الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Portal hypertension (PH) is a major complication of chronic liver disease (CLD), most frequently in cirrhosis, leading to the development of portosystemic collaterals of which the most clinically significant are those that form gastroesophageal varices.(1, 2) Variceal hemorrhage is a lethal complication of PH and liver cirrhosis, particularly in patients in whom clinical decompensation including ascites, encephalopathy, a previous episode of hemorrhage or jaundice has already developed.(5)
Gastroesophageal varices are present in approximately 50% of patients with cirrhosis. Their presence correlates with the severity of liver disease; while only 40% of Child A patients have varices, they are present in 85% of Child C patients.(6) It has also been shown that 16% of patients with hepatitis C and bridging fibrosis have esophageal varices.(8)
Development of gastroesophageal varices in cirrhotic patients occur at a rate of 7% per year.(9, 10) The 1-year rate of a first variceal hemorrhage is approximately 12% (5% for small varices and 15% for large varices).(11)
Esophagogastroduodenoscopy remains the main method for diagnosing and grading of esophageal varices (EV).(62) In the Paquet(63) classification, varix size is graded into 4 grades: grade 1 varices are small and flattened by insufflation of air; grade 2 varices are slightly larger and do not flatten by insufflations of air; grade 3 varices are larger but do not touch in the middle of the lumen; and grade 4 varices are large and touch each other in the middle of the lumen.
Portal hypertensive gastropathy (PHG) is one of sources of gastrointestinal bleeding. McCormack classified PHG into two main types, mild and severe. Mucosal changes in the mild type include fine pink speckling or scarlatina type rash, areas of raised red edematous mucosa separated by fine white reticular pattern giving the snake skin appearance and superficial reddening, especially on the surface of the rugae giving the striped appearance while in the sever type include discrete red spots and diffuse hemorrhagic lesions.(61)
Gastric varices are less prevalent than esophageal varices and are present in 5%-33% of patients with portal hypertension with a reported incidence of bleeding of about 25% in 2 years; with a higher bleeding incidence for fundal varices(57)
Management of PH is of crucial importance for patients with chronic liver disease either to prevent first attack of variceal bleeding (primary prophylaxis) or to prevent further attacks of variceal bleeding (secondary prophylaxis) as well as management of acute variceal bleeding(82).
Patients who survive an episode of acute variceal hemorrhage have a very high risk of rebleeding and death. The median rebleeding rate in untreated individuals is around 60% within 1-2 years, with a mortality of 20-35%. (11-14, 127)
Given this high recurrence rate, patients who survive an acute variceal hemorrhage should receive therapy to prevent recurrence before they are discharged from the hospital.(96, 129) Combination of endoscopic variceal ligation plus drug therapy is the current recommended regimen.(130)