DOCSLIB.ORG

Acute Gastrointestinal Bleeding: in the Clinic

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Acute Gastrointestinal Bleeding: in the Clinic In the Clinic Acute Gastrointestinal Bleeding Prevention page ITC2-2 Presentation and Diagnosis page ITC2-3 Treatment page ITC2-7 Practice Improvement page ITC2-13 Tool Kit page ITC2-14 Patient Information page ITC2-15 CME Questions page ITC2-16 Physician Writers The content of In the Clinic is drawn from the clinical information and education Meeta Prasad Kerlin, MD, MSCE resources of the American College of Physicians (ACP), including PIER (Physicians’ Jeffrey L. Tokar, MD Information and Education Resource) and MKSAP (Medical Knowledge and Self- Assessment Program). Annals of Internal Medicine editors develop In the Clinic Section Editors from these primary sources in collaboration with the ACP’s Medical Education and Deborah Cotton, MD, MPH Publishing divisions and with the assistance of science writers and physician writ- Darren Taichman, MD, PhD ers. Editorial consultants from PIER and MKSAP provide expert review of the con- Sankey Williams, MD tent. Readers who are interested in these primary resources for more detail can consult http://pier.acponline.org, http://www.acponline.org/products_services/ mksap/15/?pr31, and other resources referenced in each issue of In the Clinic. CME Objective: To review current evidence for the prevention, presentation and diagnosis, treatment, and practice improvement of acute gastrointestinal bleeding. The information contained herein should never be used as a substitute for clinical judgment. © 2013 American College of Physicians In the Clinic Downloaded From: http://annals.org/ by McGill University, Teresa Rudkin on 07/15/2016 cute gastrointestinal (GI) bleeding is common in both the outpatient setting and the emergency department. Annual U.S. incidence rates over Athe past decade are approximately 90–108 per 100 000 persons (1), lead- ing to approximately 300 000 hospitalizations annually. Most cases are due to nonvariceal sources of bleeding (e.g., peptic ulcers) and continue to be associated 1. Hreinsson JP, Kalaitza- with significant mortality (3–14%) and health economic burden (1–3). The inci- kis E, Gudmundsson dence of nonvariceal bleeding may be decreasing in the West largely because of S, Björnsson ES. Up- per gastrointestinal decreased incidence of Helicobacter pylori infection and increased awareness and bleeding: incidence, etiology and out- implementation of ulcer-prevention strategies in users of nonsteroidal anti- comes in a popula- inflammatory drugs (NSAIDs) (1). However, identifying patients with acute GI tion-based setting. Scand J Gastroen- bleeding who are in danger of serious adverse events and establishing evidence- terol. 2013;48:439-47. [PMID: 23356751] based treatment plans are essential in both primary and specialty care. 2. Yavorski RT, Wong RK, Maydonovitch C, et al. Analysis of 3,294 cases of upper gastrointesti- nal bleeding in mili- Prevention tary medical facilities. Am J Gastroenterol. Who is at risk for acute GI bleeding? with lower GI bleeding include in- 1995;90:568-73. [PMID: 7717312] Risk factors for acute GI bleeding flammatory bowel disease, infectious 3. Targownik LE, Nabal- vary according to the site and cause. amba A. Trends in colitis, neoplasia, angioectasias, and management and Upper GI bleeding most often re- benign anorectal disease (14). outcomes of acute nonvariceal upper sults from peptic ulcer disease (ap- gastrointestinal bleed- proximately one quarter of all cases), Approximately 10–20% of patients ing: 1993-2003. Clin Gastroenterol Hepatol. the primary risk factors for which with GI bleeding have “obscure” 2006;4:1459-1466. include NSAIDs and H. pylori infec- bleeding, defined as an unknown [PMID: 17101296] 4. McColl KE, el-Nujumi tion and, less commonly, increased cause despite evaluation with esopha- AM, Chittajallu RS, et gogastroduodenoscopy (EGD), al. A study of the gastric acid production (e.g., the pathogenesis of Heli- Zollinger-Ellison syndrome). Smok- colonoscopy, and radiographic small cobacter pylori nega- tive chronic duode- ing (4–6), severe physiologic stress bowel imaging. Approximately half nal ulceration. Gut. (7), and various host factors (e.g., of these patients have recurrent or 1993;34:762-8. [PMID: 8314508] genetic polymorphisms affecting cy- persistent bleeding and are further 5. Kurata JH, Nogawa subclassified as obscure-overt (pas- AN. Meta-analysis of clooxygenase and prostaglandin pro- risk factors for peptic duction) (8, 9) may increase risk for sage of visible blood with melena or ulcer. Nonsteroidal antiinflammatory peptic ulcers even in persons without hematochezia) or obscure-occult drugs, Helicobacter concomitant H. pylori infection or (iron-deficiency anemia and/or posi- pylori, and smoking. J Clin Gastroenterol. NSAID exposure. Although spicy tive for fecal occult blood) (15). 1997;24:2-17. Many such patients have bleeding [PMID: 9013343] foods may cause GI symptoms, there 6. Talamini G, Zamboni are no convincing data that they in- sources in the small intestine, now G, Cavallini G. Antral mucosal Helicobacter crease the risk for peptic ulcers. Oth- sometimes referred to as “mid-GI pylori infection densi- er risk factors for acute upper GI bleeding” (between the ligament of ty as a risk factor of duodenal ulcer. Di- bleeding include varices, esophagitis, Treitz and the ileocecal valve). An- gestion. 1997;58:211- 7. [PMID: 9243115] vascular abnormalities (e.g., angioec- gioectasia is the most common cause 7. Barkun AN, Bardou M, tasias, arteriovenous malformations, of small-bowel bleeding in the West, Pham CQ, Martel M. Proton pump in- Dieulafoy lesions), Mallory–Weiss accounting for 70–80% of cases (16). hibitors vs. histamine tear from protracted vomiting, and 2 receptor antago- Can acute GI bleeding be prevented? nists for stress-related benign and malignant neoplasms mucosal bleeding Prevention of acute GI bleeding de- prophylaxis in critical- (10–13). ly ill patients: a meta- pends on the risk factors and causes. analysis. Am J Gas- Lower GI bleeding, historically de- For example, reducing use of troenterol. 2012;107:507-20. fined as bleeding from a source distal NSAIDs and administering antacid [PMID: 22290403] 8. Arisawa T, Tahara T, to the ligament of Treitz, also results treatment with H2-inhibitors or pro- Shibata T, et al. Asso- from several causes with distinct risk ton-pump inhibitors (PPIs) prevents ciation between ge- netic polymorphisms factors. Diverticulosis is the most peptic ulcer bleeding. Prophylactic in the cyclooxyge- common cause of hematochezia, ac- acid suppression should be considered nase-1 gene promot- er and peptic ulcers counting for up to half of all cases, in selected hospitalized patients who in Japan. Int J Mol Med. 2007;20:373-8. particularly in patients older than 65 are at increased risk for gastroduode- [PMID: 17671743] years. Other risk factors associated nal ulceration and bleeding, including © 2013 American College of Physicians ITC2-2 In the Clinic Annals of Internal Medicine 6 August 2013 Downloaded From: http://annals.org/ by McGill University, Teresa Rudkin on 07/15/2016 patients who are mechanically venti- measures can prevent diverticular lated or who have coagulopathy or bleeding or bleeding related to an- thrombocytopenia, traumatic brain or gioectasias. Although high-fiber diets spinal cord injury, or a history of are often recommended, the role of burns (7, 17). In patients with chronic fiber in the pathogenesis or progres- liver disease, nonselective beta- sion of diverticulosis is debatable. Sur- blockers (such as propanolol or gical intervention for diverticulosis is nadolol) to reduce portal hypertension not routinely done for prevention, be- and endoscopic interventions, such as cause risk for diverticular bleeding is band ligation (18), can effectively pre- low relative to the morbidity of pro- vent variceal bleeding. No specific phylactic surgical resection (19). Prevention... Risk factors for, and therefore prevention of, acute GI bleeding depends on the site and cause of bleeding. In general, minimizing use and appro- priate prescribing of NSAIDs, antiplatelet agents, and anticoagulants, as well as judicious primary and secondary prophylactic acid suppression in selected pa- tients, are effective measures for ulcer-related upper GI bleeding. Nonselective beta-blockers and endoscopic therapy for esophageal and gastric varices are ef- fective for primary and secondary prevention of variceal bleeding. Few measures are helpful in preventing lower GI bleeding, except for reducing exposure to NSAIDS, anticoagulants, and antiplatelets. CLINICAL BOTTOM LINE Presentation and What are the symptoms and signs it can occur with small-bowel bleed- Diagnosis of acute GI bleeding? Can they ing and even slowly bleeding right help localize the site of bleeding? colonic lesions. The source of hema- GI bleeding can present with myriad tochezia is usually the colon. Up to signs and symptoms (Table 1). The 10% of upper GI bleeding episodes most indolent forms may present as present with hematochezia, which is 9. Malaty HM, Graham DY, Isaksson I, En- severe anemia. Manifestations include often associated with signs and symp- gstrand L, Pedersen fatigue; dizziness; pallor; and rarely NL. Are genetic influ- toms of hemodynamic instability. ences on peptic ulcer end-organ complications, such as un- dependent or inde- What are the common causes of pendent of genetic stable angina. Brisk bleeding from the influences for Heli- upper or lower GI tract can present upper and lower GI bleeding? cobacter pylori infec- tion? Arch Intern with more specific manifestations,
Load more

Recommended publications
  • Perforated Peptic Ulcer in Khartoum State
    ﺑﺴﻢ ﺍﷲ ﺍﻟﺮﲪﻦ ﺍﻟﺮﺣﻴﻢ UNIVERSITY OF KHARTOUM Faculty of Medicine Postgraduate Medical Studies Board Perforated peptic ulcer in Khartoum state By Dr. Al Fatih Mohamed Ahmed Alnajib M.B.B.S (University of Gezira) A thesis Submitted in partial fulfillment for the requirements of the Degree of Clinical MD in Surgery, October, 2002 Supervisor Prof. Mohamed El Makki Ahmed MS, FRCSI, Professor of Surgery ﺑﺴﻢ ﺍﷲ ﺍﻟﺮﲪﻦ ﺍﻟﺮﺣﻴﻢ ﻗﺎﻝ ﺍﷲ ﺗﻌﺎﻟﻰ : } ﻗﺎﻟﻮﺍ ﺳﺒﺤﺎﻧﻚ ﻻ ﻋﻠﻢ ﻟﻨﺎ ﺇﻻ ﻣﺎ ﻋﻠﻤﺘﻨﺎ ﺇﻧﻚ .{ ﺃﻧﺖ ﺍﻟﻌﻠﻴﻢ ﺍﻟﺤﻜﻴﻢ ﺻﺪﻕ ﺍﷲ ﺍﻟﻌﻈﻴﻢ CONTENTS Page Dedication I Acknowledgements II List of abbreviations III English abstract IV V Arabic abstract VI List of tables VIII List of figures CHAPTER ONE 1 Introduction and Literature review Objectives 25 CHAPTER TWO Patients & Methods 26 CHAPTER THREE Results 28 CHAPTER FOUR Discussion 58 Conclusion 65 Recommendations 67 References 68 APPENDIX Questionnaire 69 APACHE II Score 73 Dedications To my parents, teachers, Sisters & brothers ACKNOWLEDGEMENT I will always feel indebted to my supervisor Prof. Mohamed El Makki Ahmed, Professor of surgery, Faculty of Medicine, University of Khartoum, for his kind and meticulous supervision, encouragement, and guidance in this work with great patience from it’s beginning to the final touches. I would also like to express my sincere thanks and gratitude to my colleagues the registrars of surgery and the house officers who help a lot in data collection, their indefatigable efforts and cheerful co-operation are without parallel. Special thanks for all those helped or participated in this work to come to the light, not forgetting to thank Miss. Widad for help in typing and Mr.
    [Show full text]
  • Pheochromocytoma Associated with Renal Agenesis
    Case Report Open Access J Surg Volume 11 Issue 5 - June 2020 Copyright © All rights are reserved by Peterson SJ DOI: 10.19080/OAJS.2020.11.555822 A Rare Cause of Gastrointestinal Bleeding: A Jejunal Dieulafoy’s Lesion Zev Lati1, Karthik Chandrasekaran1, Fastina Khan1, Niel Dave1, Wael El Darawy1, MD Zohirul Islam1 and Stephen J Peterson1,2* 1Department of Medicine, New York Presbyterian Brooklyn Methodist Hospital, USA 2Weill Cornell Medical College, USA Received: June 01, 2020; Published: June 24, 2020 *Corresponding author: Peterson SJ, Department of Medicine, New York Presbyterian Brooklyn Methodist Hospital, New York, USA Keywords: Gastrointestinal bleed; Dieulafoy’s lesion; Jejunal bleed; End stage renal disease; Immunosuppression; Large granular lymphocytic leukemia Presentation isolated cases associated with chronic immunosuppression One in a thousand people have an acute gastrointestinal whether from underlying malignancies or medication induced (GI) hemorrhage per year [1]. There are around 300,000 [11]. hospitalizations for GI bleeds, costing an estimated $2 billion per year [2-4]. Compared to lower gastrointestinal bleeding (LGIB), More than 70% of these rare lesions are found in the stomach, upper gastrointestinal bleeding (UGIB) is associated with a much usually near the lesser curvature. The discovery of extragastric higher mortality rate, with some studies suggesting a 30-day DFL’s are infrequent, with the duodenum (14%) and colon (5%) mortality rate of up to 14% [2,3]. A majority of these UGIB (67 - being the most common locations [12-14]. The most unusual 80%) are attributed to gastric erosions/ulcers 6,17,18. However, site is the jejunum, which accounts for 1% of all DFL’s [12-14].
    [Show full text]
  • Endoscopic Diagnosis and Management of Nonvariceal Upper
    Guidelines Endoscopic diagnosis and management of nonvariceal upper gastrointestinal hemorrhage (NVUGIH): European Society of Gastrointestinal Endoscopy (ESGE) Guideline – Update 2021 Authors Ian M. Gralnek1, 2,AdrianJ.Stanley3, A. John Morris3, Marine Camus4,JamesLau5,AngelLanas6,StigB.Laursen7 , Franco Radaelli8, Ioannis S. Papanikolaou9, Tiago Cúrdia Gonçalves10,11,12,MarioDinis-Ribeiro13,14,HalimAwadie1 , Georg Braun15, Nicolette de Groot16, Marianne Udd17, Andres Sanchez-Yague18, 19,ZivNeeman2,20,JeaninE.van Hooft21 Institutions 17 Gastroenterological Surgery, University of Helsinki and 1 Institute of Gastroenterology and Hepatology, Emek Helsinki University Hospital, Helsinki, Finland Medical Center, Afula, Israel 18 Gastroenterology Unit, Hospital Costa del Sol, 2 Rappaport Faculty of Medicine, Technion-Israel Marbella, Spain Institute of Technology, Haifa, Israel 19 Gastroenterology Department, Vithas Xanit 3 Department of Gastroenterology, Glasgow Royal International Hospital, Benalmadena, Spain Infirmary, Glasgow, UK 20 Diagnostic Imaging and Nuclear Medicine Institute, 4 Sorbonne University, Endoscopic Unit, Saint Antoine Emek Medical Center, Afula, Israel Hospital Assistance Publique Hopitaux de Paris, Paris, 21 Department of Gastroenterology and Hepatology, France Leiden University Medical Center, Leiden, The 5 Department of Surgery, Prince of Wales Hospital, The Netherlands Chinese University of Hong Kong, Hong Kong SAR, China published online 10.2.2021 6 Digestive Disease Services, University Clinic Hospital, University of Zaragoza, IIS Aragón (CIBERehd), Spain Bibliography 7 Department of Gastroenterology, Odense University Endoscopy 2021; 53: 300–332 Hospital, Odense, Denmark DOI 10.1055/a-1369-5274 8 Department of Gastroenterology, Valduce Hospital, ISSN 0013-726X Como, Italy © 2021. European Society of Gastrointestinal Endoscopy 9 Hepatogastroenterology Unit, Second Department of All rights reserved. Internal Medicine – Propaedeutic, Medical School, This article ist published by Thieme.
    [Show full text]
  • 4. Pathology Esophagus and Stomach
    Pathology of esophagus and stomach. Pathology of esophagus and stomach. I. Microspecimens: № 176. Acute gastric ulcer. (H.E. stain). Indications: 1. The superficial layer of the ulcer, consisting of leukocytes and erythrocytes. 2. Necrotic masses and tissue debris in the area of the ulcer. 3. Foci of necrosis in the muscular layer of the gastric wall. 4. Leukocyte infiltration in the edges and bottom of the ulcer. A lesion in the gastric wall is observed, which involves the mucosa, the muscularis mucosa and the submucosa; the bottom of the ulcer is presented by necrotic masses with diffuse leukocyte infiltration, which extends into the muscular layer of the gastric wall; blood vessels are dilated, hyperemic; there is no granulation tissue or mature fibrocollagenous tissue. Acute gastric ulcers are located more frequently on the lesser curvature, in the antral and pyloric region, they can also be on the greater curvature. They are usually multiple, more often round in shape, diameter up to 1.0-1.5 cm, the bottom is dark brown due to the accumulation of the hemoglobinogen pigment, hydrochloric hematin. The edges and bottom have a flaccid consistency, they are not hardened, the arrangement of the folds of the adjacent mucosa is not changed. In some cases, the acute ulcer can progress with involvement of the muscular layer of the gastric wall and even the serosa, which can lead to perforation and peritonitis. Deep acute ulcers often look like a funnel, with the base facing the gastric mucosa and the tip facing the serous membrane. Another complication is gastric bleeding.
    [Show full text]
  • Endoscopic Treatment of Tracheoesophageal Fistula: Use of Stents and Endoclips
    4 Review Article Page 1 of 4 Endoscopic treatment of tracheoesophageal fistula: use of stents and endoclips Thomas Ciecierega1#, Reem Z. Sharaiha2# 1Division of Pediatric Gastroenterology and Hepatology, Department of Pediatrics, Weill Cornell Medical College/New York Presbyterian Hospital, New York, NY, USA; 2Divison of Gastroenterology and Hepatology, Weill Cornell Medicine, New York, NY, USA Contributions: (I) Conception and design: All authors; (II) Administrative support: None; (III) Provision of study materials or patients: None; (IV) Collection and assembly of data: None; (V) Data analysis and interpretation: None; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. #These authors contributed equally to this work. Correspondence to: Thomas Ciecierega, MD. New York Presbyterian, Weill Cornell medical College, New York, NY, USA. Email: [email protected]; Reem Z. Sharaiha, MD. Division of Gastroenterology and Hepatology, Weill Cornell Medicine, New York, NY, USA. Email: [email protected]. Abstract: Tracheoesophageal fistula (TEF) is a rare gastrointestinal pathology of abnormal connection or passage between the esophagus and the trachea. Most frequently, TEF is a primary (congenital) in origin and most often associated with the esophageal atresia (EA). TEF can develop as a consequence of another disease, syndrome or condition (secondary) such as infectious esophagitis, trauma, foreign body or neoplasm. Regardless of the etiology, TEF represents treatment challenge. TEF can present with wide ranging symptoms including cough, choking, gagging, poor growth and occasionally with severe complications of pulmonary aspiration. The diagnostic test of choice remains radiographic imaging. Contrast studies can usually identify majority of TEFs including their anatomical characteristics such as size, location and communication.
    [Show full text]
  • Role of Yoga in Acid Peptic Disease: a Review
    wjpmr, 2021,7(9), 133 – 136. SJIF Impact Factor: 5.922 WORLD JOURNAL OF PHARMACEUTICAL Review Article Navedita et al. World Journal of Pharmaceutical and Medical Research AND MEDICAL RESEARCH ISSN 2455-3301 www.wjpmr.com Wjpmr ROLE OF YOGA IN ACID PEPTIC DISEASE: A REVIEW *1Dr. Navedita Kumari and 2Dr. Anupam Pathak 1PG Scholar, Dept of Swasthavritta & Yoga, SriGanganagar College of Ayurvedic Science and Hospital, Tanta University, SriGanganagar. 2HOD, Dept of Swasthavritta & Yoga, SriGanganagar College of Ayurvedic Science and Hospital, Tanta University, SriGanganagar. *Corresponding Author: Dr. Navedita Kumari PG Scholar, Dept of Swasthavritta & Yoga, SriGanganagar College of Ayurvedic Science and Hospital, Tanta University, SriGanganagar. Article Received on 15/06/2021 Article Revised on 05/07/2021 Article Accepted on 25/07/2021 ABSTRACT The acid peptic diseases, also known as acid peptic disorders are a collection of diseases involving acid production in the stomach and nearby parts of the gastrointestinal tract. It includes gastroesophageal reflux disease, gastritis, gastric ulcer, duodenal ulcer, esophageal ulcer, Zollinger–Ellison syndrome and Meckel's [1] diverticulum ulcer. Acid peptic disorders are the result of distinctive, but overlapping pathogenic mechanisms [1] leading to either excessive acid secretion or diminished mucosal defense. Acid peptic disease – commonly called APD – includes a number of conditions. All these conditions are the result of damage from acid and peptic activity in gastric secretions. APD occurs when the acid starts irritating the inner cells (mucosal layer) of the stomach. Acid [2] peptic diseases mostly affect the oesophagus, stomach, and duodenum. “Acid peptic disease” is a collective term used to include many conditions such as gastro-esophageal reflux disease (GERD), gastritis, gastric ulcer, duodenal ulcer, esophageal ulcer, Zollinger Ellison Syndrome (ZES) and Meckel‟s diverticular ulcer.
    [Show full text]
  • Role of Endoscopic Clipping in the Treatment of Oesophageal Perforations
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by SZTE Publicatio Repozitórium - SZTE - Repository of Publications Submit a Manuscript: http://www.wjgnet.com/esps/ World J Gastrointest Endosc 2016 January 10; 8(1): 13-22 Help Desk: http://www.wjgnet.com/esps/helpdesk.aspx ISSN 1948-5190 (online) DOI: 10.4253/wjge.v8.i1.13 © 2016 Baishideng Publishing Group Inc. All rights reserved. REVIEW Role of endoscopic clipping in the treatment of oesophageal perforations György Lázár, Attila Paszt, Eszter Mán György Lázár, Attila Paszt, Eszter Mán, Department of through-the-scope (TTS) clip and the over-the-scope Surgery, University of Szeged, Szeged 6720, Hungary clip (OTSC). We summarized the results of oesophageal perforation closure with endoscopic clips. We processed Author contributions: Lázár G wrote the article and analyzed the data from 38 articles and 127 patients using PubMed the data; Paszt A and Mán E collected and analyzed the data and search. Based on evidence thus far, it can be stated that created the tables. both clips can be used in the treatment of early (< 24 Conflict-of-interest statement: The authors declare no conflict h), iatrogenic, spontaneous oesophageal perforations of interest. in the case of limited injury or contamination. TTS clips are efficacious in the treatment of 10 mm lesions, while Open-Access: This article is an open-access article which was bigger (< 20 mm) lesions can be treated successfully selected by an in-house editor and fully peer-reviewed by external with OTSC clips, whose effectiveness is similar to that reviewers.
    [Show full text]
  • Compatibility of Endoclips in the Gastrointestinal Tract with Magnetic Resonance Imaging Dong Yeol Shin1, Sumi Park2, Ain Kim3, Eung‑Sam Kim4* & Han Ho Jeon1*
    www.nature.com/scientificreports OPEN Compatibility of endoclips in the gastrointestinal tract with magnetic resonance imaging Dong Yeol Shin1, Sumi Park2, Ain Kim3, Eung‑Sam Kim4* & Han Ho Jeon1* There are no clear guidelines on the compatibility between endoclips that remain in the gastrointestinal (GI) tract and magnetic resonance imaging (MRI). The purpose of this study was to investigate the efect of 3T (T) MRI on endoclips placed in excised pig tissues. Two types of endoclips were assessed: Olympus EZ (HX-610-135L) and QuickClip Pro (HZ-202LR). We assessed tissue damage or perforation and detachment of endoclips under 3T MRI magnetic feld. We also evaluated the magnitude of force required to detach the endoclips from the porcine tissue. We measured the magnetic force acting on the Olympus EZ clips. QuickClip Pro clips were used as a control in this study. There was no tissue damage and no detachment of the endoclips (Olympus EZ and QuickClip Pro) during 3T MRI. The force required to detach the Olympus EZ clips ranged from 0.9 to 3.0 N. The translational magnetic force acting on the endoclips was 3.18 × 10–3 N. Ex vivo experiments showed that the magnetic feld generated by 3 MRI did not cause tissue damage or perforation and did not detach the endoclips. Olympus EZ clips and QuickClip Pro clips in the GI tract appear to be safe during 3T MRI. Endoclips are metallic clips used for hemostasis, anchoring stents, closing intraprocedural perforations, and marking tumors or other structures. During a study conducted in 2009 by Gill et al., a 1.5T (T) magnetic feld was applied to three types of endoclips (Resolution Clip, TriClip, and QuickClip) bound to a piece of gastric mucosa excised from a pig1.
    [Show full text]
  • Diagnosis and Management of Iatrogenic Endoscopic Perforations: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement
    Guideline Diagnosis and management of iatrogenic endoscopic perforations: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement Authors Gregorios A. Paspatis1, Jean-Marc Dumonceau2, Marc Barthet3, Søren Meisner4, Alessandro Repici5, Brian P. Saunders6, Antonios Vezakis7, Jean Michel Gonzalez3, Stine Ydegaard Turino4, Zacharias P. Tsiamoulos6, Paul Fockens8, Cesare Hassan9 Institutions Institutions are listed at the end of article. Bibliography This Position Paper is an official statement of the European Society of Gastrointestinal Endoscopy DOI http://dx.doi.org/ (ESGE). It addresses the diagnosis and management of iatrogenic perforation occurring during diag- 10.1055/s-0034-1377531 nostic or therapeutic digestive endoscopic procedures. Published online: 2014 Endoscopy © Georg Thieme Verlag KG Main recommendations 4 ESGE recommends that endoscopic closure Stuttgart · New York 1 ESGE recommends that each center imple- should be considered depending on the type of ISSN 0013-726X ments a written policy regarding the manage- perforation, its size, and the endoscopist exper- ment of iatrogenic perforation, including the de- tise available at the center. A switch to carbon Corresponding author Gregorios A. Paspatis, MD finition of procedures that carry a high risk of dioxide insufflation, the diversion of luminal Gastroenterology Department this complication. This policy should be shared content, and decompression of tension pneu- Benizelion General Hospital with the radiologists and surgeons at each cen- moperitoneum or
    [Show full text]
  • Peptic Ulcer Disease
    \ Lecture Two Peptic ulcer disease 432 Pathology Team Done By: Zaina Alsawah Reviewed By: Mohammed Adel GIT Block Color Index: female notes are in purple. Male notes are in Blue. Red is important. Orange is explanation. 432PathologyTeam LECTURE TWO: Peptic Ulcer Peptic Ulcer Disease Mind Map: Peptic Ulcer Disease Acute Chronic Pathophysiology Morphology Prognosis Locations Pathophysiology Imbalance Acute severe Extreme Gastric Duodenal gastritis stress hyperacidity between agrresive and defensive Musocal Due to factors increased Defenses Morphology acidity + H. Pylori infection Mucus Surface bicarbonate epithelium barrier P a g e | 1 432PathologyTeam LECTURE TWO: Peptic Ulcer Peptic Ulcer Definitions: Ulcer is breach in the mucosa of the alimentary tract extending through muscularis mucosa into submucosa or deeper. erosi on ulcer Chronic ulcers heal by Fibrosis. Erosion is a breach in the epithelium of the mucosa only. They heal by regeneration of mucosal epithelium unless erosion was very deep then it will heal by fibrosis. Types of Ulcer: 1- Acute Peptic Ulcers ( Stress ulcers ): Acutely developing gastric mucosal defects that may appear after severe stress. Pathophysiology: All new terms mentioned in the diagram are explained next page Pathophysiology of acute peptic ulcer Complication of a As a reult of Due to acute severe stress extreme gastritis response hyperacidity Mucosal e.g. Zollinger- inflammation as a Curling's ulcer Stress ulcer Cushing ulcer Ellison response to an syndrome irritant e.g. NSAID or alcohol P a g e | 2 432PathologyTeam
    [Show full text]
  • The Gastrointestinal Tract Frank A
    91731_ch13 12/8/06 8:55 PM Page 549 13 The Gastrointestinal Tract Frank A. Mitros Emanuel Rubin THE ESOPHAGUS Bezoars Anatomy THE SMALL INTESTINE Congenital Disorders Anatomy Tracheoesophageal Fistula Congenital Disorders Rings and Webs Atresia and Stenosis Esophageal Diverticula Duplications (Enteric Cysts) Motor Disorders Meckel Diverticulum Achalasia Malrotation Scleroderma Meconium Ileus Hiatal Hernia Infections of the Small Intestine Esophagitis Bacterial Diarrhea Reflux Esophagitis Viral Gastroenteritis Barrett Esophagus Intestinal Tuberculosis Eosinophilic Esophagitis Intestinal Fungi Infective Esophagitis Parasites Chemical Esophagitis Vascular Diseases of the Small Intestine Esophagitis of Systemic Illness Acute Intestinal Ischemia Iatrogenic Cancer of Esophagitis Chronic Intestinal Ischemia Esophageal Varices Malabsorption Lacerations and Perforations Luminal-Phase Malabsorption Neoplasms of the Esophagus Intestinal-Phase Malabsorption Benign tumors Laboratory Evaluation Carcinoma Lactase Deficiency Adenocarcinoma Celiac Disease THE STOMACH Whipple Disease Anatomy AbetalipoproteinemiaHypogammaglobulinemia Congenital Disorders Congenital Lymphangiectasia Pyloric Stenosis Tropical Sprue Diaphragmatic Hernia Radiation Enteritis Rare Abnormalities Mechanical Obstruction Gastritis Neoplasms Acute Hemorrhagic Gastritis Benign Tumors Chronic Gastritis Malignant Tumors MénétrierDisease Pneumatosis Cystoides Intestinalis Peptic Ulcer Disease THE LARGE INTESTINE Benign Neoplasms Anatomy Stromal Tumors Congenital Disorders Epithelial Polyps
    [Show full text]
  • Path GI – Liver – Gallbladder Paragraph Style
    Path GI – Liver – Gallbladder Paragraph Style Esophagus Congenital Hemorrhage Esophagitis Tumors Fistula Mallory‐Weiss GERD Sqaumous Cell Carcinoma Webs Esophageal Varices Barrett’s Adenocarcinoma Achalasia Chemical CONGENITAL Fistula. Fistulas often occur together with atresias. Atresias are where a tube (in this case the esophagus) ends in a blind pouch. A Fistula is where a tube connects to another tube. A Tracheoesophageal fistula is a connection between the trachea and the esophagus. Over 80% of these lesions occur with atresia of the proximal esophagus, and a fistula of the distal esophagus to the trachea. This means that when the baby swallows, the food goes into the trachea! This is pretty clear early on, presenting with dysphagia (spitting up, not vomiting, food), and Coughing + Cyanosis during feeding. Air in stomach may be seen as well. This must be surgically corrected, which is easy to do. Webs. Esophageal webs are simply extensions of mucosal epithelium into the lumen of the esophagus. They act as nets which can catch food trying to be swallowed. This presents with dysphagia and foul breath as the food that gets stuck putrefies in the esophagus. Webs are associated with Plummer‐ Vinson Syndrome from the Heme block, presenting with iron deficiency anemia and an increased risk for sqaumous cell carcinoma. These will persist into adulthood Achalasia. This is a failure of the LES to relax. When food is swallowed, it cannot pass into the stomach, causing distension of the esophagus (megaesophagus) and dysphagia. Over time, the food is pushed through the tight sphincter. It is caused by death of ganglionic cells in the LES.
    [Show full text]