Pathophysiology and prognosis of oesophageal varices.

The fundamental initiating factor in portal hypertension is an increase in resistance to portal venous flow. Portal venous pressure rises as a consequence, and collateral channels open to decompress the portal venous system. A number of secondary haemodynamic phenomena occur in animals and humans with portal hypertension. Systemic vascular resistance and mean arterial blood pressure fall and both cardiac output and splanchnic blood flow increase. Current theories suggest that increased vascular production of nitric oxide may have a principal role in the pathogenesis of these secondary haemodynamic changes. The most common causes of variceal bleeding are cirrhosis, schistosomiasis and extrahepatic portal venous obstruction. Varices develop in 90% of cirrhotic patients if follow-up is long enough. Bleeding from varices occurs in approximately 30% of patients followed up for 2-4 years, with mortality rates of 25% to 50% in those who bled. Prognosis is better in conditions where liver function is preserved, e.g. portal venous obstruction, schistosomiasis, etc.