Cirrhosis and ascites developed in a 52-year-old man with a history of chronic hepatitis C and alcohol abuse. He was hospitalized because of bleeding esophageal varices, which were successfully treated with elastic band ligation.
Cirrhosis and ascites developed in a 52-year-old man with a history of chronic hepatitis C and alcohol abuse. He was hospitalized because of bleeding esophageal varices, which were successfully treated with elastic band ligation. Seen here is an endoscopic view of the patient’s stomach with the classic macroscopic “snakeskin” appearance of portal hypertensive gastropathy-a fine reticular pattern that separates areas of erythematous mucosa. Histological examination disclosed extensive edema and submucosal vessel dilation.
The mucosa is extremely friable in those with portal hypertensive gastropathy, and it is postulated that spontaneous rupture of the ectatic vessels results in bleeding. Management of such bleeding aims to decrease the portal pressure-ideally, to less than 12 mm Hg. Therapies include portacaval shunt surgery, transjugular intrahepatic portosystemic shunt, nitrates, and β-blockers (if not contraindicated by left-sided heart failure or chronic obstructive pulmonary disease). The most frequently used drug is propranolol, given orally. The initial dosage is increased gradually until the patient’s baseline heart rate is lowered by 25% (or to about 60 to 70 beats per minute). Extreme care must be taken to prevent hypotension.
Electrocoagulation, injection laser therapy, and surgery are ineffective in controlling bleeding from portal hypertensive gastropathy. Sucralfate, proton pump inhibitors, and H2 blockers are similarly ineffective.