Cirrhotic liver disease is a condition that is caused by chronic scarring and fibrosis of the hepatic parenchyma. The causes of cirrhosis are quite varied and include alcohol abuse, metabolic diseases (α-1 antitrypsin deficiency, Wilson disease), biliary disorders (bile duct obstruction, sarcoidosis, cystic fibrosis), toxins (carbon tetrachloride, hypervitaminosis A), and infections (hepatitis A, B, or C). Regardless of the etiology, the pathophysiology and clinical findings are similar. The liver becomes enlarged on clinical examination until late in the course. There may be jaundice, hyperbilirubinemia, transaminitis, or overt liver failure. With noninvasive imaging, the liver appears nodular and may elicit stigmata of portal hypertension including splenomegaly, esophageal varices, and reversal of portal blood flow. A definitive diagnosis is usually made by liver biopsy.

Upper gastrointestinal bleeding is a common intervening finding in patients with cirrhosis and can occur from the more traditional types of lesions including gastritis, Mallory-Weiss tears, and peptic ulcer disease. An important and critical complication of portal hypertension that is responsible for nearly one third of all deaths in patients with cirrhotic liver disease is variceal bleeding. The bleeding from esophageal varices can be abrupt and massive. With the occurrence of a variceal bleed, traditional approaches to hemodynamic stabilization need to be implemented including the use of two large-bore intravenous access devices, isotonic saline infusions and blood to maintain intravascular volume, and identification of the underlying etiology. For emergent variceal bleeding, most patients can be cared for with endoscopic and pharmacologic interventions, although each of these interventions will fail between 15% and 20% of the time. When endoscopic and pharmacologic interventions fail, the use of balloon tamponade may be used as a temporizing measure to control bleeding.