Esophageal varices are a direct consequence of portal hypertension as a progressive complication of cirrhosis.
The development of bleeding carries significant morbidity and mortality.
Nonselective beta-blockers and/or endoscopic ligation can prevent the development of variceal bleeding.
Acute hemorrhage can be managed with resuscitation, a vasoactive drug or a somatostatin analog, and endoscopic ligation. Additional management may include transjugular intrahepatic shunt therapy and prophylactic antibiotics.
Diagnosis and surveillance by endoscopy is an important aspect of management.
Esophageal varices are dilated collateral blood vessels that develop as a complication of portal hypertension, usually in the setting of cirrhosis. They can be seen on endoscopy. In the US and Europe, the major cause of cirrhosis is alcoholic liver disease. Worldwide, hepatitis B virus infection and hepatitis C virus infection are the major causes of cirrhosis. Once cirrhosis has developed, increasing hepatic vein pressure gradient and deteriorating liver function may result in the formation of esophageal varices.
Rupture of esophageal varices can cause life-threatening bleeding. The most important predictor of variceal hemorrhage is the size of varices, with the highest risk of first hemorrhage occurring in patients with large varices (15% per year). Other important predictors of hemorrhage are decompensated cirrhosis (Child-Pugh B/C) and the endoscopic finding of red wale marks.
History and exam
Key diagnostic factors
- more severe liver disease
- alcohol misuse
- hepatitis B or C infection
- spider angioma
- caput medusa
- HIV coinfection
Other diagnostic factors
- portal hypertension
- large varices
- red wale marks
- Child-Pugh class
1st investigations to order
- hepatic venous pressure gradient (HPVG)
- complete blood count
- coagulation profile (INR/prothrombin time)
- serum LFTs
- BUN and creatinine
- blood typing/cross-matching
- hepatitis B surface antigen (HBsAg)
- anti-hepatitis C virus IgG (anti-HCV IgG)
- esophago-gastro-duodenoscopy (EGD)
- capsule endoscopy
decompensated cirrhosis with acute variceal hemorrhage (hepatic venous pressure gradient >12 mmHg)
decompensated cirrhosis with acute variceal hemorrhage and failed endoscopic/pharmacologic therapy
compensated cirrhosis with mild portal hypertension (hepatic venous pressure gradient >5 and <10 mmHg)
compensated cirrhosis with clinically significant portal hypertension (hepatic venous pressure gradient ≥10 mmHg): without gastroesophageal varices
compensated cirrhosis with clinically significant portal hypertension (hepatic venous pressure gradient ≥10 mmHg): with gastroesophageal varices (no bleeding)
previous variceal bleed
Grace E. Dolman, PhD, MA (Cantab), MRCP
Clinical Research Fellow
Barts Liver Centre
Barts and the London School of Medicine and Dentistry
GED declares that she has no competing interests.
Dr Grace E. Dolman would like to gratefully acknowledge Dr Gennaro D'Amico, Dr Giuseppe Malizia, Dr Vikram Boolchand, and Dr Thomas Boyer, previous contributors to this topic.
GDA, GM, VB, and TB declare that they have no competing interests.
Shreyas Saligram, MD, MRCP, FACG, FASGE
Department of Gastroenterology
University of California
SS declares that he has no competing interests.
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- Gastric varices
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- Management of anticoagulants and antiplatelets during acute gastrointestinal bleeding and the periendoscopic period
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