Portal hypertension- a major hallmark of cirrhosis is defined as a
portal pressure gradient exceeding 5-10 mm Hg. In portal hypertension,
portosystemic collaterals decompress the portal circulation and give rise to
varices. Development of esophageal varices and gastrointestinal bleeding
represents a serious consequence in patients with portal hypertension. At the
time of diagnosis of liver cirrhosis, esophageal varices are present in about
40% of patients with compensated disease and in 60% of those with
decompensated disease and ascites. In patients with liver cirrhosis who do not have detectable esophageal varices, the latter appear at a rate of nearly 5% per year. Also, the size of varices tends to increase with time. It has been estimated that among those with small esophageal varices, nearly 12% progress to large varices
annually. The annual incidence of first variceal bleeding has been estimated to
be around 4% in non-selected patients with cirrhosis of the liver who have
not bled previously. It has been shown that the risk of variceal bleeding is
related to the size of esophageal varices, 8 with large esophageal varices
being at a greater risk; this is possibly due to a higher variceal wall tension
in large esophageal varices. Thus, annual incidence of gastrointestinal
bleeding is only 1–2% in patients without varices, 5% in those with small
esophageal varices and 15–20% in patients with large esophageal varices.