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Prediction of variceal hemorrhage in patients with cirrhosis

Arun J Sanyal, MD
Jasmohan S Bajaj, MD
Section Editor
Bruce A Runyon, MD
Deputy Editor
Anne C Travis, MD, MSc, FACG, AGAF


Cirrhosis affects 3.6 out of every 1000 adults in North America, and is responsible for more than one million days of work-loss and 32,000 deaths annually. A major cause of cirrhosis-related morbidity and mortality is the development of variceal hemorrhage, a direct consequence of portal hypertension [1]. Each episode of active variceal hemorrhage is associated with 30 percent mortality [2,3]. In addition, survivors of an episode of active bleeding have a 70 percent risk of recurrent hemorrhage within one year of the bleeding episode [4].

Variceal hemorrhage occurs in 25 to 40 percent of patients with cirrhosis [5]. While several modalities are available for primary prophylaxis of variceal bleeding, many are associated with significant adverse effects.

Accurate identification of patients at highest risk of bleeding permits stratification in an attempt to avoid potentially harmful preventive treatments in the 60 to 75 percent of patients who will never have variceal bleeding.

This topic will review the formation and progression of varices and the predictive factors and risk classification for variceal bleeding. Primary prophylaxis for variceal hemorrhage, the treatment of variceal hemorrhage, and the prevention of recurrent variceal hemorrhage in patients with cirrhosis are discussed elsewhere. (See "Primary and pre-primary prophylaxis against variceal hemorrhage in patients with cirrhosis" and "General principles of the management of variceal hemorrhage" and "Prevention of recurrent variceal hemorrhage in patients with cirrhosis".)


Portal pressure is determined by the product of portal flow volume and resistance to outflow from the portal vein. Portal hypertension (defined as hydrostatic pressure >5 mmHg) results initially from obstruction to portal venous outflow. Obstruction may occur at a presinusoidal (portal vein thrombosis, portal fibrosis, or infiltrative lesions), sinusoidal (cirrhosis), or postsinusoidal (veno-occlusive disease, Budd-Chiari syndrome) level. Cirrhosis is the most common cause of portal hypertension; in these patients, elevated portal pressure results from both increased resistance to outflow through distorted hepatic sinusoids, and enhanced portal inflow due to splanchnic arteriolar vasodilation.


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Literature review current through: Sep 2016. | This topic last updated: Jul 29, 2015.
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