Acute variceal hemorrhage is a serious cause of mortality in the emergency department and can be difficult to treat. In general, upper gastrointestinal (GI) hemorrhage accounts for 102 hospitalizations per 100,000 people every year, and esophageal varices represent approximately 14% of these cases.1,2 Furthermore, esophageal varices are the most common cause of persistent and severe upper GI hemorrhage, accounting for approximately 33% of these events.3 Among patients with cirrhosis, 70% of upper GI bleeding episodes are caused by esophageal varices.4 Gastroesophageal varices exist in nearly 50% of patients with cirrhosis at the time of initial diagnosis.5
The past 2 decades have seen significant advances in the treatment of variceal bleeding, but these events remain lethal in many cases. For initial bleeding episodes from esophageal varices, 6-week mortality stands at approximately 15%, down from 40% 25 years ago.6 This high mortality rate distinguishes variceal hemorrhage from other causes of upper GI bleeding, which often resolve spontaneously and have mortality rates below 3%.3 Given the lethality of this disease, it is more vital than ever for emergency physicians to understand current therapy for gastroesophageal varices and deliver life-saving treatment.
Although the basic pathophysiology of portal hypertension and variceal disease has been well established, research is ongoing to enable us to understand the mechanisms of this disorder and uncover important therapies. In the western world, portal hypertension is caused most often by cirrhosis and leads to portosystemic shunts and enlarged blood vessels at several anatomic locations, including the distal esophagus and proximal stomach.7 As portal pressure increases, these vessels become more likely to bleed. Worsening liver failure depletes coagulation factors, increases portal hypertension, and makes bleeding more likely.8 Importantly, bacterial infection also increases the risk of hemorrhage, particularly rebleeding.9
Two main prophylactic therapies are aimed at reducing these risk factors for hemorrhage. Beta-blocker therapy is recommended for use in cirrhotic patients with known esophageal varices, and acts to reduce portal hypertension, delay the advancement of varices, and prevent hemorrhage.5 In addition, the use of prophylactic antibiotics after an episode of variceal hemorrhage decreases the likelihood of rebleeding.10