The most common presentation is hematemesis and there could also be melena. Other symptoms are abdominal pain, dysphagia, odynophagia, and other features of liver disease or underlying medical condition. They could also present in confusion secondary to hepatic encephalopathy. On physical examination, patient will be pale, hypotensive and could be in shock, with reduced urine output, and could be unconscious/subconscious. There would also be signs of liver disease and signs of overwhelming infection might also be seen.
There is a recurrence rate of about 70% and up to 33% of a recurring hemorrhage will result in death. The highest risk of fatality is during the first few days after the bleeding episode and the risk begins to decline progressively after 6 weeks. There is about 65% mortality in patients with esophageal varices that could be attributed to associated disorders of the renal, cardiovascular and immune system .
Esophageal varices are caused by anything that can cause portal hypertension. Such cause could be prehepatic like portal vein thrombosis, portal vein obstruction and increased splenic flow. It could also be intrahepatic like liver cirrhosis, hepatitis, idiopathic portal hypertension and congenital hepatic fibrosis and posthepatic like Budd-Chiari syndrome, compression from a tumor and constrictive pericarditis.
Factors are also present which increase the risk for variceal bleeding and they include malnutrition, alcohol intake, decompensation of liver disease, increased intraabdominal pressure, non-steroidal anti-inflammatory drugs (NSAIDs), bacterial infection and circadian rhythms .
Esophageal varices account for up to 30% of all cases of upper gastrointestinal hemorrhage and they are seen in over 50% of patients with liver cirrhosis. Annually, up to 8% of patient with liver cirrhosis develop esophageal varices and the varices are large enough to have a risk of bleeding in about 3% of those that develop it. Up to 30% of patients with small varices will progressively develop large varices and are also therefore at a risk of bleeding. The mortality rate from esophageal variceal bleed is about 20% at 6 weeks although, in up to 40% of patients, bleeding stops spontaneously .
Portal hypertension develops in liver disease as a consequence of an increase in vascular resistance at either the prehepatic, intrahepatic or posthepatic levels. An increase in portal venous flow also contributes to the hypertension. Esophageal varices develop as the pressure in the portal vein continues to increase. The varices are small on the outset but as the hyperdynamic circulation increases, blood flow through the varices also increases and this raises the tension within the wall. When the expanding force exceeds the maximal wall elastic limit, there is rupture which will cause variceal hemorrhage. If the pressure in the portal vein does not reduce, then there is a risk of recurrence  .
Esophageal varices are porto-systemic collaterals. They are vascular channels that link the portal and systemic venous system and they form as a result of portal hypertension and are mostly seen in the lower one-third of the esophagus. The rupture of esophageal varices and subsequent bleeding is a major complication of portal hypertension. It is usually associated with a high mortality rate .