Caused by portal hypertension resulting from increased resistance to portal flow and increased portal venous blood inflow from cirrhosis.
Portal hypertension leads to an increase in the portosystemic collateral flow as it attempts to decompress portal venous system.
The most critically important site of collateral flow is within the mucosa of the proximal stomach and distal esophagus with the development of gastroesophageal varices.
The second most common cause of upper G.I. bleeding, and is always considered in patients with a history of cirrhosis with portal hypertension.
Approximately half of patients with cirrhosis have gastroesophageal varices as a consequence of an elevated hepatic venous pressure gradient of greater than 10-12 mmHg.
The severity of underlying cirrhosis is directly related to the probability that the patient will have varices.
Depending on the severity of the bleed, patients with variceal bleeding may present with melena, hematemesis, or hematochezia.
Approximately 60% of upper G.I. bleeding cases in patients with cirrhosis are unrelated to portal hypertension.
Structural liver changes of increased vasculature fibrosis and regenerative nodules and increased dynamic hepatic vasculature tone from endothelial dysfunction and decreased nitric oxide bioavailability cause esophageal varices(Iwakiri Y).
Collateral blood vessels between the portal and systemic circulations develop when portal-pressure gradient increases.
With the development of portosystemic collateral circulation, the portal venous blood flow increases secondary to splanchnic vasodilation and increased cardiac output.
Increased portal blood flow then maintains and increases the portal hypertension.
Gastric and esophageal varices are the most important collateral blood vessels formed.
As pressure and blood flow increase in varices they grow and eventually rupture.
Gastroesophageal varices result from cirrhosis induced portal hypertension with increased resistance to portal flow, and increased portal venous blood flow.
Increased portal resistance is due to distortion of the of liver vasculature by fibrosis and regenerative nodules and by increased hepatic vascular tone due to endothelial dysfunction and decreased availability of nitric oxide (Iwakiri Y).
When the difference between portal vein pressure and hepatic vein pressure increases above a certain threshold collaterals, modulated by angiogenic factors, develop at sites of communication between portal and systemic circulation (Grozmann RJ Fernandez M, Iwakiri Y).
With the development of collateral vessels portal venous flow increases as a result of splanchic vasodilation and increased cardiac output.(Iwakiri Y).
Esophageal varices are classified as small, less than 5 mm, or large 5 mm or greater.
Esophageal varices risk of bleeding in small varices is approximately 15% per year.
In patients with large varices the risk of bleeding is as high as 40-45% each year.
Pharmacologic or endoscopic treatment for the prevention of a first variceal bleed is recommended for patients with large varices and those with small varices and significant decompensated liver disease.
Beta-blocker therapy is recommended for patients with large varices.
Beta blockers reduce the risk of initial variceal bleeding from about 45 to 22 percent.
Prevalence in cirrhosis is 60-80%.
Patients with cirrhosis and esophageal varices without previous variceal bleeding have a 25% to 40% chance of first variceal hemorrhage when they do not have effective prophylactic treatment.
Risk of first bleeding esophageal varices is related to the Child-Pugh class, the size and thickness of the varices, the hepatic venous pressure gradient and the intravariceal pressure.
Management includes primary prophylaxis to prevent the first episode of variceal bleeding, treatment of an acute bleeding episode, and secondary prophylaxis to prevent a recurrent variceal hemorrhage.
Highest rate of variceal bleeding occurs among patients with Child-Pugh Class B or C disease.
Patients at high risk for bleeding are those with red wale marks on varices.
The development and growth of gastroesophageal varices in cirrhosis occur at a rate of 7% per year (Grozmann RJ, Merli M).
The one year rate of a first variceal bleed is approximately 5% in small varices and 15% for large varices(D’amico G).
1 year rate of recurrent variceal hemorrhage in approximately 60% (Bosch J).
6 week mortality with each episode of variceal bleed is approximately 15-20%, with 0% mortality with Child class A disease and 30% with Child class C disease (Villanueva C, Albrades JG, Bosch J).