Pantoprazole Infusion Research Articles

Anaphylaxis Caused by Taking Pantoprazole: Case Series.

Pantoprazole is one of the most widely used proton pump inhibitors, but anaphylaxis occurs rarely during its use. The purpose of reporting these two cases is to show that pantoprazole is not a drug without problems; it can also cause anaphylactic reactions. A 42-year-old woman presented to the emergency department due to dyspeptic complaints. Immediately at the end of the infusion of pantoprazole, there started to be numbness of the tongue, itching all over the body, and difficulty in breathing. Half an hour after taking a pantoprazole 40 mg capsule, a 58-year-old woman started to experience redness of the face, thickening of the tongue, itching, bloating, and dizziness. Arterial pressure was 80/60 mmHg, pulse 150/minute, while saturation had dropped to 88%. In both cases, fluids, adrenaline, antihistamines, methylprednisolone, and calcium were immediately started. After the improvement of their general conditions, both patients were discharged home. The first case relates to anaphylaxis after the intravenous administration of pantoprazole, and the second case relates to the appearance of anaphylaxis after its oral administration. Health workers need to be informed about the possibility of anaphylaxis in patients taking both oral and parenteral pantoprazole. PPIs are generally safe, with a low percentage of side effects of 1-3%.Although hypersensitive reactions to PPIs are rare, cases of anaphylactoid reactions have also been reported in the literature.Anaphylaxis caused by taking pantoprazole should be considered in the differential diagnosis of anaphylaxis in both oral and parenteral administration of the drug.Doctors and pharmacists should be very careful when prescribing pantoprazole and other PPIs, especially to the elderly.

Upper GI bleeding in rural Australia: general surgery still alive and well!

The complex and critically unwell upper gastrointestinal bleeding (UGIB) patient is a common emergency presentation in Australia. Managed medically and endoscopically by rural general surgeons in rural and remote Australian hospitals which lack a gastroenterology service, this can be ameliorated by clear evidence-based guidelines. A single-centre retrospective review of adult patients who underwent emergency gastroscopy for UGIB at the Mackay Base Hospital, January 2019 to January 2022. Detailed patient data from the assessment, resuscitation, time to endoscopy, endoscopic intervention, and outcomes were compared against key international gastroenterology society safety and quality standards for UGIB. Two hundred patients had a comprehensive initial assessment and resuscitation with PRBC (39%), anticoagulation reversal (18%), pantoprazole infusion (81%), tranexamic acid (10.50%) and octreotide (16.50%). Risk scores were calculated retrospectively as none were documented. Time-to-endoscopy targets were achieved in over 70% of variceal or non-variceal UGIB patients. Bleeding was found in 59.50% of patients but 63% of patients did not require a manoeuvre to stop the bleeding. Post-operative complications were scarce. This study reflects on the need for a local multidisciplinary protocol to help expedite the current high-quality healthcare delivered by rural general surgeons in managing patients with UGIB. Implementing risk assessment scores would shorten the time to endoscopy in the initial assessment Guidelines would optimize resuscitation ensuring appropriate replacement, medication administration, anticoagulation reversal, and preventing unnecessary therapy. Despite these nuisances, the time to endoscopy, endoscopic intervention, and patient outcomes were largely in line with international quality assurance and safety targets.

Upper digestive bleeding secondary to duodenal infiltration due to pancreatic cancer: a therapeutic challenge.

A 68-year-old woman with stage IV pancreatic adenocarcinoma (liver and lymph node metastases) on first-line treatment with gemcitabine. As a non-oncological comorbidity, the patient was anticoagulated with enoxaparin 8000 IU/24 hours because she had a mitral valve prosthesis. The patient made a medical consultation for presenting vomits which looked like coffee grounds and melaena. In the complete blood count, a hemoglobin of 7.5 g/dL was detected. Transfusion support, pantoprazole infusion (80 mg in 500 cc of 0.9% SSF every 12 hours) and parenteral nutrition were prescribed. Tranexamic was not prescribed due to the patient's cardiological history.

S2282 Black Esophagus Manifesting as Upper Gastrointestinal Bleeding in Diabetic Ketoacidosis: A Case Report

Introduction: Acute esophageal necrosis, or black esophagus, is a rare clinical entity manifesting as upper gastrointestinal bleeding and complicating various conditions. However, black esophagus in the setting of diabetic ketoacidosis (DKA) has been rarely reported. We present a case of a 36-year-old male with black esophagus presenting as hematemesis complicating an episode of DKA. Case Description/Methods: A 36-year-old male with uncontrolled type 1 diabetes mellitus complicated by end-stage renal disease and hypertension presented to the emergency department with abdominal pain, nausea, and vomiting. Patient reported worsening abdominal pain and associated blood-tinged emesis. On presentation, patient was hemodynamically stable. Physical exam included an abdomen that was diffusely tender to palpation without peritoneal signs. Initial labs remarkable for serum glucose 1491, anion gap 41, bicarbonate 9, and hemoglobin 7.5. Patient was admitted to Critical Care for insulin drip and intravenous fluid resuscitation for DKA. Later, patient had an episode of hematemesis resulting in tachycardia, hypotension, and drop in hemoglobin to 5.6. Patient was further resuscitated with blood transfusions with improvement in hemodynamics and hemoglobin to 8.9. Continuous pantoprazole infusion was initiated. Upper endoscopy demonstrated severe, ulcerative necrotizing circumferential esophagitis in the middle and lower third esophagus and a medium size blood clot without evidence of active bleeding. No biopsies were taken due to concern for possible false lumen; CT chest with contrast demonstrated no signs of esophageal perforation. Following EGD, patient had several small self-limiting episodes of hematemesis and melena, while maintaining hemodynamics. He was continued on pantoprazole infusion and placed on strict nothing by mouth (NPO) precautions for 3 days with gradual advancement of diet. He received 6 days of empiric antimicrobial therapy with ampicillin-sulbactam and fluconazole. Patient reported no further episodes of hematemesis. Hemoglobin stabilized around 8.0 (Figure). Discussion: DKA is a rare but life-threatening cause of acute esophageal necrosis which may develop due to a combination of tissue hypoperfusion, impaired mucosal defenses, and gastric reflux. Upper gastrointestinal bleeding in the setting of DKA should raise suspicion for black esophagus which is a potential cause of mortality. Early diagnosis and treatment of underlying etiology are the key factors in management.Figure 1.: Severe, ulcerative necrotizing circumferential esophagitis in the middle and lower third esophagus and a medium size blood clot without evidence of active bleeding.

S709 Proton-Pump Inhibitor Infusion Misuse in the Community Hospital Setting

Introduction: Proton pump inhibitors (PPIs) are the most potent acid suppressants available. Several studies have shown that in hospitalized patients with acute upper gastrointestinal (GI) bleeding from peptic ulcer disease, high-dose PPI therapy via continuous infusion reduces the rate of high-risk bleeding lesions (active bleeding, visible vessel, adherent clot) on initial endoscopy. While the benefits of PPI infusions have been clearly described for these specific indications, they are often over-prescribed to inpatients. Our study aim was to determine the rate of misuse in a tertiary care community hospital setting. Methods: A retrospective cohort study was conducted at Lankenau Medical Center, a 370 bed community hospital. The usage of pantoprazole infusion was determined among hospitalized patients between March 1, 2018 and March 1, 2021 through review of the EPIC electronic medical record system. Appropriate candidates for pantoprazole infusion were defined as patients with hematemesis, melena, coffee-ground emesis, or hematochezia with hemodynamic instability. All other indications were categorized as inappropriate. Variables including age, sex, race, serum hemoglobin at the time of PPI infusion initiation, and antiplatelet use were collected. The rate of PPI infusion misuse was determined. Factors which significantly affected utilization of PPI infusion were determined through multivariate analysis. Results: A total of 348 pre-endoscopic PPI infusions were ordered during the three-year period. Approximately 35% of these prescriptions were ordered without an appropriate indication. The mean age of patients who were prescribed PPI infusions was 68.8 years. 48.6% were on an antiplatelet agent. The only significant variable between patients who were given a PPI infusion for an appropriate versus inappropriate indication was age, where the mean patient age was 68.8 compared to 71.1 years (p=0.04). Patient sex, race, antiplatelet use, and hemoglobin value did not significantly affect PPI infusion use. (Table) Conclusion: Pre-endoscopic PPI infusion was prescribed inappropriately in 34.8% of patients in a community hospital setting. Misuse of this drug leads to unnecessary healthcare costs and reflects poor understanding among prescribers of its appropriate clinically indicated uses. While PPIs are generally regarded as safe, misuse can increase the risk of adverse side effects. A follow-up study looking at a quality improvement intervention will follow this study. Table 1. - Characteristics and Multivariate Analysis of PPI Infusion Misuse Inappropriate PPI Infusion No Yes Total p-value n = 227 n = 121 n = 348 Age (Mean/SD) 67.6 (14.8) 71.1 (15.1) 68.8 (15.0) 0.04 Sex 0.571 Male 131 (57.7%) 66 (54.6%) 197 (56.6%) Female 96 (42.3%) 55 (45.5%) 151 (43.4%) Race 0.705 White 104 (46.0%) 59 (48.8%) 163 (47.0%) Black 112 (49.6%) 55 (45.5%) 167 (48.1%) Other 10 (4.4%) 7 (5.8%) 17 (4.9%) Ethnicity 0.12 Not Hispanic 225 (99.6%) 116 (97.5%) 341 (98.8%) Hispanic 1 (0.4%) 3 (2.5%) 4 (1.2%) Total Number of Antiplatelets 0.629 0 121 (53.3%) 58 (47.9%) 179 (51.4%) 1 70 (30.8%) 41 (33.9%) 111 (31.9%) 2 36 (15.9%) 22 (18.2%) 58 (16.7%) Antiplatelet Type (n = 169 Yes Only) Aspirin 103 (45.4%) 61 (50.4%) 164 (47.1%) 0.37 Clopidogrel 36 (15.9%) 23 (19.0%) 59 (17.0%) 0.456 Ticagrelor 4 (1.8%) 4 (3.3%) 8 (2.3%) 0.456 Prasugrel 1 (0.4%) 0 1 (0.3%) 1 Last Hemoglobin (Mean/SD, g/dl) 8.9 (2.6) 8.6 (2.9) 8.8 (2.7) 0.344 Missing Hemoglobin 19 8 27 Transfusion Units (median/IQR) 2 (0-6) 2 (0-4) 2 (0-5) 0.478

Effect of tranexamic acid on the treatment of patients with upper gastrointestinal bleeding

Objective: To determine the efficacy of tranexamic acid (TXA) in the management of acute upper gastrointestinal (GI) bleeding. Methods: A total of 70 patients with acute upper GI bleeding were included in this double-blinded randomized controlled clinical trial from September 2018 to December 2018. Patients were divided into the control group (received fluid therapy and intravenous infusion of pantoprazole, 35 cases) and the TXA group (received intravenous TXA besides the treatment of control group, 35 cases). Rebleeding, admission duration, and need for blood transfusion were compared between the two groups. Results: Fifteen patients (42.9%) in the TXA group and 10 patients (28.6%) in the control group stayed in hospital for more than 3 days during their admission (P=0.21). Rebleeding occurred in 8 patients (22.9%) and 5 patients (14.3%) of the TXA group and the control group, respectively (P=0.35). More patients in the TXA group (21 cases, 60%) received blood transfusion than the control group (8 cases, 22.9%) (P=0.02). Conclusions: TXA did not improve the outcome of patients with acute upper GI bleeding.

S2162 Hemorrhagic Shock Following a Secretin Stimulating Test

INTRODUCTION: Zollinger-Ellison Syndrome (ZES) is a rare disorder resulting from inappropriate gastrin release, which causes acid hypersecretion and the development of peptic ulcer disease (PUD), severe gastroesophageal reflux, and diarrhea. Diagnosing ZES is challenging in the age of PPIs. Furthermore, discontinuing PPI therapy in patients with suspected ZES can be dangerous and even life-threatening. CASE DESCRIPTION/METHODS: A 44 y.o. male with a history of PUD presented for evaluation for ZES. Due to concern for ZES, a secretin-stimulating test was ordered. One week prior to his test he was instructed to stop his PPI and start Ranitidine 450 mg every 6 hours until 24 hours prior to the test. Immediately following the secretin-stimulating test he presented to the emergency room with nausea, vomiting, and profuse watery diarrhea. A pantoprazole infusion at 8 mg/ hr was started. Overnight he became tachycardic and developed about 400cc of hematemesis. His Hbg dropped from 10.3 g/dL to 7.7 g/dL. He subsequently developed hemorrhagic shock requiring intubation and transfer to the ICU. On EGD, he had a large clot in the second portion of the duodenum. He had hematin in the stomach and over 10 ulcers in the duodenum (Image 1). The pantoprazole infusion was increased to 12 mg/hr with no further recurrence of hemorrhage. The secretin stim test returned, confirming the diagnosis of ZES. This was followed up with an Octreotide scan, which revealed increased radiotracer near the second portion of the duodenum, confirming the location of the gastrinoma (Image 2). DISCUSSION: This case illustrates a rare complication of a patient with suspected ZES undergoing a secretin stimulating test. In patient’s with ZES, a secretin stimulating test causes a paradoxical gastrin response to secretin, likely from secretin receptors on tumor cells (Image 3). Furthermore, PPI withdrawal can cause rebound acid secretion, which can lead to exaggerated acid hypersecretion in patient's with ZES. Our patient had an exaggerated response to secretin leading to acid hypersecretion causing PUD, diarrhea, and hemorrhagic shock. Although complications from a secretin stimulating test are rare, in patients with prior UGIB and high suspicion for ZES, a secretin-stimulating test may need to be performed in a controlled hospitalized setting to minimize complication. This case further illustrates how the diagnosis of ZES has become difficult and whether we need to propose new diagnostic criteria to avoid complications in establishing a diagnosis.Figure 1.: Image 1. Large Clot and Multiple Ulcers (Yellow Arrows) in the Duodenum.Figure 2.: Image 2. Markedly increased radiotracer uptake in a soft tissue nodule medial to the second portion of the duodenum, suggestive of a neuroendocrine tumor (confirmed to be gastrinoma by surgical resection).Figure 3.: Image 3. A. In the antrum, exogenous secretin stimulates gastrin secretion directly and concomitantly inhibits gastrin secretion by stimulating somatostatin (SST) secretion, resulting in little or no gastrin release. B. In patients with ZES, because the gastrinoma does not contain functionally coupled SST cells, the effect of secretin is solely to stimulate gastrin secretion from the tumor.

A177 AN UNUSUAL CULPRIT OF AN UPPER GASTROINTESTINAL BLEED IN A PAEDIATRIC PATIENT

Abstract Background Leiomyomas are benign tumors originating from mesenchymal cells in the muscularis propria that present equally among the sexes usually as localized lesions after the fifth decade. Though rare, esophageal leiomyomas (EL) make up the majority of benign esophageal tumors and are typically located distally. Of all known cases, 2.6% are paediatric. In this population they are 1.71 times more common in females and are often diffuse. Most are slow growing and asymptomatic but when >5cm patients describe dysphagia, vomiting, pain, cough and anorexia. Gastric leiomyomas causing upper gastrointestinal bleeding (UGIB) in adults are reported. Aims To discuss a rare cause of UGIB in a child. Methods Case report. Results We present a 16-year-old Asian boy with no significant past medical history who was transferred to our institution for an UGIB following 3 days of dark black stools, 1 day of coffee ground emesis and pre-syncope. There was no history of non-steroidal anti-inflammatory use. At presentation he was in shock and received fluid resuscitation and a pantoprazole infusion. His hemoglobin dropped to 81 from 150g/L and corrected with 2 units of packed red blood cells. He was pale, non-dysmorphic with no cutaneous lesions, abdomen was non-distended and non-tender with no masses or hepatosplenomegaly. An abdominal ultrasound showed mild bowel wall thickening in the cecum and terminal ileum. Emergent upper endoscopy identified an ulcerated sessile mass at the gastro-esophageal junction. Biopsies revealed polypoid inflamed gastric mucosa with a focal intestinal metaplasia, negative for malignancy. Magnetic resonance scan characterized a 3.8x4.3x2.5cm lesion in the stomach cardia not extending beyond the serosa with suggested causes including EL and gastrointestinal stromal tumor (GIST). Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) demonstrated a 2.8x1.8cm well circumscribed homogenous hypoechoic mass in the muscularis propria of the distal esophagus. Histopathology showed bland tumor cells with eosinophilic cytoplasm and nuclei that did not demonstrate atypia. Immunohistochemistry (IHC) stains were positive for smooth muscle actin and desmin. CD117, S-100 and DOG1 were negative. Findings were therefore in keeping with a leiomyoma and not a GIST. He was referred to the Cancer Genetics clinic for consideration of hereditary leiomyomatosis renal cell cancer and General Surgery for resection. Conclusions This case highlights a rare cause of UGIB in a child. EL are scarcely found in children and at present there are no reports of EL causing UGIB. They can be associated with Alport Syndrome or Familial Leiomyomatosis. IHC is an essential diagnostic tool, enabling differentiation of EL from GIST which is important as the latter has malignant potential. EL can be monitored with endoscopy if small but are surgically resected if symptomatic, ulcerated, or growing. Funding Agencies None

1958 An Unusual Ca(u)se of Upper Gastrointestinal Bleeding

INTRODUCTION: Duodenal varices (DVs) represent 17% of ectopic varices (EVs), have a 4-fold increased bleeding risk when compared to esophago-gastric varices (EGVs), and mortality rate up to 40%. There are no guidelines on the ideal management of DVs. We report a case of massive hemorrhage secondary to DV managed successfully with transjugular intrahepatic portosystemic shunt (TIPS). CASE DESCRIPTION/METHODS: A 69-year-old gentleman presented with hematemesis, hematochezia, dizziness and near-syncope. He was diagnosed with cryptogenic cirrhosis, non-alcoholic steatohepatitis in the past after negative autoimmune and infectious work-up. Prior doppler ultrasound showed elevated portal flow velocity; esophagogastroduodenoscopy (EGD) a month prior revealed portal hypertensive gastropathy (PHG) but no EGVs, and normal duodenum. Given prior hepatic encephalopathy, TIPS was not performed. He had abdominal surgeries in the past. He was hemodynamically unstable with benign abdominal exam. Labs revealed acute blood loss anemia with Hgb 9.1 (baseline 13), thrombocytopenia and coagulopathy. Following initial resuscitation with fluids, blood products, octreotide and pantoprazole infusion, urgent EGD was performed. There were no EGVs, but features of diffuse PHG, as well as a compressible mucosal bulge with a nipple sign representing a varix in the second portion of the duodenum were seen. Given the insufficient evidence to support endoscopic therapy in ectopic varices, interventional radiology was consulted. CT angiogram demonstrated patent portosystemic veins. TIPS was performed with a decrease in portal gradient from 16 to 2 mmHg. Rifaximin, lactulose and zinc were commenced. He remained hemodynamically stable following this and did not require further intervention. A year later, he remains free of further bleeding episodes or hepatic encephalopathy. DISCUSSION: Bleeding DVs are rare and potentially life-threatening. Diagnosis should be suspected in all cases of gastrointestinal hemorrhage, particularly in the absence of EGV or another source. Standard management has not yet been established. TIPS is a relatively safe and effective means of controlling acute DV bleeding. EVs may re-bleed despite a reduction of portosystemic pressure gradient < 12 mmHg or by 25–50% of baseline; hence the “12 mmHg rule” does not apply. Our patient recovered successfully following TIPS without needing additional therapy. Reducing the pressure gradient to very low values can result in successful outcomes with TIPS in DVs.

1946 Recurrent Lower Gastrointestinal Bleeding Secondary to Hermansky-Pudlak Syndrome

INTRODUCTION: Hermansky-Pudlak syndrome (HPS) is a rare autosomal recessive disorder with a prevalence of 1 in 1,800 in Puerto Rico. It is characterized by oculocutaneous albinism with nystagmus, variable skin hypopigmentation, loss of visual acuity, and platelet storage pool deficiency resulting in bleeding diathesis. Hematochezia in HPS primarily occurs due to inflammatory bowel disease (IBD) presenting in first to third decades. However, lower gastrointestinal bleeding can occur even without evidence of endoscopic or histological findings of colitis. CASE DESCRIPTION/METHODS: A 20-year-old Puerto Rican male with history of HPS presented with 3 to 5 episodes of bright red blood per rectum for the past one week. The patient has been experiencing intermittent hematochezia since the age of 7 years. Previous work-up with double balloon enteroscopy 4 years ago showed small bowel erosions. Colonoscopy performed during that time showed normal findings, however biopsy was not performed. Meckel’s scan did not show any evidence of Meckel’s diverticulum. He did not experience any bleeding for 2 years before this presentation. His vital signs on presentation were stable. Laboratory findings showed hemoglobin of 13 gm/dl, platelet count of 330,000/ul and white blood cell count of 8,900/µL. International normalized ratio (INR) was 1.1, prothrombin time (PT) 14.6 seconds and partial thromboplastin time (PTT) 32.3 seconds. The patient was started on intravenous fluids, pantoprazole infusion and was given one dose of aminocaproic acid. Following the dose of amino-caproic acid, the patient’s hematochezia resolved and he did not have any recurrent bleeding episodes. He was discharged after 3 days, and followed up one month later, when he did not report of recurrent bleeding episodes. DISCUSSION: Previous studies have shown that mucosal inflammation can occur in absence of endoscopic abnormalities in symptomatic patients. The likely cause of hematochezia in our patient was mucosal inflammation along with platelet dysfunction. Patients with mild intermittent episodes of hematochezia can be managed conservatively. For acute bleeding episodes, desmopressin acetate (DDAVP) or aminocaproic acid can be used and in case of severe bleeding, platelet transfusion should be performed.

ATRIO-ESOPHAGEAL FISTULA: A RARE AND GRAVE COMPLICATION OF ATRIAL FIBRILLATION ABLATION

SESSION TITLE: Tuesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Atrio-esophageal fistula (AEF) is an extremely rare, life-threatening complication of catheter radiofrequency ablation (RFA) which has an increasing incidence of > 50,000/year in the US. AEF commonly causes death via cerebral air embolism, massive gastrointestinal bleeding (GIB) and septic shock in 2 months post RFA. The associated mortality of AEF is > 80% and requires prompt diagnosis and intervention.(1) CASE PRESENTATION: An 80 year old female with heart failure with reduced ejection fraction and cardiomyopathy due to persistent atrial fibrillation (AF) despite prior interventions presented 18 days post convergent VATS, left atrial (LA) clip/LA appendage ligation with epicardial ablation of LA posterior wall, while on Eliquis to the ER after 1 episode of hematemesis. There was no history of PUD, melena, NSAID use or heavy alcohol use. She had tachycardia but other vitals were normal. Exam revealed dried blood in the mouth, generalized abdominal tenderness but was otherwise normal. Pantoprazole infusion was commenced. Esophagogastroduodenoscopy (EGD) revealed a large deep mid-esophageal ulcer with clot. Post EGD, she became lethargic with acute hypoxic respiratory failure and was intubated. Chest x-ray showed new lung infiltrate and she was started on Zosyn and vancomycin. CTA of the chest revealed a 2.5 cm thrombus in the posterior left atrium and air within the right atrium. Fluconazole was added and she was taken to the OR for LA repair. The next day she underwent esophagectomy and gastric tube placement, during which she developed hemorrhagic shock requiring multiple transfusions and vasopressor support. Blood cultures grew Rothia mucinolaginosus, B6-deficient streptococcus and lactobacillus and CT head showed an acute stroke. Unfortunately, she died after palliative extubation 10 days post admission. DISCUSSION: AEF following RFA has an incidence of < 0.03% and is thought to be multifactorial. Thermal injury during the ablation, results in fistulization of the esophagus into the atrium i.e. AEF, a 1-way valve, causing strokes more often than upper GIB. CTA chest is the modality of choice, as EGD increases the risk of air embolization resulting in stroke or death. Currently early surgical repair appears to have the best survival.(2) Preventative measures such as an esophageal temperature probe for real-time temperature monitoring was used in this case. However, there is a 0.016% incidence of esophageal perforation despite monitoring in 90% of patients.(3) Other strategies to prevent AEF include: reduced power titration while ablating the posterior LA wall, decrease delivery time and active esophageal cooling with saline. CONCLUSIONS: The incidence of RFA for AF is rapidly increasing for which AEF is a rare yet grave complication that uncommonly presents as hematemesis. Awareness is imperative for prompt diagnosis as without urgent surgical intervention mortality approaches 100%. Reference #1: Patricia C, Franz HM, Abel CD, et al. Atrioesophageal fistula following ablation procedures for atrial fibrillation: systematic review of case reports. Open Heart. 2015; 2(1), e000257. https://doi.org/10.1136/openhrt-2015- 000257. Reference #2: Singh SM, d’Avila A, Singh SK, et al. Clinical outcomes after repair of left atrial esophageal fistulas occurring after atrial fibrillation ablation procedures. Heart Rhythm. 2013; 10(11):1591–1597. Reference #3: Chirag RB, Saurabh K, Yu G, et al. Global Survey of Esophageal in Atrial Fibrillation: Characteristics and Outcomes of Esophageal Perforation and Fistula. JACC: Clinical Electrophysiology. 2016; 2(2):143-150. DISCLOSURES: No relevant relationships by Sahai Donaldson, source=Web Response No relevant relationships by Nisha Gandhi, source=Web Response No relevant relationships by Alexandra Gottdiener, source=Web Response No relevant relationships by Gene Otuonye, source=Web Response No relevant relationships by Dan Ran-Castillo, source=Web Response No relevant relationships by Matthew Tavares, source=Web Response

1989 A Rare Case of Renal Call Carcinoma With Metastasis to the Rectum and Gastric Body

INTRODUCTION: Renal Cell Carcinoma (RCC) frequently metastasizes to the lungs, lymph nodes, bones, and liver via lymphatic, hematogenous, or direct invasion. Gastrointestinal metastasis is rare. We present a case of metastatic RCC to the gastric body and rectum presenting as melena and shortness of breath. CASE DESCRIPTION/METHODS: Patient is a 68-year-old male with a history of stage IV RCC to the skin and lung status post right total nephrectomy and right upper lobe wedge resection, who presented to the hospital with a one-month history of shortness of breath and 10–15 episodes of melena per day. On presentation, his heart rate was 121 bpm and blood pressure quickly dropped from 131/81 mmHg to 110/61 mmHg. Physical exam demonstrated abdominal tenderness and cachexia. Labs demonstrated hemoglobin 6.7 g/dL, which was 4 points lower than baseline and hyponatremia of 128 mmol/L. Other labs including hepatic panel and coagulation parameters were within normal limits. Hemoccult testing was positive. The patient was started on intravenous fluids, pantoprazole infusion, and blood transfusion (2 units). CT scan of the abdomen demonstrated a metastatic lesion in the sigmoid colon suggestive of an invasive metastatic lesion. Endoscopy revealed a nodule in the duodenum and mass was visualized on the greater curvature of the gastric body. Colonoscopy revealed a single polyp in the rectum, 10 mm in size. These lesions were biopsied and treated with bipolar cauterization. Pathological reports demonstrated metastatic carcinoma consistent with a renal primary source. DISCUSSION: RCC involves malignant cell proliferation in the proximal convoluted tubules of the kidney. Post-nephrectomy, there is still an approximate 20–40% chance of distal metastasis or locally recurrent disease. Thus, strict follow up is vital. While primary colorectal cancer is common, metastasis to this site is rare. There have been approximately 10 cases reported of metastasis of RCC to the rectum. Only 0.2–0.7% of RCC cases have been found to have metastasized to the stomach. This is the first case reported of synchronous metastasis of RCC to the rectum and gastric body presenting as melena as opposed to hematochezia. Although rare, clinicians should be mindful of this scenario and this case provides a clinical reminder.

1721 Black Esophagus: A Case of Acute Esophageal Necrosis

INTRODUCTION: Acute esophageal necrosis (AEN) is a rare clinical entity characterized by diffuse, circumferential, black-appearing distal esophageal mucosa on EGD typically limited to the gastroesophageal junction. In this case, we discuss AEN in a chronically ill female precipitated by an acute low perfusion state in the setting of her preexisting vasculopathy. CASE DESCRIPTION/METHODS: A 76-year-old female with past medical history of severe coronary artery disease, high-grade distal aortic stenosis, gastroesophageal reflux disease, history of ischemic colitis presents with two-day history of melena. Patient initially presented at an outside hospital for symptomatic anemia and was transfused packed red blood cells. She was transferred to our institution and was found to have a systolic blood pressure in the 80s. Physical exam was notable for pallor and a delayed capillary refill time. Labs revealed a hemoglobin of 10.8 g/dL, white blood count of 17 uL, procalcitonin of 1.8 ng/mL, creatinine of 1.2 mg/dL, INR of 2.7, and albumin of 2.5 g/dL. CT of the chest and abdomen revealed a right lower lobe lung consolidation and a very decompressed IVC concerning for a low volume state. Patient was adequately fluid resuscitated, kept NPO and was placed on a pantoprazole (PPI) infusion. An EGD was performed which revealed diffuse severe mucosal changes characterized by ulceration with necrotizing black mucosa in the lower third of the esophagus, and non-bleeding cratered and superficial duodenal ulcers. One week later, a repeat EGD demonstrated significant esophageal mucosal healing with esophagitis and distal esophageal ulcerations. Esophageal biopsies revealed denuded submucosa, marked acute inflammation with negative HSV, CMV and fungal cultures. Given the significant improvement in symptoms and findings, her diet was advanced. She was discharged on oral PPI and sucralfate with a plan for repeat EGD in three months. DISCUSSION: The incidence of AEN ranges from 0.2% to 0.28%, however, true prevalence is underestimated given the transient nature of the insult and early tissue healing. Distal esophagus and duodenal injury are common given their similar supply from the celiac artery. This case highlights a rare disease entity with increasing prevalence owing to the increased number of comorbid conditions attributed to the disease process. It emphasizes the potential causes of the disease and timely diagnosis warranting physicians to have an understanding and awareness on potentially fatal but reversible clinical syndrome.

2001 Mastocytosis Complicated by Upper and Lower GI Bleeding

INTRODUCTION: Mastocytosis is a rare disease caused by the abnormal proliferation and accumulation of mast cells in 1 or more organs of the body and is divided into cutaneous and systemic disease. Patients have increased susceptibility to urticaria, pruritis and anaphylactic shock. GI manifestations are thought to be related to direct mast cell infiltration and release of mast cell mediators. CASE DESCRIPTION/METHODS: A 39-year-old woman with a history of cutaneous mastocytosis intolerant to cromolyn sodium, Roux-en-Y gastric bypass, gastritis, celiac disease and hemorrhoids presented with melena and hematemesis following a mastocytosis flare and concurrent pneumonia. She had no prior history of GI bleeding, PUD, H. Pylori infection, NSAID or anticoagulation use, liver disease, or family history of GI malignancies. Prior EGDs and colonoscopies were unremarkable. She was on a chronic high-dose of famotidine and prednisolone taken as needed. Physical exam showed mild epigastric and left upper quadrant tenderness, bilateral rhonchi, and hemodynamic stability. Initial laboratory findings were insignificant. She was given IV pantoprazole BID and continued to have melena while remaining stable; with Hb down-trending to 11.6 gm/dL. EGD revealed a large gastric pouch with Roux-en-Y anatomy and 2 non-bleeding cratered ulcers near the congested, erythematous gastrojejunal anastomosis. The larger ulcer (9 mm) had a visible vessel and was clipped. Pathology revealed reactive gastropathy, mild chronic inflammation without H. pylori. Jejunal biopsies showed congestive mucosa and mild acute on chronic inflammation. The patient resumed IV continuous infusion of pantoprazole for 48 hours then transitioned to oral PPI with her usual famotidine. DISCUSSION: Up to 80% of patients with systemic mastocytosis can present with a variety of GI symptoms, with the most common being diarrhea and abdominal pain. Though the etiology of diarrhea is not well understood, abdominal pain is largely attributed to dyspepsia and gastroduodenal ulcers resulting from acid hypersecretion. Symptomatic treatment for GI symptoms largely depends on anti-mediator therapy where H1 and H2 receptors are typically combined. PPIs are added to treat gastric involvement. Cromolyn sodium is a highly effective treatment for GI manifestations (100-200 mg PO up to 4 times/day). Oral corticosteroids may relieve malabsorption and ascites in the rare cases of liver involvement. Lifestyle modifications include avoidance of triggers and stress management if possible.

1960 Life-Threatening Gastrointestinal Bleeding Secondary to Kaposi’s Sarcoma of the Duodenum

INTRODUCTION: Kaposi’s sarcoma is common in patients with AIDS. Gastrointestinal involvement is not uncommon. However, a life-threatening bleeding is rare. CASE DESCRIPTION/METHODS: A 58-year-old bisexual male with a history of AIDS presented to the clinic with progressive dyspnea, dizziness and unintentional weight loss. He was found to be tachycardic and hypotensive. Physical exam revealed a non-tender, non-pruritic, dark purple skin lesions over his body, face and scalp. The patient was admitted for further evaluation. His initial labs revealed a Hb of 6.2 g/dl and a CD4 count of 120 cells/µL. CT scan of the abdomen and pelvis showed multiple enlarged lymph nodes in the peri aortic, right external iliac and porta-cava areas. He was initiated on HAART and a skin biopsy was performed. While inpatient, Hb dropped to 5.8 g/dl, which responded appropriately to 2 units of pRBCs. However, Hb dropped again and the patient started to have melena and hematochezia for which he was transferred to the ICU for close observation and resuscitation. A continuous infusion of pantoprazole 8 mg/hour was initiated. An EGD and colonoscopy were performed after resuscitation. The EGD showed erosive esophagitis, multiple non-bleeding gastric ulcers with a flat pigmented spot and non-bleeding duodenal erosions. The stomach and duodenum were biopsied. The colonoscopy showed old clotted blood in the entire examined colon. The patient underwent a second look EGD due to persistent melena and Hb drop which showed clotted blood in the gastric fundus, as well as a large, cratered gastric body ulcer, along the greater curve with adherent clot. Most of the clot was removed without bleeding or high-risk stigmata. Over the next few hours, the patient became hemodynamically unstable with increasing amounts melena. The interventional radiology team was consulted, and an urgent selective embolization was performed to the right gastroepiploic artery which was coursing through the ulcer. The patient stabilized and was eventually discharged with a plan of outpatient follow up. The biopsies from skin, stomach and duodenum showed proliferating spindle cells forming slit-like vascular channels within the lamina propria. HHV-8 immunostaining was positive. DISCUSSION: Involvement of the GI tract by Kaposi’s sarcoma is usually asymptomatic but hemorrhages, even though uncommon, have been reported. An adequate endoscopic sampling is crucial to avoid false negative results. However, severe bleeding may occur due to the hypervascularity of the lesion.

612 Impact of a Pharmacist-Managed Protocol Limiting Continuous Infusion of Proton Pump Inhibitor Use in Patients With an Upper Gastrointestinal Bleed

INTRODUCTION: In patients with an upper gastrointestinal bleed, previous reports have shown that there is no difference among clinically significant endpoints when prescribed a continuous infusion of pantoprazole versus intermittent bolus administration. Our study evaluates the impact of a pharmacist-managed protocol aimed at reducing continuous infusion proton pump inhibitor use in upper gastrointestinal bleeds. METHODS: We performed a retrospective analysis of patients receiving intravenous pantoprazole for suspected upper gastrointestinal bleeding before and after the implementation of a pharmacist managed protocol. Prior to implementation, patients were continued on pantoprazole continuous infusions (8 mg/hr) at the physician's discretion. After implementation, all hemodynamically stable patients were allowed one dose of pantoprazole as a continuous infusion (8 mg/hr for 10 hours) and then were transitioned by the pharmacist to intermittent 40 mg IV injections twice daily. The primary endpoint assessed was the incidence of upper gastrointestinal re-bleeding within 7 days of treatment. Secondary endpoints included the number of pantoprazole continuous infusions and IV push injections, number of blood transfusions, number of endoscopic interventions, length of hospital stay, and mortality. RESULTS: After screening 702 patients, 222 patients met inclusion criteria (115 in the pre-protocol group and 107 in the post-protocol group). The re-bleeding rate at day 7 was 7% in the pre-protocol group, compared to 4% in the post-protocol group (P = 0.17). As expected, use of the protocol reduced the median number of continuous infusions per patient [4 (IQR 2-4) vs 2 (IQR 1-3); P &lt; 0.001] and increased the median number of IV push injections [2 (IQR 2-4) vs 4 (IQR 2-7); P &lt; 0.001] in the pre- and post-protocol groups, respectively. There were no significant differences between the pre- and post-intervention groups regarding blood transfusions (65% vs. 63%; P = 0.78), endoscopic interventions (79% vs. 79%; P = 1.0), hospital length of stay [4 days (IQR 3-8) vs. 4 days (IQR 2-8); P = 0.521], or hospital mortality (5% vs. 2%; P = 0.28) (See Tables 1 and 2). CONCLUSION: Implementation of this pharmacy-managed protocol, allowing automatic transition from pantoprazole continuous infusions to intermittent injections in hemodynamically stable patients with an upper gastrointestinal bleed, had no detrimental effect on the incidence of re-bleeding within 7 days.

ADVERSE DRUG REACTION TO ALL PROTON PUMP INHIBITORS EXCEPT ESOMEPRAZOLE IN MEDICALLY COMPLEX PEDIATRIC PATIENT

Introduction Proton-pump inhibitors (PPIs) are commonly used for treatment of gastroesophageal reflux disease (GERD). PPIs have a favourable safety profile; however, immediate and delayed hypersensitivity reactions have been described. Case Description A six-year-old male with hypomyelination with atrophy of the basal ganglia and cerebellum (HABC) and significant medical complexity including seizure disorder, tracheostomy ventilation, severe GERD, and gastro-jejunostomy feeding, developed a papular acneiform eruption 24 hours after administration of omeprazole, lansoprazole, and rabeprazole. The lesions were not evanescent, and did not respond to antihistamine therapy. Skin testing was negative to omeprazole, lansoprazole, rabeprazole, pantoprazole, and esomeprazole. Esomeprazole was started and tolerated well up to 10mg daily, but the patient developed an upper GI bleed due to duodenal ulcer. He was urgently started on pantoprazole infusion. 24 hours later, he developed generalized coalescent erythematous macules, that resolved within 15 minutes of antihistamine administration. Upon discharge, he was continued on pantoprazole with regular antihistamines. Discussion There are three general patterns of hypersensitivity reactions with PPIs: 1) hypersensitivity to one PPI cross-reacting with all other PPIs; 2) cross-reactivity based on structure analogues; and 3) hypersensitivity to single PPI. Other patterns of reactions have been reported; however, tolerance of esomeprazole alone, with clinical reactions to others is uncommon. This was a medically fragile pediatric patient who required PPIs in both acute and chronic settings. This case demonstrates different clinical reactions in the same patient to different PPIs, and the importance of systematically evaluating all PPI options for safe alternatives.

A Fatal Case of Occult Aortoenteric Fistula

Aortoenteric fistulae (AEF) are a rare but serious cause of massive hematemesis. Due to the substantial mortality risk, it is crucial that prompt diagnosis and early management are initiated. Multiple diagnostic modalities are considered valuable in the evaluation of AEF, including endoscopy and computed tomography (CT). We present a case that highlights the limitations of these common diagnostic procedures. We describe a 58-year-old male who has a history of hypertension, dyslipidemia, and severe peripheral vascular disease (PVD). He previously underwent an aortobifemoral bypass, axillofemoral bypass, and recent hospital admission for removal of an infected aortic graft. He presented to the emergency room following massive hematemesis, and underwent urgent esophagogastroduodenoscopy (EGD). This revealed a large clot in D3 with no evidence of active bleeding. Given his significant history of PVD, a CT angiogram was obtained. The radiologist reported no evidence of aortoenteric fistula. The patient was transferred to a monitored setting, and started on a pantoprazole infusion. The next morning the patient had significant hematemesis of approximately 2L of blood, requiring CPR and urgent transfusion. He was transferred to the intensive care unit for repeat EGD. The vascular surgeon and radiologist reviewed the case and felt that despite normal imaging, the patient should be transferred emergently to the operating room. Intraoperatively, a large aortoenteric fistula was noted in D3, which was surgically managed. The patient unfortunately passed away the next day. This case highlights that even with a high index of suspicion, AEF can be difficult to identify despite gold standard diagnostic testing. The delay in diagnosis is often fatal as AEF carry high a mortality risk1. The risk is estimated to be greater than 70% in secondary AEF2,3. Endoscopy has a low sensitivity for diagnosis of AEF4. High resolution CT remains the imaging modality of choice5,6, although it carries a broad sensitivity (40-90%) and specificity (33-100%)7. In our case, the fistula likely thrombosed spontaneously resulting in a normal CT angiogram, and then subsequently exsanguinated the next day. We also want to emphasize the substantial variability of endoscopic management in the treatment of non-bleeding clots, especially in patients with a history of aortic surgery. Further research is warranted to illuminate a more reliable diagnostic and therapeutic model in these patients.1994_A Figure 1. Large clot identified in D31994_B Figure 2. CTA demonstrating no AEF (no contrast leaking into D3), as well as evidence of axillofemoral bypass

A Rare Entity of Bottle Gourd Toxicity with Multiorgan Dysfunction Syndrome

A 59 years old male was presented to our Emergency Department with complaints of multiple episode of vomiting and fresh blood in vomitus, loose stools and reddish coloured urine after consuming some home made bottle gourd juice. Later he was diagnosed as bottle gourd toxicity with a shock which led to MODS. He was aggressively managed with IV fluids, pantoprazole infusion, antibiotics and other supportive medications. He improved and was discharged in a stable condition after 7 days of hospitalization.

P033: Reducing pantoprazole infusions in ED GI bleed patients by optimizing electronic order sets

Introduction: Non-variceal upper gastrointestinal bleeding (NVUGIB) is a common presentation to the emergency department (ED) accounting for significant morbidity, mortality and health care resource usage. In Alberta, a provincial care pathway was recently developed to provide an evidence informed approach to managing patients with an UGIBs in the ED. Pantoprazole infusions are a commonly used treatment despite evidence that suggests they are generally not indicated prior to endoscopy in the ED. The goal of this project was to optimize management of patients with a NVUGIB, in particular reduce pre-endoscopy pantoprazole infusions. Methods: In July 2016, we implemented a multi-faceted intervention to optimize management of ED patients with NVUGIB including 1. de-emphasizing IV pantoprazole infusions in the ED, 2. clinical decision support (CDS) embedded (for endoscopy, disposition and transfusions) within the order set and 3. educating clinicians about the care pathway. We used a pre/post-order set design, analyzing 391 days pre and 189 days post-order set changes. Data was extracted from our fully integrated electronic health records system. The primary outcome was the % of patients receiving IV pantoprazole infusion ordered by an emergency physician (EP) among all patients with NVUGIB. Secondary outcomes included % transfused with hgb &gt;70g/L and whether using the GIB order set impacted management of NVUGIB patients. Results: In the 391 days pre-order set changes, there were 2165 patients included and in the 189 days post-order set changes, there were 901 patients. For baseline characteristics, patients in the post-order set change group were significantly older (64.4 yrs vs 60.9 yrs p-value=0.0016) and had a lower hgb (115 vs 118, p-value=0.049) but otherwise for gender, measures of severity of illness (systolic blood pressure, heart rate, CTAS, % admitted) there were no significantly differences. For the primary outcome, in the pre-order set phase, 47.1% received a pantoprazole infusion ordered by an EP, compared to 31.5% in the post-order phase, for an absolute reduction of 15.6% (p-value= &lt;0.001). For the secondary outcomes, transfusion rates were similar pre/post (22.08% vs 22.75%). Significant inter-site variability exists with respect to the reduction in pantoprazole infusion rates across the four sites (-23.3% to +6.12%). Conclusion: Our interventions resulted in a significant overall reduction in pantoprazole infusions in ED patients with NVUGIB. Reductions in pantoprazole infusions varied significantly across the different sites, future work in our department will explore and address this variability. Keys to the success of this project included engaging clinicians as well as leveraging the SCM order sets as well as the provincial care pathway. Although there were no changes in transfusion rates, it in unclear if this a function of the CDS not being effective or whether these transfusions were clinically indicated.