1. ACUTE UPPER GASTROINTESTINAL BLEEDING
ESSENTIALS OF DIAGNOSIS
Hematemesis (bright red blood or “coffee grounds”).
Melena in most cases; hematochezia in massive upper gastrointestinal bleeds.
Volume status to determine severity of blood loss; hematocrit is a poor early indicator of blood loss.
Endoscopy diagnostic and may be therapeutic.
There are over 250,000 hospitalizations a year in the United States for acute upper gastrointestinal bleeding. In the United States, the mortality rate for nonvariceal upper gastrointestinal bleeding has declined steadily over the past 20 years to 2.1% in 2009. Mortality is higher in patients who are older than age 60 years and in patients in whom bleeding develops during hospitalization. Patients seldom die of exsanguination but rather of complications from an underlying disease.
The most common presentation of upper gastrointestinal bleeding is hematemesis or melena. Hematemesis may be either bright red blood or brown “coffee grounds” material. Melena develops after as little as 50–100 mL of blood loss in the upper gastrointestinal tract, whereas hematochezia requires a loss of more than 1000 mL. Although hematochezia generally suggests a lower bleeding source (eg, colonic), severe upper gastrointestinal bleeding may present with hematochezia in 10% of cases.
Upper gastrointestinal bleeding is self-limited in 80% of patients; urgent medical therapy and endoscopic evaluation are obligatory in the rest. Patients with bleeding more than 48 hours prior to presentation have a low risk of recurrent bleeding.
Acute upper gastrointestinal bleeding may originate from a number of sources (eFigure 15–1). These are listed in order of their frequency and discussed in detail below.
Duodenal ulcer with oozing. (Used, with permission, from Kenneth McQuaid, MD.)
Peptic ulcers account for 40% of major upper gastrointestinal bleeding with an overall mortality rate of less than 5%. In North America, the incidence of bleeding from ulcers is declining due to eradication of H pylori and prophylaxis with proton pump inhibitors in high-risk patients.
Portal hypertension accounts for 10–20% of upper gastrointestinal bleeding. Bleeding usually arises from esophageal varices (eFigure 15–2) and less commonly gastric (eFigure 15–3) or duodenal varices or portal hypertensive gastropathy (eFigure 15–4). Approximately 25% of patients with cirrhosis have medium to large esophageal varices, of whom 30% experience acute variceal bleeding within a 2-year period (eFigure 15–5). Due to improved care, the hospital mortality rate has declined over the past 20 years from 40% to 15%. Nevertheless, a mortality rate of 60–80% is expected at 1–4 years due to recurrent bleeding or other complications of chronic liver disease.