The color and texture of stool or emesis (Table 48.1) can provide clues to the location of the GI bleed. Such information is vital, as it may influence the workup and management. Iron in the red blood cells, when exposed to gastric acid, becomes oxidized, resulting in a coffee-ground appearance. This oxidized blood can also be excreted in the stool, producing a tarry, blackened stool known as melena. Coffee-ground emesis and melena are both classic signs of upper GI bleeding. Bright-red blood or maroon-colored stools usually indicate bleeding in the lower GI tract. Rarely, bright-red blood per rectum is the result of massive bleeding from the upper GI tract, as large volumes of blood act as a cathartic. The rapid transit prevents the blood from being subjected to the digestive enzymes.

Increasing age (>60 years old), increased number of comorbid conditions (renal failure, liver failure, or heart failure), variceal bleeding (vs non-variceal), shock on presentation, increasing number of units of blood transfused, active bleeding during endoscopy, bleeding from a large (>2.0 cm) ulcer, recurrent bleeding, and need for emergency surgery.

Esophageal varices are dilated tortuous veins located in the submucosa of the distal third of the esophagus that form as a result of portal hypertension. Given their size, high pressure, and superficial location, they are highly prone to erode and cause life-threatening bleeding. The primary venous drainage of the esophagus is via the esophageal veins that empty into the superior vena cava. However, distal veins within the submucosa empty into the left gastric vein (also known as the coronary vein), which normally drains into the portal vein. In the presence of cirrhosis, the portal vein has much more difficulty draining its blood into the scarred liver. Blood is forced to flow in a retrograde direction, under high pressure toward the tributaries of the portal vein.

Acute gastritis is an erosive, superficial inflammation in the lining of the stomach secondary to the dysfunction of mucosal defenses. These defense mechanisms include the production of prostaglandins, bicarbonate, and somatostatin. All three reduce the inflammatory effects that gastric acid can have on the gastric mucosa. Increased hydrochloric acid secretion does not play a primary role, but low doses of alcohol have been shown to cause increased acid secretion (high doses do not) which may exacerbate erosions. NSAIDs, which are COX-1 and COX-2 inhibitors, reduce the production of prostaglandins and their protective mechanisms on the stomach lining. Consumption of corrosive materials (e.g., household cleaners, pesticides, gasoline, cosmetics) can also lead to acute gastritis.

Chronic (atrophic) gastritis is a nonerosive inflammation of the gastric mucosa. Type A or fundus-dominant chronic gastritis is associated with pernicious anemia in which the body produces autoantibodies to parietal cells leading to megaloblastic anemia and vitamin B12 deficiency. Type B or antral-dominant chronic gastritis is the most common form and is caused by a Helicobacter pylori infection leading to peptic ulcer disease and an increased risk of gastric cancer and mucosa associated lymphoid tissue (MALT) lymphoma.

Dieulafoy’s lesion is a rare cause of acute upper GI bleed. This is a vascular malformation in which a large tortuous artery that is aberrantly located in the submucosa, often in the lesser curvature of the stomach, is eroded by gastric acid. The classic finding on endoscopy is a small, pinpoint defect in the gastric mucosa which is not a primary ulcer but likely a result of the mechanical pressure from the pulsating large artery that progressively erodes through the mucosa. They are identified endoscopically and described as a visible vessel without an underlying ulcer present.

The branches of the celiac trunk (Table 48.3) may be subject to erosion leading to severe hemorrhage if an ulcer penetrates through the gastrointestinal mucosa and into the vessel.