The effects of ethanol administration on portal pressure and gastroesophageal collateral blood flow in patients with alcoholic cirrhosis

✍ Scribed by Joanna B. Ready; Kenneth F. Hossack; William G. Rector Jr.

• Publisher: John Wiley and Sons
• Year: 1990
• Tongue: English
• Weight: 394 KB
• Volume: 11
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840110422

✦ Synopsis

The pathogenesis of variceal hemorrhage is not well understood. Portal pressure and gastroesophageal collateral (azygous) blood flow are similar in patients with cirrhosis with or without a history of variceal bleeding. However, acute increases in these parameters in individual patients might predispose them to variceal rupture.

Fifteen patients with alcoholic cirrhosis and portal hypertension were evaluated to test the hypothesis that ethanol intake acutely increases portal pressure or gastroesophageal blood flow and is a possible risk factor in variceal hemorrhage. A 10% solution of ethanol in 6% dextrose in water was infused intravenously at a rate sufficient to raise the blood-alcohol level to 100 mg/d over 30 min. Eight patients received ethanol 5% dextrose in water; seven patients received a placebo (6% dextrose in water alone). Ethanol did not produce a significant change in wedged hepatic-vein pressure, free hepatic-vein pressure, azygous blood flow, mean arterial pressure or heart rate compared with the effects of 5% dextrose in water alone.

Acute administration of ethanol does not increase portal pressure or gastroesophageal blood flow. It is unlikely that acute ethanol ingestion is a risk factor for variceal hemorrhage. (HEPATOMGY 1990; 11:674-677.)

Hemorrhage from esophageal varices occurs in approximately one third of patients with cirrhosis (1, 2). An apparent risk factor for the development of this complication of chronic liver disease is the severity of portal hypertension. Portal-hepatic venous pressure gradients greater than 10 to 12 mm Hg (normal = < 5 mm Hg) are invariably present in patients with histories of variceal bleeding (3-5). Above this threshold, portal pressure does not appear to further predispose patients to bleeding. Similarly, gastroesophageal collateral blood flow, as indicated by flow in the azygous vein (6, 7), is