Esophageal varices are dilated veins at the junction of the esophagus and the stomach. This is a site of a connection between the systemic and portal venous systems (portosystemic anastomosis). Normally, the connections are closed, but in patients with cirrhosis of the liver and portal hypertension the raised pressure in the portal system causes them to open up and enlarge.
The enlarged veins protrude into the lumen of the lower esophagus (visible on endoscopy). They may burst, resulting in hematemesis, which may rapidly be fatal. Esophageal varices account for 10% of upper gastrointestinal bleeding but a higher proportion of associated mortality.
Cirrhosis is the cause of 90% of varices in the UK, but schistosomiasis (bilharzia) causing non-cirrotic prehepatic portal hypertension is the major worldwide cause. Portal vein occlusion associated with pancreatitis or umbilical vein sepsis results in left-sided portal hypertension. Themanagement of acute variceal bleeding requires resuscitation involving restoring blood volume and taking measures to stop the bleeding. Urgent endoscopy is required and vasoconstrictor drugs (e.g. terlipressin and octreotide, a somatostatin analogue) can be given.
Sclerotherapy and elastic band ligation are widely used techniques to stem the loss of blood. Both are performed by endoscopy and can help prevent re-bleeding. Sclerotherapy involves injecting the varices with a sclerosing agent to produce vessel thrombosis and arrest bleeding. Banding involves placing a tight-fitting elastic band around the varices to stop it bleeding.
Patients are often put on a beta-blocker (e.g. propranolol or carvedilol), a prophylactic measure to prevent further variceal bleeds by lowering portal blood pressure and reducing portal blood flow. Prognosis following bleeding varices is dependent on etiology and liver function: excellent in portal vein thrombosis and poor for Child’s C cirrhosis particularly when jaundice, ascites, encephalopathy or hypoalbuminaemia may be present. Overall, mortality from a first bleed from esophageal varices is 40%.
Mallory–Weiss syndrome is haematemesis from a tear at the gastro-oesophageal junction (a Mallory–Weiss tear). It is caused by prolonged retching or coughing and a sudden increase in intra-abdominal pressure. It is most common following violent retching associated with binge drinking.