hospital of Cook County/ Rush University Medical Center, Chicago, IL. The hepatitis E virus (HEV) is the most common cause of acute hepatitis and jaundice in the world, given its high incidence in highly populated regions in developing countries. Type 1 and 2 genotypes are associated with human fecal-oral transmission. Most HEV infections are clinically silent, although some patients can develop jaundice, pruritus, acholia, and choluria, accompanied by deranged liver function tests with complete resolution in most of the cases. Specific groups of patients raise concern as pregnant women (up to 20% of mortality) and immunosuppressed patients with increased potential for chronicity. 57 year-old male presenting with jaundice for 1 week associated with intermittent mild right upper quadrant pain and episodes of non-bloody emesis. His past medical history is remarkable for Coombsnegative hemolytic anemia. He emigrated from India 20 years ago; He visited his county 2 months prior to presentation. Physical exam was only remarkable by was jaundice. Laboratory work-up with hemoglobin 11.5 g/ dl, WBC 8,300/ul, total Bilirubin 24 mg/dl, direct bilirubin 20 mg/dl (baseline 2.1 and 0.5 respectively), alkaline phosphatase 135 U/l, GGT 155 U/l, AST 42 U/l, ALT 82 U/l, LDH 200 mg/dl, rest was normal.


We report a case of a 63-year-old male with chronic HCV (genotype 3; treatment naïve) and compensated liver cirrhosis (Child Pugh Score 5 Class A; MELD 15) that underwent HCV treatment. The patient is unique as he was a renal transplant recipient with concomitant CKD stage III. His baseline creatinine was 2.0 mg/dL (0.76-1.27 mg/dL) and imaging showed no signs of portal hypertension or liver de-compensation. He had a live-donor renal transplant 13 years prior. Social history revealed no evidence of tobacco, alcohol, or illicit drug abuse. Hepatitis-C treatment was initiated with sofosbuvir 400 mg daily and ribavirin (RBV) 200 mg b.i.d. Pre-treatment HCV PCR viral count was 7,170,000 IU/mL. The patient was monitored with weekly labs and his eGFR during the HCV treatment ranged from 28-32 mL/min/1.73 m2. During the treatment course, his hemoglobin acutely dropped to 6.8 g/dL (12.6-17.7). The patient underwent transfusion of two units of packed red blood cells. The anemia was attributed to a hemolytic process secondary to RBV and the dose was decreased from 200 mg b.i.d. to 200 mg daily. At that time, the patient was also started on epoetin alfa 40k units SQ weekly. The patient experienced no additional side effects during the treatment course and has successfully completed a 24-week regimen of sofosbovir and RBV. His HCV viral load was undetectable at week 12 and also at completion, week 24. He attained SVR at 6-months post treatment. Renal transplant recipients with HCV infections have a 40% chance to develop progressive liver fibrosis within the first 5 years. Furthermore, the HCV-associated glomerulopathies have the capacity to negatively impact renal graft survival. There is still controversy in the treatment of chronic HCV infection after renal transplantation since the standard treatment with pegylated-interferon and RBV is associated with acute renal insufficiency and acute graft rejection of up to 30% or more. The treatment has not been tailored to this unique population. The introduction of direct antiviral agents like sofosbuvir (GS-7977) renders the possibility of interferon-free therapies for HCV infection, and thus avoiding the myriad of complications linked to interferon therapy. Sofosbuvir has demonstrated antiviral activity in HCV genotype 3 when combined with RBV in both naïve and prior treatment experienced patients. However, there are no concrete recommendations regarding the use of sofosbuvir in renal transplant recipients, as this drug has not been fully studied in this population. We have demonstrated the effective use of sofosbuvir and RBV in treating chronic HCV in a patient with a renal transplant, compensated cirrhosis, and CKD stage III. Further studies are necessary to validate the dosing and safety profile for the use of these novel antiviral agents in this unique patient population with a renal transplant and chronic renal insufficiency.


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Hepatic Epithelioid Hemangioendothelioma Complicated by Esophageal Variceal Bleeding

Ledipasvir/Sofosbuvir in the Treatment of Hepatitis C Virus Genotype 6

Nikhil Kapila, MD, Imad Ahmad, MD, Reena Chokshi, MD, Haleh Vaziri, MD. University of Connecticut Health Center, Farmington, CT.

Andrew A. Nguyen, DO, Ilan Weisberg. Lenox Hill North Shore-LIJ Hospital System, New York, NY.

Case Report: A 39-year-old male presented with four episodes of melena. History was significant for metastatic hepatic epithelioid hemangioendothelioma (HEH) status-post three cycles of trans-arterial chemoembolization (TACE) three years prior. Patient denied significant NSAID use. He denied abdominal pain, dysphagia, unintentional weight loss, or change in appetite. He had no previous GI bleeding and no history of esophageal or gastric varices. Vital signs were stable. Physical exam demonstrated a well-nourished male with no icterus. Abdomen was soft with mild tenderness to palpation over the right upper quadrant. Liver span was 14 cm. There was no ascites. Rectal exam demonstrated melenic, hemepositive stool. The CBC demonstrated a microcytic anemia with hemoglobin of 9.8. Platelets were within normal limits, and INR was 1.4. Basic metabolic panel was within normal limits except for a BUN of 21. AST, ALT and bilirubin were normal, but alkaline phosphatase was 372. Viral hepatitis panel was unremarkable. A recent CT scan of the abdomen and pelvis showed multiple, stable hepatic lesions, consistent with the known diagnosis of HEH. A subsequent esophagogastroduodenoscopy revealed moderate to large distal esophageal varices with red whale signs. Band ligation was performed, and an octreotide drip and non-selective beta-blocker were started. Abdominal ultrasound showed a patent portal vein. He was discharged on day #7 of his hospitalization with no further episodes of bleeding. Discussion: Epithelioid hemangioendothelioma is a rare malignant neoplasm of vascular origin that may affect the soft tissue, lung, bone, brain, and liver. First described in 1982, its estimated incidence is less than 1 in 1,000,000. The etiology of primary HEH is unclear. Clinical manifestations are variable. Liver transplant can be curative in the absence of metastatic disease. Treatment for extra-hepatic disease is not clear due to limited experience with HEH and its unpredictable course. Both TACE and surgical intervention have been described. Portal hypertension may arise in HEH patients as tumor cells infiltrate the vasculature of the portal system. Post-TACE portal hypertension is transient and likely due to increased portal blood flow and endothelial dysfunction. While TACE may influence portal hemodynamics, the incidence of significant varices is variable. Bleeding is seen in approximately 1.5-8% of patients at 17-month follow up with most occurring 3 to 6 months post-TACE. Our patient, with a remote history of TACE (3yrs) presented with acute blood loss anemia due to variceal bleeding, likely as a result of significant tumor burden. This case demonstrates a unique presentation of an uncommon entity.

Chronic hepatitis C virus (HCV) is the leading cause of liver cirrhosis and the primary reason for liver transplant referral in the United States (US). In the US, most HCV infections are due to HCV genotype 1 (HCV-1), which was traditionally treated with 48 weeks of pegylated interferon (IFN) and ribavirin with a cure rate of approximately 40% and substantial treatment-related toxicity. Recently, the IFN-free single tablet regimen of ledipasvir/sofosbuvir (LDV/SOF) was approved for HCV-1 infection with cure rate >90%. The utility of LDV/SOF in less common genotypes, such as HCV genotype 6 (HCV-6), is unknown. The standard of care for patients with HCV-6 continues to be pegylated-IFN and ribavirin. Herein, we report a case of HCV-6 successfully treated with LDV/SOF. A 34-year-old Vietnamese-American woman who acquired HCV-6 through vertical transmission was found to have stage 2 fibrosis on liver biopsy. In 2010, she was treated with pegylated-IFN and ribavirin; however, therapy was discontinued at week 4 due to non-response. With the availability of direct-acting antiviral (DAA) agents she was considered for retreatment in 2014. At that time, she was asymptomatic, lab work revealed total bilirubin 0.3 mg/dL, alkaline phosphatase 41 IU/L, alanine transaminase (ALT) 133 IU/L, aspartate transaminase (AST) 75 IU/L, total protein 7.6 g/dL, albumin 4.2 g/dL, and HCV viral load (VL) 846,636 IU. She was treated off-label with 12 weeks of once-daily LDV/SOF after informed consent. By week 2, her VL was detectable, but below the limit of quantitation (< 15 IU), and her ALT and AST normalized to 32 IU/L and 24 IU/L, respectively. At treatment weeks 4 and 8, her VL was undetectable and all biochemical and hematologic parameters were normal. She had no reported treatment side effects. Off treatment VL at weeks 4 and 12 were undetectable, consistent with sustained virologic response (SVR). HCV-6 is endemic to Southeast Asia; however, in the US, is primarily found in Asian immigrants. Thus, it is important to be aware of potential treatment options for HCV-6 as the US population of Asian immigrants grows. Since IFN based therapy, with associated treatment toxicity and low cure rates, remains the standard of care for HCV-6, there exists a major unmet need to bring safer and more efficacious options to this HCV population. Here, we report the successful cure of HCV-6 with 12 weeks of LDV/SOF. With new DAA agents available, the treatment of HCV-6 is rapidly evolving.

851 An Elusive Source of Chronic Gastrointestinal Bleeding After a Whipple Procedure Kavitha Nair, MD, Anna Huguenard, Anjana Pillai, MD. Emory University School of Medicine, Atlanta, GA.

[849A] Figure 1.

Introduction: Gastrointestinal (GI) bleeding is a common cause for hospital admission and rare etiologies can be difficult to identify with conventional diagnostic techniques. Case Description: This is a 67-year-old female who underwent a Whipple procedure for a benign pancreatic cystic mucinous ductal lesion and presented with signs of occult GI bleeding requiring blood transfusions one year later. Prior to this admission, she required monthly hospitalizations and transfusions for recurrent symptomatic anemia. Despite extensive evaluation, no source was identified. During her current hospital admission, she presented with recurrent daily maroon colored stools. She underwent nuclear medicine tagged RBC scan, CT angiogram, colonoscopy, EGD and single balloon endoscopy during her two-week hospital stay but they did not identify a source of bleeding. She required daily blood transfusions to treat her symptomatic anemia. Ultimately, it was hypothesized that reconstruction of her portal vein during her Whipple surgery may have resulted in pre-hepatic portal hypertension. She was started on a trial of octreotide which stabilized her hemoglobin. On follow-up, her symptoms had greatly improved and she required one additional hospitalization since discharge. At 12 months follow-up, octreotide was discontinued successfully and her hemoglobin has remained stable. Discussion: Portal hypertension results from impaired outflow from the portal bed. Pre-hepatic etiologies include portal vein thrombosis, stricture, or invasive tumor affecting the portal vein. Etiology dictates medical and surgical options for therapy and in non-cirrhotic patients, bypassing the liver may not improve portal hypertension. In this case, the patient’s history of Whipple surgery resulted in pre-hepatic portal hypertension secondary to manipulation and diffuse damage to the portal vein. Studies have demonstrated long-term management with octreotide reduces portal pressure, sustains reduced pressure for an extended period of time, and reduces formation of collateral flow (1,2). References: [1]. Kotzampassi K, Koufogiannis D, Eleftheriadis E. Sustained reduction of potal pressure by administration of octreotide-LAR in portal hypertensive rats. Hepatol Res. 2001;19(2):108-16. [2]. Sakurabayashi S, Koh K, Chen L, Groszmann R. Octreotide ameliorates the increase in collateral blood flow during postprandial hyperemia in portal hypertensive rats. J Hepatol. 2002;36(4):507-12.

852 Goldenseal Root Powder (Hydrastis Canadensis) Associated Hepatotoxicity Dhruvan Patel, MD1, Aasim Mohammed, MD2, Aparna Basu, MD1, Ankush Asija, MBBS, MD3, Shriyanka Jain, MD1, Aditya Singh Pawar1, Mervyn Danilewitz, MD, FACG4. 1. Mercy Catholic Medical Center, Philadelphia, PA; 2. Mercy Catholic Medical Center, Yeadon, PA; 3. Mercy Catholic Medical Center, Aldan, PA; 4. Mercy Philadelphia Hospital, Philadelphia, PA.

[849B] Figure 2.


Introduction: The use of herbal supplements has increased in the United States in last decade. It may be associated with significant side effects. We report a patient with hepatotoxicity following ingestion of herbal preparation, Goldenseal root powder. Case report: A 60-year-old female was admitted to the hospital with delusional behavior. A family member had recently noticed that she was jaundiced. The patient had no prior history of liver disease. Her past medical history was significant for paranoid schizophrenia and diabetes mellitus. She denied taking any medication apart from goldenseal root powder for four months prior to admission, for general wellbeing. She did not smoke or drink alcohol. There was no history of drug abuse. Her physical examination was unremarkable apart from icteric sclera. Her liver function test showed total bilirubin of 18.8 mg/dL,


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Abstracts direct bilirubin 11.8 mg/dL, aspartate transaminase (AST) 94 U/L, alanine transaminase (ALT) 76 U/L, alkaline phosphatase 1832 U/L, albumin 2.4 g/dL, and INR 1.0. An abdominal computed tomography (CT) and liver ultrasound showed hepatomegaly without signs of cholecystitis or extra hepatic obstruction. Viral hepatitis serology, antinuclear antibody, anti-mitochondrial antibody, anti-smooth muscle antibody, liver/kidney microsome antibodies, ceruloplasmin level, and iron panel were normal. A liver biopsy showed cholestasis with canalicular and intraductular bile plugs, compatible with drug-induced cholestatic hepatitis. The patient’s jaundice improved while in the hospital. Patient was instructed to stop using goldenseal root powder. Outpatient follow-up showed continued improvement in her liver function test. Discussion: Herbal medicines are widely perceived by the public as an innocuous health aid. Goldenseal root powder is thought to be hepatoprotective in animal models by inhibiting CYP2E1 enzyme.1 However, some herbal medicines may be associated with hepatotoxicity. Our patient’s liver function improved after discontinuation of goldenseal root powder and no other etiology of cholestatic hepatitis was identified. This appears to be the first case report in english literature on goldenseal root powder associated hepatotoxicity. Our case highlights that hepatotoxicity should be considered in anyone taking goldenseal root powder. References: [1] Yamaura K, Shimada M, Nakayama N, Ueno K. Protective effects of goldenseal (hydrastis canadensis) on acetaminophen- induced hepatotoxicity through inhibition of CYP2E1 in rats. Pharmacognosy Res. 2011 Oct;3(4):250-5. doi: 10.4103/0974-8490.89745.

853 Ruptured Hepatic Hydatid Cyst: An Unusual Cause of Acute Cholangitis Geoffrey You, MD1, Sandeep Tummala2, Swati Pawa, MD2, Amy Tilara, MD2. 1. Rutgers Robert Wood Johnson Medical School, Newark, NJ; 2. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ. Introduction: Hepatic hydatid disease (HHD) is a parasitic disease of tapeworms with low incidence in the US predominantly seen in the immigrant and Native American populations. The most common complication of HHD is intrabiliary rupture, which occurs in approximately 5-25% of cases. We report an unusual case of a patient with abdominal pain and jaundice found to have ruptured HHD causing acute cholangitis. Case: A 24 year-old Bolivian male with recent travel to Mexico presented with six months of RUQ pain, nausea, vomiting, and acute onset jaundice. On admission, he was febrile and tachycardic. Exam was notable for scleral icterus, jaundice, and RUQ tenderness with liver edge palpated 4 finger breadths below costal margin. Labs revealed high white cell count, elevated liver function tests (LFTs) consistent with mixed hepatocellular and cholestatic injury. RUQ ultrasound followed by CT A/P confirmed two large cystic lesions replacing much of the left hepatic parenchyma. The larger lesion measuring 7.7x7.7 cm contained smaller cysts and appeared to be communicating with the dilated left intrahepatic bile duct. Given high suspicion for intrabiliary rupture of HHD leading to biliary obstruction and acute cholangitis, the patient was started on piperacillin and tazobactam along with albendazole. He was taken for ERCP with sphincterotomy, extraction of biliary debris, and stent placement. Due to concurrent acute cholangitis, definitive treatment with surgical resection of the cysts was deferred. The patient’s condition as well as his LFTs quickly improved, and he was discharged on oral antibiotics and albendazole with outpatient follow up for surgery. Serologic testing eventually returned positive for HHD. Discussion: Our patient presented with several classic risk factors, and characteristic physical exam and radiographic findings which collectively alluded to the rare diagnosis of a ruptured HHD causing acute cholangitis. This is a potentially fatal complication if not promptly recognized and appropriately treated by a multidisciplinary team with combined antibiotics, anthelmintic, ERCP, and surgery. The incidence of HHD-related acute cholangitis is extremely low in the US. This case emphasizes that while HHD is uncommon in the US, in certain areas of high immigrant and Native American population, the incidence may be high ranging from 1-220 cases/100,000. Therefore, US physicians must be cognizant of this disease and its rare complications when caring for at-risk populations.

[853B] Figure 2.

[853C] Figure 3.

854 A Rare Case of Focal Nodular Hyperplasia in a Man With Idiopathic Non-cirrhotic Portal Hypertension Mubeen Khan Mohammed Abdul1, Michael Hsu, MD, PhD2, Sheila Eswaran, MD, MS2. 1. Rush University Medical Center, Aurora, IL; 2. Rush University Medical Center, Chicago, IL.

[853A] Figure 1.


Idiopathic non-cirrhotic portal hypertension is a rare disorder of young adults and middle-aged women; it is even rarer in males. It is rarely seen in Western populations (3-5%), and it has increased incidence in economically disadvantaged populations. We present a case of idiopathic non-cirrhotic portal hypertension in an adult male with an incidental finding of a benign liver mass. Case Report: A 40-year old Moroccan male with no significant medical history was admitted to an outside hospital with recurrent hematemesis complicated by hemorrhagic shock requiring blood transfusions. An EGD revealed esophageal varices and banding was performed. An abdominal Doppler study was negative for portal vein thrombosis. He was transferred to our institution for consideration of liver transplantation. A transjugular liver biopsy with pressure measurements was performed which confirmed portal hypertension (HVPG = 7 mmHg) but showed no fibrosis or cirrhosis (stage 0). A venogram was normal and ruled out a post-hepatic cause of portal HTN. A CT-A/P with contrast had previously shown a 4.9 x 3.7 x 3.6 cm heterogeneously enhancing lesion in the left hepatic lobe; a targeted biopsy of the lesion revealed focal nodular hyperplasia and was unlikely responsible for his portal hypertension. His condition stabilized, and he was discharged. However, he was readmitted 11 days later with another episode of hematemesis and underwent repeat EGD with esophageal variceal banding. After his 2nd


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Discussion: Our patient presented without any of the known traditional risk factors that are associated with idiopathic portal hypertension. Although diffuse nodular hyperplasia can be associated with late stage idiopathic non-cirrhotic portal hypertension, we report a rare case of focal nodular hyperplasia in a male with idiopathic non-cirrhotic portal hypertension.

855 Obliterative Portal Venopathy Masquerading Large Bile Duct Obstruction in a Patient on Oral Contraceptive Pills Rohit Dhingra1, Asra Batool, MD2, Lee Hwa Jeong, MD1. 1. Albany Medical Center, Albany, NY; 2. Albany Medical Center, Delmar, NY.

[854A] Figure 1.

Introduction: Oral contraceptives pills (OCP) are generally safe but can cause wide range of side effects. We report a case of obliterative portal venopathy (OPV) causing large bile duct obstruction picture from OCP use and slow resolution after discontinuation of the medication. Case: A 19-year-old woman with medical history of Down`s syndrome and hypothyroidism presented with acute jaundice, pruritus and RUQ abdominal pain. She denied any fever, alcohol use, recent travel, sick contacts, new medications or herbal supplements. Her medications included levothyroxine, fexofenadine and OCP. Physical exam was remarkable for icterus and RUQ tenderness with positive Murphy’s sign. Labs showed a total bilirubin of 8.0 with direct bilirubin of 5.1, alk phos of 245, AST of 50, ALT of 100 and lipase of 23. Acute and chronic hepatitis work up was negative for acetaminophen toxicity, viral hepatitis, EBV, CMV and HSV serologies, autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, Wilson disease, hemochromatosis, α1 antitrypsin deficiency, and HIV. Urine toxicology was negative. Ultrasound showed no evidence of cholecystitis, cholelithiasis or choledocholithiasis. There was no intra or extra hepatic biliary obstruction on EUS and MRCP. CT scan was unremarkable. Alk phos progressively increased to 500 and the bilirubin slowly improved. The liver biopsy showed histologic features of large bile duct obstruction, and features suggestive of OPV and nodular regenerative hyperplasia. This was most likely thought to be due to OCP use in the absence of other etiologies. OCP was discontinued and LFT`s slowly improved with normalization in 5 months. Discussion: OCPs are currently prescribed to 62 million women of reproductive age in the US. While deemed mostly safe, they can cause hepatic and biliary dysfunction, and a small subset of women develop intrahepatic cholestasis. Liver biopsy shows bland cholestasis without significant inflammation. Obstructive picture with OPV has not been described. A prothrombotic state caused by OCP probably resulted in OPV-induced large duct injury and obstruction picture in the biopsy. This report highlights that OCP can present with OPV and secondary changes such as large duct injury due to their prothrombotic effects. OPV should be considered as a differential diagnosis if the labs and biopsy show findings suggestive of large bile duct obstruction before proceeding with invasive procedures like ERCP.

856 This Liver Abscess Seems Fishy Lorne Dindial, MD, Kasra Adham, MD, Celeste P. Pizza, MD, Vishal M. Patel, MD, Alan Brijbassie, MD. Virginia Tech Carilion School of Medicine, Roanoke, VA.

[854B] Figure 2.

Introduction: Ingestion of foreign bodies can have serious and lingering consequences that can include an atypical presentation of a pyogenic liver abscess. We present the case of a pyogenic liver abscess secondary to an ingested fish bone. Case presentation: A 77-year-old female presents with a one week history of subjective fevers, confusion, and abdominal pain. Laboratory tests revealed leukocytosis of 16.6 K/μL as well as elevated liver

[854C] Figure 3.

hospitalization, he was scheduled for an elective TIPS procedure to prevent future episodes of variceal bleeding. However, when he presented for his TIPS, he was found to have a Hgb of 4.1 and underwent another EGD with esophageal variceal banding after appropriate resuscitation in the MICU. Two days later, he was able to have the TIPS procedure with noted reduction of portosystemic pressures from 19 to 7 mmHg.


[856A] Figure 1.


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Abstracts enzymes (AST-151 IU/L, ALT-111 IU/L, Alkaline Phosphatase-137 IU/L, and Total bilirubin-2.2 mg/ dL). Cross-sectional imaging demonstrates a 7.2 cm x 6.4 cm complex cystic lesion located within the inferior medial segment of the left liver lobe. She was initially commenced on empiric broad spectrum antibiotic therapy and underwent IR guided pigtail drain placement. Cytology as well as Echinococcus and Entamoeba histolytica studies were unremarkable. Interval cross-sectional imaging demonstrates worsening of the size of the abscess with blood cultures being positive for Streptococcus anginosus; open surgical drainage was then effected for definite management. Imaging obtained 2 months after her clinical presentation defines a 3 cm long needle-shaped radio-opacity consistent with a fish bone extending from the prior hepatic abscess site into the wall of the gastric antrum with retrospective review of prior imaging demonstrating similar findings (Figure 1). Conclusion: This case illustrates the potential for infection after ingestion of penetrating foreign bodies such as fish bones. Penetration from the gastric antrum into the liver is a rare occurrence with earlier recognition on imaging with endoscopic and/or surgical removal potentially thwarting a lengthy hospitalization and prolonged antibiotic course.

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left upper quadrant around the body and tail of the pancreas, between stomach and spleen with extension to the pararenal space (figure 1). Subsequent angiogram disclosed splenic pseudoaneurysm treated by embolization and background changes to vasculature with ectatic and stenosed vessels consistent with PAN (figure 2). Hepatitis B serology was negative but she tested positive for hepatitis C, genotype 4 with viral load of 56,000. A serum cryoglobulin test was negative but perinuclear antineutrophilic cytoplasmic antibody test was positive. Serum complement levels were reduced. She was diagnosed as having classic PAN associated with hepatitis C. She was treated with pegylated interferon, and ribavirin but was a non responder at 4 weeks. She was then treated with sofosbuvir, pegylated interferon and ribavirin for 12 weeks with successful eradication of HCV with remarkable improvement in symptoms. HCV associated PAN is rare but accounts for 20 % of all HCV related vasculitis. It tends to occur more often in older females and up to 20 years from infection. Sustained remission is closely related to successful HCV clearance.It is also likely that the patients past history of B cell lymphoma was linked to HCV as well, with epidemiological studies revealing 2-3 times increased risk of B-cell lymphoma in HCV patients. Indolent disease will often respond to anti viral therapy, but aggressive disease requires traditional chemotherapy. Unfortunately our patient had never been tested for HCV prior to this presentation. In conclusion, we describe the first case of a patient with a prior history of B cell lymphoma, presenting with splenic artery pseudoaneurysm rupture from PAN from HCV successfully treated with new generation anti-viral therapy.

Polyarteritis Nodosa Associated With Hepatitis C Virus Infection: A Case Report Freeha Khan, MD, Tuyyab Hassan, MD, Sulieman Abdal Raheem, MD, Annette Kyprianou , MD. MetroHealth Medical Center/Case Western Reserve University, Cleveland, OH Polyarteritis nodosa (PAN) is a systemic necrotizing vasculitis that predominantly affects mediumsized arteries, and is often the consequence of viral infections, mainly HBV. We describe a case of Hepatitis C associated PAN in a patient who had eluded diagnosis for several years. A 55 year old Egyptian female with a history of migraine, B cell lymphoma (in remission), and depression was admitted with diffuse abdominal pain. She denied nausea, vomiting, hematochezia or fever. She had been seen in the GI clinic over many years with post prandial epigastric pain and nausea with negative imaging and endoscopic testing and had been diagnosed with functional dyspepsia. Physical examination revealed the patient looked pale and was in distress with mild tenderness to deep palpation in the left upper abdominal quadrant, with no guarding or rebound. Rectal exam was negative for masses and blood. Lab work was pertinent for a drop in Hgb from 12 g/dl to 9 g/dl. Other routine lab work was normal. After 2 visits to the ED she received a CT abdomen/pelvis, which revealed intra abdominal hemorrhage in the

858 A Case of an Oncocytoma Masquerading as a Periportal Lymph Node Geoffrey You, MD1, Swati Pawa, MD2, Amy Tilara, MD2. 1. Rutgers Robert Wood Johnson Medical School, Newark, NJ; 2. Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ. Introduction: Oncocytoma are relatively rare epithelial tumors that may arise from any organ system. They are generally considered benign tumors with low potential for metastasis. These tumors typically arise from salivary glands, endocrine tissues, and the kidneys. Oncocytoma originating from outside of these anatomical structures are exceedingly rare. We present an unusual case of an incidental periportal mass that was found to be an isolated oncocytoma. Case Report: A 67-year-old female was referred to our clinic for evaluation of an enlarged periportal lymph node found on CT abdomen and pelvis ordered for hematuria and recurrent urinary tract infection. On review of the CT, the periportal lymph node measured 1.1cm by 3.3cm without evidence of other suspicious lymph nodes or intra-abdominal pathology. The patient subsequently underwent endoscopic ultrasound and fine needle aspiration of what appeared to be a well-circumscribed, 3 cm by 3.5 cm mass-like lesion in the periportal region adjacent to the pancreatic head and 2nd portion of the duodenum. The pathology revealed cells with positive staining for CK8/18 and Anti-mitochondrial antibody, and negative staining for CK7, consistent with an oncocytic lesion. Given the pathology result, an MRI of the abdomen and pelvis was obtained to look for a primary source of the oncocytoma; however, the initial CT as well as the MRI showed no evidence of renal masses or perinephric lesions. Based on the clinical findings, it was determined that this periportal mass represent an isolated oncocytoma. Given the low risk of metastasis and the benign nature of oncocytoma, the patient is currently being closely monitored in the clinic with serial imaging. Discussion: To our knowledge, this is the first documented case of an isolated oncocytoma of neither renal nor adrenal origin presenting as a periportal mass, and as such, management is undefined. Based on review of current literature, oncocytoma as established by immunohistochemical studies have little to no potential for metastasis. However, they do have the potential to grow larger, up to 14 cm in one case report, causing compression of neighboring structures. Therefore, it is reasonable to closely monitor oncocytoma with serial imaging to ensure stability, and to consider surgical resection in cases of rapid tumor growth. Our case highlights a rare diagnosis of a common fi nding; in evaluating patients with periportal lesions, oncocytoma should be included in the differential diagnosis.

[857A] Figure 1.

[857B] Figure 2.


[858A] Figure 1.


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diagnosis of disseminated BCG. He was restarted on anti-TB therapy with INH, levofloxacin and B6. His fevers improved 5 days after initiation of therapy. He was discharged on these medications for a 6-month course. Surprisingly, 6 weeks later, initial blood and urine cultures grew M bovis. BCG is a live attenuated strain of M bovis. Intravesicular administration of BCG is commonly used as an adjuvant therapy in superficial bladder cancer. Disseminated BCG is a very rare complication following intravesicular BCG therapy. The prevalence of granulomatous hepatitis in disseminated BCG is 0.7%. Of patients with BCG-associated granulomatous hepatitis, only 10% of patients have tissue that test positive for AFB stains showing mycobacterial organisms. The mechanism by which BCG therapy can cause disseminated M bovis is not clearly understood. One thought is a Th1-mediated hypersensitivity reaction since a number of case reports demonstrated disseminated granulomas with negative AFB and no isolated organism. Our patient did have evidence of disseminated granulomas with negative AFB, but the organism was later isolated in his urine and blood, hence raising the hypothesis that the organism itself also can access the blood stream via uroepithelial cells and disseminate to other organs. In these cases, multi drug anti-TB therapy is recommended for three to six months with or without the addition of glucocorticoids.

861 A Rare Case of Fusobacterium nucleatum Liver Abscess in Immunocompetent Patient Peter Chung, MD1, Anjali Basil, MD2. 1. University of Massachusetts Medical Center, Worcester, MA; 2. UMass Memorial Health Care, Worcester, MA.

[858B] Figure 2.

859 Pancreatic Lymphoma Complicating Early Stage Chronic Hepatitis C Vicky H. Bhagat, MD, MPH1, Thomas Sepe, MD2. 1. Roger Williams Medical Center, An Affiliate of Boston University, Providence, RI; 2. Brown Medical School/University Gastroenterology, Providence, RI. Chronic infection with Hepatitis C virus (HCV) can progress to cirrhosis in 20% of cases. HCV, a single, positive strand RNA virus with great genetic variability, can replicate in peripheral blood mononuclear cells resulting in the development of lymphoproliferative disorders. Accordingly, chronic HCV infection has also been associated with many extrahepatic manifestations including the development of B cell Non-Hodgkins Lymphoma (NHL). Primary pancreatic lymphoma is very rare and comprises 2.2% of NHL and 4.9% of all pancreatic malignancies. We report a patient with early stage HCV infection who developed and died of complications from a primary pancreatic lymphoma. The patient was a 68-year-old female with a past medical history of hypertension, hypothyroidism, basal carcinoma, and hepatitis C, who presented with jaundice and dyspepsia. She had a history of hepatitis C-genotype 1b awaiting interferon-free therapy. Her liver biopsy was consistent with grade 1 inflammation and stage 1-2 fibrosis. Her HCV viral load was 3,962,429 IU/mL. She presented with abdominal distension, nausea, pruritus and jaundice. On physical exam, she had scleral icterus and an abdominal mass. CT of the abdomen revealed a large solid mass in the head of the pancreas extending to or involving the hilum of the liver. The mass measured 7.5 x 4.9 x 12.7 cm. Her labs showed T. Bili 10.0, D. Bili 5.8, ALP 160, AST 216, ALT 166, AFP 2.1, CEA 1.0, CA 19-9 46. After a failed ERCP, the patient underwent placement of internal and external biliary drains by interventional radiology. A core biopsy of the mass revealed high grade B-cell lymphoma consistent with Burkitts lymphoma with cells positive for CD20, CD10 and Bcl-6. The patient underwent chemotherapy complicated by tumor lysis syndrome with multiple complications and expired. Several studies implicate HCV infection as a risk factor for the development of B-cell NHL. Our case reflects a patient whose survival may have been impacted had she been cured of her HCV infection. Although the patient only presented with stage 1-2 fibrosis she still developed a extrahepatic lymphoproliferative disorder that progressed to a rare pancreatic lymphoma. Studies suggest that treatment of NHL with antiviral therapy for HCV can lead to a regression of lymphoproliferative disease. Following successful antiviral therapy, HCV-infected persons with non-Hodgkin lymphoma and other lymphoproliferative disorders can achieve complete or partial remission in up to 75% of cases. Consequently, there is a need to initiate antiviral therapy for all HCV patients, even in early stages of fibrosis, to prevent cirrhosis and other extrahepatic manifestations of HCV infection, lymphoma the example in our patient.

Fusobacterium nucleatum is an oropharyngeal bacteria which is associated with periodontal disease. Previous reports have described pyogenic liver abscesses due to Fusobacterium nucleatum in immunocompromised adults. However, its role as an etiological agent in liver abscesses in immunocompetent adults is poorly understood and to date, there are no case reports of Fusobacterium Nucleatum liver abscesses in the setting of liver cysts. We present a case of a fusobacterium liver abscess in an immunocompetent male in the setting of liver cysts. 51 year old male with a history of hypertension was in his usual state of health when he developed fever, chills associated with diarrhea and right-sided abdominal pain. The patient was diagnosed with infectious colitis. He was treated with Flagyl for 10 days. CT scan performed showed evidence of colitis and there were 2 liver cysts noted incidentally. The patient subsequently had a colonoscopy, which did not reveal any evidence of colitis and patient improved. However, 2 months later, pt returned with RUQ abdominal pain, and CT showed interval worsening of the size of the cysts with connection to a large 10 cm liver abscess in the right lobe of the liver. Patient did not have any history of periodontal disease. Laboratory data demonstrated borderline leukocytosis (WBC 11.9) and Tbili, AST, ALT within normal limits. Blood cultures remained negative. The patient was admitted to the hospital and had a CT-guided abscess drainage performed with drainage of about 200 ml of thick pus. Gram stain showed Gram-negative rods and grew Fusobacterium nucleatum. Patient was discharged on PO antibiotics following drainage and subsequent CT showed complete resolution of liver abscesses. This is a rare case of Fusobacterium nucleatum causing a liver abscess and notably, seemed to infect liver cysts that were asymptomatic prior to patient presentation. Patient did not have a history or oropharyngeal disease and had no tests that revealed an immunocompromised state. This case study suggests that Fusobacterium nucleatum should be considered in immunocompetent patients as a cause of liver abscess.

862 Rare Primary Hepatic Neuroendocrine Tumor: Case Report and Literature Review Sajiv Sethi, MD1, Jon Finan, MD, PhD2, Prasad Kulkarni, MD1. 1. University of South Florida, Tampa, FL; 2. Tampa General Hospital, Tampa, FL. Neuroendocrine tumors are well-differentiated low grade malignant neoplasms. Their pathogenesis is thought to be secondary to the unrestricted proliferation of neuroendocrine cells. They most commonly arise in the bronchopulmonary or gastrointestinal tract but can originate from almost any organ. While the liver is a common site of metastases, primary hepatic neuroendocrine tumors are an exceedingly rare

860 Granulomatous Hepatitis as a Consequence of Disseminated Mycobacterium bovis (M. bovis) Victor Chedid, MD1, Thomas C. Grau, MD1, Jana G. Hashash, MD2. 1. University of Pittsburgh Medical Center, Pittsburgh, PA; 2. University of Pittsburgh, Pittsburgh, PA. A 77 year-old male with history of transitional bladder cell carcinoma diagnosed 12 years ago, presented for further evaluation of recurrent fever, night sweats and weight loss of 1-month duration. Previously he was treated with 3 transurethral tumor resections (TUR) over 7 years and 18 intravesicular Bacillus Calmette-Guerin (BCG) doses. His cancer recurred recently and he underwent a TUR 2 months prior to presentation followed by 2 intravesicular BCG doses, last dose 1 day prior to fever. An extensive infectious work up in the form of blood, urine, and radiographic evaluation was obtained and was negative. Blood and urine cultures were negative. He was empirically treated for BCG cystitis with an antimycobacterial (anti-TB) regimen consisting of isoniazid (INH), rifampin (R), ethambutol and vitamin B6 (B6). His fevers resolved on this regimen and he was discharged on this regimen. He was readmitted 10 days later with fevers. Repeat blood and urine cultures had no growth. In addition, he had mildly elevated transaminases, which were attributed to the R and was substituted with ciprofloxacin. With persistently elevated transaminases, a liver biopsy was done showing granulomatous hepatitis with non-necrotizing granulomas and negative acid-fast bacilli (AFB) stain. Due to BCG therapy, this histologic finding is most consistent with BCG-associated granulomatous hepatitis confirming the


[862A] Figure 1.


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[862B] Figure 2.

[863A] Figure 1.

pathology, of which fewer than 100 cases have been described in world literature. Thus, there exists a paucity of data regarding the clinical presentation, diagnosis and management of this disease. We present a case of a 35 year old patient who presented to our facility for evaluation of a cough and cervical lymphadenopathy. Two biopsies of the lymph nodes were negative, however on workup for an occult malignancy a hypodense heterogeneous hypervascular lesion measuring 3.7cm x 2.7cm in segment IVb of the liver was noted on CT scan. The levels of laboratory studies such as LFT’s, ALP, chromogranin A, 24 hour 5-HIAA and tumor markers including AFP were not elevated. An MRI confirmed the mass, and the patient underwent CT guided biopsy of the hepatic lesion. Staining from the biopsy resulted in cells reactive for synaptophysin, chromogranin, CAM 5.2, MOC31, CD 56 wand MUC confirming a nonsecretory neuroendocrine tumor. Patient underwent octreotide scan, PET scan, CT chest, MRI head along with EUS, EGD and colonoscopy to evaluate for a primary source, however, none was found. The well localized presentation without extensive hepatic invasion made the patient a candidate for surgical resection which was successfully performed. The patient remains disease free over 25 months after initial presentation. Primary hepatic neuroendocrine tumors are an exceedingly rare entity whose variable presentation necessitates provider familiarity with this condition. Once identified, excluding other primary locations with thorough investigation and treatment with surgical resection has been shown to provide the most patient benefit.

863 Acute Right Heart Failure After Bland Embolization of Hepatocellular Carcinoma Nancy Gupta, MD1, Venkat Vuddanda, MD2, Sam McCabe, MD3, Gregg M. Lanier, MD1, Roxana Bodin, MD4. 1. Westchester Medical Center at New York Medical College, Valhalla, NY; 2. Department of Medicine, Westchester Medical Center at New York Medical College, Valhalla, NY; 3. Department of Vascular & Interventional Radiology, New York Medical College, Valhalla, NY; 4. Division of Gastroenterology and Hepatobiliary Disease, New York Medical College, Valhalla, NY.

[863B] Figure 2.

Background. Trans-arterial embolization (TAE) is widely used in the treatment of intermediate stage hepatocellular carcinoma (HCC). We report a case of acute right heart failure (RHF) related to unintended non-target embolization in a patient who underwent TAE for HCC. Case. A 56-year-old woman with mild pulmonary hypertension (pHTN) (pulmonary artery systolic pressures [PASP] before TAE: 35-47 mm Hg), hepatitis C cirrhosis, HCC was treated for hypoxic respiratory failure associated with hypotension immediately after undergoing TAE of 2.8 cm lesion in couinaud segment 8 of liver with 2cc of embozene 40-micron particles. She underwent TAE of sub-segmental branch of right hepatic artery feeding the tumor via trans-femoral approach under general anesthesia. No chemotherapeutic or lipoidol agent was used. Patient became hypotensive immediately after induction anesthesia & was supported with Phenylephrine. Bedside echocardiogram performed later demonstrated worsening right ventricle (RV) strain, elevated PASP (100 mm Hg), RV dilation, RV systolic dysfunction, moderate tricuspid regurgitation, right atrial dilation & blunted respirophasic changes of inferior vena cava, normal left ventricle function & no evidence of pericardial effusion. She was preemptively started on heparin drip, which was later discontinued when CT chest with contrast showed no evidence of PE. She remained intubated requiring high FiO2, was managed for acute severe pHTN resulting in acute RHF utilizing pulmonary artery catheter tailored therapy with diuretics/inotrope/vasopressor/endothelin receptor antagonist/phosphodiesterase-5 inhibitors. Hospital course was complicated by poly-microbial gram-negative bacteremia, septic shock and disseminated intravascular coagulation. Despite maximum medical therapy, patient went in to multi organ failure and died. Autopsy revealed diffuse alveolar damage, intra-alveolar hemorrhage, and pulmonary edema with focal microsphere emboli. Discussion. Extensive literature search revealed no case of acute RHF after TAE. Although readers might argue that phenylephrine might have contributed to the etiology in the background of pre-existing mild pulmonary hypertension. However, autopsy findings demonstrating embolized embozene particles to the lungs causing increased pressures in the vessel proximal to occlusion play an important part in raising the pulmonary artery pressures & causing acute right ventricular strain. This case imparts an important

point of being extra vigilant in the selection of patients undergoing TAE. In patients with pre-existing pHTN, embolization should be foreseen as a risk factor for acute heart failure.


864 Acute Liver Failure Due to Suspected Herpes Simplex Virus Hepatitis: A Call to Consider Empirical Acyclovir in High-risk Cases Chitharanjan Duvoor, MBBS, MD, Jagpal Singh Klair, MD, Abhishek Agarwal, Mohit Girotra, Dileep S. Atluri, Mauricio Garcia-Saenz-de-Sicilia, Farshad Aduli. University of Arkansas for Medical Sciences, Little Rock, AR. Background: Although rare, Herpes simplex virus (HSV-2) is a fatal cause of acute liver failure (ALF) if unrecognized or with delayed treatment. The accepted protocol for empirical management of ALF has a well-defined role for N-acetylcysteine (NAC), but none for antivirals. We have encountered three HSV ALF cases recently, with varying clinical courses, compelling us to highlight this unresolved issue. Case: A 25-year-old man with sickle trait presented with 1-week of fever, headache and myalgia. He claimed sexual monogamy and no medication/drug use. On admission, he was tachycardic, hypotensive, oriented mentally, with tender hepatomegaly and abdomen and lymphadenopathy in axilla/groin. Labwork suggested mild renal insufficiency, low platelets, leukopenia, coagulopathy (INR 2.4) with marked transaminasemia (AST/ALT 4009/3504), mild hyperbilirubinemia (1.8mg/dL) and LDH 4400, but negative Tylenol, salicylate and viral hepatitis panel and imaging unrevealing of cause. Patient was initiated on NAC protocol, but worsened hemodynamically, clinically and biochemically, required intubation, DIC management but eventually died due to multi-organ failure. While all serologies were negative, HSV-2 came positive (titer >1x108). Histopathology on autopsy showed HSV-2 (Fig 1).


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[864A] Figure 1.

Another woman, aged 30 years was admitted with right upper quadrant pain, headache, fever, increased transaminases in hepatocellular pattern (AST/ALT 1721/975), Hyperbilirubinemia (2.3) and LDH 3930, leukopenia, low platelets, high INR (2). The patient was initiated on NAC protocol, additionally started on empirical Acyclovir given her high-risk sexual behavior, while awaiting serologies. On day 4 of admission transaminases started to improve (AST/ALT 303/567) and so did the coagulopathy. Her HSV-2 titers resulted positive on day 3 (titer >1x10 8). Liver biopsy confirmed HSV-2 hepatitis with Cowdry type A bodies. The patient had uneventful recovery after completion of antivirals. Discussion: Mortality with HSV hepatitis progressing to ALF is high (~90%). Diagnosis is often delayed (HSV PCR), or false negative (serology) or based on Tzank smear (only if rash is present) or liver biopsy (risky because of coagulopathy). Patients can have maculopapular rash, leukopenia, thrombocytopenia, but fever and anicteric hepatitis are the hallmark features of HSV hepatitis, which if seen should serve as red flags. Based on our experiences, we urge clinicians to remain cognizant in young ALF patients to consider Acyclovir, which may be life-saving. This further raises a debate if Acylovir dose should be included as a part of ALF management protocol, while awaiting serologies, especially in high-risk patients with above mentioned suggestive clinical features.

[866A] Figure 1.

865 Hepatocellular Carcinoma: A Rare Complication of Cardiac Cirrhosis From Fontan Procedure Tyffany Ping-Yu Chen, MD1, Daniel Shue, MD1, John Daniels, MD2, Brian Kim, MD3. 1. Los Angeles County + USC Medical Center, Los Angeles, CA; 2. University of Southern California Norris Comprehensive Cancer Center, Los Angeles, CA; 3. Keck Medicine of University of Southern California, Los Angeles, CA. The cardiac Fontan operation developed in 1968 has become the procedure of choice for treatment of single-ventricle physiology. Post-Fontan liver abnormalities are well documented but their clinical significance remains poorly understood. Fifty-year-old Caucasian man with congenital right ventricular agenesis and tricuspid atresia status post classic Fontan procedure in 1974 with revision in 1996, sick sinus syndrome with pacemaker, pulmonary embolism on Coumadin, peripheral artery disease with presumed cardiac cirrhosis complicated by episodes of ascites and esophageal varices who presents with mild dyspnea. Patient received extensive work-up without evidence of acute cardiopulmonary disease, but was incidentally found to have liver lesions. Multiphase CT scan with and without contrast was obtained showing two 2-centimeter lesions in segments 3 and 7 that were arterially enhancing with delayed washout phase and concerning for hepatocellular carcinoma (HCC). His alpha fetoprotein levels were repeatedly below 6.7nl/ml. Patient had previous abdominal ultrasounds from two years ago without evidence of liver mass. To confirm the diagnosis of HCC over focal nodular dysplasia (FNH), a liver-spleen scintigraph was performed which showed photopenia of both lesions— suggesting HCC over FNH. Due to the difficult access to the lesions and multifocal disease, patient was not an ideal candidate for radiofrequency ablation or surgical resection, respectively. His extensive cardiac comorbidities would require consideration for dual heart and liver transplants. Patient declined consideration for transplant and recently underwent one round of transarterial chemoembolization with adriamycin beads to each lesion. Fontan circulation has a low hepatic perfusion pressure, chronic hypoxemia, and decreased cardiac output; these repeated injury and inflammation are thought to lead to cirrhosis. As the 20-year survival rate of Fontan patients now approaches 90%, long-term sequelae of their chronic hemodynamic alterations pose new clinical challenges. As of 2014, there were 9 reported cases of HCC after Fontan procedure, many of which were diagnosed at advanced stages or at autopsy. Surgical management of post-Fontan patients is challenging and thus seldom attempted. With the improved survival rate of Fontan patients, the number of HCC cases is expected to increase, which necessitates greater awareness and research for early detection to enable success of localized therapy.

[866B] Figure 2.

866 Acute Hepatitis E Presenting as Autoimmune Hepatitis Ishan Patel1, Rafael A. Ching Companioni, MD2, Loveleen Sidhu3, Nina Kello4, Yingxian Liu3, Ishita Rajnish3, Raghav Bansal2, Aaron Walfish, MD3, Joshua Aron3. 1. Icahn School of Medicine of Medicine (Elmhurst Program), Jackson Heights, NY; 2. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), Elmhurst, NY; 3. Elmhurst Hospital Center, Elmhurst, NY; 4. Queens Hospital Center, Jamaica , NY.

[866C] Figure 3.

Introduction: Hepatitis E virus (HEV) generally causes a self-limited acute infection, although fulminant hepatitis can develop. Chronic infection can be seen in transplant and immunosuppressed patients.



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Abstracts HEV is the second most common cause of sporadic hepatitis in the Middle East and North Africa. We discuss a case of acute HEV infection presenting as autoimmune hepatitis (AIH). Case Report: 32 year-old male with history of diabetes mellitus, hypertension and hyperlipidemia admitted to our institution for jaundice and fatigue. Patient returned back from Dubai about a month prior to the onset of his symptoms. He denied use of new medications and herbal supplements. Physical examination was remarkable for scleral icterus. The lab results revealed AST/ALT 642/1249 while ALP/GGT 152/235, protein/albumin 8.9/4.2, antinuclear antibodies 1280 and IgG 3590. Hepatitis serology positive for HEV IgM and negative for hepatitis A, B and C. Liver biopsy (see image 1; 2) findings were consistent with AIH with moderate activity, grade 3/4, stage 2-3/4 (Scheuer scheme). Pretreatment simplified score was 6 points, suggestive of probable diagnosis of AIH. In the setting of acute HEV infection, patient was not started on corticosteroids and azathioprine. The patient’s liver function test trended down significantly in a period of just 2 weeks with clinical improvement. Discussion: It has been postulated that a combination of environmental triggers, failure of immune system tolerance, and a genetic predisposition may induce a T cell–mediated immune attack against the liver. There are several scenarios which could be possible for the current presentation in our case; the presence of severe acute chronic hepatitis may be secondary to AIH decompensated by acute virus infection of HEV vs false positive results of anti-HEV antibodies in patients with chronic liver disease of autoimmune etiology vs low HEV viremia seen in minority of patients with chronic AIH highlighting the possibility of HEV also being a trigger for the trigger for AIH. It is standard practice to test for hepatitis A, B and C in patients with clinical signs of AIH. We also suggest testing for HEV in patients who immigrated or recently travelled to endemic areas. Patients who test positive for IgM should be confirmed with real time PCR technique and/or molecular liver histology and immunohistochemical testing should be performed.

[868A] Figure 1.

867 Reversal of Hepatitis B Cirrhosis Complicated by Hepatic Decompensation Monica Saumoy, MD1, David W. Wan, MD1, Jose Jessurun, MD1, Ira M. Jacobson, MD2. 1. New York Presbyterian Hospital/Weill Cornell Medical Center, New York, NY; 2. Mount Sinai Beth Israel, New York, NY. A 64-year-old man with compensated hepatitis B (HBV) cirrhosis, hepatitis B e antigen negative, on tenofovir since 2009 with complete viral suppression, history of coronary artery disease and hyperlipidemia presented with decompensated liver disease. Two months prior to presentation, the patient decompensated with new-onset portal hypertension and development of ascites despite an undetectable HBV viral load. The patient was transferred to our hospital after esophageal variceal hemorrhage that was successfully managed with endoscopic band ligation. Work up to explain his recent decompensation included negative hepatitis C and D virus, ANA, SMA, ultrasound and MRI of the liver without portal vein thrombosis or hepatocellular carcinoma. His medications included carvedilol, losartan, rosuvastatin, metformin/linagliptin, and had no change in his medications for the past year, but his atorvastatin was held as a potential hepatotoxin. He then underwent a transjugular liver biopsy which revealed a reversal of his cirrhosis and hepatoportal sclerosis thought to be either from a drug reaction or idiopathic. HVPG was 8mmHg. The patient was subsequently discharged. His new portal hypertension was managed with diuretics and prophylactic endoscopic variceal band ligation. He was maintained on tenofovir for HBV viral suppression. It has been shown that long term treatment of chronic HBV infection with antivirals can lead to regression of fibrosis and cirrhosis. As seen in our patient who received six years of tenofovir, HBV cirrhosis had regressed with successful viral suppression. However the cause of his portal hypertension was hepatoportal sclerosis, a rare cause of noncirrhotic portal hypertension. Common pathologic findings include phlebosclerosis (portal vein wall thickening and luminal obliteration), megasinusoids, and fibrosis around the portal tracts (unlike cirrhosis). Hepatoportal sclerosis has been known to result from portal vein thrombosis, drug injury (typically such as arsenic, contraceptives, steroid, ethanol, or vinyl chloride), or idiopathic. Advanced hepatoportal sclerosis is usually associated with preserved hepatic synthetic function and treatment is to relieve portal hypertension, however hepatoportal sclerosis can paradoxically cause worsening portal hypertension that necessitates liver transplant.

868 Atypical Hepatocellular Carcinoma Mimicking Hemangioma: A Case Report Prapimphan Aumpansub1, Roongruedee Chaiteerakij, MD, PhD2, Kessarin Thanapirom1, Nopavut Geratikornsupuk3, Sombat Treeprasertsuk1, Anapat Sanpavat4, Bundit Chaopathomkul5, Piyawat Komolmit1. 1. Division of Gastroenterology, Department of Medicine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Bangkok, Thailand; 2. Chulalongkorn University, Bangkok, Thailand; 3. Department of Medicine, Queen Savang Vadhana Memorial Hospital, Chonburi, Bangkok, Thailand; 4. Department of Pathology, Chulalongkorn University and King Chulalongkorn Memorial Hospital, The Thai Red Cross Society, Bangkok, Thailand; 5. Division of Diagnosis Radiology, Department of Radiology, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Bangkok, Thailand. Introduction: Hepatocellular carcinoma (HCC) is usually diagnosed by dynamic contrast computed tomography (CT) or magnetic resonance imaging showing typical contrast enhancement pattern in arterial phase and rapid washout in portovenous phase. However, large HCC may present with atypical contrast enhancement pattern mimicking benign liver masses. Case presentation: A 77-year-old female presented with right upper quadrant abdominal pain and 33-pound weight loss over the past 3 months. She was referred for further evaluation of liver mass. CT scan demonstrated liver cirrhosis with a 7.1x7.1x7.2 cm low attenuation mass in the right hepatic


[868B] Figure 2.

lobe. The mass exhibited progressive rim enhancement in arterial phase with centripetal fill-in at the central part of the mass and rapid washout at the peripheral part of the mass in portovenous and delay phase. Differential diagnoses were giant hemangioma or HCC (Figure 1). The total bilirubin was 2.8 mg/ dl, albumin was 2.2 g/dl, alpha-fetoprotein was 11 IU/ml and hepatitis B surface antigen was positive. As the peripheral part of the mass showed typical radiologic features of HCC, transarterial chemoembolization (TACE) was performed simultaneously with liver biopsy for pathological diagnosis. During TACE, angiogram confirmed the presence of a hypervascular mass fed by right hepatic artery in right lobe liver. Histopathology confirmed the diagnosis of HCC (Figure 2). The patient was diagnosed with HCC with hepatitis B related cirrhosis. Further investigation for staging of HCC revealed stage B in the Barcelona Clinic Liver Cancer Classification. The patient underwent second TACE therapy and also received tenofovir. Discussion: The diagnosis of HCC is generally made by radiologic hallmarks of dynamic contrast imaging. However large HCCs may have atypical radiologic contrast enhancement pattern, due to tumor necrosis, fibrosis, fatty change, calcification, peliotic change or portal vein thrombosis. HCCs with atypical radiologic characteristics could mimic other benign hepatic masses eg. hemangioma, large regenerative nodules or abscess. Conclusion: Progressive peripheral enhancement with centripetal fill-in can be atypical imaging pattern of HCC although it is classically described as a radiologic finding for hemangioma. With the underlying diagnosis of cirrhosis, any hypervascular lesion in the liver regardless of enhancing pattern should be considered HCC until proven otherwise.


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869 Nodular Regenerative Hyperplasia: A Case of Rare Prognosis Mindy W. Lee, Manhal Izzy, MD, Harmit Kalia, DO. Montefiore Medical Center, Bronx, NY. Nodular regenerative hyperplasia (NRH) is a known etiology of noncirrhotic portal hypertension (NCPH). About a hundred cases of biopsy- proven NRH in HIV- positive patients have been described. The long-term use of antiretroviral medications was found to be associated with the development of NRH in this patient population. While these patients often have normal synthetic liver function, several reports described cases needing liver transplantation due to liver failure. To date, there is no published data about the development of hepatocellular carcinoma in this patient population. A 26-year-old woman with history of congenital HIV on anti-retroviral therapy complicated by pneumocystis carinii pneumonia (PCP) at age 14. She had been maintained on emtricitabinetenofovir, atazanavir and ritonavir. CD4 count was >300 and viral load was undetectable. She was referred to hepatology for evaluation of splenomegaly, elevated liver function tests and thrombocytopenia. On initial presentation, she reported easy bruising and gingival oozing. Physical exam revealed splenomegaly. Imaging showed evidence of portal hypertension without associated cirrhosis. Upper endoscopy was significant for large esophageal varices without stigmata. Liver biopsy showed minimal fibrosis around the portal areas with no significant inflammation. The lobules showed focal zones of thin hepatocyte plates on reticulin stain with adjacent areas showing mild regenerative changes. The diagnosis of nodular regenerative hyperplasia was made and patient was placed on propranolol for variceal prophylaxis. Two years after the diagnosis of NRH, the patient presented with active, severe variceal bleeding warranting transjugular intrahepatic portosystemic shunt (TIPS). Post- operative course was complicated by mild encephalopathy. Subsequent screening MRI showed a 1.7 X 1.3cm lesion suggestive of HCC. The patient was deemed to be a candidate for liver transplantation and she is currently on our liver transplant list. NRH can develop in HIV patients secondary to antiretroviral medications. These cases can rarely progress to liver failure with worsening portal hypertension resulting in severe variceal bleeding that requires TIPS. Furthermore, this report describes the first case of HCC in a HIV patient with NRH. The possible association of NRH with HCC warrants further investigation.

[870B] Figure 2.

870 A Patient With Intrahepatic Cholangiocarcinoma With Large Cyst Formation Presenting With Right Flank Pain Mayu Shimaguchi1, Akihiro Kishida1, Shozo Kunizaki1, Alan Lefor2, Ken Mizokami1. 1. Tokyo Bay Urayasu Ichikawa Medical Center, Urayasu, Japan; 2. Jichi Medical University, Urayasu, Japan. We report a patient with intrahepatic cholangiocarcinoma with large cyst formation. A 60-yearold female presented with a one-day history of right flank pain. Abdominal ultrasonography and enhanced computed tomography (CT) revealed an approximately 10cm cystic mass accompanying a solid lesion. On physical examination, there was pain on percussion and slight tenderness in the right flank. Laboratory data showed slightly elevated LDH and an elevated CA19-9. Neither communication between the cystic lesion and the bile duct nor intrahepatic bile duct dilatation were observed on magnetic resonance cholangiopancreatography (MRCP). A right hepatic lobectomy was performed with a preoperative diagnosis of cystadenocarcinoma adjacent to the right hepatic vein. A 10cm cystic mass with a relatively thick wall protruding laterally and dorsally was found intraoperatively. The resected specimen contained brown turbid fluid and a 5.5x4cm solid lesion inside the cyst, and 1.8x1.5cm solid lesion in the adjacent liver. Histopathological examination showed papillary adenocarcinoma with proliferation of degenerated bile ductules contiguous with the cyst wall. This lesion was diagnosed as an intrahepatic cholangiocarcinoma with cyst formation. We must consider intrahepatic cholangiocarcinoma with cyst formation in the differential diagnosis when investigating and treating a cystic liver tumor.

[870C] Figure 3.

871 Unique Treatment of Hepatitis C, Genotype-2 Regimen in Patient With Severe Renal Insufficiency Lindsey Merritt, DO1, Darlene Negbenebor, MD2, Kirsten Hohmann, MD2, William Hines, MD2. 1. Stamford Hospital-Columbia University of Physicians and Surgeons, Greenwich, CT; 2. Stamford HospitalColumbia University of Physicians and Surgeons, Stamford, CT.

[870A] Figure 1.


Introduction: Hepatitis C virus (HCV) is the leading cause of advanced liver disease worldwide, thus the goal of treatment is aimed at preventing liver-associated morbidity and mortality. Pegylated interferon (IFN), formerly the mainstay of treatment, offered limited sustained virologic response (SVR) 54-80%, long treatment duration (24-weeks), and severe side effects. Sofosbuvir (SOF), a renally-excreted directacting antiviral (DAA) was approved for use with ribavirin (RBV) in patients with chronic genotype 2 HCV infection with SVR of 93%, providing a viable treatment option for patients with contraindications to IFN therapy (NEJM. 2013; 368:1867-1877). In mild to moderate renal impairment SOF requires no dose adjustment, but plasma concentration increases with eGFR < 30 ml/min/1.73m2 (Clin Pharma. 2014 May;53(5):409-27). Additionally, worsened creatinine has been observed in patients with


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Abstracts

[872B] Figure 2.

[871A] Figure 1.

[871B] Figure 2.

baseline renal impairment following DAA therapy (Annals. 2014 Nov 4;161(9):634-8). While reduced RBV dose is recommended in renal impairment, this significantly reduces its efficacy (Hepatology, 2003 Sep;38(3):645-52). Current guidelines are vague regarding DAAs in severe renal impairment. We describe a case of a patient with severe renal insufficiency and bipolar disorder successfully treated with SOF and reduced dose RBV. Case Report: This is a 61-year-old man with stage 4 CKD, bipolar disorder, and treatment-naïve, genotype 2b HCV infection diagnosed in 2006. Liver biopsy revealed grade 3/4 chronic hepatitis and fibrosis stage II/IV. Use of IFN was contraindicated due to mental illness and likelihood of poor response with low dose RBV. Prior to treatment initiation, HCV RNA was 7,410,000 IU/mL, eGFR was 20 ml/ min/1.73m2, and serum creatinine was 3.2 mg/dL. The patient began 12-weeks of reduced dose ribavirin (200-mg) and standard dose SOF 400-mg daily. He completed the regimen with no adverse events. HCV RNA was undetectable at 6-weeks and has remained undetectable at 6-weeks post-treatment. Creatinine and hemoglobin remained stable, +/- 0.2 mg/dL and +/-0.8 g/dL respectively, throughout treatment. Discussion: Complete clearance of virus suggests patient will achieve SVR12. As one of the first documented cases of successful treatment of chronic HCV genotype 2 in a patient with severe renal impairment using SOF and reduced dose RBV, we propose this regimen can be safe and effective in patients with chronic HCV infection and severe renal impairment.

872 Atypical Presentation of Intrahepatic Cholestasis of Pregnancy Alexander Potashinsky, MD, Tai-Ping Lee, MD. Long Island Jewish Medical Center, North Shore-LIJ Health System, Manhasset, NY. A 22 year old healthy G1P0 female at 32 weeks of gestation presented to ED complaining of nausea, diarrhea and right upper quadrant pain. Her family history was significant for her mother having pruritus during pregnancy. The patient’s vitals and physical exam were normal with a gravid, non-tender abdomen. She had elevated AST and ALT (see Table 1) with normal bilirubin, amylase, lipase and bile acids. Extensive workup ruled out Hepatitis A, B, C, E, as well as HIV, autoimmune hepatitis, hemochromatosis, Wilson’s disease, celiac disease and thyroid dysfunction. There was no proteinuria. She had a

transient mild thrombocytopenia, but there was no other evidence of hemolysis, microangiopathy or pre-eclampsia. Abdominal US, non-contrast MRI and MRCP all showed a normal biliary tree with a normal appearing liver. Her symptoms were attributed to a viral-like illness which improved with IV fluids. Two weeks later, at 34 weeks pregnant, the patient presented with recurrent nausea and right upper quadrant pain and new complaints of diffuse body itching with no rash. She again had persistently elevated AST and ALT with normal bile acids (see Figure 1). Given high index of suspicion for intrahepatic cholestasis of pregnancy (ICP), she was started on ursodeoxycholic acid. She followed up at 36 weeks of gestation with improved itching and abdominal pain. Surprisingly, bile acids were nearly 15 times the upper normal limit. The patient was induced at 37 weeks of gestation and delivered via a non-complicated vaginal delivery. She followed up four weeks post-partum with resolution of her symptoms and normalization of AST, ALT and bile acids. ICP is a poorly understood disease that classically presents in the third trimester of pregnancy with pruritus. Typically the only abnormal test is elevated bile acids, which is the most specific test for ICP and may precede physical symptoms. AST and ALT can be elevated, with ALT the more sensitive abnormality. The physical symptoms and lab abnormalities resolve quickly after delivery. Our case is unusual because the initial presentation was suggestive of a viral illness with normal bile acids and persistent elevation of liver enzymes. The bile acids remained normal even when the patient developed pruritus. Despite the use of ursodeocycholic acid there was a subsequent steep rise in bile acids. This case illustrates that high clinical suspicion for ICP should remain even with normal bile acids level to prevent adverse fetal outcomes.

873 A Giant Liver Cyst Successfully Treated With Alcohol Sclerotherapy Mohammad Hammami, MD1, Elie Chahla, MD1, Matthew Schlossberger2, Alex Befeler, MD1. 1. Saint Louis University, Saint Louis, MO; 2. Saint Louis University, St. Louis, MO. Symptoms in polycystic liver disease are due to both the number and size of cysts; treatment is usually directed at the largest cyst. Simple percutaneous cyst aspiration is associated with a high recurrence rate. Alcohol sclerotherapy, laproscpic cyst deroofing and liver resection have been used to treat cysts ranging from 5-20 cm. We report the successful treatment of symptomatic giant liver cyst with alcohol sclerotherapy. A 44 year old otherwise healthy female was evaluated for a 2-day history of worsening epigastric abdominal pain and fullness. Laboratory investigations revealed normal liver enzymes and function and mild normocytic anemia. Abdominal ultrasound (US) and computed tomography (CT) scan showed multiple hepatic cysts with a dominant cyst measuring 27 cm in diameter. The dominant cyst was treated by a CT-guided percutaneous drainage followed by alcohol sclerotherapy. A total of 5.3 liters of dark brown fluid was aspirated and 50 ml of 98 % absolute alcohol was injected as sclerosing agent. Cystic fluid analysis was unremarkable and consistent with the diagnosis of polycystic liver disease. Abdominal pain and fullness immediately and completely resolved. The procedure was well tolerated without immediate complications. The liver enzymes remained stable within normal range along with synthetic function of the liver. To our knowledge this is the largest reported liver cyst that was safely and successfully treated with CTguided percutaneous aspiration and alcohol sclerotherapy. This procedure should be considered before exploring more invasive and costly treatment options.

874 Cholestasis: A Paraneoplastic Syndrome Khalid Rasheed, MD1, Ronak Patel, MD2, Sumant Arora, MD3, Rehan Sarmad3, Gary Abrams, FACG4. 1. Team Health, Prattville, AL; 2. University of Alabama Birmingham, Montgomery, AL; 3. University of Alabama Birmingham Montgomery Campus, Montgomery, AL; 4. GHS Gastroenterology, Greenville, SC.

[872A] Figure 1.


Hodgkin’s lymphoma(HL) must be included as a differential in cases of fever of unknown origin and idiopathic cholestasis with non specific hepatitis on liver biopsy. Early bone marrow examination in such cases may allow timely therapy and improve morbidity and mortality. A 60-year-old African American man presented with a two month history of recurrent high grade fever and progressive jaundice. He was treated multiple times with empiric antibiotics. Past history was significant for hypertension, alcohol and tobacco use. He denied any history of travel, new medication intake or prior malignancy. Examination revealed pale, emaciated and weak old man with no lymphade-


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nopathy and normal chest, cardiovascular and abdominal examination. Initial lab results revealed mild normochromic anemia and cholestatic pattern of hepatic injury with normal hepatitis serology. Elevated 5-Nucleotidase levels confirmed alkaline phosphatase to be of hepatic origin. MRCP showed normal hepatobiliary system. Enhanced CT chest and abdomen revealed small confluent lymphadenopathy with calcifications in subcarinal and peri-hilar regions. On liver biopsy we found nonspecific chronic hepatitis with mild portal fibrosis and no steatosis or granulomas with no features suggestive of autoimmune hepatitis, Primary Biliary Cirrhosis , Primary Sclerosing Cholangitis or viral hepatitis. On further evaluation, bone marrow biopsy revealed hypercellular marrow with fibrohistiocytic infiltrates and large atypical cells suggestive of lymphoma. Immuno-staining of marrow confirmed large atypical cells to be ReedSternberg cells (CD 30+, CD15+, CD 45-, CD20-) confirming classical HL. Patient was started on chemotherapy and following two cycles, LFTs started to improve and normalized. Patient initially tolerated chemotherapy well until he developed septic shock and multiorgan failure and eventually passed away. HL has bimodal incidence affecting ages 15-35 and >50 years. It is associated with a diverse array of paraneoplastic syndromes ranging from complex neurological syndromes to rare entities like vanishing bile duct syndrome and idiopathic cholestasis. However, other etiologies of intrahepatic cholestasis should be ruled out like alcohol, viral , drug induced, PBC and PSC. Mortality can be as high as 65% from liver involvement. Intrahepatic cholestasis is an uncommon presentation of HL (3-13% of cases), and even more so rare are cases with negative liver biopsy despite clinical picture consistent with a cholestatic pattern of liver injury. Thus, liver biopsy may not necessary reflect the underlying etiology as highlighted by our case. Although treatment of underlying HL results in normalization of liver enzymes, however, its prognostic value remains undetermined.

875 Liver Abscess with Ulcerative Colitis: A Complication Rarely Seen George Khoudari1, Kaartik Soota1, Nayef El-Daher, MD, PhD2, Tarun Kothari, MD, FACG3, Deerajnath Lingutla4. 1. Unity Health System, Rochester, NY; 2. Rochester Regional Health, Rochester, NY; 3. Unity Hospital of Rochester Regional Health, Rochester , NY; 4. Unity Hospital, Webster, NY. Introduction: Liver abscess is a known complication of Crohn’s disease, however, they are very rarely seen in a patient with Ulcerative Colitis (UC) and only few such cases have been reported in literature so far. We will discuss about the atypical presentation of such abscess in a patient with UC which delays diagnosis and appropriate treatment. Case: A 50-year-old male with history of UC, on maintenance dose of prednisone 15mg/day, was admitted to the hospital with complaints of abdominal pain, fever and chills for 1 week. Laboratory findings were significant for leukocytosis of 15,100/mm3. Patient was started on empiric broad spectrum antibiotics for concern of sepsis. CT scan of abdomen showed 4 lesions in the liver that were absent 3 years ago and raised suspicion for metastatic disease, leading to biopsy of the lesions. On the 3rd day of hospitalization, he developed acute hypoxic respiratory failure with ARDS along with worsening of abdominal pain. Repeat CT scan of abdomen showed increase in the size of the hepatic lesions consistent with hepatic abscesses. On day 6, liver biopsy grew rare gram positive alpha hemolytic streptococci followed by absence of malignancy reported on day 8. A final diagnosis of liver abscess was made and they were drained on day 10 eventually leading to clinical improvement. Repeat CT scan 2 weeks later showed near complete resolution of the abscesses. Discussion: Liver abscess is a well-known complication of IBD. However, it is very rarely associated with UC and so far only 10 cases have been reported. High suspicion leading to early recognition is necessary to treat it appropriately. High dose of corticosteroids and active disease usually predisposes patients to develop this complication as witnessed in 9 of the 10 cases reported previously. However, our patient had well controlled symptoms with a low dose prednisone and went on to develop multiple liver abscesses. Experts recommend considering this diagnosis in febrile patients with IBD having inconsistent clinical findings for IBD exacerbation. Also, presence of multiple hepatic lesions is usually seen with metastatic cancer, as suspected in our patient, leading to delay in diagnosis and appropriate treatment which consists of drainage of the abscesses. Conclusion: Liver abscess is a very rare complication of ulcerative colitis. To our knowledge, this is the first case where multiple liver abscesses in a patient with UC was complicated with ARDS due to delay in diagnosis because of atypical presentation in a patient with well controlled UC.

[875B] Figure 2.

[875C] Figure 3.

876 Recurrent Cardiac Tamponade: An Unusual Presentation of Intrahepatic Cholangiocarcinoma Liege Diaz, MD1, Juan E. Corral, MD2, Monica Garcia-Buitrago, MD3, Paul Martin, MD3. 1. University of Miami/Jackson Memorial Hospital, Miami, FL; 2. University of Miami/Jackson Memorial Hospital, Miami, FL; 3. University of Miami, Miami, FL.

[875A] Figure 1.


A 48-year-old woman presented with 8 months of sharp mid chest pain, weight loss and new-onset shortness of breath. Vital signs and physical exam were unremarkable. Initial echocardiogram revealed a normal left ventricle with diastolic right ventricular compression, and a large pericardial effusion with diastolic right atrial collapse. (Figure 1) CT imaging of the abdomen showed a new 7.1cm hypodense mass in the right hepatic lobe. A pericardial window was performed with pericardium, xifoid cartilage and mediastinum lymph node biopsies. Bacterial, fungal, and mycobacterial smears and cultures were negative. The lymph node biopsy showed non-caseating granulomatous inflammation. b ACE levels were normal and there was no hiliar adenopathy. Anti-nuclear antibody was positive (speckled pattern 1:40). Rheumatoid factor, dsDNA, Anti Scl-70, Anti RPR, Anti Smith, Anti Jo1 and Anti centromere antibodies were negative. Hepatitis, Coxsackie, Echovirus and Brucella serologic tests were also negative. Patient was readmitted 1 month later with similar symptoms and was found to have recurrent cardiac tamponade. A second pericardial window was performed with drainage of 600mL of fluid. Epithelial membrane antigen (EMA) positive neoplastic cells were identified in the pericardial fluid. A triple phase CT scan showed persistence of the hepatic mass in segment IV A/B suggestive of cholangiocarcinoma (CCA) or a single metastatic lesion. (Figure 2,3) Workup for adenocarcinoma of


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Abstracts 877 Autoimmune Hepatitis Associated With Influenza Virus Infection Benjamin L. Bick, MD, James R. Bailey, MD, Craig Lammert, MD. Indiana University School of Medicine, Indianapolis, IN.

[876A] Figure 1.

Autoimmune hepatitis (AIH) is a complex inflammatory liver disease characterized by immune mediated destruction of hepatocytes. Disease pathogenesis is likely the result of complex interplay between both genes and environmental exposures. Infectious triggers may play an important role in immune cell activation, as several viruses have been implicated in AIH onset. Influenza is a common viral infection that results in millions of annual infections and in severe cases can have hepatic involvement. A 44-year-old Caucasian female with a history of prior cholecystectomy was referred for progressive jaundice and fatigue over a 3 week period. She also noted fevers, sinus pressure, rhinorrhea, myalgias, and tea-colored urine. Exam was notable for jaundice and RUQ abdominal tenderness. Initial studies prior to referral demonstrated a mixed hepatocellular and cholestatic pattern of injury. Repeat laboratory studies were ordered. Abnormal labs included the following: INR 1.1; alkaline phosphatase, 160 U/L; aspartate aminotransferase, 467 U/L; alanine aminotransferase, 385 U/L; total bilirubin, 9.5 mg/dL; mitochondrial Ab 27 (normal < 20); IgG 2580 mg/dL (normal 700-1500). ANA, smooth muscle Ab, L/K microsome Ab, ferritin, ceruloplasmin, and alpha 1 antitrypsin levels were normal. She tested positive for influenza B via rapid nasal swab. Serologic studies for hepatitis A, hepatitis B, hepatitis C, HSV, EBV, and CMV were negative. Abdominal ultrasound with doppler showed post-cholecystectomy changes and was otherwise normal. Liver biopsy demonstrated moderately dense inflammatory cell infiltrate with lymphocytes, plasma cells, and eosinophils with extensive periportal collapse, and focal bridging necrosis without fibrosis. She was diagnosed with autoimmune hepatitis in the setting of influenza infection. Treatment was initiated with budesonide resulting in normalization of liver enzymes within 4 weeks and a decrease in IgG levels to 1980 mg/dL. She was transitioned to azathioprine and is currently doing well. Several viruses have been implicated in the pathogenesis of autoimmune hepatitis including hepatitis viruses, herpes simplex virus, ebstein-barr virus, measles virus, and varicella zoster virus. To our knowledge, this is the first case report of influenza virus in association with autoimmune hepatitis. Although causality remains challenging, it remains possible that individual genetic predilection or mechanisms of molecular mimicry could initiate AIH.

878 A Case Report of Ceftriaxone-induced Acute Hepatitis: An Idiosyncratic Drug Reaction Patrick Avila. Brigham and Women’s Hospital, Boston, MA.

[876B] Figure 2.

[876C] Figure 3.

Case: A 65-year-old woman was admitted to the hospital for fevers, fatigue and altered mental status. She was diagnosed with S. pneumoniae bacterima secondary to pnemonia and treated with ceftriaxone 2g q12 for a planned one-month duration. Two weeks after discharge she represented with lethargy and fatigue. Physical exam was notable for a mildly tender liver without hepatomegaly or other stigmata of liver disease. A broad infectious work-up was negative. Laboratory data was significant for a transaminitis with an ALT of 1129 (IU/L), AST of 1077 (IU/L), elevated alkaline phosphatase 144 (IU/L), and a normal total bilirubin; her CBC was without eosinophilia, viral and auto-immune hepatitis panels were sent and were negative. A RUQ ultrasound showed a normal liver, patent portal and hepatic veins and no evidence of cholelithasis or cholecdocholithiasis. Given the concern for a drug reaction, her ceftriaxone was discontinued and she was switched to vancomycin. The absence of eosinophilia, lymphadenopathy, and a typical drug rash argued against drug hypersensitivity and was more consistent with drug-induced hepatitis. Within 48 hours of discontinuation the patient’s transaminases and alkaline phosphatase began to fall and two weeks later were normal. Ceftriaxone was added to the patient’s allergy list. Discussion: This case illustrates the potential of ceftriaxone to induce acute hepatitis. The exact mechanisms by which ceftriaxone results in increased hepatic transaminase levels are unknown, and thus it is considered an idiosyncratic reaction. These types of reactions typically result in direct toxic damage to hepatocytes throughout the hepatic lobule, leading to apoptosis and a variable degree of necrosis. Hepatitis symptoms may occur within days to weeks of exposure and may worsen after the agent is discontinued. In some cases, immunologic idiosyncracy, or hypersensitivity reactions involving an abnormal hepatic panel and hallmark signs of hypersensitivity (e.g., fever, rash, lymphocytosis, eosinophilia), may also explain the hepatotoxic properties of cephalosporin antibiotics. Of note, a major study of ceftriaxone’s adverse effects found an overall 5% incidence of hepatic abnormalities with ceftriaxone therapy, with abnormal AST and ALT levels in 3.1% and 3.3% of study participants. Higher dosages were associated with higher percentages of hepatocellular enzyme elevations. In conclusion, the effect of ceftriaxone as a potentially hepatotoxic drug with a delayed idiosyncratic reaction should be considered in any case of a patient treated with ceftriaxone who presents with elevated liver enzymes and hepatitis.

879 Spontaneous Liver Laceration as an Initial Presentation of Systemic Amyloidosis

unknown primary was performed including bone scan, breast US, mammogram, upper endoscopy and colonoscopy. No primary source was identified. Finally a CT guided biopsy of the liver mass confirmed moderately differentiated adenocarcinoma. Immunohistochemistry was positive for Keratin and DPC-4 suggesting intrahepatic CCA. Intrahepatic CCA is a locally aggressive disease that rapidly metastasizes to other liver segments and to the peritoneum. Patients generally succumb before developing pulmonary or brain metastases. This is the first report of CCA presenting with cardiac tamponade, surprisingly without pulmonary or mediastinal involvement. The first pericardial was non-diagnostic. This illustrates the value of repeat biopsy and immunohistochemistry when clinically indicated.


Parth J. Parekh, MD1, Luis A. Balart, MD, MACG2. 1. Tulane University School of Medicine, Gretna, LA; 2. Tulane University School of Medicine, Division of Gastroenterology and Hepatology, New Orleans, LA. Spontaneous rupture of the liver is an extremely rare complication of systemic amyloidosis. A 50-yearold male was brought to the emergency room with a reported 8-10 hour history of progressive abdominal pain and distention. He denied any trauma history. Upon arrival, he was hypotensive and severely anemic with a hemoglobin of 4.6. He was admitted several weeks prior to admission with complaints of dyspnea on exertion with anemia, for which colonoscopy / capsule endoscopy / and EGD failed to identify a source. He was admitted to the intensive care unit and resuscitated with blood products. A CT scan performed revealed a grade 2 laceration of the liver with subcapsular hematoma and intrahepatic contusion. Despite resuscitation efforts with several blood products, aggressive fluid resuscitation, and intravenous antibiotics, the patient continued to show signs of active bleeding. He was taken to the operating room on several occasions for an exploratory laparotomy, abdominal washout, packing, and wound vac changes in attempts to control the bleeding. Hepatology was consulted to determine the etiology of his spontaneous liver laceration. Hepatology recommended that a biopsy be obtained, as an extensive chart review revealed chronically elevated alkaline phosphatase levels raising concern for a possible infiltrative


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[879A] Figure 1.

embolization(TAE). Here we present a case of sarcomatoid HCC that developed without prior antineoplastic intervention. 54 M with PMH of HIV on HAART who presented to our hospital with complain of abdominal pain, nausea and vomiting. Patient had been on HAART therapy for 1 year with an absolute CD4 count of 547. He underwent a CT abdomen which showed a 5.1 x 5.6 x 5.7 cm complex, ill-defined mass in segment 8 of the liver. He subsequently underwent an abdominal MRI with liver protocol which showed 4.8 cm lesion in the liver, without enhancement. Given that the radiological finding were more consistent with an abscess patient underwent an IR guided drainage. No drainable fluid was present and the mass was solid. The patient underwent a biopsy which showed sarcomatoid carcinoma. Immunohistochemistry were positive for CAM5.2, keratin AE1/AE3, and vimentin. Focal to rare positivity was seen with CD31 and S100. Tumor cells are negative for desmin, SMA, LCA, CD34, Arginase-1, Hep-Par1, glypican-3, HHV8, and CD117. Tumor makers-CA 19-9, CEA and Alpha feto protein were negative. Patient tested postive for Hepatitis C antibody with very high RNA titires. He tested negative for Hepatitis A and B. The pathogenesis of sacrcomatoid change in HCC is unclear but is believed to be due to the degeneration and regeneration of carcinomas cells due to anticancer therapy and TAE. This causes HCC cells to become multi potent immature stem cells. But in our patient this was not the case. We propose a different mechanism. HIV and HCV are RNA viruses. HIV and HCV have both shown to cause epithelial-mesenchymal transition (EMT) of cells in vivo. EMT is a biologic process that allows a polarized epithelial cell, which normally interacts with basement membrane via its basal surface, to undergo multiple biochemical changes that enable it to assume a multi potent mesenchymal cell phenotype. Therefore we believe confections of HCV and HIV may have induced a EMT transition in HCC cells leading to sarcomatoid carcimanoma. References: [1]. Eriguchi, N. et al. Malignant Sarcomatoid Tumor of the Liver: Report of a Case. Surg Today, 31, 170-173. [2]. Sandip, B. et al. Hepatitis C Virus Induces Epithelial-Mesenchymal Transition in Primary Human Hepatocytes. 86(24), 13621-13628. [3]. Roberto, M. et al. Abdominal neoplasia with sarcomatoid features as the presenting illness of a patient with a newly diagnosed HIV infection and no AIDSrelated disorders. Case report, clinical and diagnostic features, and literature discussion. CMI 2014, 8(4), 115-120.

disease. Intra-operative biopsy revealed extensive sinusoidal amorphous hyaline deposits consistent with amyloid. In addition, Congo Red Staining revealed regional congophilia in the hyaline deposits with apple green birefringence on polarizing microscopy, characteristic of amyloid. After meeting with his family and discussing the patients’ poor prognosis, a decision was made to pursue comfort measures and the patient died shortly thereafter. We present this rare complication of amyloidosis and review the relevant up to date literature.

880 Acute Alcoholic Hepatitis Masquerading as Acute Leukemia Nisha Sharma, MD1, Mitesh Bhalala, MD2, Yuriy Israel, MD3, Roxana Bodin, MD4. 1. New York Medical College/Westchester Medical Center, Valhalla , NY; 2. Westchester Medical Center, Yonkers, NY; 3. Westchester Medical Center, White Plains, NY; 4. Division of Gastroenterology and Hepatobiliary Disease, New York Medical College, Valhalla, NY. Acute alcoholic hepatitis is commonly associated with leukocytosis. However, severe leukocytosis is rare and associated with worse outcomes. We describe a case of a 51 year old Hispanic man who presented to the Emergency Room with complaints of progressively worsening abdominal distension, shortness of breath, and bilateral lower extremity edema of two weeks’ duration. The patient did not report any other medical conditions. However, he did report heavy daily alcohol consumption. On exam he was icteric, had bibasilar pulmonary crackles, had a distended diffusely tender abdomen, and bilateral lower extremity edema. Laboratory findings were significant for a white blood cell count of 73,000/cu.mm (96% neutrophils), hemoglobin 13.4 gm/dL and platelet count 237,000/cu.mm, sodium 129 mEq/L, potassium 3.4 mEq/L, blood urea nitrogen 54 mg/dL, creatinine 1.19 mg/dL, aspartate transaminase 279 U/L, alanine transaminase 158 U/L, alkaline phosphatase 736 U/L, total bilirubin 19.1 mg/dL (direct 15.1mg/dL), lactate dehydrogenase 373 U/L and albumin 2.1 g/dL. Coagulation studies revealed prolongation of the partial thromboplastin time (36 seconds) and an elevated INR (1.67). A Maddrey’s discriminant function was calculated to be 53.82. The patient was initially admitted to the oncology service with suspicion for acute leukemia. Peripheral smear showed mature polymorphic neutrophils with toxic granulations and vacuolization, some band cells, but no blasts. Bone marrow biopsy did not reveal leukemia or lymphoma. The leukocytosis was deemed to be due to a leukemoid reaction. Ultrasound of the abdomen showed a cirrhotic-appearing liver. Viral hepatitis and atuoimmune serologies were negative. Active infection was ruled out with negative cultures, paracentesis and imaging studies. A liver biopsy revealed marked hepatocytic swelling, lobular inflammation, and prominent Mallory-Denk bodies, consistent with severe acute alcoholic hepatitis. The patient was started on IV methylprednisolone and transitioned to oral prednisolone, which led to a slow improvement in the patient’s condition. Leukocytosis in acute alcoholic hepatitis is not uncommon and may be due to inflammation or infection. However, severe leukocytosis is rarely seen and presents a diagnostic dilemma. Examination of a peripheral smear with confirmatory bone marrow biopsy along with a liver biopsy in the right clinical setting can help differentiate a leukemoid reaction due to acute alcoholic hepatitis from leukemia.

[881A] Figure 1.

881 Sarcomatoid Hepatocellular Carcinoma in a HIV and HCV-Positive Patient Without History of Prior Antineoplastic Treatment Aparna Basu, MD1, Vivek Mehta2, Dhruvan Patel, MD1, Aasim Mohammed, MD3, Bolanle Gbadamosi, MD4, Shriyanka Jain, MD1, Kamesh Parashar, MD1. 1. Mercy Catholic Medical Center, Philadelphia, PA; 2. Mercy Catholic Medical Center, Philadelphia , PA; 3. Mercy Catholic Medical Center, Yeadon, PA; 4. Mercy Health System, Aldan, PA. Sarcomatoid Hepatocellular Carcinoma is a rare neoplasm. It is seen more in the context of HCC undergoing sarcomatoid transformation following treatment with chemotherapy or transcatherial



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Abstracts 882 Abdominal Skin Rash After Transcatheter Arterial Chemoembolization Mitesh Bhalala, MD1, Prashant Nagpal2, Yuriy Israel, MD3, Sam McCabe, MD4, Roxana Bodin, MD5. 1. Westchester Medical Center, Yonkers, NY; 2. Westchester Medical Center at New York Medical College, Valhalla, NY; 3. Westchester Medical Center, White Plains, NY; 4. Department of Vascular & Interventional Radiology, New York Medical College, Valhalla, NY; 5. Division of Gastroenterology and Hepatobiliary Disease, New York Medical College, Valhalla, NY. Hepatocellular cancer (HCC) is the most common malignant hepatic tumor. Liver transplantation or surgical resection are the most curative treatments of HCC, but transcatheter arterial chemoemboliza-

tion (TACE) is considered a standard of care for intermediate-stage HCC as it has shown a survival benefit. A myriad of complications have been described related to TACE. We report a rare case of supraumblical abdominal skin rash after TACE due to embolization of the hepatic falciform artery (HFA). A 54 year-old man with history of non-alcoholic steatohepatitis (NASH) cirrhosis, diabetes mellitus presented with vague abdominal discomfort and weakness for 4 weeks. On exam, abdomen was mildly distended but non-tender with normal bowel sounds. Laboratory work-up was unremarkable. HCC protocol MRI of abdomen confirmed the presence of a 2.6 cm arterially enhancing lesion and two smaller arterially enhancing lesions in segment V concerning for HCC (Fig. 1A). A repeat MRI of the abdomen was obtained after 3 months that showed interval increase in size of the lesion to 3.2 cm (Fig. 1B), at which time the patient was referred for TACE. Selective angiography of the right hepatic artery and its branches showed a faint hypervascular area in segment V of the liver that was subsequently embolized with 75mg of doxorubicin loaded on 7250 beads. The post embolization angiogram confirmed occlusion of the branch. The patient tolerated the procedure well and was discharged. He returned a week later complaining of worsening ‘red bumps’ on his belly (Fig. 2) that appeared 4 days ago. Exam showed a few red papules with adjacent induration and ulceration in the supraumblical region predominantly on the right side. There was no pain or itching. Retrospective review of the angiogram showed that these findings could best be explained by the non-target embolization of the drug eluting beads to the patent falciform artery. The patient was started on non-steroidal anti-inflammatory medication and his symptoms gradually improved over 6 months. An abdominal wall rash after TACE is a rare complication due to non-target embolization of the HFA. We propose that when the HFA is visualized on the angiogram the tip of the microcatheter be placed distal to the origin of the HFA to prevent this complication. If distal placement is not possible, it may be useful to perform a prophylactic embolization or place icepacks near the umbilicus, especially in patients that have risk factors for relatively enlarged HFA.

[882A] Figure 1.

883 Every Other Day Treatment of Viread® in Hepatitis B Infection Tat-Kin Tsang, MD1, Grace W. Chu2. 1. North Shore University Health System, Wilmette, IL; 2. Case Western Reserve University, Mount Prospect, IL. Grace Chu1, Tat-Kin Tsang MD2,3. 1. Case Western Reserve University, Cleveland, OH; 2. University of Chicago, Chicago, IL; 3. NorthShore University Health Case System, Evanston, IL. Introduction: Tenofovir disoproxil fumarate (VIREAD) is commonly used to treat Hepatitis B (HBV). Before the development of VIREAD the treatment of HBV was not very effective. However, this medication can suppress the HBV virus, becoming undetectable. The recommended dosage for adult patients with HBV is 300 mg once daily, which can be quite expensive. Currently, there are no studies involving alternate dosages of VIREAD in HBV patients, even in those with renal impairment. Here, we present a case of an every other day treatment of VIREAD in a patient with renal insufficiency and contrast it with a daily dosage. Case 1: An 80-year old Caucasian woman was found with elevated liver function and discovered to be positive for the hepatitis B surface antigen (HBsAg). With a HBV DNA viral load greater than 170,000,000 IU/mL, she was diagnosed with HBV and prescribed VIREAD 300 mg once daily. Six months later her viral load was found to be at 20,500 IU/mL. Nine months after the diagnosis her viral load was at 552 IU/mL, which is considered to be in the normal range. Case 2: An 83-year-old Caucasian man presented with slightly elevated liver function, shortly after his wife in Case 1 was identified with HBV. While he displayed no symptoms, he was also diagnosed with the same condition. His HBV DNA viral load was discovered to be over 170,000,000 IU/mL, and he was HBsAG-positive. Because he also had a past history of renal insufficiency, he was placed on dose of VIREAD 300 mg every other day. Six months after his diagnosis his viral load dropped to 5600 IU/mL then reached 672 IU/mL at nine months. His viral load continues to do well. Discussion: While it is believed that tenofovir should be taken by HBV patients on a daily basis in order to be effective, the patient in Case 2 demonstrates an efficacious every other day treatment in patients with renal insufficiency. Tenofovir every other day study has been repeated in other treatments; HIV

[882B] Figure 2.

[883]

Table 1. HBV, Liver Function, and Kidney Function Tests Case 1

HBV Viral Load

Case 2

201402-28

2014-03-19

201409-19

2014-12-10

2015-01-23

2015-06-03

2014-03-27

2014-05-29

2014-06-23

2014-10-17

2014-12-10

201501-19

2015-06-04

—

>170 million IU/ml

20,500 IU/ ml

554 IU/ml

—

—

>170 million IU/ml

—

—

5600 IU/ml

672 IU/ml

—

—

Hep B Core Antibody

—

Positive

—

—

—

—

Positive

—

—

Negative

—

—

—

Hep B Surface Antibody

—

Negative

—

—

—

Negative

—

—

—

—

—

—

Negative

Hep B Surface Antigen

—

Positive

—

—

—

Positive

Positive

—

—

Positive

—

—

Positive

Total Protein

6.9

6.2

6.5

6.6

—

6.7

6.5

6.5

—

6.7

6.5

6.9

6.3

Albumin

3.9

3.6

3.8

3.8

—

3.9

3.6

3.5

—

3.7

3.7

3.8

3.6 0.7

Total Bilirubin

0.8

0.4

0.6

0.7

—

0.7

0.8

0.6

—

1.0

0.7

0.7

Bilirubin Direct

—

0.1

0.1

1000 EBV copies/105 peripheral blood mononuclear cells (PBMCs) in the absence of GVHD are started on Rituximab therapy as in this patient. Her transaminitis and fevers resolved after treatment. She is currently well and her EBV viral copies are undetectable. Most acute viral hepatitis are associated with serum ALT > 1000 U/L but EBV hepatitis is not. The diagnosis should be considered in all patients with inconclusive causes of hepatitis, particularly in immunocompromised hosts, and can readily be made with routine serologic testing.

896 Unilateral Cirrhotic Chylothorax: A Rare Presentation Venkata Subhash Gorrepati, MD, MPH1, Namratha Kodali, MD2, Varsha Pramil3, Ivan Nikiforov2. 1. Pinnacle Health Hospital, Mechanicsburg, PA; 2. Pinnacle Health Hospital, Harrisburg, PA; 3. Cornell University, Ithaca, NY. Background: Even though there have been 50 reported cases of bilateral cirrhotic chylothorax, unilateral cirrhotic chylothorax has never been reported in literature. We present a case with unilateral cirrhotic chylothorax and the interesting etiology behind it. Case Report: A 53 year old female presented to the emergency department with a complaint of shortness of breath. Her past medical history was significant for alcoholic cirrhosis, diabetes, congestive heart fail-

ure, and multiple abdominal revision surgeries due to rupture of tubo-ovarian abscess. Over the last year, she presented five times to the hospital with shortness of breath and right-sided pleural effusion. During these admissions, thoracocentisis was performed that showed exudative effusion with no malignant cells. The patient was symptomatically treated for presumed pneumonia and congestive heart failure each time. Physical examination showed decreased breath sounds on the right side and distended abdomen with ascitis but no organomegaly. Vital signs and initial laboratory examination were unremarkable. Chest x-ray showed an enlarging right pleural effusion occupying right hemi thorax. Due to the rapid progression and recurrent nature of the effusion, there was suspicion for a contributing structural leak. Pleural fluid demonstrated a triglyceride level of 128 mg/dL suggesting chylothorax. Follow up lymphangioscintiogrpahic images confirmed the presence of right-sided chylothorax. Patient was referred to a tertiary care centre, where lymphangiography demonstrated an injury to thoracic duct in the abdominal portion most likely caused by the earlier tubo-ovarian abscess repair. The defect allowed for the accumulation of the fluid in the right hemidiaphragm due to slow seeping. Due to patient’s multiple co morbidities, the patient was managed conservatively with a permanent indwelling pleural catheter rather than embolizing the lymphatic duct. The patients symptoms improved over the next few months. Discussion: This patient had chyloascitis that was caused by previous abdominal surgery done for repair of ruptured tubo-ovarian abscess. In this patient due to presence ascitis caused by alcoholic cirrhosis, fluid slowly leaked through the diaphragm with a preference towards right chest due to structural defects. This is similar to the pathogenesis of hepatic hydrothorax. Clinicians should be aware of unusual causes of rapidly enlarging right-sided pleural effusion in cirrhotic patients without other etiological causes.

897 Pyogenic Liver Abscesses: Incriminating Perforated Appendicitis Frank Senatore, MD1, Bhavtosh Dedania, MD2. 1. University of Connecticut Health Center, Farmington , CT; 2. University of Connecticut Health Center, Manchester, CT. We report a case of a 26 year old male with no prior medical history who presented with nausea, vomiting, abdominal pain, diarrhea and fevers for 3 weeks. Diarrhea was watery, non-bloody, occurring 2-3 times daily, associated with intermittent bilious vomiting. The patient admitted to anorexia with 15 pound unintentional weight loss over this time period. Abdominal pain was sharp, right upper quadrant, non-radiating, and progressively worsening. He denied any recent travel or sick contacts. On exam, the patient was febrile and tachycardic, with right upper quadrant tenderness. There was no rebound or tenderness at McBurney’s point, and psoas and obturator signs were negative. Laboratory investigation revealed a WBC 16,500cells/mcL, AST 111U/L, ALT 74U/L, ALP 146U/L, total bilirubin 3.5mg/dL and direct bilirubin 2.4mg/dL. Abdominal CT scan showed multiple coalescing hypoattenuated peripherally enhancing masses throughout the right hepatic lobe, superior mesenteric vein thrombus, and a conglomeration of multiple nodular masses in the right lower quadrant. The patient was started on intravenous antibiotics and heparin; however, he remained febrile and symptomatic. He subsequently underwent percutaneous drainage of the hepatic abscesses. Despite these interventions, the patient deteriorated clinically. An abdominal MRI showed 10 T2 bright lesions in the right hepatic lobe and an involuting pericecal lesion. The patient underwent exploratory laparotomy, where a perforated appendix was discovered and resected. Following surgery, the patient’s symptoms improved with no further signs of sepsis. He was treated with an extended course of antibiotics on discharge. Pyogenic liver abscesses (PLA) are rare and potentially life threatening infections. While most commonly caused by bacteria originating in biliary and portal tracts, perforated appendicitis has rarely been implicated. This case illustrates not only a rare etiology of PLA, but an unusual course of these two clinical entities. Literature indicates that patients classically present with appendicitis, undergo appendectomy, but continue to deteriorate until PLA are identified and treated. The example in this vignette suggests that physicians should be aware of perforated appendicitis as a cause for PLA in a patient not improving with antibiotics and drainage. Further, in cases where imaging studies are non-diagnostic, exploratory laparotomy should be considered for diagnostic and therapeutic implications.

[897A] Figure 1.

[895A] Figure 1.



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898 Portal Vein Thrombosis as a Cause of Massive Ascites in a Non-cirrhotic Patient Carolina Bernabe Ramirez1, Isabel Preeshagul, MD2, Jose G. Sanchez2, Jeffrey A. Shrensel, MD, MS2, Matthew Kutner3, Kristine Favila, DO2. 1. Mount Sinai Beth Israel, New York , NY; 2. Mount Sinai Beth Israel, New York, NY; 3. Mount Sinai Beth Israel, Franklin Lakes, NJ. The prevalence of portal vein thrombosis (PVT) in the general population is < 1%. Predisposing conditions associated PVT include cirrhosis, most commonly (up to 35%), hepatobiliary malignancies, abdominal infectious or inflammatory processes, abdominal trauma or myeloproliferative disorders. PVT in a non-cirrhotic patient is rare and is hypothesized to be secondary to an underlying hypercoagulable state. A 65-year-old male presented with progressive abdominal pain and distention over the past 3 months. He denied any fevers, melena or hematemesis. He consumed 1 pint of vodka daily over the last 5 years. Exam was remarkable for abdominal distention, however, there was no stigmata suggestive of cirrhosis. Labs were significant for hemoglobin 8.2 g/dL, total bilirubin 0.6mg/dl, direct bilirubin 0.4mg/dl, alkaline phosphase 88 U/L, AST 123 U/L and ALT 64 U/L. Hepatitis C antibody was positive with an undetectable viral load. Otherwise, white blood cell count (WBC), platelet count, albumin, BUN/creatinine, coagulation profile, and remaining hepatitis serologies were normal. An abdominal CT was consistent with a large amount of ascites with a normal liver and spleen size and without morphologic changes suggestive of cirrohsis. Hypodensities in the lumen of the main and right portal veins were consistant with thrombi (fig1). Paracentesis was negative for subacute bacterial perotonitis with a calculated SAAG of 2.2 g/dL. Cytology was negative for malignant cells. Hypercoagulable work-up and additional imaging were planned however not completed as that patient left against medical advice. Ascites is a common symptom in patients with portal hypertension secondary to cirrhosis, however in this case, our patient was found to have ascites secondary to PVT in the absence of cirrhosis. PVT complications include bowel ischemia, portal cholangiopathy, septic portal vein thrombosis, and portal hypertension. Management is controversial and typically depends on the acuity of the thrombi. Anticoagulation therapy is generally warranted. However, mortality rates in PVT range from 1-20% with a majority of deaths caused by variceal bleeding. Ascites, in the setting of PVT is a significant and independent prognostic factor and associated with a decreased long-term survival. It is important to recognize portal vein thrombosis as an alternative etiology of ascites in patients without evidence of cirrhosis, as this can guide further management decisions.

[899A] Figure 1.

hours prior to his presentation with hematemesis, he had undergone embolization of the right gastric and gastroduodenal arteries in preparation for Y-90 radioembolization. On endoscopy, as shown in Figure 1, he was found to have extensive gastric necrosis, extending from antrum to incisura, consistent with the embolization of these arteries. Nonsurgical treatment options have been shown to result in a reduction of the tumor burden and an increased survival benefit in patients with unresectable HCC. Of these options, Y-90 has a good safety profile with minimal complications. Prophylactic embolization of the gastric arteries before treatment of HCC with Y-90 is performed to prevent gastroduodenal ulceration. In our case, the attempted prophylactic embolization of these gastric arteries prior to the Y-90 radioembolization paradoxically resulted in gastrointestinal hemorrhage due to severe gastric necrosis. To our knowledge, this type of extensive necrosis after prophylactic embolization has not been reported in the literature.

900 Stop and Smell the “Fungus”: A Case of Cryptococcal Meningitis Victor Chedid, MD1, Jana G. Hashash, MD2. 1. University of Pittsburgh Medical Center, Pittsburgh, PA; 2. University of Pittsburgh, Pittsburgh, PA.

[898A] Figure 1.

899 A Rare Complication After Prophylactic Embolization of Right Gastric Artery Sarina Kapoor, MD1, Ashwini Anumandla, MD1, Swapna Gayam2. 1. West Virginia University Hospital / Ruby Memorial Hospital, Morgantown, WV; 2. West Virginia University School of Medicine, Morgantown, WV. The different treatment options for unresectable hepatocellular carcinoma (HCC) include: transarterial chemoembolization (TACE), radiofrequency ablation (RFA), sorafenib, and radioembolization using Yttrium 90 (Y-90) microspheres. Limited options are available for patients with tumor invasion of the portal vein. Radioembolization using intraarterial injection of Y-90 microspheres can be considered for treatment of advanced HCC with portal vein thrombosis. This report describes a 56 year old male who presents with hematemesis. He had a known history of multifocal hepatocellular carcinoma and portal vein tumor thrombosis due to Hepatitis C virus. Previous imaging had demonstrated multiple liver lesions consistent with HCC in both the right and left hepatic lobes along with portal vein invasion. He had well compensated liver disease with a MELD score of 9 and Child-Pugh Class B. His alpha-fetoprotein was greater than 200,000 ng/mL. Less than twenty-four


We present the case of a 62 yo M with hx of hepatitis C cirrhosis s/p treatment with Sofosbuvir and Ribavirin, refractory ascites, and multiple admissions for hepatic encephalopathy, presenting with blurred vision, headache and confusion. The patient has presented to the hospital with similar chief complaints over the past two months. His symptoms have been attributed to hepatic encephalopathy and lactulose noncompliance. On prior admissions, starting lactulose improves his symptoms and he gets discharged to return few days later with the same presentation. His headache is frontal and occipital, dull and not radiating, associated with blurred vision and vertigo. This was also associated with neck pain and stiffness. He also reported nausea and vomiting, with no fevers. Physical exam revealed a frail elderly male with jaundice and icteric sclerae. He had a protuberant abdomen with significant ascites. His neck was stiff. Ocular exam revealed bilateral papilledema and limited abduction of both eyes on lateral gaze. Magnetic resonance imaging (MRI) of the brain revealed subtle leptomeningeal enhancement along the cerebellar folia. Paracentesis for ascitic culutre and cell counts was unrevealing. A lumbar puncture was pursued and revealed an opening pressure of 44cm H2O. Cerebrospinal fluid (CSF) revealed white blood cell count: 21 (Neutrophils: 9, Lymphocytes: 91), red blood cells: 59, protein: 157, Glucose: < 10. CSF culture grew moderate yeast, India Ink prep revealed many encapsulated yeast and cryptococcal antigen of CSF was positive (titer 1:1024). This confirmed the diagnosis of cryptococcal meningitis. He was started on IV liposomal amphotericin B and flucytosine for induction therapy. Unfortunately he passed away from complications of amphotericin B. Cryptococcal infection in patients with cirrhosis presents most commonly as peritonitis as per Singh et al. in a case series in 2004. Cirrhosis is a chronic condition that causes immunosuppression secondary to complement deficiency and possible defective macrophages. This predisposes patients to subclinical cryptococcal infections whether in the lungs or ascitic fluid. Cryptococci disseminate hematogenously to other organ systems including the CSF causing cryptococcal meningitis. Treatment is prolonged and is divided into phases:1- Induction: Liposomal amphotericin B and flucytosine for 4 weeks, 2- Consolidation: Fluconazole 400mg for 8 weeks, 3- Suppression: Fluconazole 200mg for 8-12 months. CSF clearance should be documented at end of induction to proceed to consolidation. In our patient, his recurrent admissions for confusion and headache have been attributed to hepatic encephalopathy given the severity of his cirrhosis. It is important to keep a high index of suspicion in patients with cirrhosis specifically for opportunistic infections.


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Abstracts

901 When Liver Disease Causes HIV Tamara Brodsky, MD, Matthew Harrington, MD. Mount Sinai Beth Israel, New York, NY. Introduction: In the U.S., about 30% of HIV patients are co-infected with hepatitis C virus (HCV). The high rate of co-infection is largely due to similar routes of transmission. Sequence of infection varies by transmission route based on the efficiency of transmission. Injection drug users usually acquire HCV before HIV because HCV is so efficiently transmitted percutaneously. Alternatively, men who have sex with men are typically infected with HIV first. Due to their similar risk factors, patients with either virus should be screened for the other. Case history: 34 year old male with a history of intravenous drug use and hepatitis C infection presents to the emergency department (ED) with arm pain for 5 days. Patient stated that one week prior to admission, he had a relapse and injected heroin in his right antecubital fossa. Two days later, patient noticed redness on his right arm associated with pain, bringing him to the ED. Since then, pain worsened and became so severe that he felt he could not flex or extend his upper extremity at the elbow. Denied fevers, chills, rashes, nausea, vomiting, diarrhea, constipation, chest pain, shortness of breath, abdominal pain, urinary symptoms.Patient was admitted for treatment of abscess with overlying cellulitis with incision and drainage as well as intravenous vancomycin. Due to patient’s high-risk behaviors, HIV rapid testing was sent. Screening test was resulted as positive. Confirmatory testing was done with HIV-1/HIV-2 antibody differentiation. The result of this test was negative. HIV viral load was then checked which was also negative. Discussion: False negative results for anti-HCV tests have been reported in HIV infected patients. Recommendations exist to additionally check for viral load as a confirmatory test in these patients. However, false positive HIV results in hepatitis C patients has been less well-documented. Because hepatitis C is generally asymptomatic for a long period of time, diagnosis is made later compared to HIV where patients can become acutely symptomatic. Given new recommendations to increase screening for hepatitis C virus in asymptomatic patients of a certain age, hepatitis C diagnosis will start to be made earlier. All patients with hepatitis C should also be screened for HIV given their similar risk factors and routes of transmission. The possibility of false positive results raises the question of appropriate tests for screening in this population.

upper quadrant (RUQ) pain and 20 lb weight loss. Five years prior to presentation, an abdominal MRI done for RUQ pain revealed a heterogeneous right liver lobe with mixed attenuation partially cystic focal lesions, punctate calcifications and peripheral biliary ductal dilatation concerning for neoplasm. She was subsequently lost to follow up. Upon re-presentation, her exam was notable for RUQ tenderness to palpation. Labs revealed total bilirubin 1.1 mg/dL, AST 169 U/L, ALT 280 U/L, and alkaline phosphatase 496 U/L. Serologic evaluation for underlying liver disease, HIV and infectious agents were negative except TB quantiferon was positive. Chest CT demonstrated scattered bilateral pulmonary nodules and a prominent right hilar lymph node. Abdominal CT revealed a complex mass in the right hepatic lobe with associated biliary ductal dilatation and calcifications concerning for metastatic malignancy. Sputum acid fast bacilli (AFB) stain and culture were negative. Fine needle aspiration of the liver mass revealed extensive granulomatous inflammation. Stains and cultures for fungi and AFB were negative. Core biopsy of the liver mass was performed, again yielding negative AFB stains and culture. Ultimately, TB PCR from the core samples returned positive. She was initiated on rifampin, isoniazid, pyrazinamide and ethambutol with continued follow up in TB clinic. This case highlights the diagnostic challenges associated with hepatic TB. While AFB stain and culture should be performed to evaluate for this entity, these are highly insensitive tests with culture yielding organisms in less than 10% of cases. TB PCR has demonstrated sensitivity of 53% with specificity of 96%, resulting in 90% positive and 76% negative predictive value. While PCR is not an ideal test, it’s improved sensitivity over culture makes it extremely valuable in making the diagnosis of hepatic TB.

902 Vertical Sleeve Gastrectomy Is Ineffective for Treatment of Serum Transaminase Elevations in a Morbidly Obese Individual With Hepatitis C/HIV Coinfection William Hsueh, MD1, Iman Andalib, MD2, Timothy R. Shope, MD3, Timothy R. Koch, MD, FACG3. 1. MedStar Washington Hospital Cetner, Washington , DC; 2. MedStar Washington Hospital Cetner, Washington, DC; 3. Center for Advanced Laparoscopic & Bariatric Surgery, MedStar-Washington Hospital Center and Georgetown University School of Medicine, Washington, DC. It is not clear whether treatment of nonalcoholic fatty liver disease can reduce ongoing hepatic inflammation in individuals with hepatitis C/HIV coinfection. We report a case of a patient with hepatitis C/HIV coinfection and serum transaminase elevations who underwent bariatric surgery for treatment of medically-complicated morbid obesity. This is a 59 year-old female with diabetes mellitus, hypertension, morbid obesity (BMI 40.5 kg/m2), and HIV/Hepatitis C co-infection. She was receiving for treatment of HIV: Darunavir, EmtricitabineTenofovir, Ritonavir, and Raltegravir. Two years prior to her Bariatric Clinic evaluation, at an outside facility she underwent a percutaneous liver biopsy that revealed grade II activity, stage III fibrosis, patches of macrosteatosis and microsteatosis, balloon degeneration and hydropic changes. She was not considered to be a candidate for hepatitis C antiviral therapy. The patient was seen in Medical-Surgical Bariatric Clinic for consideration of surgical therapy for medically-complicated morbid obesity. Her serum transaminase levels were elevated at twice normal levels. The patient underwent vertical sleeve gastrectomy, and a liver biopsy demonstrated chronic hepatitis with moderate activity (grade II) and severe stage fibrosis (stage IV). Although she had lost 31% of her total body weight at her 18 month follow up visit, her serum transaminases levels were unchanged. She was then again seen at an outside facility and was started on Ledipasvir-Sofosbovir for 12 weeks, which resulted normalization of her serum transaminase levels within 2 weeks of initiation of treatment; her hepatitis C viral load remained undetectable after the 12 weeks of treatment. Obesity can result in elevated serum transaminase levels, the presence of steatohepatitis, and progression to chronic liver disease including cirrhosis. Bariatric surgery is the most effective strategy to achieve long term weight loss in obese individuals. Results from recent studies have demonstrated a positive correlation between resolution of elevated serum transaminase levels and weight loss in individuals who underwent bariatric surgery. In our present patient, despite significant weight loss after vertical sleeve gastrectomy, the serum transaminase levels did not normalize until after antiviral therapy for hepatitis C was initiated. These findings suggest that bariatric surgery may be not helpful for improving elevated serum transaminase levels in patients with hepatitis C/HIV coinfection.

903 Hepatic Tuberculosis: A Rare Cause of a Liver Mass in an Immunocompetent Host Courtney B. Sherman, MD, Neil Mehta, MD. University of California San Francisco, San Francisco, CA. Hepatic tuberculosis (TB) is an uncommon clinical entity seen in immunocompetent hosts and its diagnosis may be challenging. Hepatic TB may present in three main forms: diffuse hepatic involvement associated with miliary or pulmonary TB, granulomatous hepatitis, or tuberculoma/abscess that may mimic malignancy. Clinicians must maintain a high index of suspicion in order to avoid missing or delaying this diagnosis. A 24-year-old woman from the Philippines presented for evaluation of right


[903A] Figure 1.

904 A Fatal Cause of Fever and Pancytopenia in a Patient With Ulcerative Colitis Treated With Azathioprine Amen I. Javaid1, Katherine J. Hahn, MD, MPH2, Ryan M. Kwok, MD3, Mohammed Albugeaey, MD4, Amol S. Rangnekar, MD3, Rohit S. Satoskar, MD3. 1. MedStar Georgetown University Hospital, Department of Internal Medicine, Alexandria, VA; 2. MedStar Georgetown University Hospital, Department of Internal Medicine, Washington, DC; 3. MedStar Georgetown University Hospital, Department of Hepatology, Washington, DC; 4. MedStar Georgetown University Hospital, Department of Gastroenterology, Washington, DC. Hemophagocytic lymphohisitiocytosis (HLH) is a rare, life threatening disease caused by excess activation of lymphocytes and macrophages. Acquired forms of HLH are trigged by infection, immunosuppression, or malignancy resulting in uncontrolled cell proliferation. Patients with inflammatory bowel disease (IBD) are at an increased risk of developing HLH due to a chronic inflammatory state and chronic exposure to immunosuppression. Further, thiopurine therapy increases the risk of lymphoproliferative disorders. A 33-year-old male with ulcerative colitis on mesalamine and azathioprine was admitted to an outside hospital with three weeks of fevers. Initial work up revealed pancytopenia and elevated liver enzymes. Serologic evaluation including viral hepatitis, autoantibodies, ceruloplasmin, and alpha-1-anti-trypsin was negative. Ultrasound showed patent hepatic and portal vessels with nonspecific hepatosplenomegaly. MRCP showed no biliary abnormalities. Despite broad spectrum antibiotics and discontinuation of azathioprine the patient continued to be febrile and was transferred to our institution. On transfer, the patient continued to be febrile and pancytopenic (WBC 2.5, Hemoglobin 5.4, platelets 41). Liver related tests were also elevated: AST 277 U/L, ALT 116 U/L, alkaline phosphate 406 U/L, total bilirubin of 9.6mg/dL, with an INR 3.4. Further studies showed a ferritin of 25,268 (units?) and fibrinogen < 60 mg/dL. Antibiotics were stopped and hematology was consulted. Additional labs revealed an EBV PCR of > 2 million. Bone marrow biopsy revealed both an EBV associated B cell lymphoproliferative disorder and evidence of hemophagocytic lymphohisitiocytosis. The patient’s soluble IL-2r was greater than 15,000 units. Despite aggressive supportive therapy and treatment with decadron and etoposide the patient developed complications including bacteremia and passed. Prolonged use of thiopurines in treatment of IBD has been shown to decrease cell-mediated immunity and blunt humoral response. The resulting immunosuppression increases susceptibility to infection, to include EBV. EBV infection can result in fatal, acquired HLH. Early treatment of HLH can be life-saving but the challenge in diagnosis can lead to delays in therapy. Screening for HLH should be considered in IBD patients on thiopurine therapy presenting with fevers and pancytopenia.


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905 Spontaneous Bacterial Empyema (SBEM) Treated With Antibiotic Therapy Followed by TIPS Mindy M. Sampson, DO, Alison J. Burt, MD, Kellee L. Oller, MD. University of South Florida, Morsani College of Medicine, Tampa, FL. Introduction: Hepatic hydrothorax is a complication of liver failure occurring in 5-12% of cirrhotic patients. Infection of the pleural fluid of a hepatic hydrothorax is referred to as spontaneous bacterial empyema (SBEM). We describe a case of spontaneous bacterial empyema in a patient with recurrent hepatic hydrothorax in which transjugular intrahepatic portopulmonary shunt (TIPS) was utilized in addition to antibiotic therapy to assist with symptom control. Case Report: A 64 year old female with a history of alcoholic cirrhosis complicated by esophageal varices, mild hepatic encephalopathy, and recurrent hepatic hydrothorax presented for abrupt worsening dyspnea and cough. She had three previous admissions over the last two months for hepatic hydrothorax requiring thoracentesis. On physical exam she was afebrile, hypotensive, hypoxic, with decreased breath sounds on the right hemithorax. Computed tomography of the chest, demonstrated large right pleural effusion with collapse of the right, middle, and lower lobes. There was no evidence of pneumonic process. A repeat thoracentesis was performed which was consistent with SBEM (Table 1). Pleural fluid gram stain and culture were negative. She was treated with levofloxacin for a total of 4 weeks. She required repeated thoracentesis every 2-3 days secondary to dyspnea and after eight days of antibiotics she underwent TIPS procedure. She required two further thoracenteses prior to discharge. She completed her antibiotic therapy, and did not require further thoracentesis for the last six months. Discussion: SBEM is diagnosed when a patient with known hepatic hydrothorax develops pleural fluid with polymorphonuclear predominance (PMN > 500 cells/mm3 or > 250 cells/mm3 with positive fluid culture) without evidence of pneumonia at the time of diagnosis. Light’s criteria is not useful for diagnosis, as pleural fluid can remain transudative. Treatment of SBEM parallels that of spontaneous bacterial peritonitis and relies on antibiotic therapy. Unlike a parapneumonic empyema chest tube drainage is contraindicated. The use of TIPS in patients recovering from SBEM has not been specifically studied, but can be considered in patients with refractory hepatic hydrothorax.

[905]

Table 1. Laboratory Work Up

Test

Results Prior Labs

Current Admission

182

629

Body Fluids Nucleated cells (cell/ul) Neutrophils (%)

5

80

250/ mm3 with a positive culture and absence of pneumonia by chest imaging. It occurs without SBP in about 40-50% of cases and thus requires a high index of suspicion in cirrhotics who present with fever. Our patient did not have any radiographic evidence of pneumonia. He was treated with appropriate antibiotics and diuretics. Tube thoracostomy was not performed. A follow up chest X-ray 8 weeks later demonstrated almost complete resolution of the pleural effusion.

913 Intrahepatic Cholestasis in the Setting of Recurrent Prostate Cancer: A Paraneoplastic Syndrome Hayley Walter, MD, Nancy Backus, MD, George Aragon, MD. Mercer University School of Medicine, Savannah, GA. Through well-known mechanisms such as bile duct obstruction and hepatic infiltration, malignancies can cause cholestasis and intrahepatic symptoms and signs. Through unclear mechanisms, and in the absence of infection, obstruction, and infiltration, paraneoplastic syndromes may also cause intrahepatic cholestasis and jaundice. Though usually described in association with renal cell carcinoma (known as Stauffer’s syndrome), cholestasis and jaundice may occur in association with other malignancies, including prostate cancer. We present a rare variant of Stauffer’s syndrome involving recurrent prostate cancer.

[913]

Table 1. Select Laboratory Findings on Admission

Alkaline Phosphatase

1061 IU/l

Total Bilirubin

8.2 mg/dl

AST (SGOT) ALT (SGPT) Prostate Specific Antigen

[913]

175 IU/l 124 IU/l 4364 ng/ml

Table 2. Select Laboratory Findings 5 Months After Therapy with Leuprolide

Alkaline Phosphatase Total Bilirubin AST (SGOT) ALT (SGPT) Prostate Specific Antigen

383 IU/l 0.8 mg/dl

[913B] Figure 2.

A 72-year-old man who had undergone prostatectomy for prostate cancer 8 years prior presented with back pain and jaundice. The patient was found to have recurrent prostate cancer with metastatic disease to the bone. Laboratory values (Table 1) included elevations in prostate specific antigen (PSA), bilirubin, aspartate aminotransferase, alkaline phosphatase. Hepatitis profile and HIV screen were negative. Liver ultrasound and magnetic resonance cholangiopancreatography (Figure 1) demonstrated no obstruction or masses. Liver biopsy, negative for metastatic prostate cancer, revealed intrahepatic cholestasis and extensive extramedullary hematopoeisis (Figure 2). We prescribed ursodiol and pentoxifylline, and planned hormonal therapy for prostate cancer. The patient was discharged in good condition and followed up with gastroenterology and oncology as an outpatient. The patient began leuprolide injections every 3 months. Liver function tests dramatically decreased and, with the exception of alkaline phosphatase, returned to normal limits (Table 2). Stauffer’s syndrome variant seen with prostate cancer is rare with only 6 reported cases in the literature. Case reports of cholestasis attributed to prostate cancer-related paraneoplastic syndromes have documented improvement in cholestasis following treatment of the underlying malignancy. Therefore, we have reason to believe that our patient’s cholestasis and jaundice resolved due to treatment of the underlying malignancy. We theorize the alkaline phosphatase remains elevated secondary to bony metastasis. This case illustrates the importance of considering malignancy during evaluation of unexplained cholestasis and jaundice. Through paraneoplastic syndromes, malignancies can produce symptoms at locations far from the primary lesion or metastases, and by mechanisms other than direct organ infiltration or local obstruction. In the proper clinical setting, patients who present with nonobstructive cholestatic jaundice should be evaluated for nongastrointestinal malignancies, including prostate cancer.

19 IU/l 18 IU/l 62 ng/ml

914 Isolated High Alkaline Phosphatase: Diagnostic Dilemma Muznay Khawaja1, Shriyanka Jain2, Aasim Mohammed2, Jayamohan Nair2, William Mcnamee2, Dhruvan Patel, MD3, Uzma Khan2. 1. Mercy Catholic Medical Center/ Drexel University School of Medicine, Secane, PA; 2. Mercy Catholic Medical Center/ Drexel University School of Medicine, Darby, PA; 3. Mercy Catholic Medical Center, Philadelphia, PA.

[913A] Figure 1.


53 year old male from Haiti with medical history of hypertension, diabetes mellitus type 2, systolic congestive heart failure, end stage renal disease (on hemodialysis), presented to the hospital with nausea and vomiting for a few days. He had a fever of 101.2 and reported marked weight loss. On exam, his abdomen was not distended. Liver edge was palpable 6 cm below the costal margin, and was soft and mildly tender. He had markedly elevated alkaline phosphatase (947) and gamma glutamyl transpeptidase (904) but normal transaminases. CT scan of abdomen showed moderate ascites and right pleural eff usion, no splenomegaly and nodular contour suggestive of cirrhosis; ascites and pleural effusion were drained. Ascitic fluid analysis showed low SAAG. Keeping infiltrative disaeses in differential, liver was biopsied and showed non caseating granuloma in peri portal areas. Microorganisms were not identified by various stains. Later, PCR for tuberculosis was performed on liver biopsy specimen, which was negative. A cardiac MRI did not show strong evidence of cardiac sarcoid. A quantiferon gold test for tuberculosis was positive but it did not clarify if tuberculosis was active. Chest Xray was normal. Sputum and urine gram stain and culture were negative for acid fast bacilli. Anti tubercular therapy was started empirically. To rule out sarcoidosis, whole body gallium scan was performed to identify another site for sarcoid, however it was negative. Since patients fevers started to improve after initiating TB treatment, he was discharged on anti TB drugs. In this case, hepatomegaly and markedly elevated alkaline phosphatase/GGT raised concern for an infiltrative disease of liver. A low SAAG was against portal hypertension related ascites. Our differentials were amyloidosis, sarcoidosis, hemachromatosis, granulomatous hepatitis. Relevant labwork for these diseases was negative. In setting of recurrent exudative ascites, weight loss, night sweats and being from an endemic area, suspicion for TB was high, and positive quantiferon led to initiation of TB therapy. Although liver biopsy was highly suggestive of sarcoidosis, lack of evidence of another site of sarcoidosis on gallium scan led to final diagnosis of liver tuberculosis. This case illustrates the importance of keeping infiltrative liver diseases high in differentials in setting of high alkaline phosphatase, and reminds us of the management strategy when faced with diagnostic dilemma of sarcoidosis vs tuberculosis.


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Abstracts 915 Chronic Use of Social Alcohol: Is It Really Safe? Rifat Mamun, MD1, Dovid S. Moradi, MD 2, Krystle Hernandez, MD3, Neil Theise, MD3, Ira M. Jacobson, MD3. 1. Mount Sinai Beth Israel, New York , NY; 2. Mount Sinai Beth Israel, Hillside , NJ; 3. Mount Sinai Beth Israel, New York, NY. Learning objective #1 : Reviewing characteristics of significant alcohol abuse. Learning objective #2 : Reviewing diagnosis of alcoholic liver disease. Case Report: 67 year old female with no medical history presented to the emergency department for new ascites. Over the previous month, increasing abdominal girth and dyspnea were noticed. She denied smoking or illicit drugs, but admitted to 1-3 glasses of wine with dinner. CAGE questionnaire was negative. She was up to date with cancer screening. Paracentesis was performed, and 6 liters of ascites was drained. Labs showed Tbili 2.3, Alk phos 223, AST 116, ALT 29, WBC 19.9, HGB 11.1, MCV 108.6, and INR 1.8. Ascitic fluid was transudative and negative for infection. Viral hepatitis and autoimmune panels were negative. Endoscopy showed grade 3 esophageal varices and portal hypertensive gastropathy. Liver biopsy showed all three components of alcoholic liver disease (ALD): 1. steatosis; 2. extensive steatohepatitis in the forms of hepatocyte ballooning with prominent Mallory-Denk bodies and neutrophilic infiltration; and, 3. steatofibrosis (transition to cirrhosis with prominent central-portal linking and pericellular fibrosis). Discussion: We present a case of biopsy proven severe ALD in a patient without clear history of heavy alcohol use or overt signs of alcoholism. Although almost 60% of Americans consume alcohol, medical under diagnosis of excessive alcohol use is common. Barriers to diagnosis include: reliance on patient self reporting, stereotyping of an alcoholic patient, and lack of time for screening. Although transaminases are critical in diagnosis of acute hepatitis and alcohol use, there is no objective screening test for alcohol abuse. Regular discussion of patient alcohol use is needed as it is unclear as to what amount and duration of alcohol consumption may lead to significant hepatotoxicity. A wide range of amounts (20-80g of ethanol/ day) has been suggested as harmful. Female gender and the practice of binge drinking have been shown to increase risk of development of ALD. Furthermore, it is unclear which patients will develop simple reversible steatosis and who will develop alcoholic steatohepatitis and/or steatofibrosis that ultimately

leads to cirrhosis. Low grade alcohol use that may be perceived as “harmless” or even beneficial, may in actuality, as in this patient, cause significant injury. It is important, therefore, to regularly and accurately evaluate patient alcohol use and discuss inherent risks of over-consumption. Physicians have a unique opportunity to prevent progression of serious alcohol associated liver-disease.

916 Small Duct Primary Sclerosing Cholangitis: A Rare Entity Vinod Kumar, MD1, Shobha Shahani, MD2, Simranjit Singh, MD1, Ihab Hammoud, MD3. 1. University of Illinois at Urbana-Champaign, Internal Medicine Residency Program, Champaign, IL; 2. University of Illinois at Urbana-Champaign, Champaign, IL; 3. Christie Clinic, Champaign, IL. 26 years old male, recently diagnosed with Ulcerative colitis (UC) presented with elevated liver enzymes. With the history of UC, Primary Sclerosing Cholangitis (PSC) was suspected. Right upper quadrant Ultrasound was noted for only slight dilatation of common bile duct. Patient underwent Magnetic Resonance Cholangiopancreatograpy (MRCP) which showed abnormal fullness at the junction of the head and body of the pancreas but normal bile ducts. Endoscopic Ultrasound was done which suggested normal bile ducts and pancreatic head lymph node enlargement but cytology was negative for malignancy. Patient continued to have persistent elevation of liver enzymes. MRCP was repeated, showing same fullness in pancreas without extrahepatic biliary abnormality. Meanwhile extensive immunological and infectious work up was negative. Finally Liver biopsy was done which revealed intrahepatic biliary injury and obstruction consistent with small duct Primary sclerosing cholangitis. Discussion: Small duct primary sclerosing cholangitis or pericholangitis is variant of PSC involving small caliber bile ducts. It has biochemical and histological features similar to classic PSC. Only a small number of patients with small duct PSC have so far been reported. It has been proposed that patients with small duct PSC would eventually develop large duct PSC but may have better prognosis than classic PSC. The most common criteria for diagnosis of small duct PSC that have been proposed are occurrence of biochemical features of chronic cholestasis, liver histology compatible with PSC, normal cholangiogram, and concomitant IBD. An important part of the mortality in PSC is due to cholangiocarcinoma but there have been different studies with contradictory reports of association of cholangiocarcinoma with small duct PSC and further large scale studies are needed. Conclusion: Small duct PCS should be considered as differential when patient with IBD has abnormal liver function tests but unremarkable imaging studies. Patients with small duct PSC seem to have a good prognosis in terms of risk of progression of liver disease and cholangiocarcinoma.

917 Fatal Hyperammonemia: A Case of Urea Cycle Disorder Unmasked After Roux-en-Y Gastric Bypass Katherine J. Hahn, MD1, Philip Sarges, MD1, Kathy P. Bull-Henry, MD2. 1. MedStar Georgetown University Hospital, Washington, DC; 2. Georgetown University, Washington, DC.

[915A] Figure 1.

Introduction: Urea cycle disorders (UCD) are caused by defects in the nitrogen disposal system, which converts ammonia into excretable urea. Typically in newborns, UCD is increasingly reported in adults. Adults with a partial enzyme deficiency remain asymptomatic until a stressor, such as Roux-en-Y gastric bypass (RYGB), triggers a hyperammonemic crisis. Clinical Case: A 41-year-old obese female s/p gastric bypass in 2004, with history of fatty liver disease, was admitted for nausea. On day 2, the patient became encephalopathic and neurologically unresponsive. Her initial serum ammonia concentration was 446μmol/L; AST and ALT were 62 U/L and 46 U/L. Serum thiamine level was 79nmol/L. Soon after, the patient began to have seizures. CT head revealed cerebral edema. Lumbar punctures and blood cultures were negative. Urine cultures were positive for enterococcus faecalis and sputum showed pseudomonas. The patient was placed on antibiotics without improvement. The patient remained in status epilepticus and phenobarbital was initiated, which controlled the seizures. She was started on dialysis and ammonul, an ammonia binder. She was given a specialized diet with Cyclinex-2 (amino acid modified food) and supplemented with citrulline. Her ammonia level decreased to < 100 μmol/L. Multiple serum amino acid levels were elevated, consistent with UCD. Most notably, glutamine was 1998 nmol/ml (normal 205-756). Testing for ornithine transcarbamylase (OTC) and carbamoyl-phopshate synthase-1 gene mutations were negative. Despite treatment, the patient remained unconsciousness and died. Discussion: UCD, caused by a defect in 1 of 5 urea cycle enzymes, alters the metabolism of nitrogen. Adults with subclinical disease are difficult to diagnose. Women are at risk of silent disease due to X-linked transmission of the OTC gene and chromosome inactivation. In this patient, like most, no genetic mutation was found. Non-genetic pathways can unmask UCD in RYGB patients. Increased nitrogen turnover caused by protein catabolism from rapid weight loss and caloric reduction, combined with augmented nutritional protein load in the protein-dense post surgical diet result in a nitrogen imbalance. This can cause cerebral edema, seizures, and encephalopathy. Early diagnosis can lead to life-saving treatment. Mild UCD can present years after RYGB, but the reason is unknown. As gastric bypass becomes more prevalent, urea cycle disorders must be considered in patients with altered mental status.

918 Is the Liver a Glutton When It Comes to Gluten? Reviewing the Relation Between Celiac Disease and Cirrhosis Karan Gupta, Phillip A. Aleksiejuk, Aditya Kalakonda, David Lehmann. SUNY Upstate Medical University, Syracuse, NY.

[915B] Figure 2.


We have recently started to establish the relationship between Celiac disease (CD) and liver dysfunction, most notably the association with autoimmune disorders such as primary biliary cirrhosis. The balance of gut microbiome, intestinal permeability, hepatocyte function and Kupffer cell activation is critical for good health, and the breakdown of this equilibrium triggers the development of intestinal and liver disorder. We will discuss a case to review the approach to liver dysfunction and review the true nature of CD and cirrhosis.


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[918A] Figure 1.

of the greater omentum, and more rarely, torsion of the fatty appendage of the falciform ligament. Isolated infarction of the falciform ligament, without any underlying anatomical distortion or torsion, makes this case even more unique. We found that only 2 cases were ever reported; this case is the first reported within the United States. A 28-year old male patient with a PMH of HTN presented with the complaint of epigastric and RUQ pain. This pain presented one day prior to admission while at work. The patient could not characterize this pain but stated that it was of moderate severity. It was exacerbated by movement and alleviated with rest and as-needed morphine. No fever, fatigue, or N/V/C/D was present. Physicial exam was remarkable for epigastric and RUQ tenderness with palpation and guarding. Lab data was positive for a CRP of 1.8. A RUQ US revealed only a contracted gallbladder. A CT scan of his abdomen with/without IV contrast was positive for inflammatory changes in the inferior falciform ligament consistent with infarction of fatty appendage of the falciform ligament. An arterial and venous abdominal US was negative, and a follow-up CTA scan of his abdomen showed patent vascularity without thrombosis. EGD was positive for antral gastritis and PPI therapy was started QD. Hem-onc was consulted for etiology workup, and a hypercoagulable panel resulted negative. The patient’s symptoms soon resolved with supportive management. Our case demonstrates the first ever report on infarction of the falciform ligament in the United States. This is an extraordinarily rare case with the previous two reports occurring in Europe. It’s the rarest entity under the general term IFFI, which covers a variety of other conditions such as epiploic appendagitis and omental fat infarction. While it’s known that the underlying pathological development is due to infarction of the fatty tissue, the actual etiology is unknown. Due to its rarity, epidemiological data is limited; however, the reported cases involve males under the age of 50 with past medical histories significant for HTN, a possible risk factor. Possible causes could include an underlying hypercoagulable state such as malignancy, which should be further investigated. The correct diagnosis is of upmost importance as this disease resembles other pathology managed differently. Unfortunately, it’s frequently misdiagnosed with invasive interventions undertaken, such as surgery. Instead, the correct diagnosis can negate these invasive methods and the patient can be managed conservatively as described in our case.

920 Herpes Simplex Hepatitis Ofor Ewelukwa, MD, MSc, Roniel Cabrera, MD, MS. University of Florida, Division of Gastroenterology, Department of Internal Medicine, Gainesville, FL.

[918B] Figure 2.

We present a 23 year old female who presents for new gastroenterology consultation for elevated AST and ALT. On review of systems she elicits 4 months of increasing fatigue, a history of alcohol consumption of 4 drinks (56 grams) 3 days per week for the last year. She denies any transfusions or IV drug use and has multiple tattoos. Viral serologies and abdominal ultrasound obtained on follow up in one month, at which time AST 599 u/L, ALT 355 u/L, Hepatitis B surface Ab positive, and on ultrasound has multiple hyperechoic regions. Workup for congenital and autoimmune hepatitis obtained and advised to abstain from alcohol. She returned in one month with complete abstinence from alcohol, AST 347u/L, ALT 292 u/L, positivity for IgG and IgM of both gliadin and tissue transglutaminase. MRI performed and showed diffuse nodularity of liver. EGD is performed revealing severe loss of villous architecture and increased intraepithelial lymphocytes in the lamina propria. Liver biopsy performed and consistent with focal nodular hyperplasia. She is strongly advised to refrain from all gluten products as well as continue to refrain from alcohol. Given clinical decompensation since, she is now awaiting transplant. Studies illustrate that celiac disease causes disruption of the gut-liver axis and due to increased bacterial translocation and cytokine cascades, can present as transient transaminitis which resolves with gluten abstinence. However, we are learning of the strong relation of autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis with CD. Unfortunately, as in our patient, we are learning of idiopathic cirrhosis associated with CD, and her lack of classic symptomatology hindered her earlier diagnosis. Our outpatient workup nicely illustrates the stepwise approach to such cases and what we would like to emphasize is the early screening for celiac disease in young patients with mild transamintis.

919 A Rare Case of Isolated Falciform Ligament Infarction Dominic M. Colella, DO1, Ranje (RJ) Mohamadameen, DO1, Joseph Salhab, DO2, Michael Valladares, DO1, Steven Selub3, Javier Sobrado, MD1. 1. Nova Southeastern University-Larkin Hospital, Miami, FL; 2. Nova Southeastern University-Larkin Hospital, Tampa, FL; 3. Nova Southeastern University-Palmetto Hospital, Hialeah, FL. Infarction of the falciform ligament is an incredibly rare event that can manifest as acute abdominal pain. The most common forms of intraperitoneal focal fat infarction (IFFI) are epiploic appendigitis, infarction


Introduction: Herpes Simplex Virus Hepatitis (HSVH) is a severe form of viral hepatitis with very high mortality that can be averted if diagnosed and treated early as seen in the patient below. Case: A 59 y/o M with history of diabetes mellitus (DM), hypertension and seizures was admitted with 2-week history of abdominal pain, fever and mild confusion. He denied recent sexual activity, genital/ oral rash, new medications, chronic liver disease or alcohol use. Labs: AST/ALT gradually increased from baseline normal to 1670/800, leukopenia and thrombocytopenia (L&T), negative for ALP, bilirubin, INR, toxicology, hepatitis A/B/C, autoimmune hepatitis panel, septic screen, HIV, CT head, liver CT/ ultrasound. HSV IgM and IgG were positive. Liver biopsy revealed 30% patchy lobular necrosis containing nuclei with HSV I&II viral cytopathic effects including ground glass changes and margination of the chromatin but was negative for CMV and adenovirus. He was started on Acyclovir and showed dramatic improvement in mentation and improvement of AST/ALT and L&T back to normal. Discussion: HSVH first described in 1969, is a rare, cause of acute liver failure (ALF) that often leads to liver transplantation or death. It accounts for < 1% of all causes of ALF and < 2% of all viral causes of ALF. It is often seen in immunocompromised patients as seen in our patient with poorly controlled DM (A1c 10.6) and pregnant women. It is associated with impaired cellular and macrophage immunity with consequent antigen dissemination. It is a diagnostic challenge due to lack of specificity of symptoms and signs with about 58% of diagnosis made post-mortem. Mucocutaneous lesions are often lacking in > half of cases of HSVH as seen in our patient. When present, skin biopsy in the appropriate clinical setting can provide a definitive diagnosis especially when coagulopathy precludes liver biopsy. Elevated transaminases often > 1000 occur during the acute stages due to hepatic necrosis. L&T are often present but resolve with treatment as seen in our case. HSV serum serologies are insensitive even in advanced disease. Radiological findings are usually non-specific. Liver biopsy is the gold standard for diagnosis. Early treatment with Acyclovir decreases mortality. Conclusion: HSVH is a rare, potentially fatal viral cause of ALF that can be appropriately treated if detected and treated early. A high index of suspicion should be maintained especially in the appropriate clinical setting.

921 Development of Non-alcoholic Fatty Liver Disease Following Pancreatectomy Mindy M. Sampson, DO, Cuc Mai, MD. University of South Florida, Morsani College of Medicine, Tampa, FL. Introduction: Non-alcoholic fatty liver disease (NAFLD) is defined as fat in the hepatocytes in excess of 5% of total liver weight or fatty degeneration of more than one-third of the total number of cells in the liver with the absence of alcohol use. NAFLD is usually associated with obesity, hyperlipidemia, or insulin resistance. The development of NAFLD may be due to pancreatic exocrine dysfunction and NAFLD has been shown to be influenced by the volume of remnant pancreas. We present a case of a patient with NAFLD after a pancreatectomy. Case Report: A 36 year old female presented with refractory epigastric and left upper quadrant abdominal pain associated with 2 days of vomiting and inability to tolerate a diet. Her past medical history is significant for diabetes mellitus type 1 (present since childhood, last Hgb A1C: 6.6), and chronic pancreatitis secondary to sphincter of oddi dysfunction which required a total pancreatectomy 6 months prior. Following her pancreatectomy the patient was symptom free for 3 months, after which she developed recurrent and persistent abdominal pain with nausea, vomiting, and diarrhea. She admitted to a weight loss of more than 50 pounds since her surgery. She denied alcohol intake and stated compliance with medications including insulin and pancreatic enzymes. On evaluation her vital signs included a blood pressure of 105/54, heart rate of 80, and temperature of 36.3C. Her BMI had decreased from 31 prior to the surgery to 22 after the surgery. Her abdomen was soft but she had tenderness to palpation in the epigastric area and bilateral upper quadrants with hepatomegaly. Her laboratory studies were significant


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Abstracts for elevated AST and ALT of 98 and 71 respectively, which were normal prior to surgery. Her lipid panel revealed triglycerides, 93; cholesterol, 59; HDL, 16; and LDL, 27. Computed tomography of the abdomen was performed and showed new hepatomegaly with the largest diameter of 25 cm with fat deposition. She was treated with in an increase in pancreatic enzymes. Discussion: This case illustrates a less common cause of NAFLD. Patients with post pancreatectomy NAFLD can develop non-alcoholic steatohepatitis (NASH) and should be monitored for progression of this disease. Further research is needed to evaluate etiology and treatment options in this unique population, as there are currently limited recommendations for treatment.

922 Recurrent Post-partum Jaundice: Rare Genetic Disorder With Novel Genetic Mutations Identified Manraj Khosla, MD1, Devin Dunatov2, Anita Kohli, MD3, Ann Moore, NP3, Ashley Hepner, NP3, Justin Reynolds, MD3, Robert Gish, MD3, Richard Manch, MD3. 1. St. Joseph’s Hospital and Medical Center, Phoenix, AZ; 2. Creighton University School of Medicine, Phoenix, AZ; 3. St. Joseph’s Hospital and Medical Center, Phoenix, AZ. Defective secretion of bile salts results in the accumulation of bile salts and toxic by-products in hepatocytes, as well as plasma, which leads to progressive liver fibrosis and/or cirrhosis. Mutations in the ABCB11 gene, encoding BSEP (bile salt export pump), are associated with benign recurrent intrahepatic cholestasis type 2 (BRIC2) and progressive familial intrahepatic cholestasis type 2 (PFIC2), both rare genetic diseases with an incidence of 1/50,000 to 1/100,000 births. We report two novel mutations in the ABCB11 gene resulting in severe bile salt export deficiency in a patient with recurrent episodes of jaundice and liver failure after multiple subsequent pregnancies. A 27-year-old G4P4 female developed worsening jaundice, pruritus, and abdominal pain 8 weeks after her fourth pregnancy. Laboratory results were significant for elevated total bilirubin of 17.1 mg/dL, direct bilirubin of 12.6 mg/dL, AST 76 IU/L, ALT 45 IU/L, and ALP 358 IU/L. GGT levels were within normal limits at 16 IU/L, INR 1.4, PT 14.2 and albumin 4.1 g/dL. The patient had a history of four successful pregnancies with uncomplicated deliveries. 5-8 weeks after each delivery she developed severe jaundice and liver dysfunction characterized by a similar pattern of laboratory abnormalities. Each episode of jaundice after pregnancy lasted progressively longer, ranging from 4 weeks to 10 months. Our patient underwent an extensive workup for infectious, autoimmune, obstructive, and drug-induced etiologies of disease including multiple liver biopsies, cholecystectomy, and bile duct stenting. After the third pregnancy the patient underwent genetic testing where a heterozygous frameshift mutation, c.2542delG, and a heterozygous missense variant, c.245T>C, were detected in the ABCB11 gene, which encodes for BSEP. We describe two novel mutations in the ABCB11 gene associated with the development of BRIC in a 27 yo female patient with recurrent postpartum jaundice. There have been no reported cases of BRIC2 presenting after pregnancy in a consistent manner as observed in our patient. One explanation could be linked to the estrogen-induced cholestasis in the presence of estradiol-17B-glucuronide (E217G), a cholestatic estrogen metabolite that could exacerbate the onset of postpartum jaundice and cholestasis. BRIC should be considered in the differential diagnosis of patients with recurrent jaundice of unknown etiology.

923 A Rare Case of Hepatoduodenal Abscess With Fistula Damodar Pandey, MD1, Didem Uzunaslan2, Kamran Zahid, MD3, Nejat Kiyici, MD4. 1. Montefiore Medical Cente-Wakefield, Bronx, NY; 2. Cleveland Clinic, Cleveland, OH; 3. Montefiore Medical Center, Bronx, NY; 4. Division of Gastroenterology, Montefiore Medical Center, Wakefield Division, Bronx, NY. Introduction: A hepatic abscess can be complicated by hepatoduodenal fistula. We present a case with a hepatic abscess which was in continuation with duodenum, revealed during upper endoscopy. Case: A 76 year-old male with a history of diabetes mellitus, hypertension, atrial fibrillation and pancreatic stent placement for duodenal adenoma two years ago presented with intermittent nausea, vomiting and abdominal pain for 3 to 4 weeks, associated with several episodes of non bilious vomiting for 2 days. Physical examination showed a mild epigastric tenderness with abdominal distension. Patient was found to have leukocytosis (18.2) and signs of gastric outlet obstruction with noncontrast CT abdomen and pelvis showing 4.2 x 4.8 x 4.4 cm lesion extending from the lateral aspect of the pylorus/proximal duodenum, with surrounding inflammatory stranding, contiguous with 8.3 cm intrahepatic collection. He underwent upper endoscopy that showed a space occupying extrinsic compression in the duodenal bulb, which upon biopsy revealed purulent matrials with bile droplets. Repeated deeper biopsy of extrinsic bulge in the bulb drained a large amount of purulent materials into the small intesine. Duodenal biopsies showed marked acute and chronic duodenitis with granulation tissue formation, numerous intraepithelial neutrophils, and reactive epithelial changes. Post procedure CT abdomen and pelvis showed smaller hepatic collection with airfluid level without pneumoperitoneum, Patient responded very well with total of two weeks of antiobiotics. Repeat CT abdomen and pelvis in 3 weeks and 3 months showed near complete and complete resolution of hepatic collection and adjacent duodenal wall thickening respectively. Discussion: There are few case reports published about liver abscess with hepatoenteric fistula, managed operatively. This is a rare case where patient had a complete response with enodoscopic drainage and antibiotics. Complete recovery can be achieved with endoscopic drainage of abscess and intravenous antibiotics in patients with hepatoduodenal abscess as in our case. References: [1]. Mowji P J et al: Liver abscess with hepatoduodenal fistula. AM J Gastroenterol. 1987 Jun; 82(6):558-9. [2]. Akira I. et al. A case of liver abscess associated with hepatoduodenal fistula.Nihon Rinsho Geka Gakkai Zasshi (Journal of Japan Surgical Association). Vol. 61 (2000) No. 10 P 2724-2728.

agulable states, chronic infections or inflammatory conditions or hematological disorders. Our case is unique as patient was diagnosed with BCS without any known risk factors. Case report: A 54 year old Cambodian male with a history of decompensated cirrhosis secondary to alcohol abuse and chronic hepatitis B complicated by esophageal variceal bleeding and ascites presented for evaluation of abdominal pain. On examination revealed mild ascites but no jaundice, hepatomegaly or signs of right sided heart failure. Labs were notable for normal liver tests, renal function, and coagulation profile. MRI abdomen revealed a cirrhotic liver with evidence of portal hypertension and chronic left and middle hepatic vein thrombi and collaterals draining into the inferior vena cava. Within one year, the patient developed extensive thrombosis involving the hepatic veins, main portal vein and superior mesenteric vein. Comprehensive hypercoaguable work up including Factor V Leiden, Protein C and S deficiency, antiphospholipid syndrome, and paroxysmal nocturnal hemoglobinuria were negative. Patient was not started on anticoagulation in view of his risk for bleeding from esophageal varices and was managed conservatively. Ultimately the patient received transjugular intrahepatic portosystemic shunt (TIPS), which was also complicated by occlusion, but was successfully revised and he is now listed for orthotopic liver transplantation. Discussion: BCS is a rare but clinically challenging disorder defined as any pathophysiologic process resulting in hepatic venous outflow obstruction in the absence of cardiac disease, pericardial disease or sinusoidal obstruction. It is more common in women and most commonly occurs in the third or fourth decade of life. Patients usually present with fever, abdominal pain, distension, lower extremity edema, jaundice, gastrointestinal bleeding from varices or portal gastropathy, or hepatic encephalopathy. Sometimes it is discovered incidently.It can be categorized as acute, subacute, chronic, or fulminant, depending on the rapidity and severity of the development of symptoms.BCS causes post-hepatic portal hypertension leading to complications similar to those in cirrhosis. Treatment options include anticoagulation,treatment of the underlying cause, recanalization, TIPS, and OLT. This case is unique as the patient had no known risk factors for BCS. Moreover, BCS has not been shown to be associated with chronic hepatitis B, alcoholism or demographically with Cambodian male population.

925 Echinacea Induced Acute Hepatitis Transitioning to Autoimmune Hepatitis Varun Kesar, MBBS1, Jawad Ahmad, MD2, Joseph Odin , MD, PhD3, Vivek Kesar4. 1. Lenox Hill Hospital/ Mount Sinai Hospital, New York, NY; 2. Mount Sinai Hospital, New York, NY; 3. Icahn School of Medicine, New York, NY; 4. Lenox Hill Hospital, New York, NY. Introduction: The use of herbal and dietary supplements (HDS) in the United States is increasing and there is growing evidence of HDS associated hepatotoxicity. Echinacea purpurea is a very widely used herbal supplement recommended as a common cold remedy. Echinacea has only once been associated with hepatoxicity (1). We report a second case of Echinacea associated acute hepatotoxicity. Case A 58 year old Caucasian woman with a history of hypertension presented with abdominal pain, jaundice, and dark urine for 2 days. She denied fever, nausea, vomiting, chills, change in bowel habits, rash, joint pains, muscle aches, abdominal swelling, or confusion. She denied alcohol or drug abuse, recent travel, and any new medications. She was only taking enalapril for hypertension for 18 years. On examination, she was icteric, alert, and had no stigmata of chronic liver disease. Her total bilirubin was 12.7 mg/dL, AST 1466 U/L, ALT 1486 U/L, Alk phos 303 U/L. Serologies for viral hepatitis were negative. Her ANA was 1:160, but her IgG level was only 1.61 g/dL. Abdominal imaging was negative for any biliary abnormalities. Careful history revealed that she had taken Echinacea for approximately 10 days for common cold type symptoms during the month before presentation. A liver biopsy showed active hepatitis with eosinophils, many ceroid filled macrophages, and only rare plasma cells consistent with drug induced liver injury. She stopped all HDS and her liver biochemistries initially improved. Her liver biochemistries started to rise again 4 months after presentation (Table). A repeat liver biopsy showed few ceroid filled macrophages and sheets of plasma cells with severe interphase hepatitis consistent with autoimmune hepatitis. Prednisone was started with gradual improvement in liver biochemistries after two months.Discussion: This appears to be a rare case of Echinacea induced liver injury. Both cases resulted in autoimmune hepatitis. This case highlights the need to consider all HDS as a potential cause of liver injury.

[925]

Table 1. PMID: 18249315

Labs

Day 0 (date of presentation)

Day 10

Day 77

Day 136

Day 203

AST (1–50 U/l)

1466

889

469

602

151

ALT(1–53 U/l)

1486

866

466

557

228 235

Alkaline Phosphatase (30–110 U/l)

303

244

325

357

Total Bilirubin (0.1–1.2 mg/dl)

12.7

10.9

2.6

2.8

1.0

ANA

N/A

1:160

1:160

1:320

N/A

926 A Textbook Case: The Multiple Sequelae of Hepatitis C Virus-Related Mixed Cryoglobulinemia in 1Patient Katherine J. Hahn, MD. MedStar Georgetown University Hospital, Washington, DC.

924 Budd Chiari Syndrome in an Atypical Patient Annu Gupta, MD1, Swathi Gopalakrishnan, MD2, Harmit Kalia, DO2. 1. Montefiore Medical Center, SCARSDALE, NY; 2. Montefiore Medical Center, Bronx, NY. Introduction: Budd-Chiari syndrome (BCS) is defined as venous outflow obstruction of the liver,occurring as a consequence of thrombosis of the hepatic veins usually in patients with hyperco-


Introduction: Hepatitis C virus (HCV) infected individuals are at risk for extrahepatic manifestations. Autoimmune pathologies, such as mixed cryoglobulinemia, are among the most commonly reported systemic symptoms. The result of immune complex deposition, HCV related cryoglobulinemia causes dermatologic, rheumatologic, and renal complications. It is rare, however, to see all these in one patient. Clinical case: A 56-year-old man with past medical history of diabetes presented to an outside hospital with myalgias and a new rash that had presented four months prior. On physical exam, the patient had diffuse non-tender, non-blanching, palpable purpuric rash on his lower extremities. Laboratory testing revealed elevated AST and ALT of 502 U/L and 365 U/L, as well as a serum creatinine of 2 (baseline of


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0.8). The patient’s only risk factor was a new tattoo. Given the patient’s elevated liver enzymes, he was transferred to our hospital. On admission, the patient had normal blood count and thyroid function tests, but was found on routine urine analysis to have microscopic hematuria and red cell casts. His creatinine had now increased to 2.4 and his AST/ALT to 615 and 422. Autoimmune markers, including ANCA and dsDNA were found to be normal, but rheumatoid factor was elevated. In addition, complement levels (specifically C4), were significantly decreased at a level of 4 mg/dL. Serum cryoglobulins were tested and detected. Hepatitis C virus RNA PCR showed a viral load of 8,562,493 IU/mL. A diagnostic punch biopsy of the lower extremity by dermatology diagnosed a leukocytoclastic vasculitis. Given the positive serum cryoglobulins, low complement, and biopsy proven leukocytoclastic vasculitis – diagnosis of hepatitis C related cryoglobulinemia with cutaneous vasculitis was made. Since the patient also had positive rheumatoid factor, hematuria, and elevated creatinine, a diagnosis of HCV associated glomerulonephritis was also made. Discussion: The association between HCV and mixed cryoglobulinemia is quite common, occurring in about 50% of cases. Most patients present with palpable purpura. Less common though more pressing, the renal manifestations of cryoglobulinemia HCV are often diagnosed as membranoproliferative glomerulonephritis (MPGN). Early diagnosis and treatment of MPGN is imperative in preventing renal failure. As HCV treatment improves, patients with multiple sequelae of HCV should be diagnosed quickly and treatment initiated promptly.

vancomycin, zosyn, and levofloxacin. Chest x-ray showed cardiomegaly and increased interstitial markings likely related to cardiac decompensation. CT abdomen and pelvis without contrast showed airspace opacity in the right lung base, enlarged liver with nodular contour compatible with cirrhosis, moderate amount of loculated perihepatic collection, and a calcified failed right sided kidney transplant. Laboratory data included a white blood cell count of 62,700, neutrophil percentage of 90.1%, and 14% bands on manual differential. Lactic acid 4.3 mm/l, procalcitonin 91.46 ng/ml, ammonia 64 μM/l. The patient’s hepatic panel showed an albumin of 2.7 gm/dl, alkaline phosphatase 193 mu/ml, alanine transaminase 98 mu/ml, aspartate transaminase 242 mu/ml, direct bilirubin 5.9 mg/dl, and total bilirubin 10.9 mg/dl. The patient had a CT-guided drainage of the inferior perihepatic fluid collection. Approximately 200cc of amber colored fluid was removed and a drainage bag was placed. Fluid analysis and chemistries were consistent with exudative process. Infectious diseases was consulted for documented blood culture positivity for Lactococcus and Escherichia coli, with recommendation to continue vancomycin and zosyn, discontinue levofloxacin, and send perihepatic fluid for gram stain, culture, and cytology. The patient’s fevers resolved and his white blood cell count continued to trend downwards from a peak of 62, 700. He was transferred from the medical intensive care unit to the medical floor for further management.

929 927

A Rare Case of Lamivudine Induced Neuromyopathy Causing Respiratory Failure in a Post-liver Transplant Patient

Cutaneous Metastasis From Hepatocellular Carcinoma to the Abdomen

Arvind R. Murali, MD, Michael D. Voigt, MD. University of Iowa Hospitals and Clinics, Iowa City, IA.

Jamil S. Alsahhar, MD. Baylor University Medical Center, Murphy, TX.

58 year old male received Liver Transplantation (LT) for NASH cirrhosis, with refractory ascites, hepatic encephalopathy and hepatorenal syndrome type 2. He was hepatitis B core antibody positive, surface antigen negative and surface antibody positive. During LT he was dialyzed for volume overload. Induction immunosuppression was with basiliximab, methylprednisolone and mycophenolate. Tacrolimus was then added but was switched to cyclosporine due to delirium with tacrolimus. Hepatitis B core antibody positivity was treated with HBIG (Hep B immune globulin) and Lamivudine150mg daily. Serum creatinine improved to new baseline of 2.0 mg/dl and he was discharged to rehab facility. He was re-admitted 2 weeks later for dyspnea and weakness. He was volume overloaded and was started on diuretics. He remained weak and only intermittently left skilled care facility, with multiple readmissions for dyspnea and weakness. 6 months post-LT he presented again with severe dyspnea and muscle weakness. He had ascites, pleural eff usion and pedal edema. Liver doppler US showed patent vessels. Echocardiogram was normal. Liver biopsy was normal except for sinusoidal dilation. Portal pressures were normal. Pleural effusion was managed adequately and resolved. However his respiratory status declined. Arterial blood gas before intubation showed ph 7.3, pCo2 71, pO2: 88, HCO3 33; indicating hypercapnic respiratory failure from alveolar hypoventilation. Excellent mentation ruled out central respiratory depression. EMG/ NCS showed sensorimotor neuropathy. Lamivudine was discontinued with remarkable improvement in respiratory function within a week after discontinuation. He was discharged on entecavir. He has had no issues since and doing well at 1 year post-LT follow up. Lamivudine, a nucleoside analogue has been used in combination with HBIG to prevent Hepatitis B re-activation post-LT. Lamivudine can induce severe mitochondrial dysfunction, which can rarely lead to serious complications. In our patient, lamivudine toxicity (possibly from high levels of lamivudine as a result of renal failure) caused neuromuscular weakness of respiratory muscles, leading to respiratory failure. Myasthenia gravis and primary carnitine deficiency were ruled out. Pleural effusion was small and insufficient to cause a restrictive defect by itself. Our case illustrates that nucleoside analogues can rarely result in severe side effects and a high index of suspicion is needed to make a timely diagnosis.

Introduction: Hepatocellular carcinoma (HCC) is the sixth most prevalent cancer and the third most leading cause of cancer mortality worldwide. Patients with cirrhosis are at highest risk of developing this malignant disease. Metastases are most commonly seen in the lung, abdominal lymph nodes, and bones. Cutaneous metastases of HCC are uncommon. Case presentation: We report a case of a 54-year-old Caucasian male with a history of HCC, for which he received six rounds of trans-arterial chemoembolization followed by CyberKnife therapy, hepatitis C cirrhosis, and diabetes mellitus, who presented with complaints of abdominal rash and pain. Examination revealed multiple erythematous, firm and well-circumscribed, dry, subcutaneous nodules surrounding the umbilicus and left abdomen. The nodules were tender to palpation. The patient was initially started on antibiotics as the rash was concerning for cellulitis. A histopathological analysis of the nodules was consistent with high-grade adenocarcinoma of hepatobiliary origin. Electron beam therapy was utilized for palliative measures. Discussion: HCC often metastasizes to the lungs, abdominal lymph nodes, and bones. Literature review shows that cutaneous metastasis of HCC to the abdomen are rare, with the majority occurring at sites of previous biliary drains or biopsies. Conclusion: Cutaneous nodules presenting in patients with HCC or hepatobiliary malignancies should be biopsied to assess for possible metastases.

930 Giant Intrahepatic Biliary Cystadenoma Harish Guddati, MD1, Damodar Pandey, MD2, Kamran Zahid, MD2, Hilary Hertan, MD, FACG2. 1. Montefiore Medical Center, Bronx, NY; 2. Montefiore Medical Cente-Wakefield, Bronx, NY.

[927A] Figure 1.

928 Lactococcus Septicemia With Perihepatic Fluid Collection in End-Stage Renal Disease Patient Tyrrell Jenkins, MD, MPH1, Constance Mere, MD2. 1. Howard University College of Medicine, Washington, DC; 2. Howard University Hospital, Washington , DC. A 38 year old African American male presented to the emergency room with complaints of having chills, fever, and shortness of breath. His past medical history was significant for sickle cell disease SS-type, end-stage renal disease dialysis dependent, diastolic congestive heart failure, and hemochromatosis. The patient stated that while receiving dialysis he started having the above symptoms. Blood cultures were taken at the dialysis center, and he was administered vancomycin and gentamicin. His temperature was recorded as 101.1, and he was hypotensive. The patient also admitted to gradual onset of abdominal pain, primarily on the right side and dull in nature;also, he had productive cough and rhinorrhea that started 3 to 4 days prior to admission. Of significance, this patient was in a hospital 2 weeks prior for symptomatic anemia and shortness of breath. He was admitted for severe sepsis perhaps secondary to healthcare-associated pneumonia and transaminitis possibly secondary to hemochromatosis vs hypoperfusion due to sepsis. He received hemodialysis, additional blood cultures were drawn, and placed on broad spectrum antibiotics, which included


Introduction: Hepatobiliary cystadenomas are rare cystic neoplasms, accounting for upto 1 – 5 % of total hepatic cysts. We present a case of giant intrahepatic cystadenoma that required complete surgical resection. Case: A 48 year old female with no significant comorbidities presented with one week history of upper abdominal discomfort. She was afebrile and physical examination revealed a large firm nontender liver mass extending to right lower quadrant. Laboratory tests revealed alkaline phosphatase 334 U/L, AST 162, ALT 411 U/L, total bilirubin 0.8, INR 0.9, hemoglobin 10.9 gm/dl and WBC of 12.4 K/ UL.Ultrasound abdomen showed a complex, large cystic mass with approximately 17 x 13 x 18 cm in size, extending from the liver to the pelvis. CT abdomen and pelvis revealed a large cystic, multiloculated, septated liver mass with mass effect on distal stomach and duodenum. Hepatitis A, B and C were negative for acute or chronic infection. Echinococcus antibody was negative. Patient was initially thought to have a simple hepatic cyst with some septations, and underwent laparoscopic cyst marsupialization. Biopsy of the cyst was consistent with a benign mucinous cystadenoma. Patient then underwent liver cyst excision, left hepatectomy and Roux-en-Y biliary reconstruction. Final pathology revealed benign mucinous cyst, consistent with hepatobiliary cystadenoma. No dysplasia was seen with normal uninvolved liver parenchyma. Liver chemistries were within normal limit after surgery. Discussion: Intrahepatic biliary cystadenomas are congenitally derived, aberrant hepatobiliary duct remnants. These are mostly asymptomatic, and may have symptoms from mass effect including anorexia, nausea or abdominal pain. Differential diagnosis includes simple cyst, echinococcal cyst, hemangioma and cystadenocarcinoma etc. They are thought to be precursors of adenocarcinoma. Ultrasonogram can help to differentiate from simple hepatic cysts where as CT or MRI is very useful in further characterization of the cystic mass contents. Histological confirmation is necessary to confirm the diagnosis in a large cyst, as in our case. The definitive treatment is complete resection to prevent mass effect, rupture or malignant transformation. In our case, left hepatectomy with complete cyst resection was performed in view of the large size and nature of the tumor.


| OCTOBER 2015

www.amjgastro.com

Abstracts 111 U/L, total bilirubin 13.3 mg/dl, direct bilirubin 9 mg/dl and INR 1.3. Hepatitis A, B, C and E, EBV, CMV were negative for acute or chronic infection. ANA and antimitochondrial antibody were negative, but antismooth muscle antibody was positive. Serum acetaminophen, salicylate and alcohol levels were negative. Ultrasound abdomen showed hepatosplenomegaly with no biliary ductal dilatation or gall stone. Liver biopsy showed moderate to severe active hepatitis with moderate mixed portal inflammation with lymphocytes, eosinophils and scattered plasma cells, with moderate interface activity as well as ductular proliferation and neutrophils. The findings were suggestive of possible drug-induced autoimmune hepatitis. He was started on prednisone and was discharged after improvement of liver test. During outpatient follow up, attempts to taper prednisone were not successful with reversal of elevated liver tests. Azathioprine was then added and liver tests signifanctly improved to normal limit. Discussion: Herbalife has been widely used for the purpose of weight loss. There are several case reports of liver injury caused by herbalife. Patient in our case was taking herbalife for about 3-4 years for weight loss. It is difficulty to identify any specific ingredient or any other factors including processing, preservatives or contamination that is responsible to cause liver injury. This is a rare case of herbalife induced autoimmune hepatitis with cholestatic pattern and patient responded very well to prednisone and azathioprine. Conclusion: While no evidence based or randomized study is available to show the effectiveness of herbalife in reducing weight, close monitoring while on the herbal supplements as well as state regulation is necessary to prevent the potential serious adverse effect and health care burden as in our case.

CLINICAL VIGNETTES/CASE REPORTS - PEDIATRICS [930A] Figure 1.

933 931 A Rare Case Series Demonstrating the Mixed Pattern of Metformin Induced Hepatotoxicity Sandeep Dayanand, MD1, Pradeep Dayanand, MBBS2, Jasmin Martinez, MD1, Michael Monzel, MD, FACG3. 1. University of Miami/JFK Medical Center Palm Beach Regional GME Consortium, West Palm Beach, FL; 2. Mamata Medical College, Hyderabad, India; 3. Palm West Hospital/JFK Medical Center, Loxahatchee, FL. Introduction: Metformin is one of the most commonly prescribed medications in the management of type 2 Diabetes Mellitus (DM). It is not known to be hepatotoxic, as it is not metabolized by the liver. However, very few case reports of metformin-induced hepatotoxicity have been reported to date. Here in, we report a case series of two patients with clinical presentations consistent with metformin-induced hepatotoxicity. Case series: Case 1: A 56 y/o male presented with a one-week history of right-sided abdominal discomfort and jaundice. A month prior to presentation he was placed on metformin for his type II DM. Laboratory work up revealed aspartate transaminase (AST) of 4422 U/L, alanine transaminase (ALT) of 4701 U/L, total bilirubin (TB) of 20.7 mg/dl, direct bilirubin (DB) of 17mg/dl and alkaline phosphatase of 192 U/L. Serological work up for hepatitis A, B and C were negative. Case 2: A 61 y/o male presented with worsening pruritus and jaundice. Patient had a medical history of chronic hepatitis C and type II DM for which he was prescribed metformin 2 months prior to admission. Laboratory tests revealed TB of 25.6 mg/dl with direct bilirubin of 20 mg/dl, alkaline phosphatase 916 U/L, AST of 916 U/L, ALT of 1269 U/L consistent with a mixed hepatocellular and cholestatic pattern of liver injury. Hepatitis C viral load by PCR revealed a titer of 7 IU/ml, which was unlikely to be the etiology of his acute presentation. Both patients denied any contributing social and family history. Diagnostic workup ruled out autoimmune and metabolic disease in both patients. Imaging showed normal liver parenchyma, ductal architecture and normal gall bladder in both patients. Liver biopsy was performed. In case one liver biopsy was consistent with markedly active lobular and portal hepatitis. There were no viral inclusions identified. Biopsy in case two revealed a cholestatic hepatitis unlikely to be secondary to a viral etiology and suggestive of a drug induced hepatitis. Metformin induced hepatotoxicity was thought to be the most probable diagnosis and metformin was held. Rapid resolution of signs and symptoms with normalization of liver enzymes was noted during hospital stay and subsequent follow up. Conclusion: Metformin induced hepatotoxicity is a rare drug induced idiosyncratic reaction. As metformin is a widely used drug, physicians should be aware of this potential adverse reaction. Early recognition and cessation of medication is crucial in reversal of this adverse effect.

Fecal Microbiota Transplantation in Refractory Clostridium difficile Infection in Children: Case Report and Review of the Literature Janese Laster, MD1, Mohamed Sultan, MD2, Mark Mattar, MD3. 1. Georgetown University Hospital, Washington, DC; 2. MedStar Georgetown University Hospital, Arlington , VA; 3. Georgetown University Hospital, Washington , DC. The human gastrointestinal tract evolves gradually from being sterile as neonates to being populated with trillions of bacterial species existing symbiotically for proper colonic function [1]. Disruption of homeostasis predisposes the gastrointestinal tract to increased incidence of enteric infections. Antibiotic use and immunocompromised states have been associated with an increased incidence of Clostridium difficile infection (CDI). Although approximately 35% of children’s guts are colonized with CDI, it rarely causes symptoms [5]. Antibiotic therapy is considered first line for CDI; however, fecal microbiota transplantation (FMT) has recently gained favorable results for refractory and recurrent cases [6]. This involves reintroducing typical microbiota to reestablish balance of the gut flora [6,7]. We report a case of refractory CDI affecting half of an immunocompromised child’s life that was cured with single FMT treatment. A 4-year-old male born via cesarean section at 37 weeks was diagnosed with a genetic disorder, Kabuki syndrome. His early life was complicated by recurrent infections, requiring several courses of antibiotics. As a result, he developed refractory CDI that lasted for 30 months, affecting his growth. His parents sought alternative options in which he was evaluated for FMT. He underwent FMT with his father as the stool donor. A 250mL aliquot of stool slurry was infused into the terminal ileum via colonoscopy, according to our institution’s protocol. The child recovered from CDI with decreased bowel movements within 24 hours. He remained CDI negative and asymptomatic at 8 weeks after the procedure. Antibiotic use and immunocompromised states have been associated with an increased incidence of CDI [6]. CDI causes profuse diarrhea and may progress to colitis or complications including multi-organ failure and sepsis [6]. Recurrence after initial treatment course with antibiotics is noted to be as high as 20% [8]. In this case, Kabuki syndrome predisposed this patient to multiple infections requiring several courses of antibiotics. Each course of antibiotics caused an additional insult to the homeostasis of the gut microbiome, leading to refractory CDI. FMT has been reported to successfully treat patients with recurrent CDI in immunocompetent patients; however, there have been no reported cases of FMT in the immunocompromised pediatric population with Kabuki syndrome and CDI. The success in this case should prompt consideration of FMT in he pediatric population.

934 932 Herbalife Induced Autoimmune Hepatitis With Cholestatic Pattern Damodar Pandey, MD, Venu Gopal Kankani, MD, Kamran Zahid, MD, Hilary Hertan, MD, FACG. Montefiore Medical Cente-Wakefield, Bronx, NY. Introduction: Herbal supplement has been commonly used in the community. There are several case reports of liver injury caused by herbalife. We report a rare case of autoimmune hepatitis with cholesatic pattern induced by herbalife. Case: A 40 year old male with no significant comorbidities presented with few days history of abdominal pain and yellowish discoloration of eye. He was afebrile and was hemodynamically stable. Physical examination was nonsignificant except jaundice. Patient denied recent travel, heavy alcohol use, substance or intraveou drug use, and family history of liver disease. He had been using Herbalife supplement for 3-4 years to loose weight. Initial blood tests showed AST 1327 U/L, ALT 2362 U/L , alkaline phosphatase


Masquerading Meckel’s? Gastrointestinal PEComa Causing Hematochezia in 9-Year-Old Girl Aileen Har, MD1, Amit Srivastava2, Jennifer Thorn, MD3, Yi Zeng, MD, PhD4, Beth L. Braunhut, MD1. 1. University of Arizona, Tucson, AZ; 2. University of Arizona, Gilbert, AZ; 3. Banner - University Medical Center, Tucson, AZ; 4. Pediatric Hematology/Oncology/BMT, University of Arizona, Tucson, AZ. Background: Perivascular endothelial cell neoplasms (PEComas) are rare mesenchymal tumors that occur in variety of anatomic locations including abdominopelvic and retroperitoneal sites, visceral organs and soft tissues of extremities, skin and bones. Coined in 1996, PEComas are smooth muscle and melanocytic marker positive (smooth muscle actin, HMB45, Melan-A, MiTF) and are part of a family of tumors which include angiomyolipomas, lymphangioleiomyomatosis, clear cell “sugar” tumor of the lung, extrapulmonary clear cell “sugar” tumor, and clear cell myomelanocytic tumor. Most recent reviews estimate pediatric PEComa cases involving the GI tract to be under 20. Due to their relative rarity, no formal system currently exists regarding classification, associated prognostic factors, and treatment.


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Case: A 9 year old previously healthy female presented with 2 episodes of hematochezia. Her hemoglobin decreased from 12.7 (g/dL) to 9.5 in the first 35 hours then down to 6.9 in the following 24 hours. Presentation of massive painless rectal bleeding with currant jelly stools appeared classic for Meckel’s diverticulum and patient was taken to the OR without Meckel’s scan. Surgical evaluation did not note the presence of a diverticulum; appendix was removed per parents request. Patient hemoglobin continued downtrending post-operation and tagged red blood cell scan was performed, revealing physiologic distribution of tracer and no abnormal radiotracer pooling consistent with no active gastrointestinal bleeding. Decision was made for an esophagogastroduodenoscopy and colonoscopy; colonoscopy revealed a 2.5 cm multilobulated polyp at the hepatic flexure. Location of the polyp was tattooed endoscopically and later removed surgically. Histopathology was consistent with PEComa with no features of malignancy, confirmed from several independent histopathology labs. Although patient’s PEComa showed no features of malignancy the margins were not clear; a repeat colonoscopy was performed 6 months postresection did not reveal recurrence of the lesion and her hemoglobin has since been stable. Conclusion: Although rare in presentation, diagnosis of gastrointestinal PEComa should be entertained in cases of hematochezia without an obvious source of bleeding. Patients with a negative Meckel’s scan or seemingly atypical presentation of a Meckel’s diverticulum may warrant additional workup.

935 Bizarre Bezoar: An Unusual Cause of Abdominal Pain and Vomiting in a Pediatric Patient Stephen Nanton, MD, Joelle Roskens, RN, Sarah Feit, CMA. Avera McKennan Hospital and University Health Center, Sioux Falls, SD. 15 year old female presented with a 1 day history of severe LUQ abdominal pain associated with one episode of non-bloody, non-bilious vomiting. Her pain was described as sharp 6-8/10 in severity, non radiating and persistent. She denied hematemesis, melena or blood in stools. Her past medical history was significant for depression . She did report that 3 years ago she went through a phase of eating and chewing her hair and also swallowing a large amount of chewing gum. She denied any current episodes of pica.

[935C] Figure 3.

Abdominal CT demonstrated a large mass like structure within the gastric lumen with the appearance of undigested particulate matter suggestive of gastric bezoar. There is some thickening of the wall of the stomach suggesting chronic inflammation. No dilated small bowel. No free air. Normal air-filled nondistended appendix. Endoscopy findings demonstrated a large gastric bezoar consisting of human hair and chewing gum in a cemented mass almost occupying the full volume of the stomach. Multiple gastric ulcers, non-bleeding, in the gastric body and antrum. Multiple attempts were used to achieve endoscopic removal; however, the gastric bezoar was too large and hard to pass through the GE junction. Hence, surgical removal was indicated. The patient was therefore referred for surgical management. Attempts at laparoscopic removal of the gastric bezoar failed due to its large size; therefore a small laparotomy was needed to remove the bezoar which was removed piecemeal. The surgeon noted that the hair bezoar was large in size and took up almost half the stomach. The patient recovered uneventfully. Conclusion: This case demonstrates an unusual etiology of left upper quadrant pain and vomiting.

936 Timeline of Progression From Autoimmune Hepatitis to Overlap Syndrome in a 9-Year-Old Pediatric Patient Stephen Nanton, MD, Joelle Roskens, RN, Sarah Feit, CMA. Avera McKennan Hospital and University Health Center, Sioux Falls, SD.

[935A] Figure 1.

A 9 year old male presented with fatigue and elevated liver function tests including; Alkaline Phosphatase at 430 U/L, AST at 888 U/L, and ALT at 1300 U/L. The total bilirubin was normal at 0.5 mg/dL. Smooth Muscle antibody IgG was elevated at 99 units, gliadin IgG elevated at 21 units and liver kidney microsomal (LKM) antybody was normal. An initial MRCP was normal.

[936A] Figure 1.



| OCTOBER 2015

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Abstracts

[936B] Figure 2. [937A] Figure 1. A liver biopsy revealed moderate interface hepatitis with lobular disarray, consistent with autoimmune hepatitis (AIH), Grade 3, Stage III. Negative for cirrhosis and malignancy. The patient initially responded well to glucocorticoid therapy with AST decreasing from 887 U/L to 54 U/L over a 6 week period. His ALT also decreased from 1316 U/L to 103 U/L over a that same time frame. The patient subsequently developed loss of response to glucocorticoid therapy with increasing GGT and transaminases. The patient did not respond to the addition of immunomodulator (6-MP) despite therapeutic levels. Repeat MRCP revealed a new finding of mild intra and extrahepatic biliary dilations with irregularity and nodularity of the intrahepatic bile ducts. The walls of the common hepatic and bile ducts and the proximal central bile ducts were mildly thickened with slight enhancement. The appearance was consistent with cholangitis (Primary Sclerosing Cholangitis). The child was diagnosed with AIH-PSC Overlap Syndrome. The patient was than treated with Vancomycin 125mg TID x 4 weeks, then BID thereafter. The patient had a prompt response with improving (AST) from 164U/L to 25 U/L and (ALT) from 361 U/L to 39 U/L in 2 months. The GGT also normalized. Patient was successfully weaned off glucocorticoid and is currently in remission over the past 4 months. Conclusion: AIH and PSC may be sequential in their occurrence in children. Our case documents the sequential nature of this overlap syndrome. Sequential progression to PSC or overlap syndrome should be considered in children with AIH who lose response to standard therapy.

937 Autoimmune Pancreatitis: Case Report of a 9-Year-Old Female and Review of Literature Zinal Patel, MD1, Suril Patel, MD2, Prateek Chapalamadugu, MD3, Tuvia Marciano, DO3, Sohail Husain, MD4, James Grendell, MD3. 1. Winthrop University Hospital, Albertson, NY; 2. Winthrop University Hospital, Hempstead, NY; 3. Winthrop University Hospital, Mineola, NY; 4. Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA. We report a case of autoimmune pancreatitis in a 9-year-old female who presented with persistent epigastric pain for 3 weeks. Magnetic resonance cholangiopancreatography (MRCP) showed both intrahepatic and extrahepatic biliary ductal dilatation. The common bile duct, along with the pancreatic duct, was noted to be dilated. Labs showed normal IgG and IgG4 levels and were negative for autoimmune antibodies. Endoscopic ultrasound revealed the pancreatic head to be enlarged and surrounded by hypoechoic and lobulated lymph nodes. Biopsy of the pancreatic head showed chronic mildly active inflammation with fibrosis, acinar atrophy, and lymphocytic infiltrate consistent with autoimmune pancreatitis. She was diagnosed with autoimmune pancreatitis, and treated with prednisone. Repeat MRCP showed resolution of inflammatory changes and intrahepatic and pancreatic ductal dilatation.

[937]

Table 1. Reported Cases of AIP in Pediatrics

Type of Autoimmune Pancreatitis

Number of Reported Cases

Definitive Type 2 AIP

8

Definitive Type 1 AIP

2

Probable Type 2 AIP

1

Unspecified AIP

5


[937B] Figure 2.

938 Superior Mesenteric Artery Syndrome Secondary to Placement of a Large-Caliber Gastro-Jejunostomy Tube in a Young Child Naser Tolaymat, MD, FACG. Children’s Hospital at Lehigh Valley Health Network, Allentown, PA. Introduction: Superior Mesenteric Artery Syndrome (SMAS) is typically associated with weight loss in the literature, but this case demonstrated that it can be caused by placement of a large size gastrojejunostomy (GJ) tube for feeding. Symptoms and radiographic appearance of SMAS resolved after removing the GJ tube. Case Presentation: An 18-month-old female with caudal regression syndrome who was referred to us from another institution. Previously, at 6 months of age, she had a fundoplication and gastrostomy tube placed for feeding. G tube was converted to GJ tube (16 Fr size) 3 months prior to her hospitalization. At the time of presentation, the patient was experiencing recurrent bilious emesis and drainage around her gastrostomy (G) tube site. She was fed via the jejunostomy tube continuously. There was no weight loss. Her weight was 5.9 kg; height, 64.5 cm; BMI was 13. Barium upper gastrointestinal (UGI) series via G tube revealed dilated duodenum with apparent cutoff of the barium column at midline and delayed passage to the 3rd segment of duodenum. An interventional radiology physician changed the GJ tube to 18 Fr. size. She was treated conservatively with positioning and continuous feeding through the jejunostomy site. After 6 weeks, the patient showed no improvement of her symptoms and had gained only 50 g. Repeat barium UGI series yielded similar results and showing reflux of barium to stomach. The GJ tube was removed and replaced with a standard G tube. After 3 days, a barium UGI series done via the G tube showed significantly decreased distention of proximal duodenum, rapid progress of barium into the 3rd portion of duodenum, and no further midline obstruction. She was discharged home with slow G-tube feedings, which she tolerated well.


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Discussion: SMAS is a rare condition in children, usually reported after significant weight loss, which did not occur in our patient. To obtain the diagnosis, it was necessary to reevaluate her UGI anatomy without the presence of the GJ tube. In this case, SMAS occurrence was secondary to placing a largecaliber GJ tube in a small child, causing a compression of duodenum against the spine. Caution should be taken when placing a GJ tube in young children; we recommend exploring other unusual causes of persistent vomiting when emesis persists following GJ tube placement.

939 Incidental Diagnosis of MEN1 Syndrome by Endoscopic Ultrasound in a Pediatric Patient Presenting With Obstructive Jaundice and Abdominal Pain Jason D. Jones, MD1, Jason D. Conway, MD2, Brent Cengia, MD1, Andrew Johnsen, MD3, Shashank Suresh4, Rishi Pawa, MBBS2. 1. Wake Forest School of Medicine, Department of Internal Medicine, Winston-Salem, NC; 2. Wake Forest School of Medicine, Department of Gastroenterology, Winston-Salem, NC; 3. Wake Forest School of Medicine, Department of Pathology, Winston-Salem, NC; 4. Wake Forest School of Medicine, Winston-Salem, NC. Introduction: Pancreatic endocrine neoplasms are a rare malignancy which can be associated with the MEN1 syndrome and diagnosis can be difficult without clinical suspicion. Case presentation: A 16 year old male presented with one week of jaundice, nausea, vomiting, and epigastric abdominal pain. Pertinent labs on presentation included AST 374, ALT 779, Total Bilirubin 3.27, and Alkaline Phosphatase 162. Abdominal ultrasound was performed and revealed cholelithiasis and a common bile duct(CBD) diameter of 6mm. Due to high suspicion of distal CBD stone, endoscopic ultrasound performed and discovered several hypoechoic lesions in the uncinate, neck, body, and tail of the pancreas, the largest of which was a homogenous 10mm x 12mm lesion with well defined borders. FNA was performed on the largest lesion and revealed a well differentiated pancreatic endocrine neoplasm. The patient’s jaundice and gastrointestinal symptoms improved with time and were likely secondary to a biliary stone which spontaneously passed. History was significant for hypercalcemia and increased PTH of unknown etiology and MRI later found a sellar microadenoma. The constellation of his imaging findings and pathology results, in the setting of an elevated PTH, confirmed the MEN1 syndrome.

[939C] Figure 3.

Discussion: Multiple endocrine neoplasia type 1 (MEN1) is a genetic syndrome manifested most commonly as neoplasms of the anterior pituitary, parathyroid glands, and pancreas. Diagnosis is made by the presence of one of the following: ≥ 2 associated tumors in an individual, ≥1 associated tumor in a first degree relative of an afflicted individual, indicative genetic analyses. Our case is unique in that our patient was young and his diagnosis was an incidental discovery based on his presentation of obstructive jaundice. Pancreatic islet cell tumors are present in 30-80% of patients with the MEN1 syndrome, however pancreatic endocrine neoplasms have an annual incidence of less than 1 per 100,000 and are most frequently diagnosed in the sixth and seventh decades of life. Discovery of these lesions can be difficult and endoscopic ultrasound is one of the most sensitive means of detection. Treatment varies based on tumor location, but generally involves surgical resection. Lastly, genetic screening, focused on analysis of chromosome 11q13, plays a large role in care once a diagnosis of MEN1 is made.

940 Malrotation With Volvulus Presenting as Recurrent Pancreatitis Kevin Fang, MD, Quin Liu, MD, Mark Corden, MD. Children’s Hospital Los Angeles, Los Angeles, CA.

[939A] Figure 1.

[939B] Figure 2.


Case Report: An 11-year-old obese girl with a history of hospitalization for dehydration from persistent vomiting at four years of age was admitted for epigastric abdominal pain, non-bilious emesis and a lipase of 1207 units/L (normal < 300 u/L). Abdominal X-ray showed a paucity of bowel gas in the right lower quadrant but was non-specific. After four days of medical management for pancreatitis, she was discharged. The next day, she was re-admitted for severe abdominal pain, non-bilious emesis and a lipase of 1385 units/L. Abdominal ultrasound showed echogenicity of the pancreas without gallstones. Although her lipase down-trended more slowly than expected (Figure 1), her abdominal pain resolved with bowel rest, and she was discharged. Ten days later, she returned with abdominal pain without emesis and a lipase of 989 units/L. A magnetic resonance cholangiopancreatography was obtained, showing a normal-appearing pancreas and dilation

[940A] Figure 1.


| OCTOBER 2015

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Abstracts At the time of PTLD diagnosis, serum specimens collected from the patient were positive for HHV-6b DNA, and in 2 months, levels increased from 10^3 copies/ml to 10^6 copies/ml, evidence of patient lymphocytes harboring the HHV-6b virus. PCR results of donor and recipient liver showed the patient’s native liver to have elevated levels of ciHHV-6b compared to negative levels in the donor liver tissue. The PTLD tissue tested showed significantly elevated levels of HHV-6b. Tissue from the patient and liver donor allowed us to conclude that native reactivation of ciHHV-6b likely resulted in PTLD in this EBV serum negative patient. In the setting of low (or absent) EBV serum titers, this clinical scenario illustrates the diagnostic complexities associated with ciHHV-6b in liver transplant recipients, and the need for further investigation of this viruses potential role in the development of PTLD.

942 Choledocholithiasis: A Rare Entity in Children With a Rare Presentation Wendy Rabbenou, Sammy Ho, MD. Montefiore Medical Center, Bronx, NY.

[940B] Figure 2.

of the proximal duodenum with swirling around the superior mesenteric artery. A fluoroscopic study confirmed malrotation with volvulus (Figure 2). The patient underwent an open Ladd procedure. Discussion: Only 10% of cases of malrotation are diagnosed beyond infancy. Symptoms can be vague (abdominal pain, non-bilious emesis), leading to a delay in diagnosis. We report a case of malrotation in an 11-year-old girl where diagnosis was delayed because she was initially thought only to have pancreatitis. Five case reports exist of malrotation presenting as pancreatitis. Lipase levels were not reported in those cases. Hyperlipasemia can be due to non-pancreatic causes, including gastric/duodenal ulcers, cholecystitis, enteritis and small bowel obstruction. However, lipase values greater than three times normal are 98% specific for pancreatitis. Because of her high lipase levels, we suspect our patient likely had pancreatitis in the setting of her malrotation with volvulus. There may be an association between the two conditions due to the inability of the pancreas to secrete against increased intraluminal pressure caused by an obstruction. If this were true, these would be the highest lipase levels ever reported in a case of small bowel obstruction. In cases of idiopathic pancreatitis that fail to respond to standard medical management, anatomic causes such as malrotation should be considered.

941 Origin of Chromosomally Integrated HHV6B After Liver Transplant in a Child With Post-Transplant Lymphoproliferative Disorder Jessica Barry, MD1, Johanna Goldfarb, MD2, Belinda Yen-Lieberman, PhD3, Marsha Kay, MD4, Philip Pellett, PhD5. 1. Cleveland Clinic Children’s, Cleveland, OH; 2. Cleveland Clinic Children’s, Dept of Infectious Disease, Cleveland, OH; 3. Molecular Virology, Serology, and Cellular Immunology, Cleveland Clinic, Cleveland, OH; 4. Pediatric Gastroenterology, Cleveland Clinic Children’s, Cleveland, OH; 5. Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI. Human herpesvirus-6b (HHV-6b) is a viral pathogen that infects nearly all children by age 2, remaining latent in adulthood. Reactivation of this virus has been documented following cord blood transplantation with majority of cases being self limited and a minority developing active disease (notably encephalitis). Recent studies show a 16% HHV-6 PCR detection rate among pediatric patients post liver transplant, with rate of active infection 2.6%. In 1-2% of cases, HHV-6b can be chromosomally integrated (ciHHV-6b), leading to vertical transmission of the virus, and is suspected when elevated copy numbers of the virus (>6 log10copies/ml whole blood) are persistently detected by PCR. Studies have investigated genomic integration of HHV-6b from donor to recipient in stem cell transplants, but this has yet to be studied in pediatric patients post liver transplant. Post-transplant lymphoproliferative disease (PTLD) in pediatric liver transplant is a significant source of morbidity and mortality (incidence 6-20%), thought to be caused by the interplay between immunosuppression and Epstein Barr virus (EBV) infection. The role of ciHHV-6b in PTLD among solid organ transplants is unknown. We propose that ciHHV-6b is analogous to EBV’s role in PTLD by its presence in our serum EBV negative patient diagnosed with PTLD following liver transplant. We investigated the case of a 10 year old boy with Caroli disease (serum EBV negative donor/recipient status) who developed EBV chromogenic in situ hybridization (EBER-CISH) positive PTLD with low serum EBV titers (452 copies-Low (ref < 500 copies) 5 months post liver transplantation, in the setting of extraordinarily high levels of HHV-6b that emerged after liver transplantation. To determine the origin of chromosomally integrated HHV-6b, parental and organ donor tissue, and whole blood were examined using PCR, along with fluorescence in situ hybridization (FISH) analysis of chromosomes from white blood cells.


This patient is a 22 month old female with a history of a 3 month NICU hospitalization for necrotizing enterocolitis, presenting with generalized pruritis. The patient required TPN for the first 3 months of life while in the NICU. Her hospital course was complicated by cholestasis, necrotizing enterocolitis with perforation, and a 5cm jejunal resection, followed by re-anastomosis. Upon discharge and cessation of TPN, her cholestasis resolved. All developmental milestones were met appropriately. Six months prior to admission, her mother began noticing whole body itching, often to the point of bleeding from excoriation. The patient was diagnosed with eczema and treated with diphenhydramine along with oral and topical steroids. The pruritis worsened and medication doses were increased. Two months later, the mother noticed yellowing of the patient’s eyes, followed by pale stools the next month. The patient was seen by a gastroenterologist. Labs were notable for elevated total and direct bilirubin 8.6 and 5.1 mg/dl; AST and ALT ~180 IU/L; GGT >1000 IU/L, and normal renal function. Magnetic resonance cholangiopancreatography (MRCP) showed a dilated common bile duct (CBD) to 6 mm, a 2 mm stone in the mid-CBD, and a distended gallbladder containing sludge. The liver parenchyma and size was normal. The mother denied any change in oral intake, fever, chills, cough, congestion, vomiting, diarrhea, constipation. She was eating regular food and Pregestimil. The patient was referred to our hospital for an endoscopic retrograde cholangeopancreatography (ERCP). At ERCP, one stone was removed via sphincterotomy and balloon sweeps. Three days following the procedure, her pruritis resolved, jaundice improved, and the patient was discharged home. There are few studies published on the development of choledocholithiasis in children less than 2 years old. Reif et al. reported no cases among 50 children with gallstones. Kumar et al. performed a retrospective study on the incidence of gallstones and choledocholithiasis in infancy and childhood from 1979-1996 in Australia. A total of 102 infants and children were identified. 18% had choledocholithiasis, of whom over 80% initially presented with jaundice with or without abdominal pain. The remainder presented with abdominal pain alone. Our case of choledocholithiasis is unique in that the initial presentation was pruritis, rather than abdominal pain and jaundice. The patient was misdiagnosed and incorrectly treated for over 4 months, until icterus was noted. This case report emphasizes that choledocholithiasis should be in the differential diagnosis even when evaluating the toddler with generalized pruritis.

943 A Case of Crohn’s Disease With Pulmonary Manifestation Kinjal Suryawala, MD1, Marilyn Steele, MD2, Judith O’Connor, MD2. 1. Oklahoma University Children’s Hospital, Department of Pediatric Gastroenterology Hepatology and Nutrition, Oklahoma City, OK; 2. Oklahoma University Children’s Hospital, Department of Pediatric Gastroenterology, Hepatology and Nutrition, Oklahoma City, OK. Extraintestinal manifestations (EIM) of inflammatory bowel disease (IBD) are increasingly identified. The most common manifestations in both Crohn’s disease (CD) and Ulcerative colitis (UC), include arthropathies, mucocutaneous, ophthalmological and hepatobiliary conditions. Although occurring less frequently, new onset pulmonary symptoms should be considered as EIM of IBD. We present a patient with new diagnosis of CD with pulmonary manifestations. A 16 year old male was diagnosed with CD one week prior to presentation at an outside hospital with no treatment initiation. He was admitted for shortness of breath, non-productive cough, chest pain and fever. Chest x-ray showed bilateral lower infiltrative process and clindamycin was initiated. A CT scan of the chest revealed nodular areas of consolidation within the left lung suggestive of a multifocal infectious process versus granulomatous lesions. Extensive infectious work up was negative for other granulomatous diseases. He had normal PPD, ACE levels, serum immunoglobulins, ANA and negative stool cultures. It was hypothesized that his pulmonary findings may be an EIM of CD. Diagnosis of CD was confirmed endoscopically and histologically and clindamycin was discontinued. A bronchoalveolar lavage (BAL) was negative for gram stain, fungal culture, AFB stain, Pneumatosis J. and mycoplasma. It showed elevated lymphocytes with an increase CD4/CD8 ratio of 8.6 (normal: 0.7-3.5) suggesting an inflammatory process. The increase CD4/CD8 ratio is generally seen in conditions like sarcoidosis, rheumatoid arthritis, asbestosis or CD. He had a dramatic clinical improvement in his respiratory status after starting IV solumedrol with resolution of respiratory distress and improvement on chest x-ray. The pathogenesis of pulmonary disease associated with IBD is unknown. However, the inflammatory changes in the lungs are thought to represent the same type of inflammatory changes that occur in the bowel. Colonic and respiratory epithelia share embryogenic origin and both contain submucosal lymphoid tissue that plays a role in host mucosal defense. It is hypothesized that these similarities in mucosal immune system cause the same inflammatory changes in the lungs as seen in inflammatory bowel disease.


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CLINICAL VIGNETTES/CASE REPORTS SMALL INTESTINE/UNCLASSIFIED 944 A Case of PRESS Syndrome Presenting With Nausea, Vomiting, and Abdominal Pain Rovin Saxena1, Olaitan Adeniji, MD, FACG2. 1. International American University College of Medicine, Ann Arbor, MI; 2. Atlanta Gastroenterology Associates, Lawrenceville, GA. A 68 year-old, Caucasian female presented to the emergency department with 4 day history of nausea, vomiting and generalised abdominal pain associated with delusions, confusion, agitation, and stupor. She had no history of illicit drug use, alcohol abuse, recent medication change, hypoglycemia, falls or psychiatric illness. On examination, she had a Blood pressure 206/145 with a pulse of 84 and normal respiration. She was able to ambulate with an unsteady gait and upper extremity apraxia.The rest of her examination was otherwise normal. EEG failed to show features suggesting any underlying seizure activity. CT scan of the brain was negative for hemorrhages. MRI of the brain demonstrated volume loss of periventricular white matter disease and abnormal symmetric patchy foci of increased signal in cortex, subcortical white matter of the posterior frontal and occipital lobes. MRA was normal. The patient responded well to conservative measures including anti-emetics and anti-hypertensive therapy. Her agitation, aggression, confusion and disorientation and gastrointestinal symptoms resolved. Based on clinical course and radiological findings, it was concluded that this patient had Posterior Reversible Encephalopathy Syndrome (PRES) also known as Reversible Posterior Leukoencephalopathy Syndrome (RPLS). PRES is a radiologically diagnosed condition. Imaging shows posterior brain hyperintensities which translates to vasogenic edema, frequently seen in the white matter junctions. Most common locations of involvement are the occipital lobes, parietal lobes, and posterior frontal lobes. Clinically, it is associated with accelerated/malignant hypertension, eclampsia, renal disease, seizures, autoimmune disorders, and immunosuppressive therapy, but these conditions do not demonstrate causality. Pathophysiology of the syndrome is uncertain, although hypotheses of endothelial dysfunction, autonomic dysregulation, and cerebral ischemia have been postulated to be at the root of the problem. Prevalence is high in women. Clinicians most often see patients manifesting with mental status changes, constant headaches, seizures, and vision impairment. Gastrointestinal symptoms usually resolves with conservative measures. Diagnosis relies on a combination of clinical presentation and imaging, but emphasis is on neurological imaging. Treatment of the condition starts with early detection and diagnosis, which requires early recognition of the constellation of symptoms, associated conditions and MRI scanning of the brain. Removal of the offensive agent(s) prevents further progression of PRES and reverses the vasogenic edema present in the brain, which in turn, avoids permanent neurological impairment.

[946A] Figure 1.

945 Small Bowel Obstruction Successfully Treated With Lubiprostone Ayman Founas, DO1, Zuie Wakade, DO1, Poorna Ramachanran2, Armita Ghodoussi, DO1, Jack Tocco, DO1, Jacqueline Moore, DO1, Joseph Kinzie1. 1. Henry Ford Macomb Hospital, Charter Township of Clinton, MI; 2. Henry Ford Macomb Hospital, Clinton Township, MI. Introduction: Lubiprostone is a medication used to treat constipation predominant irritable bowel syndrome and chronic idiopathic constipation. It exerts its effects via chloride secretion from the chloride channel type-2 and cystic fibrosis transmembrane conductance regulator channels. Contraindications of lubiprostone include its use in gastrointestinal obstruction. Herein, we present a case where a small bowel obstruction caused by multiple bezoars was treated successfully with lubiprostone. Case presentation: A 74-year-old woman with a relevant past medical history of clostridium difficile treated with fecal transplant presented with a chief complaint of abdominal pain. Patient admitted to increasing her cholestyramine dosage over the past two weeks because mucous was noted in her stool. Work up included a computed tomography scan that revealed a small bowel obstruction and a colonoscopy that revealed multiple pharmacobezoars. Initial attempts to facilitate a bowel movement were unsuccessful with enemas, suppositories, and polyethylene glycol. Lubiprostone was initiated and in the subsequent two days she began to pass flatus and had several bowel movements. Her symptoms completely resolved prior to discharge. Discussion: Although lubiprostone’s use has been contraindicated in a gastrointestinal obstruction, we believe that understanding the etiology of the obstruction allows its spectrum of use to be broadened. The patient had a mechanical cause for her obstruction and allowing her body to stimulate a bowel movement seemed appropriate for treatment. The passing of the pharmacobezoars with lubiprostone was facilitated by a net secretory effect by chloride ions causing increased intestinal motility and allowed enhanced transit. Recent literature has suggested that lubiprostone may also promote gastrointestinal motility via increasing circular smooth muscle cell intestinal activity. Treatment of an ileus or chronic pseudo-obstruction may be possible with lubiprostone because of its ability to cause prostaglandin E receptor 1 mediated increase in circular muscle activity in the gastrointestinal tract. Lubiprostone’s use may be limited by its lack of long-term studies. We suggest more research be performed utilizing lubiprostone in the treatment of a bowel obstruction caused by pharmacobezoars.

946 A Rare Case of a Dedifferentiated Gastrointestinal Stromal Tumor Arising de novo Hirsh D. Trivedi, MD1, Blanca Lizaola, MD1, Olga Kozyreva, MD2. 1. St. Elizabeth’s Medical Center, Brighton, MA; 2. Dana-Farber Cancer Institute at St. Elizabeth’s Medical Center, Brighton, MA. Gastrointestinal stromal tumors (GIST), the most common mesenchymal tumors of the gastrointestinal (GI) tract, can very rarely present as dedifferentiated tumors arising de novo. We present an extremely


[946B] Figure 2.

rare case of a retroperitoneal dedifferentiated GIST arising de novo and presenting with inferior vena caval (IVC) compression and thrombosis. An 80 year-old male came in with complaints of dark colored stool. He was stable with a normal physical exam. His labs were notable for WBC 13.4 k/cmm, hemoglobin 4.6 g/dL, hematocrit 16%, platelets 232 k/cmm, INR 1.2, BUN 29 mg/dL, creatinine 0.9 mg/dL, lipase 43 U/L, and normal liver enzymes. He was resuscitated with blood, started on a pantoprazole drip and underwent an upper endoscopy, which was normal. A Computed Tomography scan showed a large, 12.4cm by 9.8cm, multilobed, exophytic retroperitoneal mass communicating with the duodenum. The largest part of the mass had an enhancing wall containing air from a fistulous tract communicating with the duodenum. The mass was compressing the IVC, which showed thrombosis extending into the iliac veins and right gonadal vein. A small bowel enteroscopy showed a large extrinsic impression along the greater curvature in the gastric antrum, a partially obstructing extrinsic impression in the duodenum, and a hemicircumferential mass with central ulceration and mild oozing of blood in the second and third portions of the duodenum. Endoscopic Ultrasound showed a large heterogeneous retroperitoneal mass with air in one of the lobes suggesting a fistulous communication with the duodenum. The mass also involved the pancreatic head, ampulla and duodenal wall, and was compressing the portal vein. Biopsy showed a high-grade malignant neoplasm with some spindle cells and numerous pleomorphic epitheloid cells, a high mitotic rate, and a weak positivity for CD117 (KIT) consistent with a pleomorphic sarcoma favoring a dedifferentiated GIST. There are about 5000 new GIST cases in the United States per year. CD117, or c-kit, and PDGFRA are immunohistochemical markers that are positive in 80-95% of cases. The remaining GISTs, termed as dedifferentiated GISTs, do not have a detectable KIT or PDGFRA mutation and do not stain positive for CD117, making their diagnosis and treatment extremely difficult. This variant of the tumor has been reported only in a handful of cases, and was initially thought to be only associated with prolonged use of Imatinib, a tyrosine kinase inhibitor used for the treatment of c-kit positive GISTs. Dedifferentiated GISTs arising de novo, without previous Imatinib therapy, as in our patient, have recently been reported and are even more rare. A heightened awareness of these tumors is essential as they pose a diagnostic challenge and have an unclear response to targeted molecular therapy compared to their c-kit positive counterparts.


| OCTOBER 2015

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Abstracts 947 Median Arcuate Ligament Syndrome and Successful Robotic-Assisted Intervention Cari Sorrell, MD, Tisha N. Lunsford, MD, FACG, Kent Van Sickle, MD, Abhijit Sunnapwar, MD. University of Texas Health Science Center, San Antonio, TX. Introduction: Median arcuate ligament syndrome (MALS) is a rare disorder defined by chronic, recurrent abdominal pain related to compression of the celiac artery by the median arcuate ligament. It is often an elusive diagnosis made only after an exhaustive work-up which can delay diagnosis. We present here a healthy 33-year old female, her diagnostic evaluation and the successful, novel use of robotic-assisted intervention as a cure. Case report: A 33 year-old female with no history of chronic medical problems presented with a complaint of progressive, severe, postprandial epigastric pain accompanied by nausea, loose stools, sitophobia and weight loss. Two years prior, she was diagnosed with irritable bowel syndrome and lactose intolerance based on clinical history and a basic workup. Despite extensive dietary restrictions she continued to have progressive, severe post-prandial pain and weight loss cultimating in further evaluation in an emergent situation. On physical exam, her only positive finding was a soft abdominal bruit. A detailed workup was non-revealing including an esophagogastroduodenoscopy and colonoscopy with biopsies of the small and large intestine, hepatobiliary scan, upper gastrointestinal series with small bowel follow through, CT scan of the abdomen and pelvis with contrast and wireless capsule endoscopy. Liver enzymes and celiac serologies were normal as well. Because of the abdominal bruit and worsening of symptoms, an abdominal MRI was performed revealing a narrowing at the origin of the celiac trunk with classical hook shaped contouring and post-stentoic dilation pathognomonic for median arcuate ligament syndrome. Digital subtraction angiography confirmed extrinsic compression of the celiac artery on expiration consistent with MALS. Subsequent robotic-assisted minimally invasive release of the median arcuate ligament using the da Vinci® Surgical System by our surgical colleagues resulted in complete resolution of all of her symptoms. Discussion: MALS is a rare disorder with a multifactorial pathophysiology, which is poorly understood. The median arcuate ligament is a fibrous arch that unites the diaphragmatic crura on either side of the aortic hiatus and usually passes superior to the origin of the celiac artery. However, in patients with MALS, the ligament may lie abnormally low, causing compression of the celiac artery and thus symptoms of severe abdominal pain. MALS is an elusive diagnosis often discovered only after an extensive work-up, high clinical suspicion and a multidisciplinary effort. We present above an example of successful intervention using an emerging technology for an evasive clinical entity.

A 67 year-old male presented to the emergency department with lightheadedness and a 10-day history of melena. He was further admitted for the evaluation of symptomatic anemia. He had a hemoglobin of 7.1 g/dL, however was in no apparent distress. Rectal exam revealed no evidence of bright red blood or melena. His medical history included malignant melanoma, diagnosed a year prior to admission after a sentinel node biopsy was done because of a suspicious 2 cm lesion on his back. The lesion was removed via wide local excision and bilateral axillary lymphadenectomy was also performed. Ultimately, no malignancy was found in the axillary nodes and he was reported to have no evidence of disease. During this admission, complaints of ongoing neck pain led to obtaining a positron emission tomography-computed tomography which showed suspicion for metastasis to the cervical spine, lungs and peritoneal lymph nodes likely due to recurrence of malignant melanoma. Upper endoscopy and colonoscopy did not reveal a source of bleeding. Video capsule endoscopy revealed multiple large ulcers throughout the small bowel. The ulcers were noted to be clean-based and had rolled edges. Deep enteroscopy revealed ulcers in the duodenum and jejunum. Biopsies of the edges of the ulcers were positive for malignant spindle cell neoplasm, consistent with a diagnosis of metastatic melanoma. The presentation of clean-based ulcers and overt GI bleeding in the setting of malignant melanoma is not a common endoscopic or clinical presentation. The most common presentation of metastasis to the small bowel is obstruction or intussusception. Obscure overt GI bleeding in the setting of melanoma is a rare presentation of metastatic disease. References: [1]. K.V. Liang, et al. Metastatic malignant melanoma of the gastrointestinal tract. Mayo Clin Proc, 81 (2006), 511-516. [2]. Shenoy, I, et al. Metastatic melanoma to the gastrointestinal tract: role of surgery as palliative treatment.W V Med J. (2013),109:30-33. [3]. I. Panagiotou, et al. Malignant melanoma metastatic to the gastrointestinal tract. Melanoma research,12.2 (2002),169-173.

948 An Unusual Case of Enteropathy Syed Amer, MBBS1, Jennifer L. Horsley-Silva, MD2, Shannon Myers3, Lucinda Harris, MD3. 1. Division of Internal Medicine, Mayo Clinic, Phoenix, AZ; 2. Mayo Clinic, Phoenix, AZ; 3. Mayo Clinic, Phoenix , AZ. Olmesartan is an angiotensin II receptor antagonist commonly used in the treatment of hypertension. A growing amount of evidence and literature has shown this medication to be associated with a severe form of spruelike enteropathy. A 54 year-old lady presented with chief complain of diarrhea for the past 18 months. She described severe, intractable diarrhea up to 20 loose watery bowel movements a day, 50 pound weight loss, and significant malnutrition. She had undergone an extensive work up at another institution including negative investigations for infectious causes - clostridium difficile, ova and parasites, microsporidia, cryptosporidium and cyclospora. Her EGD revealed subtle scalloping of proximal duodenum with biopsies revealing villous blunting. She was tested for celiac disease and was found to be positive for tissue transglutaminase antibodies, negative for endomysial antibody, and positive for HLA DQ 2. A diagnosis of celiac disease was made based on these results and patient was advised to follow a gluten free diet. Despite strict adherence to the diet her symptoms continued to worsen. She was admitted to the hospital with severe intractable diarrhea and protein energy malnutrition, with some improvement after initiating IV solumedrol. She was thought to have refractory celiac disease. She was then switched to high dose oral prednisone, but upon tapering her symptoms returned. She continued to be malnourished and had developed severe steroid induced myopathy. At our facility, on further review of her medications she was found to be on olmesartan for her hypertension. Since olmesartan has been associated with enteropathy, she was advised to discontinue the medication. Within 12 weeks of stopping olmesartan her symptoms improved drastically to the point where she had complete resolution of her diarrhea with 1-2 formed bowel movements a day, and gained 10 pounds. Repeat EGD was normal and small bowel biopsy revealed normal villi with no evidence of celiac disease. Olmesartan-induced enteropathy can develop months to years after the initiation of therapy, and in severe cases, can lead to hospitalization. Because of the time lag between olmesartan initiation and symptom development, the mechanism of enteropathy is unlikely to be an allergic type-1 hyper-sensitivity response. A possible mechanism is a cell-mediated immune response. Olmesartan or other angiotensin receptor antagonists (ARBs) should be discontinued in patients presenting with severe diarrhea, even if these drugs have been used for several months or years. If undiagnosed, this unusual adverse effect can lead to significant investigations, hospitalization costs and serious clinical consequences.

[949A] Figure 1.

949 Metastatic Melanoma to the Jejunum Presenting as Obscure Overt Gastrointestinal Bleeding Stephanie H. Mai, MD1, Christian S. Jackson, MD2. 1. Loma Linda University Medical Center/ Loma Linda VA Health System, Loma Linda, CA; 2. Loma Linda VA Healthcare System, Loma Linda, CA. Metastatic spread of a cutaneous malignancy to the small intestine is a rare phenomenon but is commonly seen with malignant melanoma. Metastasis to the gastrointestinal (GI) tract (most commonly ileum and jejunum) occurs in as many as 50-60% cases postmortem, however the clinical diagnosis is only made in about 2-4.7% of patients, antemortum.1,3 Metastatic melanoma to the GI tract is usually undetectable early in its presentation and may arise at the time of primary diagnosis or may be a recurring event, decades later.2 Clinical symptoms of metastasis to the GI tract include abdominal pain, bleeding, weight loss, melena and anemia.2 We present a case of an unusual occurrence of melanoma with metastasis to the jejunum.


[949B] Figure 2.


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950 Chronic Antibody Refractory Pouchitis Associated With Abdominal Mesh in a 49-Year-Old Woman Donelle Cummings, MD1, Jean Ashburn, MD2, Bo Shen, MD, FACG3. 1. Medicine Institute, Cleveland Clinic Foundation, Cleveland, OH; 2. Digestive Diseae Institute, Cleveland Clinic Foundation, Cleveland, OH; 3. Digestive Disease Institute, Cleveland Clinic Foundation, Cleveland, OH. Restorative proctocolectomy with ilealoanal pouch-anal anastomosis (IPAA) is the standard surgical therapy for patients with medically refractory ulcerative colitis (UC), UC with dysplasia, or familial adenomatous polyposis. Complications of IPAA are common and include chronic antibiotic-refractory pouchitis (CARP), which may lead to pouch failure. The etiology and pathogenesis of CARP are illdefined. A 49-year-old woman with IPAA presented to our Pouch Center in September, 2013 with worsening pouchitis symptoms including increased bowel frequency and abdominal pain. She was diagnosed with UC in 1984. She underwent proctocolectomy 2-stage IPAA for steroid-dependent UC in 1995. In 1997 and 2007 she developed a small bowel obstruction (SBO) requiring exploratory laparotomy, adhesiolysis and ventral herniorrhaphy. During the 2007 surgery, partial pouch prolapse with volvulus was noted, prompting sacral pouchpexy involving the small bowel mesentery. Postoperative pouchoscopy showed no active inflammation. In 2009, she underwent elective herniorrhaphy with abdominal mesh placement for incisional hernia. She subsequently developed recurrent pouchitis and cuffitis and initially responded to oral rifaximin. She then developed CARP without response to rifaximin, ciprofloxacin, budesonide or suppositories of belladonna/opium, tincture of opium and hydrocortisone/lidocaine. Abdominal imaging in 2013 showed bulging of the mesh containing unobstructed small bowel loops. Pouchoscopy in May, 2014 revealed chronic pouchitis with mucosal edema, ulcers, and pouch stiffness. Due to medical refractoriness and timing, we believed that her CARP resulted from herniorrhaphy with mesh placement. She underwent diversion ileostomy, adhesiolysis, and mesh removal in August, 2014. The pouchitis symptoms resolved without further medical therapy. She underwent ileostomy reversal in December, 2014 and was without clinical or endoscopic recurrence of pouchitis and has been doing well ever since. This is the first documented association of abdominal herniorrhaphy with mesh placement and CARP in the medical literature. Despite unclear pathogenesis, a variant of ischemic pouchitis due to chronic compromise of mesenteric blood flow or foreign body reaction is possible. Risks and benefits of herniorrhaphy with mesh placement in patients with ileal pouch must be carefully balanced.

[950B] Figure 2.

[950C] Figure 3.

951 HIV Enteropathy: A Rare Cause of Severe Diarrhea in HIV Patients Vipin Verma, MBBS1, Barinder Chana, MD2, Won Cho, MD3, Christian J. Woods, MD4. 1. Internal Medicine, Georgetown University Hospital / Washington Hospital Center, Silver Spring, MD; 2. Internal Medicine, Georgetown University Hospital / Washington Hospital Center, Washington, DC; 3. MedStar Washington Hospital Center, Washington, DC; 4. MedStar Washington Hospital Cetner, Washington, DC.

[950A] Figure 1.


HIV enteropathy is an idiopathic, pathogen-negative form of diarrhea in HIV patients with unknown incidence rates. Several studies have shown that 20-50% of HIV patients have non-infectious chronic diarrhea1. We present a case of HIV enteropathy treated with Crofelemer.


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Abstracts A 30 year-old African-American male with AIDS (non-compliance with HAART) presented with diarrhea, nausea and occasional vomiting for 11 days. Initial emergency department work up revealed potassium 1.5 (3.5 - 5.1 mmol/L), bicarbonate 12 (22-30 mmol/L), creatinine 2.19 (0.66-1.5 MG/DL, baseline of 0.7), BUN 31 (9-20 MG/DL), venous pH 7.02 (7.32-7.42) and CD4 count of 5 (527-1380 cells/ UL). His stool output ranged between 5-9 L/day and required a total of 181 L of IV fluids. He required 1300mEq of potassium supplement with aggressive electrolytes replacement in the first 5 of 20 days of hospitalization. Stool studies (C. difficile, ova/parasites, bacteria/viral/ AFB culture, Rotavirus Ag, Cryptosporidium, Isospora, Microspora, Cyclospora, CMV PCR/culture), serum studies (gliadin IgA/IgM, transglutaminase IgA, norovirus) and CT abdomen/pelvis were negative. Endoscopy revealed esophagitis and scalloped mucosa in the duodenum. Colonoscopy demonstrated congested, erythematous and ulcerated mucosa in the transverse colon. Biopsies were non-specific without any infectious etiology identified. Notable findings included low serum zinc/cortisol and positive serum CMV IgM/IgG (no response to valganciclovir). The patient was started on Crofelemer, loperamide and stool bulking agents with resolution of diarrhea. HIV enteropathy is diagnosis of exclusion. Treatment options ultimately focus on stopping further destruction of CD4+ T lymphocytes and the initiation of HAART along with supportive care. Antimotility agents, antisecretory, adsorbents and opioids are other appropriate adjuvant treatments. Crofelemer should be considered in HIV positive patients with diarrhea not responding to HAART and supportive care. Our case is unique given extent of supportive care required for the patient and resolution of diarrhea with a relatively new FDA approved medication, Crofelemer, stool bulking agents and HAART. References: MacArthur et al. Noninfectious Diarrhea in HIV Seropositive Individuals: a Review of Prevalence Rates, Etiology, and Management in the Era of Combination Antiretroviral Therapy. Clin Infect Dis. 2012 Sep;55(6):860-7.

[952B] Figure 2.

952 Gastrointestinal Bleeding: A Rare Presentation of Gastrointestinal Metastases From Primary Carcinoma of the Lung Carmine Catalano, MD1, Samarth Patel2, Vivek Trivedi2. 1. Icahn School of Medicine at Mount Sinai (Elmhurst Hospital Center), East Rockaway, NY; 2. Elmhurst Hospital Center, Elmhurst, NY. Lung cancer has the highest mortality rate amongst any other cancer. About half of patients with primary lung cancer have metastases at the time of diagnosis. Metastases to the gastrointestinal tract (GI) are rare but when they do occur manifestations from bowel perforation are common and GI hemorrhage is exceedingly rare. We present two cases of patients who presented with overt gastrointestinal bleeding secondary to metastatic lung cancer involving the proximal small bowel. Case1: A 54-year-old male and active smoker presented to the emergency department with complaints of fatigue and black stool for 1 week. The patient also noted 20 pound unintentional weight loss in the last 4 months. Denied any prior endoscopies. Physical exam remarkable for melena on digital rectal exam. Labs notable for anemia with hemoglobin of 6.0 gm/dL. An emergent esophagogastroduodenoscopy (EGD) revealed a 10 millimeter, doughnut-shaped, ulcerated nodule in the duodenum with dried blood (see Figure 1). Pathology showed a metastatic poorly differentiated pulmonary adenocarcinoma. Colonoscopy was unremarkable. A Computed Tomography (CT) scan of the chest showed a large mass in the left upper lung lobe and pathology revealed poorly differentiated pulmonary adenocarcinoma. Case 2: A 78-year-old Chinese male and active smoker, presented to the emergency department with generalized weakness, dark stools, and 15 pound unintentional weight loss over the last 2 months. Normal EGD and virtual colonoscopy 3 months prior. Physical exam remarkable for melena on digital rectal exam. Labs notable for anemia with hemoglobin of 6.2gm/dL. An EGD and a colonoscopy were performed and were unremarkable. Capsule endoscopy revealed a bleeding jejunal mass. A push enteroscopy showed a circumferential, necrotic mass in the proximal jejunal that was partially obstructing the lumen and actively oozing blood. An exploratory laparotomy found a necrotic mass in the proximal jejunum that was penetrating the serosa and adherent to the mid transverse colon (see Figure 2). A segmental resection of the penetrating small bowel mass and mid transverse colon was performed. Pathology revealed metastatic, poorly differenti-

[952A] Figure 1.


ated pulmonary adenocarcinoma with neuroendocrine differentiation. A CT scan of chest showed a large mass in the left upper lung lobe and pathology revealed a non-small-cell undifferentiated carcinoma of the lung with neuroendocrine expression. This was consistent with the jejunal lesions being metastases from primary lung carcinoma. Our cases are unique since this is the first reported case series of undiagnosed metastatic lung cancer involving the proximal small bowel in patients admitted with overt gastrointestinal bleeding. In both cases diagnosis of lung cancer was made by histological examination of the gastrointestinal lesions, which prompted further pulmonary work-up.

953 Pyogenic Granuloma: A Rare Cause of Obscure Gastrointestinal Bleeding Sujaata Dwadasi, MD1, Rahul Maheshwari, MD1, Yue Xue, MD2, Nikrad Shahnavaz, MD1. 1. Emory University, Atlanta, GA; 2. Emory University Hospital, Atlanta, GA. Pyogenic granuloma is a lobular capillary hemangioma that occurs mostly on the skin, and occasionally on the mucosal surface of the oral cavity, but very rarely in the gastrointestinal tract. We report a case of a 63-year-old man who suffered from iron deficiency anemia with multiple syncopal episodes and intermittent melenic stools for the past 1 year. Multiple studies at various centers including esophagogastroduodenoscopies (EGDs), push enteroscopies, colonoscopies, bleeding scintigraphies, and abdominal CT scans during this time period could not reveal the bleeding source. He had not received medical treatment except for oral iron. The patient was transferred to our University hospital for further assessment after he presented to an outside facility with presycope, moderate volume melena, and a hemoglobin of 4.0 g/dl. Initially, a colonoscopy was done which only showed a scant amount of dark blood in the terminal ileum. Next, a video capsule endoscopy revealed a bleeding focus in the jejunum without a distinct etiology. Afterwards, antegrade and retrograde single balloon enteroscopies were planned to locate the source. During retrograde single balloon enteroscopy, a 15 mm pedunculated polypoid mass, with active

[953A] Figure 1.


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albumin of 3.5 mg g/dL. Basic metabolic panel, rest of liver profile, lipase, ESR, AFP, CEA, Ca19-9 and urinalysis were all within normal limits. Chest X ray revealed mild right pleural effusion and CT of the abdomen showed significant ascites. Peritoneal fluid analysis found leukocytes of 0-1, protein of 3.4 g/dL and albumin of 3 g/dL, giving a SAAG score of 0.5. BK and cultures were both negative and pathology was negative for malignancy. Upper endoscopy was unremarkable while colonoscopy revealed active pancolitis. Histology showed mild evidence of neutrophilic activity in vessel wall and lamina propia. Autoimmune disease was considered high in the differential as we had a young female patient, with pan serositis and chronic abdominal pain. Rheumathoid factor was within normal limits, anti Smith Antibody was elevated at 102 U, C3 and C4 were decreased at 23 mg/dL and 1.2 mg/dL respectively, anti-dsDNA Antibody elevated at >800, ANA: positive and transthoracic echochardiogram revealed mild pericarditis with ejection fraction of 55%. After initial inpatient intravenous methylprednisolone 1mg for three days, she was discharged with improved symptoms and to continue taking prednisone 40mg orally daily. She returned to the clinic 1 week later with decreased abdominal pain and improved appetite. Patient has been told to return for outpatient gastroenterology and rheumatology follow up in one month. Ascites as first manifestation of SLE is rare. It is a diagnosis of exclusion and other more common causes for non portal hypertension ascites such as peritoneal carcinomatosis, primary mesothelioma, peritoneal tuberculosis, and nephrotic syndrome should be considered first. The astute clinician should be aware of this entity and the utility of steroids in its resolution.

955 Mesenteric Lymphangioma Encasing Small Bowel

[953B] Figure 2.

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bleeding, was found in the small intestine 90 cm away from the ileocecal valve (Image 1 and Image 2). The bleeding was controlled with epinephrine injection and hemoclip placement. The following day, surgical resection of the small bowel segment was performed. The histological features revealed a capillary hemangioma with a pyogenic granuloma pattern (Image 3). Shortly after resection, the patient’s anemia improved and he had no further bleeding episodes. The small bowel is the source of gastrointestinal bleeding in 2% to 10% of all bleeding episodes. Vascular tumors of the small bowel are very rare, accounting for only 7% to 10% of all benign tumors of the small bowel. Pyogenic granulomas of the small bowel are difficult to diagnose, as they are usually inaccessible via conventional endoscopic techniques. This patient underwent a total of 8 endoscopic and radiologic procedures prior to finally visualizing this rare source of bleeding. This case demonstrates the challenges in the diagnosis and management of obscure GI bleeding. One should be aware of the rare causes of obscure GI bleeding such as pyogenic granuloma and utilize the appropriate diagnostic modalities such as capsule endoscopy and balloon-assisted enteroscopy in finding the source.

Kevin Kuppler, MD1, Katherine Jeong, MD, MS2, Trevor Rose, MD2, Brian Morse, MD2, Daniel Jeong, MD, MS3. 1. University of South Florida, Tampa, FL; 2. Moffitt Cancer Center, Tampa, FL; 3. Moffitt Cancer Center, University of South Florida, Tampa, FL. Introduction: Lymphangiomas are benign lesions arising from lymphatic vessels. These typically arise in the head, neck, and upper thorax though they can rarely involve the small bowel mesentery. Additionally, lymphangiomas are most commonly found in children, but can also be seen in adults. Lymphangiomas comprise 3% of benign small bowel or mesenteric tumors and are usually discovered incidentally on imaging workup given their asymptomatic nature. However, they have also been reported as the cause for acute GI bleeding or abdominal pain. Case report: A 56 year old female with a past medical history of hysterectomy and bilateral salpingooophorectomy and previous bariatric sleeve surgery presented with chronic intermittent cramping abdominal pain associated with bowel movements. A contrast enhanced CT demonstrated a fluid density (15 Hounsfield units) lobulated mass measuring 12.1 x 10.9 cm completely encasing a loop of lower abdominal small bowel. No post contrast enhancement or calcifications were appreciated. Oral contrast passed distal to the affected loop of small bowel and there was no evidence of obstruction. The mass abutted an adjacent portion of sigmoid colon. The mass was biopsied and pathologic findings were compatible with lymphangioma. Given the patient’s relatively mild symptoms and aversion to additional surgery, the decision was made to start with low dose radiation therapy. Follow up imaging 3 months post radiation (not shown) showed stable size of the mesenteric mass corresponding with a mild decrease in the patient’s symptoms. Discussion: Mesenteric lymphangiomas are rare cystic neoplasms which are often detected incidentally on imaging. They are known to have a very soft cystic configuration which can insinuate between loops of bowel and are easily indented by surrounding structures including mesenteric vessels. Mesenteric lymphangiomas can range from a few millimeters to 45 cm in size and typically have simple fluid density. The imaging differential includes: loculated ascites, gastrointenstinal duplication cyst, and peritoneal inclusion cyst. It is helpful to exclude a visceral origin of the cystic lesion by identifying whether adjacent organs demonstrate a claw sign with the lesion. The claw sign refers to sharp angles on either side of the mass made by visceral parenchyma from which the mass originates. Histologic sampling is the gold

954 SLE Ascites: An Uncommon Initial Presentation Eduardo A. Rodriguez, MD1, Vanessa R. Rodriguez, MD2, Diana Otero, MD3, Marcelo Larsen, MD4. 1. University of Miami Palm Beach Campus, West Palm Beach, FL; 2. Universidad de San Martin de Porres/ Hospital Nacional Sergio Bernales, Lima, Peru; 3. Mount Sinai Bronx Program, Bronx, NY; 4. University of Miami, Miami, FL. Ascites is uncommon in systemic lupus erythematosus (SLE) and it may be secondary to common causes such as nephrotic syndrome or malignancies, however it may also be associated with active SLE inflammation. When recognized early and properly treated, the clinical course may be benign, as exemplified in the following report. 46 year old female patient, without significant medical history, came to the clinic complaining of 3 months of worsening diffuse colicky abdominal pain, associated with abdominal distention and decreased appetite. She denied constitutional symptoms, change in bowel movement or abnormal vaginal bleeding. Vital signs were within normal limits. Breath sounds were decreased bilaterally at the bases. Abdominal was mildly distended and tympanitic, with decreased bowel sounds, no tenderness, rebound or guarding. She had a hemoglobin of 11.8g/dL, leukopenia at 3000 uL (Netrophils: 68%, Lymphocytes:28%) and


[955A] Figure 1.


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Abstracts standard for diagnosis and total surgical resection is the standard treatment for symptomatic small bowel and mesenteric lymphangiomas. However, previous authors have shown that radiotherapy represents a viable alternative to surgery in unresectable benign lymphatic tumors.

956 Recurrent Ileal Intussusception Due to a Large Polyp Containing Pancreatic and Gastric Heterotopia Removed by Double-Balloon Enteroscopy F. Otis. Stephen, MD. Woodland Hills, CA. Small bowel intussusception in adults usually occurs as a result of various mucosal abnormalities including polyps and neoplasms. Surgical resection of the affected area of intestine is often required. Pancreatic and gastric heterotopias are uncommon clinical entities rarely identified in the distal small bowel. The following is a unique case of a large heterotopic polypoid lesion in the ileum causing recurrent ileal intussusception that was successfully removed endoscopically. An otherwise healthy 38 year-old female presented for evaluation of new onset hematochezia and episodic lower abdominal pain. Colonoscopy revealed a 2 cm rectal polyp located 5 cm from the anal verge. Biopsies of this lesion revealed adenocarcinoma. This tumor was completely resected via trans-anal surgical excision, and there was no evidence of concurrent lymphovascular invasion. Despite resection of the tumor, she continued to experience intermittent abdominal pain. A more detailed history revealed a 29-year history of episodic lower abdominal pain accompanied by nausea and vomiting. A contrastenhanced CT scan obtained for cancer staging revealed an unusual polypoid mass in the ileum. Retrograde Double-balloon enteroscopy was performed to assess this lesion, and revealed a 7.0 X 2.5 cm elongated polypoid lesion with multiple surface erosions in the distal ileum. This lesion was removed via snare cautery after submucosal injection. There were no procedure-related complications. Pathology revealed diffuse circular submucosal adipose tissue surrounded by pancreatic acini ducts, islets of Langerhans and a minute focal area of gastric fundic-type epithelium within the enteric mucosa, consistent with a submucosal lipoma surrounded by heterotopic pancreatic and gastric tissue. Follow-up evaluation six months after resection revealed no further episodes of abdominal pain, nausea, and vomiting, and a weight gain of 15 lbs. This is an unusual case of a large 7 cm polypoid lesion in the distal ileum consisting of both pancreatic and gastric heterotropic tissue, encompassing a lipoma. Description of a histologically similar ileal lesion was not identified in the literature; thus, this appears to be the first report of such a lesion. Despite its large size and unusual location, this lesion was safely and successfully removed endoscopically, demonstrating that in certain situations, endoscopic resection may be a safe alternative to surgery for similar lesions.

autoimmune work-ups were negative. After failing an empiric trial of antibiotics, Esophagastroduodenoscopy (EGD) and Colonoscopy (CF) were performed with unremarkable endoscopic findings. Duodenum, colon and ileum biopsies were interpreted as normal per the assigned pathologist. Four months later, the patient presented to our clinic seeking a second opinion. The prior EGD and CF biopsies were reviewed with an expert GI pathologist. CF biopsies were interpreted as normal. However, the duodenal biopsies were significant for moderate villous blunting and increased intraepithelial lymphocytosis consistent with indeterminate sprue. Having no relief with a gluten free diet and given his risk of TS, Doxycycline and folic acid were started, resulting in immediate improvement. He has since returned to his regular body weight and feels well. Conclusion: Our case highlights two important details. TS must be kept in the differential diagnosis for persons traveling to countries at risk for this infection. A high level of clinical suspicion must be maintained when diagnosing TS, as serologic testing does not exist and histopathology can be misleading. In addition, reviewing biopsies with a dedicated GI pathologist for patients with any GI disorder is imperative not only to improve our own knowledge base but to assure that our patients receive the best care possible.

958 A Rare Case of Clostridium difficile Enteritis and Small Bowel Obstruction Noah Settergren, DO1, Colin Wolslegel, DO2, Henrique Fernandez, MD2. 1. Parkview Medical Center, Colorado Springs, CO; 2. Parkview Medical Center, Pueblo, CO. There have been less than one-hundred reported cases of Clostridium difficile enteritis, demonstrating the rarity of our case. To date, there is no consensus on the treatment of C.difficile enteritis. Understanding the cause for C.diff enteritis and initial treatment is important to quickly identify and prevent potential associated complications.

[958A] Figure 1.

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957 Lessons from Paradise: The Many Subtleties of Tropical Sprue David M. Pinn, MD1, Jeffrey A. Shrensel, MD, MS2, Andrew S. Korman, MD3, Gabriel Levi4, David L. Carr-Locke, MD, FACG3. 1. Mount Sinai Beth Israel Medical Center, Department of Medicine, New York, NY; 2. Mount Sinai Beth Israel, New York, NY; 3. Mount Sinai Beth Israel Medical Center, New York, NY; 4. Mount Sinai Beth Israel, New York , NY. Tropical Sprue (TS) classically presents as chronic diarrhea and symptoms of malabsorption in countries located within 30 degrees latitude of the equator, mostly affecting the indigenous population. Although the etiology is unclear, bacterial overgrowth, toxigenic bacterial species, and viral sources have all been theorized to play roles in the disease pathogenesis. Duodenal biopsies are the gold standard. However, TS is often a diagnosis of exclusion and histopathologic findings can mimic celiac disease. Timely diagnosis may be assisted by a dedicated GI pathologist when clinical suspicion for TS is high. Long term treatment with folic acid and broad spectrum antibiotics are the mainstay of therapy. We present a case of TS in a man visiting Haiti whose diagnosis was initially delayed due to misdiagnosis. Case: A 61 year old man with a medical history of Chronic Lymphocytic Leukemia presented after a six week trip to Haiti with watery, non-bloody diarrhea associated with bloating and a 20lb weight loss. From another GI provider, stool studies and routine blood-work were unremarkable and infectious and


[958B] Figure 2.


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Abstracts

A sixty-four year-old male with familial adenomatosis polyposis s/p colectomy and J-pouch presented with recurrent gastrointestinal bleeding, abdominal pain, and diarrhea. A recent EGD and RBC scan failed to identify a bleeding source. An abdominal/pelvis CT performed two days prior to admission was significant for small bowel distention. Repeat abdominal/pelvis CT found enteritis of the J-pouch and fluid-filled bowel loops. A C. difficile antigen test was positive. Initial treatment with oral metronidazole was unsuccessful. Antibiotics were changed to intravenous metronidazole and oral vancomycin and finally oral vancomycin for two weeks. The diarrhea improved and repeat C.difficile antigen testing was negative. Following treatment, the abdominal pain and nausea persisted and the patient was unable to tolerate a colonoscopy prep. An abdominal x-ray revealed multiple loops of small bowel with air-fluid levels of discordant heights. Due to concerns for a small bowel obstruction an NG tube was inserted. An exploratory laparotomy with lysis of adhesions and pouch endoscopy were performed revealing an internal closed loop obstruction and a distal pouch obstruction due to anal stenosis, which was dilated. The constipation continued following the operation and a rectal tube was placed. A repeat enteroscopy two weeks after the laparotomy found an ileoanal stricture above the J-pouch and was dilated. Afterwards, the bowel obstruction and patient’s condition improved. This case illustrates the delay in diagnosis of the cause of a small bowel obstruction following C.difficile enteritis leading to an extended hospital stay. This case raises the question of whether the stricture may have have been prevented with either earlier or more aggressive antibiotic therapy. Further, with no consensus for treatment of C.difficile enteritis, is aggressive initial antibiotic therapy necessary as compared to standard treatment for C.difficile colitis?

959 EBV Negative NK/T-Cell PTLD of the Distal Ileum in a Renal Transplant Recipient Meghan Steiner, Elvira Umyarova. Medical University of South Carolina, Charleston, SC. Post-transplant lymphoproliferative disorder (PTLD) represents a spectrum of Epstein–Barr virusrelated (EBV) clinical diseases from a benign mononucleosis-like illness to a fulminant non-Hodgkin’s lymphoma. We describe a case of a PTLD in a patient with renal transplant. 21 yo male with congenital nephrotic syndrome and living donor renal transplant was diagnosed with polymorphic PTLD 2 years ago. He presented with fatigue, anemia, back pain and recurrent sinus infections. Staging CT scans revealed cervical and mesenteric lymphadenopathy. Patient underwent excisional cervical lymph node biopsy with pathology positive for polyclonal PTLD. His EBV viral load was above 100,000. Patient’s immunosuppression was decreased and he received 6 cycles of chemotherapy with cyclophosphamide, rituximab and prednisone. Post-treatment re-staging scans showed no evidence of the disease.Three months later patient presented with a new onset of back pain and signs of bowel obstruction. Images showed a soft tissue density in right mid-abdomen. He was found to have a 4cm distal ileum mass with caecal intussusception and underwent a resection with an end-end anastomosis. Pathology report was consistent with monomorphic PTLD: DLBCL type.During recovery period he presented with weight loss, back pain, and an enlarged lymph node in anterior chest. Restaging PET/CT scan revealed diffuse hypermetabolic activity in multiple lesions of the neck, chest, abdomen, pelvis and bones. Serum EBV viral load was negative. Previous surgical specimen was reviewed and final diagnosis changed to EBV negative NK/T-cell PTLD. Patient was started on systemic chemotherapy regimen with SMILE (dexamethasone, methotrexate, ifosfamide, l-aspariginase, etoposide) and tolerated treatment well.PTLD is a rare complication after stem cell or solid organ transplantation and is related to unbalance between EBV-infected B lymphocytes and specific T cells of response. Revised WHO classification includes early lesions, classic HL-type, polymorphic and monomorphic PTLD. The majority of monomorphic PTLD are of B-cell origin: diff use large B-cell lymphoma (DLBCL) or Burkitt lymphoma. 5% of cases are T-cell types and around 1% represent the NK/T-cell type.The incidence of PTLD following renal transplant is approximately 1% at 10 years, with greater than 80% of cases occurring within the first year following transplant.Our patient had unusual presentation: he had EBV negative monomorphic PTLD NK/T-cell lymphoma - the type of disease which is exquisitely rare. He also had a long time interval before malignant transformation and an unusual site of involvement.Clinicians need to have a high level of suspicion for malignancy in stem cell and solid organ transplant recipients. Rarely patient’s symptoms of intussusception might be related to NK/T cell lymphoma.

960 Fever of Unknown Origin: An Unlikely Culprit Ijagha Eme, MD1, George Mount, MD2, Christina Schofield, MD3. 1. Madigan Army Medical Center, DuPont, WA; 2. Madigan Army Medical Center, Tacoma, WA; 3. Madigan Army Medical Center, Tacoma, WA, Wallis and Futuna. CPT Ijagha Eme, MD (Associate), LTC George Mount, MD (FACP), Christina Schofield, MD (FACP), COL Mark Cumings, MD (FACP). Madigan Army Medical Center, Tacoma, WA. Introduction: Mesenteric panniculitis is a rare inflammatory condition manifested by chronic and nonspecific inflammation of the adipose tissue of the intestinal mesentery. It is an uncommon presentation for a fever of unknown origin. Case: A 46-year-old female presented with a 2-year history of recurrent fevers up to 38.9°C, fatigue, muscle weakness, joint stiffness, and extreme headache lasting approximately 30 hours. Her past surgical history was notable for gastric sleeve around the start of these febrile episodes. Her exam was unremarkable with normal vital signs. Laboratory data revealed a microcytic anemia, whereas comprehensive metabolic panel, HIV antibody, inflammatory markers, quantiferon TB gold, blood cultures, LDH, ANA and SPEP were all within normal limits. CT of the abdomen and pelvis showed a misty appearance of the mesentery in the left hemiabdomen with multiple enlarged mesenteric lymph nodes consistent with mesenteric panniculitis. In retrospect, this was seen on several CT scans spanning over 2 years following her gastric sleeve and onset of fevers. Gastroenterology consult was obtained and a mesenteric biopsy was obtained. Initiation of corticosteroids was considered


following confirmatory biopsy. Patient continues to endorse symptoms and is being followed closely from a multi-disciplinary approach. Discussion: Mesenteric panniculitis is a rare inflammatory condition manifest by chronic and nonspecific inflammation of the adipose tissue of the intestinal mesentery. There is a 2-3:1 predilection for men versus women with incidence increasing with age. A precise etiology remains unclear although a history of abdominal surgery or trauma has been reported. Fever, abdominal pain and malaise are common symptoms although the disease is usually asymptomatic. Therapy is individualized with drugs such as steroids, thalidomide, cyclophosphamide, progesterone, colchicine, azathioprine, tamoxifen, antibiotics or radiotherapy used with various degrees of success. This case suggests that mesenteric panniculitis should be considered as a rare etiology of fever of unknown origin in a patient with a history of abdominal surgery.

961 Successful Management of Bouveret’s Syndrome With Severe Esophagitis in a High-Risk Surgical Patient Mohsen Pourmorteza, MD1, Charles Rives2, Mehdi Pourmorteza, DO1, John Litchfield, DO3, Jason Mckinney, DO2, Mark Young, MD4. 1. Department of Internal Medicine, East Tennessee State University, Johnson City, TN; 2. East Tennessee State University, Johnson City , TN; 3. East Tennessee State University, Department of Internal Medicine, Division of Gastroenterology, Johnson City, TN; 4. East Tennessee State University, Johnson City, TN. Introduction: Bouveret’s syndrome is a rare variant accounting for 1–3% of gallstone ileus.Management and treatment modalities consist of endoscopy and surgery such as enterolithotomy or gastrostomy with or without cholecystectomy and fistula repair.We describe a successful management of a unique variant of chronic Bouveret’s syndrome with a rare association of severe esophagitis. Case report: An 84 year old Caucasian male with a history of sick sinus syndrome status post AICD placement was admitted to the hospital for multiple episodes of coffee-ground emesis of 1 day duration and 3 day history of decreased oral intake. On examination patient was in mild distress, pale with dry membrane mucosa and elevated creatinine/BUN level (0.94/34). He denied any fever/chills, weight loss or recent travel but had noticed a 2 day history of melena and diffuse epigastric abdominal pain with mild leukocytosis 12.2 (k/uL). Abdominal examination revealed epigastric tenderness and hypoactive bowel sounds without any rigidity or guarding. Initial blood investigations demonstrated Potassium 3.6mmol/L, sodium 139mmol/L and Chloride 106mmol/L. Blood count showed hemoglobin of 15.1g/ dL, platelet count of 203k/mcl, Liver enzymes AST U/L 15; ALT U/L 10; Total Bilirubin 0.7 mg/dl. Computed tomography (CT) abdoman with IV contrasts revealed high-grade distal small bowel obstruction with air in the gallbladder consitant with gallstone ileus. Esophagogastro-duodenoscopy (EGD) was performed during which an embedded large stone was unretrievable from the duodenal bulb. There was also evidence of severe esophagitis, gastric polyps and extensive stasis ulceration at the point where the stone was impacted. Surgery was consulted as they proceeded with a stage 2 laparoscopic enterolithotomy with successful removal of a 4 cm stone. Discussion: Bouveret’s syndrome is an uncommon form of gallstone ileus comprising only 1-3% of cases of gallstone ileus. It presents as a clinically distinct form due to the proximal GI obstruction.Such obstruction commonly occurs at the distal small intestine due to the smaller diameter of the lumen. Symptoms include nausea/vomiting (86%), abdominal pain (71%); less commonly with hematemesis, weight loss,anorexia, while only 2% of Bouveret’s syndrome cases present with esophagitis. Endoscopy is considered the first line of treatment. However, the success rate of endoscopic extraction is dependent on stone size. Stones larger than 2.5 cm are more difficult to extract endoscopically. If endoscopic treatment fails, surgical managemen is required. In our case a stage 2 procedure was sufficient relief of intestinal obstruction with no post op complication in a high risk surgical patient.

962 Beer Belly Without the Beer: Tense Ascites as a Presenting Manifestation of SLE Daniel K. Hodge, MD1, Samuel J. Kallus, MD2, Matthew Tuck, MD3. 1. Department of Medicine, Walter Reed National Military Medical Center, Bethesda, MD; 2. Department of Medicine, Georgetown University Hospital/Veterans Affairs Medical Center, Washington, DC; 3. Department of Medicine, Veterans Affairs Medical Center, Washington, DC. Introduction: Ascites is an exceedingly rare initial presentation of systemic lupus erythematosus (SLE). Hallmarked by its varied clinical presentation, this multisystem inflammatory disease represents a diagnostic challenge. We present a rare case of acute onset ascites as the presenting symptom of lupus peritonitis (LP) in an adult male. Case: A 57-year-old male with history of Grave’s disease presents with progressive abdominal distension over three weeks. He reported early satiety, occasional non-bloody emesis, and weight loss during this time. Patient denied fevers, chills, and night sweats. Past medical history significant for alcohol abuse, but was not currently drinking. He was a prior smoker with history of incarceration. On physical examination, patient was afebrile and normotensive. He was cachectic with temporal wasting and a tightly distended abdomen with flank dullness and positive fluid wave. No stigmata of chronic liver disease were evident. Abdominal ultrasound confirmed the presence of ascites without evidence of cirrhosis or portal vein thrombosis. Remarkable serum labs demonstrated leukopenia, positive ANA (1: 2560), positive dsDNA (>1000 IU/ ml), positive anti-smith antibody, and low complement. Diagnostic paracentesis yielded serum-ascitesalbumin gradient (SAAG 0.8 g/dL), negative adenosine deaminase, and negative cultures including culture for acid fast bacilli. Patient was diagnosed with LP and started on treatment. Discussion: Tense ascites is an exceedingly rare initial presentation of SLE. While serositis, most commonly pericarditis and pleuritis, develops in approximately 13% of patients with SLE during the course of the disease, peritoneal serositis is an uncommon clinical manifestation and extremely rare initial presentation of SLE.


| OCTOBER 2015

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Abstracts

[961A] Figure 1.

[962]

Table 1. Serum-Ascites Albumin Gradient (SAAG)

High Gradient ( 1.1 g/dl)

Low Gradient (