bluuebunny/crossref_metadata_2025 huggingface dataset:
1269 Massive Life-Threatening Hemobilia Managed Successfully at ERCP: The Importance of Teamwork and Appropriate Interventions in a Catastrophic Situation!
Authors: Enslin Sarah , Tariq Raseen , Pisharoty Anil , Kothari Truptesh , Ullah Asad , Kothari Shivangi , Kaul Vivek
Published: October 2019

INTRODUCTION:

Clinically significant bleeding at ERCP is encountered in 0.1% to 2% cases. Hemobilia is relatively uncommon and usually mild. Here we present a case of successful management of massive life-threatening hemobilia during ERCP.

CASE DESCRIPTION/METHODS:

A 79-year male with T2N0 pancreatic tail adenocarcinoma s/p distal pancreatectomy in 2007, cirrhosis and portal hypertension developed obstructive jaundice due to recurrent pancreatic head malignancy 11 years later. ERCP with placement of an uncovered 10 mm × 40 mm SEMS was performed. Recurrent cholangitis 4 months later required repeat ERCP, revealing extension of stricture to the CHD. A 10 F × 12 cm plastic biliary stent was placed through the metal stent into the right hepatic duct. At repeat ERCP six weeks later, the plastic biliary stent was removed easily with snare. Approximately one minute later, massive hemobilia ensued with complete occlusion of endoscopic visual field. Due to volume and rapidity of bleeding, it was suspected that bleeding was from tumor erosion of intraductal varices. Approximately 1.2 liters of blood was lost in less than 5 minutes resulting in hemodynamic instability. During this time, the following decisions and events were put into motion: 1. Anesthesia attending took charge of patient's hemodynamics, central venous access, pressor support and PRBC transfusion, 2. Charge nurse alerted ICU team, sent additional nursing and tech resources to room, 3. The endoscopist focused on clearing the duodenal luminal field with aim to re-establish biliary access, however this was very difficult due to amount of blood/clot in the visual field, 4. Two additional endoscopists helped re-position patient to left lateral position, enabling visualization & biliary access, 5. Per consensus, placement of a fully covered SEMS was the only endoscopic option that could achieve hemostasis, 6. A10 mm × 60 mm fully covered SEMS was placed into the CBD/CHD with tamponade of hemobilia and restoration of biliary drainage, 7. Patient was transferred to PACU, extubated, recovered uneventfully and discharged home × 48 hrs.

DISCUSSION:

Massive, life threatening hemobilia can occur from friable tumors/intraductal varices even with minimal manipulation. Teamwork and correct medical decision making are critical to a successful outcome during such catastrophic endoscopic events. Placement of a fully covered metal biliary stent served a dual purpose of tamponading hemobilia and relieving biliary obstruction in this case.
1276 Acute Pancreatitis Causing Multiple Aortic Thrombi and Multi-Organ Infarcts
Authors: Faris Mohamed M. , Balanchivadze Nina , Sherertz Robert , Edmison John
Published: October 2019

INTRODUCTION:

There have not been many case reports of acute pancreatitis causing aortic thrombi. In this vignette we illustrate this rare but noteworthy clinical scenario.

CASE DESCRIPTION/METHODS:

A 44-year-old homeless man with a history of chronic pancreatitis and alcoholism presented with acute, sharp, diffuse abdominal pain. Vital signs were notable for hypotension and tachycardia. Abdominal examination revealed a diffusely tender abdomen with guarding and rigidity. Neurological examination revealed bilateral upper extremity weakness. White blood cell count, lipase, ESR, CRP, and D-dimer were all markedly elevated A CT abdomen revealed acute pancreatitis with diffuse acute multiple thrombi in the aorta with hepatic, splenic, bowel, and bilateral renal infarcts. There was diffuse ascites of the abdomen and pelvis with bilateral pleural effusions. Cervical MRI revealed C4-C6 cord infarct with diffusely abnormal signal. Brain MRI revealed two acute ischemic infarcts in the right occipital lobe. CTA chest revealed multiple large exophytic thrombi in the descending aorta with no evidence of pulmonary embolism. Duplex ultrasound of all extremities and echocardiogram with contrast were non-revealingHypercoagulability studies revealed mildly decreased factor II, antithrombin III, and protein C levels. Anticoagulation was started with IV heparin and later switched to a direct oral anticoagulant. Paracentesis revealed pancreatic ascites. The patient's abdominal pain resolved and he was transferred to a higher tertiary care center where he was found to have a pancreatic duct leak requiring stenting.

DISCUSSION:

There are only a few reports in the literature of acute pancreatitis causing aortic thrombosis. The pathophysiology remains unclear. However, there are a few hypotheses. First, proteolytic enzymes released in the setting of acute pancreatitis cause direct injury to the aortic wall, resulting in a nidus for mural thrombus formation. Second, trypsin released during acute pancreatitis causes the activation of several thrombogenic factors such as platelets and fibrinogens. Lastly, hypovolemia caused by acute pancreatitis increases the risk of vascular stasis and vasospasm. In conclusion, this is a rare case of acute pancreatitis complicated by multiple aortic thrombi and multi-organ infarcts in the setting of a mild coagulation disorder. The patient responded well to supportive measures for acute pancreatitis and direct oral anticoagulants thereafter.
1277 Female Predominance in Metronidazole-Induced Acute Pancreatitis: A Case Report and Review of Literature
Authors: Chang Eileen , Vaishnani Marvin , Chang Ian , Jennings Whitney
Published: October 2019

INTRODUCTION:

Acute pancreatitis is a relatively common condition in the hospital. About 75% of cases are associated with excessive alcohol use or gallstones, and only 0.1 to 2% are drug-induced. The clinical and pathologic findings are similar regardless of the inciting cause. We have suspicion that metronidazole-induced pancreatitis occurs at a significantly higher incidence, or maybe exclusively, in females.

CASE DESCRIPTION/METHODS:

A 68-year-old Caucasian female with history of hyperlipidemia, cardiomyopathy and hypothyroidism presents to the ED with chief complaint of epigastric pain. Symptoms started few days prior with back pain that progressed to epigastric tenderness and fullness. Associated symptoms include nausea and vomiting. She denies fever, chest pain, hematemesis, hematochezia, melena or recent injury. She denies alcohol or tobacco use. About 2 weeks ago, patient underwent upper endoscopy for ongoing epigastric pain and family history of sister who passed away in her 50s from gastric cancer. EGD showed numerous pedunculated and sessile hyperplastic appearing gastric polyps in the fundus and body; biopsy was obtained. Pathology report revealed no dysplasia or malignancy. She completed a short course of metronidazole for abdominal bloating and diarrhea 4 days prior to hospital presentation. On admission, lipase was 10,347 with normal triglyceride and calcium levels. CT imaging demonstrated stranding around the pancreatic head and uncinate process. She was placed on bowel rest, IV hydration and supportive care. MRCP was performed to assess the pancreatic duct; it revealed acute pancreatitis, but no cholelithiaisis, choledocholithiasis or other complicating features. Repeat lipase was 2,533. Patient recovered well and was discharged home.

DISCUSSION:

Metronidazole-induced acute pancreatitis has been reported in prior English literature; in which all 8 cases involved female patients (O'Halloran E, et al. HPB Surgery, pp. 1–4, 2010). Proposed mechanisms include free radical production and immune-mediated inflammatory response. In a population-based case control study, there was a significantly increased risk of acute pancreatitis within 30 days exposure to metronidazole, especially when used in combination with other agents for H. pylori eradication (Barbulescu A, et al. Clinical Epidemiology, pp. 1573–1581, 2018). Physicians should maintain a high index of suspicion when prescribing metronidazole and avoid rechallenge. Further investigation may help reduce morbidity related with this phenomenon.
1281 Duodenobiliary Fistula: A Rare Complication of Peptic Ulcer Disease
Authors: Larson Brian , Bank Jeffrey S. , Walker Michael J.
Published: October 2019

INTRODUCTION:

Spontaneous biliary enteric fistulas are usually late complications of cholelithiasis or choledocholitiasis. The incidence of biliary enteric fistulas in this population ranges from 0.3 – 0.9%. Biliary enteric fistula formation is usually occurs from a gallstone ulcer perforating into the normal duodenum. However in rare circumstances (3.5-10% of cases) fistula's can form from a duodenal ulcer penetrating into the biliary tree, as is the case with biliary enteric fistula's due to peptic ulcer disease (PUD). These fistula's often present with abdominal pain, malaise and/or hematemesis. We discuss a rare case of a duodenobiliary fistula as a result of long standing peptic ulcer disease.

CASE DESCRIPTION/METHODS:

A 57-year-old male with long standing abdominal pain who recently immigrated to the United States from the Democratic Republic of Congo presented to the ED with acute on chronic epigastric abdominal pain. He denied previous surgery. Notably, he had tested positive for h. pylori a few months prior and was questionably compliant with prescribed antibiotics. He was admitted with hypokalemia and renal failure. Persistent symptoms prompted a computed tomography (CT) of his abdomen and pelvis. Findings from the CT demonstrated air and oral contrast material within the common bile duct and intrahepatic bile ducts with a fistulous connection to the second portion of the duodenum. Endoscopic evaluation demonstrated esophagitis, gastritis and severe pyloric stenosis likely due to long-standing PUD. The standard endoscope was unable to traverse this stenosis, but was successfully traversed with an ultrathin scope. The ampulla was briefly visualized and was grossly normal. There was no definitive fistulous tract identified. The patient was placed upon high dose proton pump inhibitor therapy. A repeat CT of the abdomen and pelvis was done 6 weeks later and was unchanged. The patient was referred to surgical oncology for definitive management.

DISCUSSION:

Historically, biliary enteric fistulas were often diagnosed during surgical interventions. Currently, CT can often diagnose these fistulas by detecting minimal pneumobilia. Endoscopic evaluation may or may not demonstrate a biliary enteric fistula due to duodenal narrowing or edema. Antiulcer therapy usually allows clinical improvement and fistula closure for PUD associated fistulas. Surgery is reserved for cases refractory to medical care, poorly controlled symptoms, hemorrhage or biliary obstruction.
1282 Abrupt Onset of Acute Pancreatitis Following the Ingestion of Eluxadoline
Authors: Gonzaga Ernesto Robalino , Borgan Saif , Sourial Kirolus , Vanar Vishwas
Published: October 2019

INTRODUCTION:

Acute pancreatitis is a common condition in the US, with high mortality and burden on the health care system. In the US, it is one of the main causes of gastrointestinal related admissions with more than 291,000 hospitalization per year. The most common causes are alcohol use (30%) and gallstones (40%). Less frequently, drug induced. Interestingly, drug induced pancreatitis has excellent prognosis and low mortality. The mechanisms of drug induced pancreatitis include immunologic reactions, direct toxic effect, accumulation of toxic metabolites, ischemia, and intravascular thrombosis.

CASE DESCRIPTION/METHODS:

A 78-year-old woman with surgical history of cholecystectomy presented to the emergency room with a sudden onset of sharp epigastric pain radiating to the back, that was associated with vomiting, 60 minutes after taking Eluxadoline for the first time. She had a history of hypertension, diabetes mellitus, and irritable bowel syndrome with diarrhea (IBS-D) for which Eluxadoline was prescribed. On exam, she was hemodynamically stable and had epigastric tenderness without rebound. Laboratory tests remarkable for elevated lipase, 2754 U/L. Based on the Revised Atlanta criteria, patient had mild pancreatitis. A computed tomography of the abdomen and pelvis was unremarkable without biliary pathology. She was admitted for acute pancreatitis presumed secondary to Eluxadoline ingestion. The patient was treated conservatively and Eluxadoline was discontinued. Five hours later, her lipase was 68 U/L and symptoms resolved. She was advised to discontinue Eluxadoline and discharged home.

DISCUSSION:

The diagnosis of drug induced pancreatitis requires first the diagnosis of acute pancreatitis based on symptoms, biomarkers or imaging. Common causes, such as alcohol use and gallstones, must be ruled out. A medication review should be conducted to look for potential culprits. Any medication of suspect should be discontinued and resolution of pancreatitis should be appreciated. Eluxadoline is used in treatment of IBS-D. It reduces abdominal pain and lessens diarrhea frequency, but has been noted to be associated with acute pancreatitis in 82% of patients who has previously underwent cholecystectomy. It is thought to be due to spasms in the sphincter of oddi, leading to pancreatic duct hypertension. The FDA has suggested to avoid the use of this medication in these cases. Careful attention should be made to the potential adverse events, especially acute pancreatitis, in those patients on Eluxadoline.
1285 Elevated CEA and CA 19-9 Producing Carcinoma: Think Beyond the Digestive System!
Authors: Bhardwaj Gaurav , Shahid Tamoor , Hertan Hilary
Published: October 2019

INTRODUCTION:

Carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA 19-9) are validated and well-known tumor markers for colorectal and pancreatic malignancies but data concerning these markers in bladder carcinoma are limited. We report a rare case of bladder carcinoma with metastasis to the bone marrow producing very high serum levels of CEA and CA 19-9.

CASE DESCRIPTION/METHODS:

A 68-year-old man with a medical history of hypertension, COPD presented with altered mental status. The patient further reported anorexia, unintentional weight loss of 50 lbs and intermittent hematuria over the last few months. He was confused but hemodynamically stable on presentation. Initial laboratory data showed pancytopenia, ALP of 712 U/L with normal transaminases and bilirubin, urine microscopy showed >100 red blood cells/HPF. A CT scan of the abdomen showed bilateral hydronephrosis with thickening of the urinary bladder and diffusely abnormal bone marrow. Bone marrow biopsy showed poorly differentiated metastatic carcinoma with positive immunohistochemical (IHC) stains for cytokeratin (CK)7 and CK20. In addition, very high levels of tumor markers CA19-9 42,635 U/ml, CEA 347 ng/ml raised a possibility of origin from the gastrointestinal or pancreatobiliary system. Subsequently, upper endoscopy, colonoscopy, EUS, and magnetic resonance cholangiopancreatography (MRCP) were performed and results were unremarkable. Finally, a cystoscopy was performed showing multiple papillary tumors throughout the bladder. Unfortunately, the patient died before any further workup and therapeutic interventions were initiated.

DISCUSSION:

Elevated levels of CEA and CA19-9 have been demonstrated in TCC of the bladder. The specificity of CEA for diagnosis of colorectal cancer is 89 percent while the specificity of CA 19-9 for pancreatic cancer goes up to 85% at a serum level >37 U/ml but neither are useful tools in the primary diagnosis of TCC. The pattern of staining with the CK20 and CK7 may be helpful in narrowing the diagnostic spectrum, but both can show positivity in pancreatobiliary and urothelial cancers. IHC allows limited determination of the tissue of origin in poorly differentiated carcinomas due to atypical staining patterns. In conclusion, when CEA and CA19-9 serum levels are elevated, a gastrointestinal malignancy should be excluded and one should be mindful of the existence of CEA and CA19-9 producing TCC and thus examine the urologic tract.
1286 Chylous Ascites in the Setting of Metastatic Pancreatic Cancer: A Case Report
Authors: Gribbin Caitlin , Martin Tracey , Wan David
Published: October 2019

INTRODUCTION:

Chylous ascites, or milky-appearing peritoneal fluid rich in triglycerides, is an uncommon finding that occurs in the presence of lymph in the abdominal cavity. The incidence has been reported as one in 20,000 hospital admissions though this number may be increasing due to improved survival in the setting of gastrointestinal malignancies. Etiology is most commonly associated with malignancy and other causes include cirrhosis, congenital malformations, traumatic causes as well as postoperative complications, and infectious or inflammatory diseases.

CASE DESCRIPTION/METHODS:

A 52-year-old woman with a history of pancreatic cancer with metastases to the spine status-post C3-6 laminectomy and fusion as well as polycystic kidney disease (PCKD) status-post renal transplant presented with abdominal distension and fever. The patient underwent a paracentesis to rule-out spontaneous bacterial peritonitis (SBP) and was noted to have chylous ascites with a triglyceride level of 1323 mg/dL in the ascites fluid. The patient remained hemodynamically stable and received treatment with piperacillin/tazobactam for presumed pneumonia versus urinary tract infection underlying the patient's fever. Following rule-out of tuberculosis, the presence of chylous ascites was presumed to be secondary to tumor burden within the abdominal cavity and the patient was continued follow-up with oncology without further intervention from the gastrointestinal team.

DISCUSSION:

Chylous ascites is a rare finding associated with disruption of the lymphatic system in either the abdominal or thoracic cavity. It is most commonly associated with malignancy but can also be seen situations involving cirrhosis, trauma, postoperative complications, or congenital malformations. Occasionally, chylous ascites may be seen in inflammatory or infectious diseases, which must be ruled out if suspected. Associated symptoms include abdominal pain and distention, weight gain, and dyspnea. The condition is typically not suspected prior to performing a paracentesis, which is diagnostic. Treatment is aimed at correcting the underlying cause as well as addition of a low-fat, high-protein diet and therapeutic paracentesis as needed. In this case, the patient continued treatment with oncology alongside palliative measures to alleviate associated symptoms.
1290 Years of Undiagnosed Recurrent Hypoglycemia in a Child
Authors: Desai Koosh , Mehta Minesh
Published: October 2019

INTRODUCTION:

Below we present a case of a child with an insulinoma, a rare and difficult to diagnose cause of hypogylcemia.

CASE DESCRIPTION/METHODS:

A previously healthy 12-year-old child presented to the emergency department with an unresponsive episode. Her father found her in bed, “unable to open her eyes” and extremely lethargic. Her blood sugar was noted to be less than 20 and she had ketones in her urine. Her glucose improved with oral intake and was discharged with a presumptive diagnosis of a well known cause of hypoglycemia in this age group, ketotic hypoglycemia. She remained well for around a year but then returned to the ED with lethargy. She was deemed have symptoms consistent with her originally diagnosed condition and was discharged. After an illness free period of 18 months, she presented to the ED with a low glucose of 33, high insulin of 14, and high c-peptide of 3.3. She had a negative CT scan was again discharged home. For the next few months, she having daily symptoms of fatigue and “cranky” behaviors, with only partial response to glucose intake. At age 16, after being seen by an endocrinologist, an insulinoma was considered as a possible diagnosis. MRI was ordered, but didn't detect a mass in the pancreas. Thus, GI was consulted for endoscopic ultrasound (EUS) and a 2 cm mass in the uncinate process was detected. FN-B of the pancreatic mass was consistent with neuroendocrine tumor. The patient had a surgical resection and, eventually, complete resolution of symptoms.

DISCUSSION:

Insulinomas are a very rare cause of hypoglycemia, with around 1 to 4 new cases occurring per million persons per year, and particularly uncommon in children with only limited number of published case reports. Classically, the “Whipple's triad” is expected with insulinoma: a low plasma glucose, symptoms consistent with hypoglycemia, relief of symptoms when the glucose is raised to normal. This patient did have certain aspects of the triad of symptoms, but she didn't always respond to glucose thus complicating diagnosis. This case is a reminder that, while rare, insulinoma is a important cause of hyperinsulinemic hypoglycemia in the pediatric population. Also important to know I is that while CT is generally considered first line for diagnosis of insulinoma and has good sensitivity and specificity and MRI has even better accuracy, neither test is perfect, thus EUS is sometimes required to identify lesions.
1291 Pancreatico-Biliary Stricture by Benign Hepatic Cysts
Authors: Kim Hyaehwan , Beck Gregory
Published: October 2019

INTRODUCTION:

Hepatic cysts are frequently identified incidentally, and usually do not require any follow up. We present a case of benign, large hepatic cysts which were extrinsically compressing on biliary ductal system and caused a fusiform-dilitation of the hepatic ducts, distal dilation of the common bile duct (CBD) and a narrowing of the pancreatic duct.

CASE DESCRIPTION/METHODS:

A 77-year-old male presented to our facility for drainage of a large liver cyst. Initial discovery was incidental, but follow up imaging showed increased solid component in one of the cysts. At the time of presentation he was completely asymptomatic and laboratory studies were all within normal range. Computed Tomography (CT)-guided drainage of the hepatic cyst yielded 250 cc of brown fluid. The cytology was benign. Patient then presented to one-month follow up appointment with painless jaundice, and elevated total bilirubin of 6.7 mg/dL. Magnetic Resonance Cholangiopancreatography (MRCP) was performed and showed filling defects of the CBD and bilateral hepatic ducts. Elective Endoscopic Retrograde Cholangiopancreatography (ERCP) a few days later showed dilated CBD and strictures of biliary duct at the bifurcation and pancreatic duct at the neck. The stricture appeared to be from extrinsic compression. We were concerned about infected cyst, and repeated cyst drainage. Previsouly drained cyst yielded 200 cc for purulent fluid; the adjacent cyst was also drained and it yielded >1 L of clear fluid. At this time, patient had leukocytosis of 13.7 K, total bilirubin 6.2 mg/dL, ALP 433 IU/L. Patient was admitted post-procedure and was placed on broad-spectrum antibiotics. Culture grew Actinomyces species, and patient was discharged to home on long term oral antibiotics. ERCP was repeated two weeks later, and it showed fusiform dilation of intrahepatic duct, though stricture of the biliary tract and pancreatic duct were now resolved. There was no communication between the biliary tract and the hepatic cysts. CT of the abdomen showed persistent fluid collections, the patient ultimately underwent laparoscopic resection of hepatic cyst with partial hepatectomy, cyst fenestration and cholecystectomy. Pathology confirmed that it was indeed a benign cyst.

DISCUSSION:

It appears that due to close abutment of two large cysts caused compression of the ductal system. This unusual presentation of benign liver cyst leading to stricture of bile and pancreatic duct by extrinsic compression is worth a report.
1292 Combined Postcholecystectomy Bile Leak and Benign Biliary Stricture—Should a Temporary Placement of Fully Covered Self-Expanding Metal Stent Be the First Choice?
Authors: Al-Chalabi Ahmed , Kobeissy Abdallah , Javaid Toseef , Nawras Ali
Published: October 2019

INTRODUCTION:

Bile leaks are common complications seen after cholecystectomy. Endoscopic Retrograde Cholangiopancreatography (ERCP) with the establishment of an enhanced transpapillary flow – through biliary stent placement and/or sphincterotomy – is considered the standard of care and usually has high success rates. Failure of initial endoscopic therapy (complex bile leak) can be managed with the placement of a fully covered self-expanding metal stent (FCSEMS) or surgery. We present a patient in which large postcholecystectomy biloma developed despite the presence of biliary plastic stent in place.

CASE DESCRIPTION/METHODS:

48-year-old female with history of chronic pancreatitis and benign distal biliary stricture was admitted with worsening abdominal pain for the last 2 days. One month prior to this episode, the patient was admitted with the diagnosis of acute on chronic pancreatitis. She underwent ERCP with balloon dilatation and placement of plastic biliary (10 Fr × 10 cm) and pancreatic duct (5 Fr × 7 cm) stents. She had cholecystectomy prior to her discharge. Her abdominal pain on readmission was associated with nausea, vomiting, loss of appetite. She has chronic loose stools, which remained unchanged. She denied fevers, chills, or hematemesis. Her vital signs were within normal range. Abdominal exam revealed sluggish bowel sounds and right upper quadrant abdominal tenderness. She had elevated white cell count at 13,900/µL. The rest of the labs including kidney and liver function tests were unremarkable. CT scan of the abdomen showed moderate to large subcapsular and intraperitoneal fluid. There was mild dilatation of the common bile duct with the biliary and pancreatic duct stents in place. Findings were consistent with post-cholecystectomy biliary leak. A right upper quadrant pigtail drain was placed followed by ERCP. Cystic duct stump bile leak was diagnosed and treated with placement of FCSEMS. The patient tolerated the procedure well with improvement of symptoms. Bile leak resolved and FCSEMS was removed after three months.

DISCUSSION:

Patients with postcholecystectomy bile leak superimposed on a benign biliary stricture are probably appropriate candidates for endoscopic therapy with FCSEMS. Despite their higher costs, initial temporary placement of FCSEMS may obviate additional ERCP sessions in cases of failure of plastic stents. FCSEMS improve drainage since they have larger lumens. They should be considered especially in the presence of biliary prestenotic duct dilatation and high-grade leaks.
1293 Non-Steroidal Anti-Inflammatory Drug-Induced Acute Pancreatitis: A Case Report
Authors: Reyes Jonathan M. , Gonzalez Manuel O. , Patel Bhavin , Malik Fahad , Weissman Simcha
Published: October 2019

INTRODUCTION:

Ibuprofen-induced acute pancreatitis, a diagnosis secondary to the use of non-steroidal anti-inflammatory drugs (NSAID) is an extremely rare occurrence. Common culprits such as obstruction, alcohol consumption, infection, direct trauma, and medication (sans NSAID) adverse effect can be attributable to the majority of cases reported. The following case report describes a patient with acute pancreatitis secondary to a 3-week use of Ibuprofen for chronic shoulder pain. Alternative causes of acute pancreatitis were excluded through the patient's clinical history, laboratory findings, and diagnostic imaging. Although a rare risk factor, our aim is to further demonstrate that patients with chronic NSAID use can develop these complications and should be considered among the differential diagnoses.

CASE DESCRIPTION/METHODS:

Our patient was a 44 yo F with significant past medical history of hyperlipidemia, cholelithiasis status post cholecystectomy (2003), and acute pancreatitis (2010) secondary to choledocholithiasis who presented with a 2-week history of abdominal pain. The pain was described as an intermittent burning pain, rated 8/10 that radiated to the back. It was associated with nausea, vomiting and diarrhea but not associated with eating. She reported that she did not use any palliative measures for the pain, but indicated that she had been taking 800 mg Ibuprofen every 8 hours for the past 3 weeks for an acute flare of chronic right shoulder pain. She denied recent travel, sick contacts at home, or any change in eating habits. She also denied Ibuprofen use during the last episode of acute pancreatitis in 2010. She was a non-tobacco smoker, non-alcohol drinker, and did not use any illicit drugs.

DISCUSSION:

The incidence of drug-induced pancreatitis is low and generally includes HMG-CoA Reductase Inhibitors, ACE Inhibitors, Oral Contraceptives/Hormone Replacement Therapy, diuretics, HAART therapy, and Valproic acid as some of the more common offending agents. The mechanisms of these drugs are not well known but one case report of ibuprofen – induced pancreatitis suggests a possible mechanism related to a reduction in systemic glutathione, which therefore prevents an appropriate response against oxidative stresses. In this case of suspected diagnosis of Ibuprofen-induced acute pancreatitis, we did not perform a re-challenge test on the patient to confirm the suspected diagnosis; however, the patient demonstrated no other contributing factors that could be linked to the condition.
1297 Cheers to Budd: Pyogenic Liver Abscess Complicated by Acute Budd-Chiari Syndrome
Authors: Gupta Kamesh , Hans Bandhul , Rawat Saumya , Jobbins Kathryn
Published: October 2019

INTRODUCTION:

Amebic liver abscess (ALA) is the most common extraintestinal manifestation of amebiasis with high mortality rates (20%). Complications include rupture; superinfection; anemia; and rarely vascular thrombosis. Budd-Chiari syndrome is characterized by post-sinusoidal portal hypertension caused by obstruction of either major hepatic veins or the inferior vena cava.

CASE DESCRIPTION/METHODS:

A 54-year-old alcoholic male, with a history of recent travel to India, presented with 2 weeks of fever, vomiting and abdominal pain. On exam, he was febrile, icteric, with generalized abdominal tenderness. Chemistries revealed WBCs 12000/mm3, total/direct bilirubin 6.5/3 mg/dL, AST/ALT 410/318 U/L, and ALP 310 U/L. USG RUQ showed hepatomegaly with multiple, thick-walled areas of central low attenuation, suspicious for LA. CT confirmed the presence of multiple ALAs along with rupture and delayed filling in the left and middle hepatic veins. Under USG guidance, brownish fluid (anchovy sauce-like) was aspirated and a pigtail catheter was placed. He was started on ceftriaxone and metronidazole for the treatment of pyogenic LA. Fluid serology was positive for Entamoeba histolytica and only metronidazole was continued for 21 days, along with rivaroxaban for six months for the treatment of Budd Chiari syndrome. His liver enzymes normalized in 21 days and a follow-up USG after 48 days of treatment with rivaroxaban showed no evidence of thrombosis in hepatic veins and IVC.

DISCUSSION:

ALA should be suspected in patients with fever & jaundice with a history of recent travel to an endemic area. The rates of complications are high, commonest being an abscess rupture. Thrombosis of IVC, hepatic and sometimes right atrium, are rare complications, caused by either direct spread of inflammation or external mechanical compression by the abscess. A diagnosis of Budd-Chiari syndrome should be considered in cases of prolonged fever unresponsive to treatment or ascites with leg edema and collateral abdominal venous circulation. Underlying prothrombotic affection must be excluded. To conclude, identifying a treatable cause of Budd-Chiari syndrome, such as liver abscess, can result in early, effective, and life-saving treatment.
1301 Bleeding Pancreaticoduodenal Fistula: An Unusual Case of Melena
Authors: Ahmed Zarir , Al-Taee Ahmad M. , Boumitri Christine
Published: October 2019

INTRODUCTION:

Pancreatic fistulas have been described in the setting of pancreatic resection, trauma, and less commonly in acute or chronic pancreatitis (CP). Spontaneous pancreatic fistulas resulting in gastrointestinal (GI) bleeding are rare.

CASE DESCRIPTION/METHODS:

An 80 year-old woman presented to the emergency room with shortness of breath and melena. She was afebrile, normotensive, and had a heart rate of 93. Labs showed hemoglobin (Hgb) of 5.2 g/dL. EGD showed a 2 mm clean-based duodenal ulcer. As this did not account for melena, she had a colonoscopy and video capsule endoscopy which did not show a clear source of bleeding. As she continued to have melena with drop in Hgb, she had an abdominal CT scan showing a retroperitoneal fluid collection medial to the 2nd and 3rd portions of the duodenum, hyperattenuating material in the 2nd portion of the duodenum concerning for bleeding, and signs of CP with a pancreatic duct (PD) diameter of 14 mm. A second look EGD showed a duodenal mucosal defect suspicious for a fistulous opening into the PD with evidence of active bleeding (Figures 1 and 2). Repeat CT scan revealed extraluminal contrast extravasation into the retroperitoneum medial to the 2nd part of the duodenum and close in proximity to the superior mesenteric vein (SMV) (Figure 3). Abdominal MRI showed signs of CP and multiple small pseudocysts in the body and tail. Patient's melena resolved and Hgb stabilized prior to discharge.

DISCUSSION:

Bleeding is a rare complication of CP and occurs in 10-15% of CP patients. Pancreatic structures can be destroyed by enzyme digestion and necrosis. This may create pseudoaneurysms which may create cavities, fistulas, or rupture if they involve arterial or venous structures. The splenic and gastroduodenal artery are most commonly involved. Clinical presentation varies depending on location and severity of bleeding. Diagnosis involves abdominal CT and EGD, however laparotomy may sometimes be needed. Management involves embolization or surgery. Our patient's pancreaticoduodenal fistula was the result of previously undiagnosed CP. Bleeding may have resulted from spontaneous hemorrhage into the cystic cavity or as a result of erosion into the SMV given proximity on imaging. This case highlights the need to maintain a high clinical suspicion for pancreaticoduodenal fistulas in patients with a history of pancreatic disease presenting with GI bleeding.
1302 Bouveret's Syndrome: An Overlooked Cause of Duodenal Obstruction
Authors: Kothari Shana , Kobeszko Matthew , Kalinowski Michael , Almouradi Tarek
Published: October 2019

INTRODUCTION:

Bouveret's syndrome is a rare clinical entity of gastric outlet obstruction from an impacted gallstone in the pyloric channel or duodenum. The stone travels from the biliary tree via a fistulous tract, formed in the setting of cholecystitis or pericholecystic inflammation. Diagnosis is typically made by computed tomography or magnetic resonance imaging, and treatment is focused on disimpaction via endoscopic, laparoscopic, or open intervention. We report a case of Bouveret's syndrome causing duodenal obstruction that was endoscopically managed with fusion lithotripsy basket extraction.

CASE DESCRIPTION/METHODS:

Patient is an 85 year-old male with a history of hypertension and coronary artery bypass grafting that presented with severe upper abdominal pain, vomiting, and melenic stools for three days. Vital signs were within normal limits. Laboratory data was significant for mild leukocytosis (11.7 thousand/mcl) and anemia (11.7 gm/dL; baseline 13 gm/dL). Abdominal ultrasound and computed tomography without contrast of the abdomen/pelvis revealed large gallstones, suspicious biliary air with intrahepatic ductal extension, superimposed gallbladder wall thickening suggestive of possible cholecystitis, and inflammatory changes extending to the distal stomach. Antibiotic therapy with piperacillin-tazobactam was initiated. Patient underwent esophagogastroduodenoscopy for evaluation of melena, which showed ulcerative esophagitis, erosive gastritis, and a large gallstone in the duodenal sweep with surrounding ulceration causing duodenal obstruction. Endoscopic lithotripsy with stone crushing basket was performed to fragment the large gallstone in smaller retractable pieces. For further evaluation, endoscopic retrograde cholangiopancreatography was performed and notable for a cholecystoduodenal fistula. Given his clinical state, the patient was not a surgical candidate during the hospitalization, but was recommended to follow up with general surgery outpatient.

DISCUSSION:

Bouveret's syndrome is commonly missed in clinical practice when it is not considered in the setting of intestinal obstruction, especially in males with no history of gallstone disease as seen in our patient. There are no formal management guidelines of this condition. However, endoscopic extraction with or without lithotripsy is preferable, particularly in cases when the patient is a poor candidate for surgical enterolithotomy. It is imperative to facilitate early diagnosis to improve prognosis and prevent adverse outcomes.
1305 A Genetically Rare Cancer Singled Out Just in Time: Pancreatic Neuroendocrine Tumor
Authors: Alegre-Boschetti Sergio M. , Betancourt-Guzmán Natalia , Diaz Carolina , De Jesús Henry , Fernández Carlos , Magno Priscilla
Published: October 2019

INTRODUCTION:

Pancreatic neuroendocrine tumors (PNETs) are rare neoplasms that account for 1-2% of all pancreatic tumors. PNETs can manifest at any age, although, they occur commonly after the fourth decade of life. We herein report a patient diagnosed and managed for nonfunctioning PNET. It is important to acknowledge that these malignant tumors might have an insidious presentation.

CASE DESCRIPTION/METHODS:

46-year-old male patient presented with unintentional 25-lb weight loss over 8 months with associated symptoms of weakness and decreased oral intake. Patient without major medical history and family history of gastric cancer, as well as, breast cancer. His physical examination was unremarkable. Initial laboratory workup including CBC, CMP, serum CA-19-9, IgG4, serum chromogranin A and serum neuron specific enolase were unremarkable. CT scan of the abdomen and pelvis, ordered for evaluation of unexplained weight loss, demonstrated a large lobulated mass replacing most of the pancreatic body and tail with loss of cobblestoning with several distinct peripancreatic soft tissue nodules. PET/CT revealed severe hypermetabolic lesion involving the body and tail of the pancreas. An endoscopic ultrasound with fine-needle biopsy of the pancreatic mass (3 cm × 2 cm) revealed a PNET. Immunohistochemical panel such as CK7, synaptophysin, and chromogranin were positive and CD34 as well as Pan-CK were non-contributory. Patient underwent a successful distal pancreatectomy, splenectomy, and removal of regional nodes without any complications. Histology confirmed a well differentiated PNET intermediate-grade (G2) with 2-20 mitosis/2 mm2, Ki-67 index of 3%-20%, and the tumor only involved the pancreas. A somatostatin receptor scintigraphy scan, using octreotide, was normal without evidence of any somatostatin avid lesions. The patient is currently under the care of the Gastroenterology and Hematology & Oncology service.

DISCUSSION:

PNETs are generally indolent malignancies and clinical manifestations can vary from abdominal pain, weight loss, anorexia, nausea, jaundice, palpable mass on physical exam or symptoms attributed to metastatic disease. No risk factors like smoking, diabetes, nor history of chronic pancreatitis were identified. It is of great importance to raise awareness of malignancy symptoms. This case demonstrates how a complete history and physical exam can lead to early identification of a curable malignancy, having a positive impact on the patient survival and quality of life.
1314 Lemmel Syndrome in a Centenarian
Authors: Mirza Zeyn , Fernández Carlos , Tirado Francisco , Martin-Ortiz Jose
Published: October 2019

INTRODUCTION:

Obstructive jaundice can be caused by intraluminal forces (choledocholithiasis), extraluminal forces (carcinoma) or transmural forces (choledochal cysts). In addition to the above, a rare cause of obstructive jaundice includes periampullary diverticula - Lemmel's syndrome. This syndrome involves a periampullary duodenal diverticulum that can compress the common bile duct resulting in obstructive jaundice. These diverticula are extraluminal and their prevalence increases with age and given that the majority are asymptomatic, they can be overlooked in imaging studies. It is estimated that 5% of patients experience acute symptomatology due to these diverticula.

CASE DESCRIPTION/METHODS:

This is the case of an over 90-year-old male with medical history of hypertension and Alzheimer's dementia who came to the ER due to right upper quadrant abdominal pain the day prior to admission. Physical wasexam remarkable for epigastric and right upper quadrant tenderness. Labs with transaminitis (ALT:1294 U/L, AST: 1166 U/L), alkaline phosphatase 366 U/L, total bilirubin 3.2 mg/dL, amylase: 123 U/L, lipase: 98 U/L). Abd/pelvic CT scan reported prominence of the intrahepatic and extrahepatic biliary system. The common bile duct measuring 8-9 mm, proximal pancreatic duct dilated approximately 4 mm, and the common bile duct extending to a large duodenal diverticulum without evidence of choledocholithiasis. Considering the patients advanced age, he was treated with conservative medical management including antibiotic therapy.

DISCUSSION:

This case highlights the importance of taking a holistic approach to patient care especially patients of advanced age who may have findings suggestive of a diagnosis that is overlooked as it is uncommon. The literature states that the detection rate of duodenal diverticula ranges from 1% to 27%. In addition, the majority of peri-ampullar diverticula are asymptomatic however 5% of cases can present with bleeding, jaundice or intestinal obstruction. Misdiagnosis of this condition may lead to erroneous management and delay in treatment in patients who are able to receive aggressive management.
1316 A Rare Congenital Anomaly Unveiled in an Octogenarian
Authors: Mirza Zeyn , De Jesús Henry , Estremera Rodolfo , Martin-Ortiz Jose , Toro-Lugo Doris
Published: October 2019

INTRODUCTION:

Congenital agenesis of the gallbladder is a rare anomaly that occurs during embryonic development with an average incidence of 0.02% at birth. The clinical presentation is varied as patients may be asymptomatic; therefore, isolated gallbladder agenesis is usually discovered incidentally on imaging. Up to 50% of patients may present with symptoms similar to a biliary colic, such as right upper quadrant pain, nausea, vomiting and jaundice. We present an interesting case of an octogenarian who was first diagnosed with gallbladder agenesis after presenting with obstructive jaundice due to choledocholithiasis.

CASE DESCRIPTION/METHODS:

This is the case of an 88 year-old male with past medical history of hypertension and chronic kidney disease, presented to the emergency department with right upper quadrant abdominal pain, nausea and non-bloody vomits. He appeared acutely ill with pain in the right upper quadrant. Laboratory tests were remarkable for a cholestatic pattern. Total bilirubin 5.1 mg/dL, alkaline phosphatase 676  IU/L, AST 167 IU/L, and ALT 111 IU/L. There was prior history of exposure to Hepatitis A. Hepatitis B and Hepatitis C were negative. In view of the clinical presentation, an abdominal ultrasound was done. There was evidence of choledocholithiasis with extensive intra and extrahepatic duct dilation. At the gallbladder fossa, there was “WES sign” indicating a gallbladder full of stones. The patient was admitted to the hospital and underwent ERCP with a sphincterotomy with stones extraction. The gallbladder was not visualized. An abdominopelvic CT and HIDA scan confirmed its absence.

DISCUSSION:

Gallbladder agenesis is a rare entity and seldomly diagnosed for the first time in the ninth decade of life. It is estimated that 25%-50% of this subset of patients may develop choledocholithiasis. The association between these two entities is hypothesized to be similar to post-cholecystectomy syndrome: biliary dyskinesia may favor stone formation. In addition, hypertonic contractions of the sphincter of Oddi may lead to common duct dilation, biliary stasis and also predispose to calculi formation. This case provides an important point to increasing awareness of this condition to avoid misdiagnosis, unnecessary procedures and prolonged hospitalizations. In patients who present with biliary colic, jaundice with equivocal gallbladder imaging findings, the possibility of gallbladder agenesis should be entertained.
1318 Pancreaticopleural Fistula in a Patient With Recurrent Alcoholic Pancreatitis: Combined Endoscopic and Medical Management
Authors: Ferreira Kaio S. , Arsenault John J. , Pan Jason , Harmatz Alexander , Moss Steven F.
Published: October 2019

INTRODUCTION:

Pancreaticopleural fistula (PPF) is a rare complication of pancreatitis, resulting from disruption of the pancreatic duct. This injury may be secondary to acute/chronic pancreatitis, trauma, or surgery. Here we describe a patient with a PPF, and our workup and treatment for this rare condition.

CASE DESCRIPTION/METHODS:

A 61-year-old male with COPD, alcohol misuse, and history of recurrent acute alcoholic pancreatitis complicated by pseudocysts was admitted with one month of worsening shortness of breath from a large left pleural effusion, which reaccumulated within four days after a 1.6 L thoracentesis. On examination he had mild abdominal tenderness in the RUQ and epigastrium. Labs were notable for serum amylase 1105 U/L, lipase >1000 U/L, and WBC 10.8. He underwent another thoracentesis, removing 1.5 L of fluid which was an exudate with amylase greater than 2000 U/L. CT of the chest and abdomen showed a subdiaphragmatic LUQ fluid collection with communication to the pancreatic body and duct. A chest tube was then placed to prevent fluid re-accumulation. MRCP confirmed a PPF from the proximal pancreatic body duct to the left pleura. He was started on octreotide. ERCP confirmed a fistula originating from the distal pancreatic duct but attempts to pass a wire into the dorsal pancreatic duct were unsuccessful, and a ventral pancreatic sphincterotomy was performed. His chest tube was removed after one day, and he was discharged to continue octreotide at home. Unfortunately, he returned the following day with complaints of dyspnea. Pancrelipase was then added in an attempt to minimize pancreatic exocrine secretions. On follow-up 1 and 2 months later, the pleural fluid is much smaller, and the patient's dyspnea has resolved.

DISCUSSION:

Here we present a novel management of PPF without pancreatic duct stent placement and instead with pancreatic sphincterotomy to divert pancreatic secretions away from the fistula tract and medical therapy (octreotide and pancrelipase) to reduce the pancreatic secretion. The diagnosis was reached through a combination of clinical history, lab studies (particularly, the elevated amylase in the pleural fluid), and CT and MR imaging. This was further confirmed with ERCP, which is useful especially if a stent can be placed to divert secretions away from fistula tract. Ultimately, this diagnosis requires a high index of suspicion, particularly in patients who present with recurrent effusions in the setting of pancreatitis.