Portal hypertension: the management of esophageal/gastric varices, portal hypertensive gastropathy or hypertensive colopathy

10.2217/14750708.4.1.91 © 20 Portal hypertension is one of the main consequences of cirrhosis. Esophageal varices are most often a consequence of portal hypertension, although they can also be formed in other areas of the body, including the stomach, duodenum, colon and/or rectum. Patients with esophageal varices have a strong tendency to develop bleeding. Conversely, varices do not bleed if the hepatic venous pressure gradient is below 12 mmHg. Approximately 30–50% of patients with esophageal varices will bleeding within the first year of diagnosis. Once a patient experiences bleeding, the risk of rebleeding is high, reaching 80% within 1 year. The mortality rate for esophageal variceal bleeding, on the first event, is between 40 and 70%. Endoscopy can be useful in searching for varices with respect to primary prophylaxis and treatment of bleeding in cirrhotics. The treatment of esophageal varices can be pharmacologic, endoscopic or surgical. Three different clinical situations must be distinguished: in primary prophylaxis of esophageal variceal bleeding, the use of β-blocker treatment is only recommended in patients at high risk; in treatment of acute variceal hemorrhage, combining pharmacotherapy for 3–5 days with endoscopic therapy reduces rebleeding compared with either measure alone; in secondary prophylaxis of esophageal variceal bleeding, the treatment of choice is eradication of esophageal varices with band ligation. When the bleeding is refractory, the use of balloon tamponade may stop hemorrhage at least temporarily. If bleeding is uncontrolled, transjugular intrahepatic portosystemic shunt or nonselective portosystemic shunt may be suitable in patients with cirrhosis, provided that the liver dysfunction is not too severe. None of these measures, while being effective in stopping bleeding, have been shown to affect surveillance.