Esophageal Varices



The portal vein carries approximately 1500 mL/min of blood from the small and large bowel, the spleen, and the stomach to the liver. Obstruction of portal venous flow, whatever the etiology, results in a rise in portal venous pressure. The response to increased venous pressure is the development of a collateral circulation diverting the obstructed blood flow to the systemic veins. These portosystemic collaterals form by the opening and dilatation of preexisting vascular channels connecting the portal venous system and the superior and inferior vena cava.[1, 2, 3]

High portal pressure is the main cause of the development of portosystemic collaterals; however, other factors such as active angiogenesis may also be involved. The most important portosystemic anastomoses are the gastroesophageal collaterals. Draining into the azygos vein, these collaterals include esophageal varices, which are responsible for the main complication of portal hypertension -- massive upper gastrointestinal (GI) hemorrhage.

The most common causes of upper GI bleeding are duodenal (35%) and gastric ulcers (20%). Bleeding from esophageal varices is responsible for only 5-11% upper GI bleeding (incidence varies depending on geographic location). Other causes for upper GI bleeding are acute gastric erosions/hemorrhagic gastritis (18%), Mallory-Weiss tears (10%), gastric carcinoma (6%), and other causes (6%).

For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center, Liver, Gallbladder, and Pancreas Center, and Heartburn/GERD/Reflux Center. Also, see eMedicine's patient education articles Gastrointestinal Bleeding, Cirrhosis, and Gastritis.


Obstruction of the portal venous system at any level leads to increased portal pressure. Normal pressure in the portal vein is 5-10 mm Hg because the vascular resistance in the hepatic sinusoids is low. An elevated portal venous pressure (>10 mm Hg) distends the veins proximal to the site of the block and increases capillary pressure in organs drained by the obstructed veins.

Because the portal venous system lacks valves, resistance at any level between the right side of the heart and the splanchnic vessels results in retrograde flow of blood and transmission of elevated pressure. The anastomoses connecting the portal and systemic circulation may enlarge to allow blood to bypass the obstruction and pass directly into the systemic circulation.

Studies have demonstrated the role of endothelin-1 (ET-1) and nitric oxide (NO) in the pathogenesis of portal hypertension and esophageal varices.[2, 4] ET-1 is a powerful vasoconstrictor synthesized by sinusoidal endothelial cells that has been implicated in the increased hepatic vascular resistance of cirrhosis and in the development of liver fibrosis. NO is a vasodilator substance that is synthesized by sinusoidal endothelial cells. In the cirrhotic liver, the production of NO is decreased, and endothelial nitric oxide synthase (eNOS) activity and nitrite production by sinusoidal endothelial cells are reduced.

Obstruction and increased resistance can occur at 3 levels in relation to hepatic sinusoids, as follows:

Gastroesophageal varices have 2 main inflows, the first is the left gastric or coronary vein. The other major route of inflow is the splenic hilus, through the short gastric veins. The gastroesophageal varices are important because of their propensity to bleed.

Studies of hepatic microcirculation have identified several mechanisms that may explain the increased intrahepatic vascular resistance. These mechanisms may be summarized as follows:

The following are risk factors for variceal hemorrhage:

A well-documented association exists between variceal hemorrhage and bacterial infections, and this may represent a causal relationship. Infection could trigger variceal bleeding by a number of mechanisms, including the following:



United States

In Western countries, alcoholic and viral cirrhosis are the leading causes of portal hypertension and esophageal varices.


Hepatitis B is endemic in the Far East and Southeast Asia, particularly, as well as South America, North Africa, Egypt, and other countries in the Middle East. Schistosomiasis is an important cause of portal hypertension in Egypt, Sudan, and other African countries. Hepatitis C is becoming a major cause of liver cirrhosis worldwide.


Patients who have bled once from esophageal varices have a 70% chance of rebleeding, and approximately one third of further bleeding episodes are fatal. The risk of death is maximal during the first few days after the bleeding episode and decreases slowly over the first 6 weeks. Mortality rates in the setting of surgical intervention for acute variceal bleeding are high.

Associated abnormalities in the renal, pulmonary, cardiovascular, and immune systems in patients with esophageal varices contribute to 20-65% of mortality.






Diseases that interfere with portal blood flow can result in portal hypertension and the formation of esophageal varices. Causes of portal hypertension usually are classified as prehepatic, intrahepatic, and posthepatic.

Laboratory Studies

Imaging Studies

Other Tests


Medical Care

Surgical Care

Surgical care and therapeutic radiologic procedures for variceal hemorrhage

Approximately 5-10% of patients with esophageal variceal hemorrhage have conditions that cannot be controlled by endoscopic and/or pharmacologic treatment. Balloon tamponade (eg, Minnesota tube, Sengstaken-Blakemore tube, Linton-Nachlas tube) may be used as a temporary option in the management of these patients. Definitive salvage options may include the following:

Role of liver transplantation

Liver transplantation is indicated for patients with end-stage liver disease resulting in cirrhosis (viral hepatitis, alcoholic, nonalcoholic steatohepatitis, cholestatic liver disease), fulminate liver failure, and early stage hepatocellular carcinoma. Careful assessment of patients for liver transplantation is required. However, this procedure has revolutionalized the management of patients with end-stage liver disorders.


Consider early consultation with a gastroenterologist and a surgeon, particularly for patients with active bleeding from esophageal varices.


In patients with hemodynamically significant upper GI tract bleeding, a nasogastric tube should be in place for 24 hours to assist in identifying any rebleeding. Gastric lavage may be performed frequently through the nasogastric tube, and the volume and appearance of material aspirated from the stomach should be recorded. Do not allow any food by mouth.

Medication Summary

Two major categories of drugs (vasoconstrictors and vasodilators) are used to treat acute bleeding related to portal hypertension.

The main advantages to using vasoactive agents include the ability to treat variceal bleeding in the emergency department, lowering of the portal pressure, and offering the endoscopist a clearer view of varices because of less active bleeding. Vasoactive agents represent an ideal treatment for sources of portal hypertensive bleeding other than esophageal varices (eg, gastric varices >2 cm below the gastroesophageal junction or portal hypertensive gastropathy).

In the treatment of acute variceal bleeding, somatostatin, terlipressin, or octreotide is now the preferred therapy before performing endoscopy. Intravenous infusions of octreotide will lower portal blood pressure and can prevent rebleeding during the patient's initial hospitalization.

Vasopressin (Pitressin)

Clinical Context:  Has vasopressor and antidiuretic hormone (ADH) activity. Increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). However, vasoconstriction is also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels. Decreases portal pressure in portal hypertension.

Notable adverse effect is coronary artery constriction that may dispose patients with coronary artery disease to cardiac ischemia. This can be prevented with concurrent use of nitrates. Rarely used.

Terlipressin (Glypressin)

Clinical Context:  Synthetic analogue of vasopressin. Only pharmacologic agent shown to reduce mortality from variceal bleeding.

Widely used in Europe. In the United States, has orphan drug status to treat bleeding esophageal varices.

Has longer biologic activity compared with vasopressin.

Significantly reduces portal and variceal pressure and azygos flow. Beneficial when combined with sclerotherapy. Also has advantage of preserving renal function (particularly important in patients with cirrhosis).

Class Summary

Vasoconstrictors reduce portal blood flow and/or increase resistance to variceal blood flow inside the varices. Therefore, these drugs reduce blood flow in the gastroesophageal collaterals because of their vasoactive effects on the splanchnic vascular system.

Somatostatin (Zecnil)

Clinical Context:  Naturally occurring tetradecapeptide isolated from the hypothalamus and pancreatic and enteric epithelial cells. Diminishes blood flow to portal system due to vasoconstriction, thus decreasing variceal bleeding. Has similar effects as vasopressin but does not cause coronary vasoconstriction. Rapidly cleared from the circulation, with an initial half-life of 1-3 min.

Octreotide (Sandostatin)

Clinical Context:  Synthetic octapeptide. Compared with somatostatin, has similar pharmacologic actions with greater potency and longer duration of action.

Class Summary

Antisecretory agents are used as adjuncts to nonoperative management of secreting cutaneous fistulas of the stomach, duodenum, small intestine (jejunum and ileum), or pancreas.

Propranolol (Inderal)

Clinical Context:  Competitive nonselective beta-adrenergic receptor antagonist without intrinsic sympathomimetic activity. Competes with adrenergic neurotransmitters (eg, catecholamines) for binding at sympathetic receptor sites. Similar to atenolol and metoprolol, propranolol blocks sympathetic stimulation mediated by beta1-adrenergic receptors in the heart and vascular smooth muscles.

Class Summary

Beta-adrenergic blockers may block the effect of vasodilators, decrease platelet adhesiveness and aggregation, and increase the release of oxygen to tissues.

Nitroglycerin PO (Nitro-Bid, Nitrostat, Deponit)

Clinical Context:  Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is a decrease in blood pressure.

Class Summary

Vasodilators reduce the intrahepatic vascular resistance without decreasing peripheral or portal-collateral resistance.

Further Inpatient Care

Further Outpatient Care

Inpatient & Outpatient Medications





Samy A Azer, MD, PhD, MPH, Professor of Medical Education and Head of Curriculum Development Unit, King Saud University, Riyadh, Saudi Arabia; Visiting Professor of Medical Education, Faculty of Medicine, University of Toyama, Japan; former Professor of Medical Education, Chair of Medical Education Research and Development Unit, Faculty of Medicine, Universiti Teknologi MARA, Malaysia; former Consultant to the Victorian Postgraduate Medical Foundation, Melbourne, Australia; former Senior Lecturer in Medical Education, Faculty Education Unit, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne and University of Sydney, Australia

Disclosure: Nothing to disclose.

Specialty Editors

Waqar A Qureshi, MD, Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP, Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania

Disclosure: Nothing to disclose.


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