Ruptured gastroesophageal varices are the most severe and frequent causes of upper gastrointestinal bleeding in patients suffering from liver cirrhosis, accounting for 80% of all bleeding episodes. Despite recent progress in treatment strategies, variceal bleeding is still considered the most severe type of gastrointestinal bleeding associated with a mortality of 20% at 6 weeks. The most widely accepted explanation for the rupture is the "explosion hypothesis": bleeding is a result of the elevated intravariceal pressure and increased wall-straining due to a rapid increase in the portal pressure gradient. The rupture of the varices and the early rebleeding cannot be attributed solely to mechanical changes. Furthermore, the factors involved in the sudden increase of portal pressure gradient are yet to be discovered. Recently it was postulated that various humoral factors may also play an important role in the pathomechanism of the rupture. The pivotal role of bacterial infection and consequent endotoxaemia must be emphasized. Passage of both viable microbes and microbial products, such as endotoxins from the intestinal lumen to peripheral and portal circulation in cirrhotic patients can be explained by the intestinal bacterial overgrowth, the intestinal dysmotility and the increased intestinal permeability. Endotoxaemia can be a critical factor that triggers a cascade of humoral events, resulting in a further increase of portal pressure, impairment of liver function and worsening of haemostasis, and eventually leads to variceal bleeding. Early administration of prophylactic antibiotics to variceal bleeders recently became an integral and important part of therapeutic strategy. Antibiotics are not only useful in the prevention of early rebleeding but also they are proven to significantly decrease the rate of mortality. The improvement in mortality is equivalent to that seen with terlipressine.