Upper GI Bleeding



Up to 90 per cent of upper GI bleeding is at­tributable to peptic ulceration, erosive gastritis, or esophagogastric varices.
Peptic Ulcer. Bleeding may occur from duo­denal, gastric, and post-surgical anastomotic ul­cers. A typical history of ulcer pain or dyspepsia may be absent, with bleeding being the first man­ifestation of peptic ulcer disease.

Gastritis. Erosive gastritis may result from ingestion of alcohol or anti-inflammatory drugs, such as aspirin or indomethacin. Gastric erosions also frequently develop as so-called stress gastritis in hospitalized patients with major trauma, severe systemic illness, extensive burns, or head injury. Since the risk of bleeding from erosive gastritis is recognized as being high (about 20 per cent) with a high mortality rate in such severely ill hospi­talized patients, preventive measures aimed mainly at raising gastric pH above 4 are usually instituted through the hourly administration of antacids. Although clearly successful in prevent­ing bleeding, these measures do not affect mor­tality in these critically ill patients.

Esophagogastric Varices. Bleeding occurs most frequently from varices in the esophagus and is characteristically abrupt and massive. Varices arise mainly as a result of portal hypertension sec­ondary to cirrhosis. Alcoholic cirrhosis is by far the commonest cause of variceal bleeding in the United States, although any cause of portal hy­pertension (e.g., portal venous thrombosis, schis­tosomiasis) may lead to variceal hemorrhage. Three factors complicate the course of GI bleeding in patients with cirrhosis. (1) Although varices are usually suspected as the cause of bleeding, other causes (e.g., gastritis, ulcers) actually account for up to 50 per cent of bleeding lesions in these pa­tients. These other causes of bleeding must in­variably be considered in the diagnostic work-up of the cirrhotic patient. (2) Sustained portal hy­pertension leads to recurrent bleeding in 70 per cent of patients with cirrhosis. Thus portal de­compression by means of a surgically created por­tosystemic shunt is the only absolutely effective means for preventing recurrence of bleeding. This in turn carries a high morbidity and appreciable mortality, especially when performed as an emer­gency procedure. (3) Cirrhosis often leads to the development of encephalopathy, which may manifest or exacerbate during bleeding, as well as to the development of coagulation defects, which contribute to continued bleeding. Because of these three factors, GI bleeding in patients with cirrhosis often poses difficult therapeutic prob­lems.

Other Lesions. The Mallory-Weiss syndrome, which refers to hemorrhagic laceration of the mu­cosa of the esophagogastric junction produced by vomiting, is characterized by a history of retching and nonbloody vomiting followed by hemate-mesis. Several other lesions of the upper GI tract, including esophagitis, carcinoma, and other tu­mors of the stomach, generally cause chronic blood loss but may also produce massive bleed­ing. Arterial-enteric fistulae may occur as a result of the use of synthetic bypass grafts for aortic aneurysms and must be suspected in any patient who has had such a bypass and presents with GI bleeding.