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• W2040804906 abstract "A 72-year-old woman presents to the emergency room after 2 episodes of coffee-ground emesis and a 1-day history of melena. She has no other gastrointestinal (GI) symptoms. She complains of dizziness when standing, but denies shortness of breath and chest pain. She has a history of hypertension, diabetes, and coronary artery disease. Three weeks ago, she sustained a myocardial infarction and had 3 drug-eluting coronary artery stents placed. She takes insulin, metformin, metoprolol, aspirin, and clopidogrel. Her vital signs at presentation show orthostasis with a heart rate of 98 supine and 120 upright. Her blood pressure is 135/80 supine and 100/55 upright. The physical examination is unremarkable except for melenic stool on rectal examination. Relevant laboratory values include a hemoglobin level of 8.1, platelet count of 215, blood urea nitrogen level of 38, creatinine level of 1.2, and a normal international normalized ratio. The use of antiplatelet therapy is prevalent and likely will increase because an abundance of data support the benefits of antiplatelet therapy for primary and secondary management strategies of cardiovascular diseases. Dual antiplatelet therapy (DAT) with aspirin and clopidogrel has been shown to decrease the mortality associated with acute coronary syndrome (ACS) (ie, unstable angina and myocardial infarction). Administration of DAT also is indicated after percutaneous coronary intervention, whether or not a stent has been placed. After coronary artery stent placement, DAT has been shown to reduce the risk of stent thrombosis, which carries with it a high incidence of myocardial infarction and death. The risk of stent occlusion appears to be highest in the first year after placement, prompting the American College of Cardiology and the American Heart Association to recommend continuous DAT for at least 1 year after stent placement. Several case series have reported improved survival of patients who received DAT beyond 1 year, as compared with patients who only had a single year of DAT after drug-eluting coronary artery stent placement. Although the cardiovascular benefits of DAT are clear, the agents prescribed for DAT are associated with a high risk of GI injury and of bleeding from such lesions. Aspirin irreversibly inhibits cyclooxygenase, thereby decreasing prostaglandin production and resulting in gut injury. Endoscopic evaluation of the upper GI tract within 12 weeks of initiating aspirin therapy will reveal an ulcer in 7% to 10% of patients, and erosive disease in up to 47% of patients. The mucosal toxicity of aspirin is compounded by its antithrombotic effect. Inhibition of thromboxane A2 leads to decreased platelet aggregation and prolongation of bleeding time. Low-dose aspirin (<166 mg/d) is associated with a 2 to 4-fold increased risk of upper GI hemorrhage. Factors thought to increase this risk further include old age, history of peptic ulcer disease, Helicobacter pylori infection, chronic renal failure, diabetes mellitus, and concomitant use of other antiplatelet agents, anticoagulants, or nonsteroidal anti-inflammatory drugs. The thienopyridine clopidogrel is a commonly used antiplatelet agent that inhibits platelet aggregation by irreversibly antagonizing adenosine diphosphate. The use of clopidogrel alone increases the risk of GI hemorrhage, especially in patients with a history of peptic ulcer disease. DAT with combination aspirin and clopidogrel increases the incidence of GI hemorrhage as compared with either agent alone. Data from the Management of A Therothrombosis With Clopidogrel in High Risk Patients (MATCH) and Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) studies show that the risk of GI hemorrhage within the first 30 days of DAT is 1.3%, and increases to 12% in patients with a prior history of peptic ulcer disease or GI hemorrhage. Not only are patients using DAT at high risk of developing adverse GI events, they are also at increased risk of poor outcomes because of their underlying medical conditions. The challenge for the clinician is to adequately manage the bleeding event while minimizing the risk of cardiovascular complications associated with acute blood loss, withholding antiplatelet agents, and sedation administered during endoscopy. The initial approach to a patient with acute GI hemorrhage using DAT is similar to that of other patients. Adequate resuscitation and risk stratification should occur immediately upon presentation. Volume replacement with isotonic intravenous (IV) fluid and/or blood products will improve oxygen delivery to the myocardium. Although the threshold for blood transfusions has not been determined, a recent Cochrane database review suggested that a liberal transfusion policy for patients with cardiac disease is reasonable. Risk stratification and prognostication is important for all patients with acute GI hemorrhage and any number of risk schema can be used that incorporate presenting clinical characteristics, endoscopic findings, or initial response to therapy. By using pre-endoscopic criteria alone, patients with active coronary artery disease and orthostasis have a moderate risk of 30-day mortality. Patients with ACS, in particular, are at much higher risk of adverse events if hypovolemia is significant. Data specifically from patients with ACS and acute blood loss owing to GI hemorrhage suggest that in-hospital mortality is increased 4- to 7-fold as compared with patients with ACS without GI hemorrhage. Endoscopy for patients with acute upper GI hemorrhage is indicated whether or not antiplatelet agents are being used. Early upper endoscopy is an important tool for diagnosing the source of hemorrhage, risk stratification, and for therapy of high-risk lesions. When deciding whether to perform endoscopy, the clinician should consider the benefits and risks of the procedure in that particular scenario. Factors to account for include the likelihood of an improved outcome owing to endoscopic identification and treatment of findings, the risk of adverse events associated with endoscopy, and the risk of discontinuing or reversing the effect of antiplatelet agents in a patient taking DAT. Multiple randomized clinical trials have shown that early endoscopy for patients with acute upper GI hemorrhage results in overall improved outcomes. A recent meta-analysis of 75 randomized clinical trials for endoscopic hemostasis of gastroduodenal ulcers reported lower rates of recurrent bleeding, transfusion requirement, and need for surgical intervention in patients randomized to hemostasis. Although few studies have shown an improvement in mortality as a result of endoscopic hemostasis, the hospital length of stay and recurrent admission rates are considerably lower when compared with patients who do not undergo endoscopic hemostasis. Early endoscopy provides valuable information that helps guide patient management, even when hemostasis is not performed. For example, in a patient with ACS or a recently placed drug-eluting coronary artery stent who has a clean base ulcer or flat stigmata of recent hemorrhage, one could consider continuing antiplatelet therapy because the short-term mortality due to withholding antiplatelet agents in high-risk cardiovascular patients is likely greater than the risk of recurrent hemorrhage from low-risk lesions if DAT is maintained. Diagnostic endoscopy, with or without biopsy, for patients using antiplatelet agents is safe. Several observational studies reported no significant increase in bleeding complications for patients undergoing upper endoscopy, colonoscopy, or enteroscopy. Consensus expert opinion by the American Society for Gastrointestinal Endoscopy and British Society of Gastroenterology suggests that endoscopic hemostasis also is effective and appears safe in the setting of antiplatelet agents. The data to support these opinions are less robust than the data for diagnostic endoscopy, and are extrapolated from studies evaluating the safety of polypectomy in patients using aspirin, or from endoscopic hemostasis in anticoagulated patients. Although successful hemostasis of peptic ulcers has been shown to be effective in retrospective studies of patients with international normalized ratio values ranging from 1.5 to greater than 4.0, the applicability of these data to patients taking DAT is unclear. Although DAT has been associated with an increased risk of postpolypectomy bleeding, data from a very small study reported successful endoscopic hemostasis in 17 patients with bleeding ulcers taking DAT. The overall rate of complications of upper GI endoscopy or colonoscopy within 30 days of ACS is 7.5% to 12%. The mortality in this setting is 1% to 2%, and usually is limited to patients with severe myocardial compromise, complex tachyarrhythmias, or a high Acute Physiology and Health Evaluation II score. Although the mortality from acute GI hemorrhage is 10-fold higher in patients with ACS than in those without ACS, the benefits of proceeding with endoscopic evaluation likely outweigh the risks. No randomized data support this conclusion, but in a recent decision analysis, Yachimski et al showed the benefits of upper endoscopy for acute GI hemorrhage after a myocardial infarction. The investigators reported that patients who undergo esophagogastroduodenoscopy before cardiac catheterization would have a reduction in mortality from 600 per 10,000 patients, to 97 per 10,000 patients. Similar benefits could not be shown for patients with ACS and occult GI hemorrhage. The decision to continue or discontinue antiplatelet agents must be individualized based on an assessment of the risk of thromboembolic events if these agents are withheld versus the risk of further GI hemorrhage associated with continuation of these medications. Most investigators recommend stopping DAT upon presentation with acute GI hemorrhage, but there are no randomized clinical trials comparing continuous use of DAT with temporarily withholding DAT. In a retrospective study of acute GI hemorrhage in the setting of DAT, Ng et al reported that no recurrent bleeding occurred in 33 of 106 patients who received DAT continuously, or in the 24 patients who had DAT stopped for fewer than 7 days. As described earlier, the mortality associated with discontinuing DAT in patients with ACS or recently placed coronary stents is high. Thus, an alternative strategy may be to determine DAT therapy after complete clinical and endoscopic risk assessment. Patients with severe ongoing hemorrhage or those with GI lesions requiring endoscopic hemostasis may benefit from having DAT withheld for several days. Patients with stable vital signs and low-risk endoscopic findings may continue uninterrupted use of DAT. A proposed algorithm for initial management of DAT in the setting of acute GI hemorrhage is shown in Figure 1. Randomized clinical trials and meta-analyses of peptic ulcer bleeding show improved rates of rebleeding and mortality in patients randomized to a proton pump inhibitor (PPI) after endoscopic hemostasis. Prevention of recurrent hemorrhage consists of healing mucosal lesions, eradicating H pylori, and avoiding offending agents, whenever possible. Patients who require continued use of antiplatelet agents present a dilemma. Several randomized clinical trials have addressed this specific issue. In one trial, 156 patients were randomized either to PPI and early resumption of aspirin after endoscopic hemostasis of peptic ulcer disease or to PPI and placebo. Although the aspirin group had a higher rate of recurrent bleeding than the placebo group (18.9% vs 11%), 30-day all-cause mortality was significantly lower (1.7% vs 14.5%). An earlier trial randomized 129 patients with low-risk peptic disease to early resumption of aspirin and omeprazole, or to clopidogrel and omeprazole. No patient had rebleeding, and the rate of recurrent ulceration at 8 weeks was 5% in both groups. Although these were fairly small trials, the data support the re-initiation of antiplatelet agents along with a PPI after acute GI hemorrhage caused by ulcer disease. For patients requiring cardiac prophylaxis after bleeding from a peptic ulcer, use of clopidogrel alone has been shown in 2 randomized trials to have a higher risk of GI adverse events than aspirin combined with a PPI. Therefore, if antiplatelet agents are needed, consideration should be given to aspirin with PPI co-therapy in patients at higher risk for recurrent bleeding. Decisions regarding continuing antiplatelet agents and timing of endoscopic interventions for elective endoscopy also must be individualized in the same manner as for urgent endoscopy. There is ample evidence that upper GI endoscopy and colonoscopy with biopsies or with polypectomy can be performed safely without discontinuing aspirin. Endoscopic biopsy for patients using clopidogrel also appears safe, but data for polypectomy and clopidogrel are limited. Therefore, consideration should be given to postponing elective procedures (including screening colonoscopy, during which polypectomy may be necessary) until clopidogrel can be withheld (eg, until after the first year of DAT for coronary artery stents). The lack of randomized clinical trials leaves many questions unanswered and mandates reliance on expert opinion for many recommendations. Research is still necessary to clarify several key issues. The effect of clopidogrel on the GI mucosa and on the incidence of recurrent bleeding is unclear. Clopidogrel may delay ulcer healing by interfering with angiogenesis, but endoscopic findings for patients using clopidogrel have been no different from patients taking placebo. Conversely, a recent trial showed that the 6-month risk of recurrent ulcers in patients with a history of peptic ulcer disease was 11% in patients randomized to clopidogrel alone, versus 1.2% for those randomized to clopidogrel and esomeprazole. Endoscopic hemostasis is recommended for lesions at high risk of recurrent hemorrhage, but the efficacy and safety of hemostasis during active use of DAT has not been studied adequately. In a recent meta-analysis, Laine and McQuaid reported that the pooled rate of inducing bleeding with endoscopic hemostasis is 0.5%. None of these clinical trials allowed continued use of antiplatelet agents, thus it is unknown whether the risk of induced bleeding as a result of endoscopic hemostasis would be higher with these medications. Should all antiplatelet agents be withheld when patients present with acute GI hemorrhage, and when should treatment be resumed? As detailed earlier, there are no randomized trials evaluating a strategy of continuous DAT for patients with acute GI hemorrhage. Two clinical trials resumed aspirin 1 to 3 days after successful endoscopic hemostasis and showed survival benefit for patients randomized to aspirin compared with withholding aspirin for 8 weeks. Whether this time interval is optimal to balance the cardiovascular risks of discontinuing antiplatelet therapy in ACS patients and the mucosal toxicity of these agents is unknown. Lastly, if aspirin is re-introduced after major GI hemorrhage, should a very low dose of aspirin be prescribed? Although Sung et al showed lower overall mortality for patients randomized to aspirin and PPI compared with those randomized to placebo, the rebleeding rate in the aspirin group was not insignificant (14%). Is there a lower dose of aspirin that still may confer cardioprotection but avoid the risk of serious GI adverse events? Several practice guidelines and expert consensus statements published since 2008 address the subject of GI hemorrhage and the use of antiplatelet agents. The American Society of Gastrointestinal Endoscopy and the British Society of Gastroenterology discuss recommendations for management of antithrombotic agents for patients undergoing endoscopic procedures. A multisociety consensus document by the American College of Cardiology, American College of Gastroenterology, and the American Heart Association focuses on reducing the GI risk of antiplatelet therapy and nonsteroidal anti-inflammatory drug use. Finally, an international conference group updated a 2003 consensus recommendation document on the management of patients with nonvariceal upper GI bleeding and devoted several sections to the management of patients using antiplatelet agents and nonsteroidal anti-inflammatory drugs. These groups provide similar recommendations with regard to managing GI hemorrhage in patients with increased coronary risk, although some were more explicit than others. The decision to discontinue antiplatelet agents in the setting of acute GI hemorrhage should be individualized according to the cardiac risks and severity of hemorrhage. If the bleeding is life-threatening, consider transfusing platelets at initial presentation. Endoscopic evaluation of this patient population should be performed. For patients at high cardiac risk (eg, ACS, recent coronary stents), antiplatelet agents should be resumed as soon as the cardiac benefits appear to outweigh the risk of GI events. Monotherapy with clopidogrel carries a higher risk of GI toxicity than monotherapy with aspirin and a PPI. Patients should be tested for H pylori after an episode of GI hemorrhage owing to ulcer disease, and treated if infection is shown. The patient was given supplemental oxygen and resuscitated in the emergency room with IV fluids and 2 units of packed red blood cells. A bolus of IV PPI followed by a continuous infusion was provided. She was transferred to the intensive care unit, and 6 hours after presentation underwent upper endoscopy. A 1.5-cm duodenal ulcer with a nonbleeding visible vessel was identified and treated with a heater probe. Antral biopsies were performed to search for H pylori. IV PPI therapy was continued and after consultation with her cardiologist we decided to hold the aspirin and clopidogrel. She remained stable and was transferred to a regular bed 24 hours later. On day 3 of her hospitalization she was tolerating a regular diet. Low-dose aspirin and clopidogrel were resumed and the IV PPI was changed to once-daily oral dosing. Antral biopsy showed gastritis, but no H pylori. Given the possibility of a false-negative result in this setting, blood was sent for H pylori antibody determination. She was discharged home after 4 days of hospitalization feeling well, and with a stable hemoglobin level. The serum H pylori antibody was positive, and thus eradication therapy for H pylori was prescribed at the 2-week follow-up evaluation by her gastroenterologist. This material is the result of work supported in part by resources from the VA Puget Sound Health Care System (Seattle, Washington). CME Activities–Exams 1 and 2Clinical Gastroenterology and HepatologyVol. 9Issue 8Preview Full-Text PDF" @default.
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• W2040804906 title "Acute Upper Gastrointestinal Hemorrhage in an Elderly Woman Taking Aspirin and Clopidogrel" @default.
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