Either nonselective β-blockers or esophageal variceal ligation can be first-line treatment for primary prophylaxis of variceal hemorrhage in patients with medium to large esophageal and high-risk small varices.
Endoscopic variceal ligation (EVL) is an alternative to pharmacologic therapy for patients intolerant to β-blockers.
Management of acute variceal hemorrhage includes resuscitation, antibiotic prophylaxis, use of vasoactive agents, and endoscopic treatment with band ligation. Early transjugular intrahepatic portosystemic shunt (TIPS) should be considered for high-risk patients.
Balloon tamponade can be used as a bridge to TIPS or surgical shunt therapy.
The combination of a nonselective β-blocker and esophageal variceal ligation is first-line treatment for prevention of recurrent variceal hemorrhage.
Hepatic venous pressure gradient (HVPG) measurements have prognostic and therapeutic value.
TIPS, surgical shunt procedures, or liver transplantation are treatment options for patients who do not respond to medical therapy.
Gastric varices that are contiguous with esophageal varices can be treated as esophageal varices; those below the gastroesophageal junction are best treated with endoscopic injection of glue.
TIPS is the preferred rescue procedure for uncontrolled variceal bleeding and can be first-line therapy for high-risk patients.
Portal hypertensive gastropathy (PHG) is usually mild and stops spontaneously.
Chronic bleeding from PHG is treated with β-blockers or TIPS based on the severity of hemorrhage.
Chronic liver disease and cirrhosis are the 12th leading causes of mortality in the United States. Portal hypertension and its consequences are progressively debilitating complications of cirrhosis (Table 48–1). Variceal hemorrhage, spontaneous bacterial peritonitis, and the hepatorenal syndrome are chiefly responsible for the high morbidity and mortality rates in patients with cirrhosis.
Table 48–1.Causes of portal hypertension. |Favorite Table|Download (.pdf) Table 48–1. Causes of portal hypertension.
| ||Presinusoidal ||Sinusoidal or Mixed |
|Infectious (other than hepatitis) ||Schistosomiasis ||— |
|Toxin-mediated || |
Chronic arsenic ingestion
|Cirrhotic ||Early biliary cirrhosis || |
Primary biliary cirrhosis
|Autoimmune, oncologic, primary fibrotic || |
Congenital hepatic fibrosis
Early primary sclerosing cholangitis
Incomplete septal fibrosis
Nodular regenerative hyperplasia
Primary sclerosing cholangitis
|Vascular || |
Splenic vein thrombosis
Portal vein thrombosis
Cavernous transformation of the portal vein
Extrinsic compression of the portal vein
|Other ||Idiopathic portal hypertension ||— |
Esophageal varices develop at a rate of 5–8% per year in patients with cirrhosis and portal hypertension, and up to 80% of patients with cirrhosis will eventually develop this complication. Variceal hemorrhage occurs in 25–35% of patients with cirrhosis and large esophagogastric varices. The majority of bleeding episodes occur within the first year of diagnosis of varices. Bleeding from esophageal varices is associated with 15–20% early mortality and accounts for one-third of all deaths. If no long-term therapy is instituted after control of acute ...