[108] Chahal P, Tarnasky PR, Petersen BT, et al. Short 5Fr vs long 3Fr pancreatic stents in patients at risk for post-endoscopic retrograde cholangiopancreatography pancreatitis. Clin Gastroenterol Hepatol. 2009; 7(8):834–839
[109] Zolotarevsky E, Fehmi SM, Anderson MA, et al. Prophylactic 5-Fr pancreatic duct stents are superior to 3-Fr stents: a randomized controlled trial. Endoscopy. 2011; 43(4):325–330
[110] Tarnasky PR, Palesch YY, Cunningham JT, et al. Pancreatic stenting prevents pancreatitis after biliary sphincterotomy in patients with sphincter of Oddi dysfunction. Gastroenterology. 1998; 115(6):1518–1524
[111] Harewood GC, Pochron NL, Gostout CJ. Prospective, randomized, controlled trial of prophylactic pancreatic stent placement for endoscopic snare excision of the duodenal ampulla. Gastrointest Endosc. 2005; 62(3):367–370
[112] Yaghoobi M, Pauls Q, Durkalski V, et al. Incidence and predictors of post-ERCP pancreatitis in patients with suspected sphincter of Oddi dysfunction undergoing biliary or dual sphincterotomy: results from the EPISOD prospective multicenter randomized sham-controlled study. Endoscopy. 2015; 47(10):884–890
[113] Alvarez-Sánchez MV, Jenssen C, Faiss S, Napoléon B. Interventional endoscopic ultrasonography: an overview of safety and complications. Surg Endosc. 2014; 28(3):712–734
[114] Chantarojanasiri T, Aswakul P, Prachayakul V. Uncommon complications of therapeutic endoscopic ultrasonography: What, why, and how to prevent. World J Gastrointest Endosc. 2015; 7(10):960–968
[115] Varadarajulu S, Bang JY, Sutton BS, et al. Equal efficacy of endoscopic and surgical cystogastrostomy for pancreatic pseudocyst drainage in a randomized trial. Gastroenterology. 2013; 145(3):583–90.e1
[116] Hookey LC, Debroux S, Delhaye M, et al. Endoscopic drainage of pancreatic-fluid collections in 116 patients: a comparison of etiologies, drainage techniques, and outcomes. Gastrointest Endosc. 2006; 63(4):635–643
[117] Bang JY, Hasan M, Navaneethan U, et al. Lumen-apposing metal stents (LAMS) for pancreatic fluid collection (PFC) drainage: may not be business as usual. Gut. 2016; 0:1–3. doi:10.1136/gutjnl-2016–312812
[118] Arvanitakis M, Delhaye M, Bali MA, et al. Pancreatic-fluid collections: a randomized controlled trial regarding stent removal after endoscopic transmural drainage. Gastrointest Endosc. 2007; 65(4):609–619
[119] Zhang X-C, Zhou P-H. Major perioperative complications of POEM: experience based on 1680 patients. Gastrointest Endosc. 2016; 83:1000
[120] Bechara R, Onimaru M, Ikeda H, Inoue H. Per-oral endoscopic myotomy, 1000 cases later: pearls, pitfalls, and practical considerations. Gastrointest Endosc. 2016; 84:330–338
11 Anticoagulation and Endoscopy
Eduardo Rodrigues-Pinto and Todd H. Baron
11.1 Introduction
Anticoagulation and endoscopy often go hand in hand, and management of antithrombotic therapy in patients undergoing endoscopic procedures can be challenging. The risk of endoscopy in patients on antithrombotics depends on the risks of procedural hemorrhage and thrombosis due to discontinuation of therapy. The decision-making process is challenging when moderate-to high-risk patients, for thrombosis off anticoagulation, undergo high-risk bleeding procedures. Management also differs between elective and emergency procedures. Appropriate decision making requires knowledge of thrombotic risk, procedure-related bleeding risk, concepts of bridging anticoagulation, and timing of cessation and reinitiation of antithrombotic agents. A discussion between clinicians specializing in preoperative management of antithrombotic agents and coagulation disorders, primary providers prescribing these agents, and the proceduralist is essential. Ideally, this communication should occur well in advance of the procedure to increase patient safety and facilitate patient education. In this chapter, we review antiplatelet agents, anticoagulants, procedure risks, assessment of thrombotic risk, antithrombotic management, postprocedure care, and endoscopy procedures in the actively bleeding patient on antithrombotic therapy.
A large number of patients require long-term treatment with anticoagulant and antiplatelet agents (APAs), collectively known as antithrombotic agents. Antithrombotics are prescribed to reduce the risk of thromboembolic complications in patients with certain cardiovascular and thromboembolic conditions.1 In addition, dual antiplatelet therapy (DAPT; combination treatment with aspirin and a thienopyridine) after coronary-artery stent placement has dramatically increased.2
In patients undergoing elective endoscopic procedures in whom the decision is made to discontinue these agents, familiarity with these medications is required to optimize the timing of cessation before, and reinitiation after procedures. The absolute risk of an embolic event in patients whose anticoagulation is interrupted for 4 to 7 days is approximately 1%.3 In addition to drug cessation, the risk of thromboembolism might be increased by dehydration caused by preparation for endoscopic examinations.4 Similarly, in those patients for whom the decision is made to continue antithrombotic agents for elective procedures, the clinician must understand the risk that these agents impart on procedural-induced bleeding. Finally, it is important to understand how to manage these agents in the setting of urgent/emergent endoscopic procedures and in the presence of acute gastrointestinal bleeding (GIB).
The goal is to minimize thromboembolic events and major hemorrhage in the periprocedural period. For patients taking antithrombotics who require endoscopy, the urgency of the procedure, its bleeding risks, the effect of the antithrombotic drug(s) on the bleeding risk, and the risk of a thromboembolic event related to periprocedural interruption of antithrombotic agents must be considered.5
Although guidelines from major Gastroenterological societies provide a framework for management of antithrombotics, the decision-making process may not always be straightforward.6,7,8
11.2 Antithrombotics
11.2.1 Antiplatelet Agents
APAs decrease platelet aggregation, thus preventing thrombus formation. APAs are usually used in patients with ischemic heart disease, coronary stents, and cerebrovascular disease. Aspirin causes irreversible inhibition of the cyclooxygenase 1 and 2 enzyme systems; after cessation of aspirin, 7 to 9 days are required to regain full platelet function.9 Clopidogrel (Plavix, Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership, Bridgewater, New Jersey, United States), prasugrel (Effient, Eli Lilly and Company, Indianapolis, Indiana, United States), ticlopidine (Ticlid, Roche Pharmaceuticals, Nutley, New Jersey, United States), and ticagrelor (Brilinta, AstraZeneca, Wilmington, Delaware, United States) are thienopyridines, which inhibit the P2Y12 component of the adenosine diphosphate (ADP) receptors, preventing activation of the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor complex.10,11 Restoration of normal platelet aggregation requires 5 to 7 days for clopidogrel and prasugrel and 3 to 5 days for ticagrelor. Dipyridamole (Persantine, Teva Pharmaceuticals USA, Sellersville, Pennsylvania, United States) reversibly inhibits platelet aggregation; its duration of action is about 2 days after discontinuation. Abciximab (ReoPro, Eli Lilly and Company, Indianapolis, Indiana, United States), eptifibatide (Integrilin, Merck Sharp & Dohme Corp, Whitehouse Station, New Jersey, United States), and tirofiban (Aggrastat, Medicure Pharma, Inc, Somerset, New Jersey, United States) are GPIIb/IIIa receptor inhibitors that limit platelet aggregation, respectively, for 24 hours, 4 hours, and 1 to 2 seconds after discontinuation.10,11
11.2.2 Anticoagulants Agents
Anticoagulants prevent the clotting of blood by interfering with the native clotting cascade. Warfarin (Coumadin, Bristol-My-ers Squibb Company, Princeton, New Jersey, United States) is an oral anticoagulant that