Skip to Main Content


Gastrointestinal (GI) bleeding is an important cause of mortality for emergency department (ED) and critically ill patients. Upper gastrointestinal bleeding (UGIB) is defined as a gastrointestinal bleeding source proximal to the ligament of Treitz, whereas lower gastrointestinal bleeding (LGIB) is defined as bleeding distal to the ligament of Treitz (Figure 23-1). This chapter discusses the epidemiology, clinical presentation, and etiology of UGIB and LGIB, followed by a discussion of the management of patients with GI bleeding.


(A) The ligament of Treitz attaches the third and fourth part of the duodenum to connective tissue around the superior mesenteric artery. It demarcates the end of the upper gastrointestinal tract and the beginning of the lower gastrointestinal tract. (B) The gastric parietal cells generate an acidic environment via the H-K-ATPase. The mucosal epithelial cells balance the acidity and protect the gastric lining by secreting mucus and bicarbonate. Ingested protein present in the stomach stimulates G-cells to produce gastrin, which stimulate parietal cells to secrete H+ ions. An acidic environment provides negative feedback via somatostatin from D-cells. Enterochromaffin-like (ECL) cells are located in gastric glands in the gastric mucosa and have multiple receptors, receiving positive input from the enteric nervous system (M1) and negative input via somatostatin. When stimulated, ECL cells produce histamine (H2) which stimulate parietal cells to secrete H+ ions. Peptic ulcer disease (PUD) is caused by NSAIDs and H. pylori infection. NSAIDs inhibit the cyclooxygenase (COX) enzyme which produces prostaglandins from arachidonic acid (AA). Prostaglandins promote mucus and bicarbonate secretion from mucosal epithelial cells. NSAID use decreases the presence of these protective elements. H. pylori infection, again, inhibits the secretion of bicarbonate and mucus, but also activates the parietal cells and the ECL cells, causing an acidic environment, resulting in PUD. (C) The portal vein conducts blood from the gastrointestinal tract and spleen to the liver. Hepatic cirrhosis leads to increased hepatic resistance, resulting in portal vein hypertension and increased portal blood flow. This increase in portal pressure causes dilation of existing vessels and the formation of portocaval anastomoses, such as esophageal varices. These highly vascularized anastomoses are under elevated pressures and liable to bleeding in the gastrointestinal tract.



In the United States, UGIB occurs in 50 to 150 cases per 100,000 adults per year, and accounts for 400,000 hospital admissions and 30,000 deaths annually.13 With a mortality rate ranging from 3% to 16%, UGIB is an important cause of mortality in the ED.411

Hospital inpatients presenting with UGIB have a 2- to 6-fold increase in mortality compared with their ED counterparts.411 Increased risk of mortality is associated with increased age, severe comorbidity, hypotension, shock, rebleeding, and the timing of the bleeding ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.