Chapter 042. Gastrointestinal Bleeding (Part 2)

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Peptic Ulcers In addition to clinical features, characteristics of an ulcer at endoscopy provide important prognostic information. One-third of patients with active bleeding or a nonbleeding visible vessel have further bleeding that requires urgent surgery if they are treated conservatively. These patients clearly benefit from endoscopic therapy with bipolar electrocoagulation, heater probe, injection therapy (e.g., absolute alcohol, 1:10,000 epinephrine), and/or clips with reductions in bleeding, hospital stay, mortality rate, and costs. In contrast, patients with clean-based ulcers have rates of recurrent bleeding approaching zero. If there is no other reason for hospitalization, such patients may be discharged on the...

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Chapter 042. Gastrointestinal Bleeding (Part 2) Peptic Ulcers In addition to clinical features, characteristics of an ulcer at endoscopy provide important prognostic information. One-third of patients with active bleeding or a nonbleeding visible vessel have further bleeding that requires urgent surgery if they are treated conservatively. These patients clearly benefit from endoscopic therapy with bipolar electrocoagulation, heater probe, injection therapy (e.g., absolute alcohol, 1:10,000 epinephrine), and/or clips with reductions in bleeding, hospital stay, mortality rate, and costs. In contrast, patients with clean-based ulcers have rates of recurrent bleeding approaching zero. If there is no other reason for hospitalization, such patients may be discharged on the first
hospital day, following stabilization. Patients without clean-based ulcers should usually remain in the hospital for 3 days, as most episodes of recurrent bleeding occur within 3 days. Randomized controlled trials document that a high-dose constant-infusion IV proton pump inhibitor (PPI) (e.g., omeprazole 80-mg bolus and 8-mg/h infusion), designed to sustain intragastric pH > 6 and enhance clot stability, decreases further bleeding (but not mortality), in patients with high-risk ulcers (active bleeding, nonbleeding visible vessel, adherent clot), even after appropriate endoscopic therapy. Institution of therapy at presentation in all patients with UGIB does not significantly improve outcomes such as further bleeding, transfusions, or mortality as compared to initiating therapy only when high-risk ulcers are identified at the time of endoscopy. One-third of patients with a bleeding ulcer will rebleed within the next 1–2 years. Prevention of recurrent bleeding focuses on the three main factors in ulcer pathogenesis, H. pylori, NSAIDs, and acid. Eradication of H. pylori in patients with bleeding ulcers decreases rates of rebleeding to
but PPIs are more commonly used due to less frequent dosing (once daily) and fewer side effects (e.g., diarrhea). However, either PPI co-therapy alone or use of a coxib alone is associated with an annual rebleeding rate of ~10% in high-risk patients (i.e., a recent bleeding ulcer). Combination of a coxib and PPI provides a further significant decrease in ulcers and recurrent bleeding and should be employed in very high-risk patients. Patients with bleeding ulcers unrelated to H. pylori or NSAIDs should remain on full-dose antisecretory therapy indefinitely. Peptic ulcers are discussed in Chap. 287. Mallory-Weiss Tears The classic history is vomiting, retching, or coughing preceding hematemesis, especially in an alcoholic patient. Bleeding from these tears, which are usually on the gastric side of the gastroesophageal junction, stops spontaneously in 80–90% of patients and recurs in only 0–7%. Endoscopic therapy is indicated for actively bleeding Mallory-Weiss tears. Angiographic therapy with embolization and operative therapy with oversewing of the tear are rarely required. Mallory-Weiss tears are discussed in Chap. 286. Esophageal Varices Patients with variceal hemorrhage have poorer outcomes than patients with other sources of UGIB. Endoscopic therapy for acute bleeding and repeated sessions of endoscopic therapy to eradicate esophageal varices significantly
reduce rebleeding and mortality. Ligation is the endoscopic therapy of choice for esophageal varices because it has less rebleeding, a lower mortality rate, fewer local complications, and requires fewer treatment sessions to achieve variceal eradication than sclerotherapy. Octreotide (50-µg bolus and 50-µg/h IV infusion for 2–5 days) further helps in the control of acute bleeding when used in combination with endoscopic therapy. Other vasoactive agents such as somatostatin and terlipressin, available outside the United States, are also effective. Antibiotic therapy (e.g., quinolones) is also recommended for patients with cirrhosis presenting with UGIB, as antibiotics decrease bacterial infections and mortality in this population. Over the long term, treatment with nonselective beta blockers decreases recurrent bleeding from esophageal varices. Chronic therapy with beta blockers plus endoscopic ligation is recommended for prevention of recurrent esophageal variceal bleeding. In patients who have persistent or recurrent bleeding despite endoscopic and medical therapy, more invasive therapy is warranted. Transjugular intrahepatic portosystemic shunt (TIPS) decreases rebleeding more effectively than endoscopic therapy, although hepatic encephalopathy is more common and the mortality rates are comparable. Most patients with TIPS have shunt stenosis within 1–2 years and require reintervention to maintain shunt patency, although the use of coated stents appears to markedly decrease shunt dysfunction, at least in the first year. A randomized comparison of TIPS and distal splenorenal shunt in
Child-Pugh class A or B cirrhotic patients with refractory variceal bleeding revealed no significant difference in rebleeding, encephalopathy, or survival, but a much higher rate of reintervention with TIPS (82% vs. 11%). Therefore, TIPS is most appropriate in patients with more severe liver disease and those in whom transplant is anticipated. Patients with milder, well-compensated cirrhosis should require fewer re-interventions with decompressive surgery, although the higher initial risks of surgery must also be considered. Portal hypertension is also responsible for bleeding from gastric varices, varices in the small and large intestine, and portal hypertensive gastropathy and enterocolopathy.