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,