Frequency of Variceal Upper Gastrointestinal Bleeding (UGIB) in Patients with Established Varices

Abstract

Older literature suggests that 53% of patients with known varices presenting with acute UGIB have a nonvariceal source; bleeding peptic ulcers and erosions account for almost 40% (Dagradi, Am J Gastroenterol 1970). These proportions may have changed with advances in endoscopic evaluation and overall management. Methods: All patients presenting with definitive acute UGIB and varices on upper endoscopy were eligible for inclusion. Inpatient charts were reviewed to confirm the source of acute UGIB and corroborate the diagnosis of portal hypertension. Variceal bleeding was diagnosed if active bleeding or red wale sign were visualized. Nonvariceal etiologies required the presence of stigmata of bleeding (active bleeding or adherent clot). Multiple bleeding presentations within a 30 day period were considered part of one bleeding episode. Results: Over a 2-year period, varices were visualized on endoscopy in 143 consecutive patients (55±1.1 yr, 50F:93M) presenting with 173 distinct episodes of acute UGIB. Bleeding presentation included hematemesis (bloody or coffee ground emesis) in 65 instances (37%), melena in 41 (24%) and both in 67 (39%). The source of UGIB was conclusively localized in 137 bleeding episodes (79%). A variceal source was identified in 115 instances (66%), 108 from esophageal varices, and 7 from gastric varices. Nonvariceal bleeding accounted for 22 bleeding episodes (13%), and included peptic ulcers and erosions (9 episodes, 5%), angioectasia including gastric antral vascular ectasia (9, 5%), Mallory-Weiss tear (1, 0.6%), oozing portal hypertensive gastropathy (1, 0.6%), and oro- and nasopharyngeal sources (2, 1%). The bleeding source could not be definitively identified in 36 instances (21%); endoscopic findings included Grade II or larger varices in 10 (4 underwent band ligation), peptic ulcers and erosions in 9, nonbleeding angioectasia in 4 (3 treated), esophagitis in 4 and Mallory Weiss tears in 2. All patients with angioectasia had melena but no hematemesis, and all patients with gastric variceal bleeding had bloody emesis. However, bleeding presentation did not predict source of UGIB (p=NS). Conclusions: Using strict criteria to establish the bleeding source, variceal bleeding accounts for as many as two-thirds of patients with known varices presenting with UGIB - a significant change from older reports. Peptic ulcers are uncommon sources of bleeding in this population in the present day. Bleeding presentation cannot be used to predict the most likely source of UGIB.