eMedicine Specialties > Gastroenterology > Esophagus

Esophageal Varices: Treatment & Medication

Author: Samy A Azer, MD, PhD, MPH, Professor of Medical Education, Chair of Medical Education Research and Development Unit, Faculty of Medicine, Universiti Teknologi MARA, Malaysia; Visiting Professor of Medical Education, Faculty of Medicine, University of Toyama, Japan; Former Senior Lecturer in Medical Education, Faculty Education Unit, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne and University of Sydney, Australia
Contributor Information and Disclosures

Updated: Jan 4, 2010

Treatment

Medical Care

• Esophageal varices with no history of bleeding
  • Patients with esophageal varices and no previous history of variceal hemorrhage should be treated with nonselective beta-adrenergic blockers (eg, propranolol, nadolol, timolol), provided that the use of beta-blockers is not contraindicated (eg, because of insulin-dependent diabetes mellitus, severe chronic obstructive lung disease, congestive heart failure).^1,5,6,7,8
  • The dose of nonselective beta-blockers is determined by a 25% decrease in resting heart rate or a decrease in heart rate to 55 beats per minute or the development of adverse effects.
  • The use of beta-blockers decreases the risk of initial variceal bleeding by approximately 45%.
  • If contraindications to using beta-blockers exist, long-acting nitrates (eg, isosorbide 5-mononitrate) are alternatives.
  • Treatment with beta-blockers should be continued indefinitely.
  • The role of endoscopic sclerotherapy or variceal ligation for prevention of esophageal variceal hemorrhage is as effective as treatment with propranolol in decreasing the incidence of first variceal bleeding and death in cirrhotic patients with higher-risks of bleeding from esophageal varices. Kumar et al investigated whether endoscopic variceal ligation alone or a combination of endoscopic variceal ligation plus propranolol and isosorbide mononitrate was more effective for secondary prophylaxis in patients with previous variceal bleeding.⁹ Patients were randomly assigned to receive endoscopic variceal ligation alone (n = 89) or the combination therapy (n = 88). No difference between the groups was observed for rebleeding 2 years after initial therapy (P = 0.822).⁹ The authors concluded that endoscopic variceal ligation alone is sufficient to prevent variceal rebleeding, whereas addition of propranolol and isosorbide mononitrate to endoscopic variceal ligation may increase risk for adverse effects.
  • Combined sclerotherapy and treatment with nonselective beta-blockers offer no advantages over the use of beta-blockers alone for prevention of esophageal varices hemorrhage.
  • Approximately 50% of patients with NASH with severe fibrosis had esophageal varices. NASH patients with esophagogastric varices need to be followed up carefully like patients with other chronic liver disorders.
• Bleeding esophageal varices
  • Assess the rate and volume of bleeding. Check blood pressure and pulse with the patient in the supine position and with the patient in a sitting position.
  • Gain venous access and obtain blood for immediate hematocrit measurement. Obtain a type and cross-match. Measure the platelet count and prothrombin time. Send blood for renal and liver function tests and measure serum electrolytes.
  • Provide emergency treatment as outlined below.
• Emergency treatment
  • Promptly resuscitate and restore the circulating blood volume of patients with suspected cirrhosis and variceal hemorrhage.
  • Establish intravenous access for blood transfusion. While the blood is being cross-matched, start rapid infusion of 5% dextrose and colloid solution until the blood pressure is restored and urine output is adequate.
  • Establish airway protection in patients with massive upper GI tract bleeding, especially if the patient is not fully conscious.
  • If indicated, correct clotting factor deficiencies with fresh frozen plasma, fresh blood, and vitamin K-1.
  • Insert a nasogastric tube to assess the severity of the bleeding and to lavage gastric contents before performing endoscopy.
  • Consider pharmacologic therapy (octreotide or somatostatin) and endoscopy as soon as the patient has been resuscitated. The aim is to establish the cause of and to control the bleeding.
  • Endoscopic therapy probably has replaced balloon tamponade as the initial therapy for variceal bleeding. Balloon tamponade is now rarely necessary, and, when it is used, it must be performed by experienced personnel because the procedure is potentially dangerous.
• Endoscopic therapy
  • Endoscopic sclerotherapy
    • Endoscopic sclerotherapy is successful in controlling acute esophageal variceal bleeding in up to 90% of patients. Hemorrhagic control should be obtained with 1-2 sessions. Patients continuing to bleed after 2 sessions should be considered for alternative methods to control their bleeding.
    • In the United States, sodium tetradecyl sulfate or sodium morrhuate has generally been used as a sclerosant, whereas polidocanol or ethanolamine has been more popular in Europe. Variations in the technique or the sclerosant used have not been shown to influence the outcome.
    • Serious complications related to sclerotherapy have been reported in 15-20% of patients, with an associated mortality rate of 2%.
    • Complications of sclerotherapy may include mucosal ulceration, bleeding, esophageal perforation, mediastinitis, and pulmonary complications. Long-term complications, such as esophageal stricture formation, may also occur.
  • Endoscopic variceal ligation (banding)^10,11
    • Endoscopic variceal ligation is based on the widely used technique of rubber-band ligation of hemorrhoids. The esophageal mucosa and the submucosa containing varices are ensnared, causing subsequent strangulation, sloughing, and eventual fibrosis, resulting in obliteration of the varices.
    • Rebleeding occurs less frequently with endoscopic variceal ligation (26%) than with endoscopic sclerotherapy (45%).
    • Endoscopic ligation requires placement of an opaque cylinder over the end of the endoscope. This decreases the endoscopic field of view and may allow pooling of blood. Thus, in patients with active bleeding, visualization may be impaired more with ligation than with sclerotherapy.
    • Clinical trials have demonstrated that ligation and sclerotherapy achieved similar rates of initial hemostasis in patients whose varices were actively bleeding at the time of treatment.
    • Local complications are less common with ligation compared with sclerotherapy. For example, esophageal strictures were found to be less common with ligation compared with sclerotherapy. Systemic complications, such as pulmonary infections and bacterial peritonitis, were not significantly different between the 2 groups. However, a trend was observed toward a decrease in these 2 complications in patients treated with ligation.

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:

• Surgical interventions include the following:
  • Portosystemic shunt
  • Devascularization (transabdominal devascularization of the lower 5 cm of the esophagus and the upper two thirds of the stomach, with staple gun transection of the lower esophagus) is rarely performed but may have a role in patients with portal and splenic vein thrombosis who are not suitable candidates for shunt procedures and who continue to have variceal bleeding despite endoscopic and pharmacologic treatment.
  • Orthotopic liver transplantation is the treatment of choice in patients with advanced liver disease.
• Therapeutic radiologic procedures include the following:
  • Percutaneous transhepatic embolization (PTE) of gastroesophageal varices involves catheterization of the gastric collaterals that supply blood to varices via the transhepatic route. A variety of agents had been used, with varying degrees of success in controlling acute bleeding. Generally, PTE is less effective than endoscopic sclerotherapy for treatment of variceal hemorrhage, and it is much less effective compared with medical and surgical options. Thus, it should be reserved for situations in which acute variceal bleeding is not controlled by pharmaceutical treatment, endoscopic sclerotherapy, or endoscopic variceal ligation and in which contraindications for surgical management are present.
  • Transjugular intrahepatic portosystemic shunt (TIPS) placement is an effective salvage procedure for stopping acute variceal hemorrhage after failure of medical and endoscopic treatment. However, this procedure is associated with a number of complications; 20% of patients develop encephalopathy, and 50% may occlude their shunt within 1 year. Thus, TIPS placement should be considered as a bridge to subsequent liver transplantation.

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.

Consultations

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

Diet

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

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.

Vasoconstrictors

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.

Vasopressin (Pitressin)

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)

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).

Antisecretory Agents

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

Somatostatin (Zecnil)

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)

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

Beta-adrenergic Blockers

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

Propranolol (Inderal)

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.

Vasodilators

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

Nitroglycerin (Nitro-Bid, Nitrostat, Deponit)

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

• Search for CME/CE on This Topic »

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