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Primary prevention of bleeding from esophageal varices in patients with cirrhosis

Primary prevention of bleeding from esophageal varices in patients with cirrhosis
Literature review current through: May 2024.
This topic last updated: Dec 18, 2023.

INTRODUCTION — Patients with cirrhosis who develop portal hypertension (ie, increased pressure within the portal venous system) are at risk for complications, including bleeding from esophageal varices. Portal hypertension is the result of resistance to portal blood flow, which most often occurs in the liver. When esophageal varices rupture, bleeding may be severe and life-threatening. In addition, variceal bleeding is a decompensating event. Thus, strategies to prevent the first episode of variceal bleeding are important for patients with cirrhosis and portal hypertension.

This topic will discuss screening for esophageal varices in patients with cirrhosis in addition to strategies for preventing the first episode of bleeding (ie, primary prophylaxis). The discussion that follows is largely consistent with society guidelines [1-4].  

The prevention of recurrent bleeding from esophageal varices (ie, secondary prophylaxis) is discussed separately. (See "Prevention of recurrent bleeding from esophageal varices in patients with cirrhosis".)

Management of acute bleeding from esophageal varices is discussed separately. (See "Overview of the management of patients with variceal bleeding" and "Methods to achieve hemostasis in patients with acute variceal hemorrhage".)

Prevention and management of other complications of cirrhosis and portal hypertension are discussed separately:

(See "Cirrhosis in adults: Overview of complications, general management, and prognosis".)

(See "Ascites in adults with cirrhosis: Initial therapy" and "Ascites in adults with cirrhosis: Diuretic-resistant ascites".)

(See "Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis".)

(See "Portal hypertensive gastropathy".)

PORTAL HEMODYNAMICS — A normal pressure gradient between the portal and hepatic veins (ie, the hepatic venous pressure gradient or HVPG) is 1 to 5 mmHg. Esophageal varices develop when HVPG is at least 10 mmHg, whereas the risk of bleeding from esophageal varices is associated with HVPG ≥12 mmHg [5,6]. Patients with cirrhosis and clinically significant portal hypertension (CSPH; defined as HVPG ≥10 mmHg) are also at risk for other complications such as ascites and portal hypertensive gastropathy. Thus, therapies aimed at decreasing portal hypertension may decrease both the risk of variceal bleeding and the risk of developing other complications. (See "Pathogenesis of ascites in patients with cirrhosis" and "Portal hypertension in adults".)

Although CSPH is defined by HVPG measurement, such testing is not commonly performed because it is invasive and requires specialized equipment and clinical expertise. In most centers, noninvasive assessments such as platelet count and liver stiffness measurement by transient elastography are used to evaluate for CSPH [7]. (See "Noninvasive assessment of hepatic fibrosis: Ultrasound-based elastography", section on 'Transient elastography'.)

Elevated portal pressure results from a combination of increased portal inflow, due to splanchnic arteriolar vasodilation, and elevated intrahepatic resistance to portal blood flow. The intrahepatic increase in resistance is due to the architectural alterations of the hepatic parenchyma (mainly fibrosis) and to an increase in the intrahepatic vascular tone. Splanchnic vasodilation and the intrahepatic increase in vascular tone are both factors that may respond to medical therapy [8-10].

SCREENING FOR ESOPHAGEAL VARICES

Rationale — The rationale for screening for esophageal varices is to identify patients at risk for bleeding from esophageal varices and to prevent bleeding and improve survival in such patients.

The reported annual rate of a first bleeding episode among those with varices is 12 percent, and each episode of variceal bleeding is associated with up to a 20 percent risk of mortality [11-14]. In addition, the reported rate of decompensation (ie, developing ascites, gastrointestinal bleeding, or encephalopathy) in patients with clinically significant portal hypertension (CSPH) is 40 percent at five years, whereas the rate of decompensation is less than 10 percent in those without CSPH [15].

Indications — Screening for esophageal varices is indicated for patients with CSPH and includes the following groups [3,16] (see 'Portal hemodynamics' above and "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'Prognosis'):

All patients with decompensated cirrhosis (ie, patients with cirrhosis and at least one complication)

Patients with compensated cirrhosis and either liver stiffness measurement (LSM) >20 kPa or platelet count <150,000/microL

For patients with compensated cirrhosis, LSM ≤20 kPa, and platelet count >150,000/microL, we do not routinely screen for varices because studies suggest that such patients are unlikely to have varices at risk for bleeding [3,17,18]. As an example, in a study including 518 patients with compensated cirrhosis who had noninvasive testing for fibrosis and underwent endoscopic screening, patients with LSM ≤20 kPa and platelet count >150,000/microL had very low rates (<5 percent) of having either large varices or small varices with red signs [17].

For patients who do not meet criteria for screening, the frequency of repeating noninvasive testing is individualized and informed by the patient's baseline assessment, activity of underlying liver disease, and clinician preference. We typically perform transient elastography to measure liver stiffness and obtain a platelet count on a yearly basis. If LSM increases (>20 kPa) or platelet count declines (<150,000/microL), we perform screening upper endoscopy (algorithm 1). In addition, if a patient develops a new complication (eg, ascites, hepatocellular carcinoma), we repeat the upper endoscopy.

For patients with cirrhosis who are already taking a nonselective beta blocker to prevent decompensation or for other indications, we do not perform screening upper endoscopy because the presence of varices will not modify management [3]. (See 'Preventing other decompensating events' below.)

General management of patients with cirrhosis is discussed in more detail separately. (See "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'Preventing complications'.)

Measuring spleen stiffness is an emerging method that may be an alternative to measuring liver stiffness with transient elastography for predicting CSPH. In a study including 100 patients with chronic hepatitis C virus infection who had not received antiviral therapy, a spleen stiffness measurement (SSM) >50 kPa was associated with an increased risk of having CSPH and esophageal varices [19]. Further studies are needed before spleen stiffness measurements are routinely used in clinical practice.

Endoscopic evaluation — For patients in whom screening for varices is indicated, we perform upper endoscopy. (See 'Indications' above and "Overview of upper gastrointestinal endoscopy (esophagogastroduodenoscopy)".)

For patients with esophageal varices, we insufflate the esophageal lumen when assessing varix appearance and size. Varices are typically categorized as large or small. However, estimating varix size is subjective and based on clinical experience.

Features that are associated with higher risk for bleeding include [20,21]:

Large esophageal varices with or without a tortuous, coiled appearance

Esophageal varices of any size with red signs (eg, red wale markings, erythematous raised spots [also referred to as cherry red spots]) (picture 1) or in patients with decompensated cirrhosis (see "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'Prognosis')

Small, straight varices without red signs in patients with compensated cirrhosis have a lower risk of bleeding.

Although other screening methods such as capsule endoscopy have been studied, alternatives to upper endoscopy are not routinely used because they are less sensitive [22].

Surveillance intervals — For patients with cirrhosis but without high-risk esophageal varices on screening upper endoscopy, surveillance intervals are informed by the endoscopic findings and activity of the patient's liver disease (algorithm 1) (see 'Endoscopic evaluation' above):

For patients with compensated cirrhosis with ongoing liver inflammation (eg, untreated viral hepatitis, active alcohol use disorder, metabolic syndrome) and small varices without red signs, upper endoscopy is repeated in one year.

For patients with compensated cirrhosis but no active liver inflammation and small varices without red signs, upper endoscopy is repeated in two years.

For patients with cirrhosis with ongoing liver inflammation and no varices, upper endoscopy is repeated in two years.

For patients with cirrhosis but no active liver inflammation and no varices, upper endoscopy is repeated in three years.

PREVENTIVE STRATEGIES

General measures — General measures to prevent the first episode of variceal bleeding include:

Manage underlying liver disease – Patients with cirrhosis are evaluated for interventions that will slow or reverse the progression of liver disease (ie, avoiding alcohol) and prevent additional insults to the liver (eg, adjusting medications, immunizing against hepatitis A virus and hepatitis B virus). The general management of patients with cirrhosis is discussed separately. (See "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'General management'.)

Refer patients with decompensated cirrhosis for transplantation evaluation – We refer patients with decompensated cirrhosis for liver transplantation evaluation because transplantation is effective long-term therapy for preventing variceal bleeding and other complications of portal hypertension. Selecting patients for liver transplantation and the pretransplant evaluation are discussed separately. (See "Liver transplantation in adults: Patient selection and pretransplantation evaluation" and "Model for End-stage Liver Disease (MELD)".)

Goals of prophylaxis — The goals of prevention for patients with esophageal varices at risk for bleeding include [23]:

Prevent variceal bleeding

Improve survival

Prevent other complications of portal hypertension (eg, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy) (see "Portal hypertension in adults")

Selecting a strategy — Selecting a preventive strategy for patients with esophageal varices at risk for bleeding takes into account the efficacy, risks, and burden of the interventions, available endoscopic expertise, and patient characteristics that may limit the use of beta blockers. Our preferred strategy is pharmacologic prophylaxis with a nonselective beta blocker for patients without contraindications to beta blockers. An alternative approach for patients who do not tolerate beta blockers is endoscopic variceal ligation (EVL). (See 'Pharmacologic prophylaxis' below and "Endoscopic variceal ligation".)

We do not initiate beta blockers in patients with any of the following conditions because of increased risk of adverse events (eg, decreased cardiac output, increased mortality) [24]:

Hyponatremia (serum sodium concentration <130 mEq/L). (See "Hyponatremia in patients with cirrhosis", section on 'Discontinue beta blockers and other antihypertensive drugs'.)

Acute kidney injury [25]. (See "Overview of the management of acute kidney injury (AKI) in adults".).

Spontaneous bacterial peritonitis – Beta blocker therapy in patients with active spontaneous bacterial peritonitis is associated with higher mortality risk [26]. (See "Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis", section on 'Discontinue nonselective beta blockers'.)

Severe alcoholic hepatitis – Beta blockers increase the risk of acute kidney injury (AKI) in this setting [27]. (See "Alcoholic hepatitis: Clinical manifestations and diagnosis", section on 'Assessing disease severity' and "Management and prognosis of alcoholic hepatitis", section on 'Renal failure and acute kidney injury'.)

History of adverse effects with beta blockers – Patients with a prior history of adverse effects related to beta blockers are not candidates for therapy (eg, bronchoconstriction, heart failure, acute kidney injury). (See "Major side effects of beta blockers".).

Systolic blood pressure <90 mmHg; this threshold is supported by consensus statement only [4]. Some UpToDate contributors for this topic use mean arterial pressure (MAP) ≤82 mmHg as the threshold for avoiding beta blockers because MAP ≤82 mmHg predicts mortality in patients with cirrhosis and ascites (calculator 1) [28].

Primary prophylaxis with a nonselective beta blocker or with EVL is supported by randomized trials demonstrating similar survival benefits with each strategy [29,30]. In a meta-analysis of 17 trials including 1640 patients with cirrhosis, the risk of mortality was not significantly different for patients who had EVL compared with beta blocker prophylaxis after 8 to 60 months of follow-up (HR 1.05, 95% CI 0.80-1.38) [30]. In the same meta-analysis, beta blocker prophylaxis resulted in lower risk of mortality compared with no intervention (21 versus 43 percent, hazard ratio [HR] 0.59, 95% CI 0.42-0.83) [30]. In another meta-analysis of 32 trials including 3362 patients with cirrhosis, EVL resulted in lower risk of an initial episode of variceal bleeding compared with beta blocker prophylaxis (10 versus 19 percent, HR 0.52, 95% CI 0.35-0.78) [29]. However, rates of treatment-related serious adverse events (eg, death, esophageal perforation, bleeding esophageal ulcers) were numerically higher with EVL compared with beta blockers (4 versus 1 percent). (See 'Options' below.)

Options

Pharmacologic prophylaxis — Nonselective beta blockers are the cornerstone of pharmacologic prophylaxis for patients with cirrhosis and esophageal varices who do not have a contraindication or intolerance to beta blockers. (See 'Selecting a strategy' above.)

The goal of prevention with beta blockers is to lower the portal pressure by reducing portal blood flow, which is accomplished by vasoconstricting the splanchnic circulation [31].

Options for prophylaxis with a nonselective beta blocker include carvedilol, nadolol, and propranolol. Carvedilol is a nonselective beta blocker that also has mild anti-alpha 1 adrenergic activity [2]. In addition to reducing portal venous inflow through nonselective beta blockade, the anti-alpha 1 adrenergic activity lowers hepatic vascular tone and hepatic resistance. This results in greater reduction in portal pressure [32].

The choice of nonselective beta blocker is informed by the severity of cirrhosis (see "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'Prognosis'):

Patients with compensated cirrhosis – For patients with compensated cirrhosis, carvedilol is first-line prophylaxis, provided that there are no contraindications to beta blockers. (See 'Selecting a strategy' above.)

The initial dose of carvedilol is 3.125 mg twice daily. After a minimum of three to four days of carvedilol therapy, the dose may be gradually increased to a maximum dose of 6.25 mg twice daily while maintaining a MAP >82 mmHg and a target resting heart rate ranging from 55 to 60 beats per minute. For most patients, a low blood pressure prevents achieving the maximum carvedilol dose, whereas the heart rate often remains above the target range. We continue therapy indefinitely while monitoring for adverse effects (ie, hypotension).

Multiple home blood pressure values are more useful than a single blood pressure measurement taken during an office visit. Instructing patients and/or care givers how to measure blood pressure can help ensure compliance with medical therapy.

Data from randomized trials and observational studies suggest that carvedilol is effective for preventing variceal bleeding and may provide a survival benefit [33-36]. In a trial including 152 patients with cirrhosis and medium/large esophageal varices, carvedilol resulted in lower rates of variceal bleeding compared with EVL after a median follow-up of 20 months (10 versus 23 percent, relative hazard ratio [HR] 0.41, 95% CI 0.19-0.96) [35]. There was no statistically significant difference in rates of overall mortality or bleeding-related mortality between groups. However, in a retrospective analysis of these 152 patients after a longer follow-up, carvedilol was associated with greater median overall survival compared with EVL (7.8 versus 4.2 years), whereas liver-related mortality and rates of decompensation were not significantly different between groups [33].

Patients with decompensated cirrhosis For patients with decompensated cirrhosis, we typically initiate a low-dose nonselective beta blocker that does not have anti-alpha 1 adrenergic activity (eg, nadolol, propranolol). We titrate the beta blocker dose to a target resting heart rate ranging from 55 to 60 beats per minute. We continue therapy indefinitely while monitoring for adverse effects (ie, hypotension).

As an example, the initial dose of nadolol (where available) is 20 mg daily, and the dose is gradually increased after a minimum of three to four days to achieve a resting heart rate of 55 to 60 beats per minute, provided that the mean arterial pressure is >82 mmHg (calculator 1). The maximum daily dose of nadolol is 160 to 240 mg daily. (See "Prevention of recurrent bleeding from esophageal varices in patients with cirrhosis", section on 'Selecting a strategy'.)

We do not use carvedilol as a first-line agent in patients with decompensated cirrhosis because it may produce greater reduction in mean arterial pressure than other beta blockers due to its vasodilating properties [37]. However, for selected patients with decompensated cirrhosis (eg, those with ascites only), we may use carvedilol provided that the systolic blood pressure remains >90 mmHg [3].

We monitor patients for adverse effects associated with beta blockers including hypotension, shortness of breath, fatigue, bronchoconstriction, and heart failure. Despite the inability of nadolol to cross the blood-brain barrier due to its hydrophilic nature (in contrast to the highly lipophilic propranolol), central nervous system side effects of the two medications do not differ. (See "Major side effects of beta blockers".)

Patients with cirrhosis on beta blocker prophylaxis require long-term follow-up, and some centers use a multidisciplinary approach involving hepatologists and pharmacists.

For additional drug prescribing information, please refer to the drug interactions program.

Endoscopic variceal ligation — The goal of EVL is to eradicate varices, and it may be performed during the screening endoscopy and repeated every two to four weeks until esophageal varices are no longer visible endoscopically with insufflation of the esophageal lumen. In most patients, this is achieved with three to four EVL sessions.

During an upper endoscopy, EVL is performed by attaching a device loaded with rubber bands to the tip of the endoscope. A varix is suctioned into the device and then the rubber band is deployed around the base of the varix, which results in occlusion. Adverse events associated with EVL include dysphagia, band-related esophageal ulcerations, bleeding, and strictures [38]. The technical aspects and adverse events associated with EVL are discussed in more detail separately. (See "Endoscopic variceal ligation".)

For patients in whom esophageal varices have been eradicated, we perform surveillance upper endoscopy every three to six months for one year and then once annually thereafter. If esophageal varices recur, EVL can be performed again.

Evidence from clinical trials suggested that EVL reduced the risk of variceal bleeding and mortality [29,39,40]. In a meta-analysis of 32 trials including 3362 patients with cirrhosis and large varices but without history of bleeding, EVL resulted in lower risk of variceal bleeding (odds ratio [OR] 0.36, 95% CI 0.14-0.92) and lower risk of mortality (OR 0.48, 95% CI 0.28-0.80) compared with placebo [29].

Strategies to avoid — We do not use the following strategies for prophylaxis:

Endoscopic sclerotherapy – Endoscopic sclerotherapy (ie, endoscopic injection of a sclerosant solution into the varices) is not used because of the risk of transmural injury to the esophageal wall that often occurs after sclerotherapy. (See "Endoscopic variceal ligation".)

Shunt intervention – Shunt interventions (eg, surgical shunts, transjugular intrahepatic portosystemic shunt) are not used because of the risk of hepatic encephalopathy [41]. (See "Transjugular intrahepatic portosystemic shunts: Postprocedure care and complications", section on 'Postprocedure complications'.)

Cardioselective beta blockers – Cardioselective beta blockers are not used for lowering portal pressure because they selectively block beta-1 receptors with little or no effect on beta-2 receptors. In addition, published evidence supporting their use is lacking.

PREVENTING OTHER DECOMPENSATING EVENTS — For patients with cirrhosis and clinically significant portal hypertension but without high-risk esophageal varices, nonselective beta blockers are being studied for preventing any decompensating event (eg, ascites, bleeding) [23,33,42]. As an example, in a trial including 201 patients with compensated cirrhosis, beta blocker therapy reduced the risk of decompensation (defined as developing ascites, hepatic encephalopathy, or bleeding) compared with placebo (16 versus 27 percent; HR 0.51, 95% CI 0.26-0.97) [23].

General management of patients with cirrhosis and portal hypertension is discussed separately. (See "Cirrhosis in adults: Overview of complications, general management, and prognosis".)

SPECIAL POPULATIONS

Patients with gastric varices — The approach to pharmacologic prophylaxis in patients with cirrhosis and nonbleeding gastric varices is similar to the approach for patients with esophageal varices [4]. While nonselective beta blockers are the cornerstone of prevention in clinical practice, data from randomized trials in patients with gastric varices are limited [43]. (See 'Pharmacologic prophylaxis' above.)

We do not use any of the following strategies because evidence supporting the safety and efficacy of these interventions for primary prophylaxis in patients with gastric varices is very limited: cyanoacrylate injection, endoscopic ultrasound-guided coil placement, balloon-occluded retrograde transvenous obliteration, balloon-occluded anterograde transvenous obliteration, or transjugular intrahepatic portosystemic shunt. Management of patients with bleeding gastric varices is presented separately. (See "Methods to achieve hemostasis in patients with acute variceal hemorrhage", section on 'Management of gastric varices'.)

Patients with cirrhosis related to viral hepatitis — For patients with cirrhosis related to chronic viral hepatitis who have responded to antiviral therapy, we agree with society guidelines that use liver stiffness measurement (LSM) and platelet count to determine whether screening upper endoscopy is indicated [3,44,45]. (See 'Screening for esophageal varices' above.)

Emerging data suggest that noninvasive tests can accurately predict the risk of decompensation in patients with viral hepatitis who responded to antiviral therapy. In a study including 418 patients treated for chronic hepatitis C infection who had sustained virological response, patients with a LSM <12 kPa and platelet count >150,000/microL had negligible risk of hepatic decompensation during three years of follow-up [46]. This study also suggested that some patients who respond to antiviral therapy may no longer need an evaluation for esophageal varices, however, additional studies are needed to confirm these findings.

The management of patients with chronic viral hepatitis is presented separately. (See "Hepatitis B virus: Overview of management" and "Overview of the management of chronic hepatitis C virus infection".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cirrhosis" and "Society guideline links: Gastrointestinal bleeding in adults".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Esophageal varices (The Basics)")

Beyond the Basics topics (see "Patient education: Esophageal varices (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

General principles Patients with cirrhosis who develop portal hypertension (ie, increased pressure within the portal venous system) are at risk for complications, including the development of esophageal varices. When esophageal varices rupture, bleeding may be severe and life-threatening. Thus, strategies to prevent the first episode of variceal bleeding are important for such patients. (See "Portal hypertension in adults".)

Screening – The rationale for screening for esophageal varices is to identify patients at risk for variceal bleeding, to prevent bleeding, and to improve survival (see 'Screening for esophageal varices' above):

Indications – Screening for esophageal varices with upper endoscopy is indicated for patients with clinically significant portal hypertension (CSPH) and includes the following groups:

-All patients with decompensated cirrhosis

-Patients with compensated cirrhosis and either liver stiffness measurement (LSM) >20 kPa by transient elastography or platelet count <150,000/microL

Surveillance intervals For patients with no varices or with small varices at low risk for bleeding, surveillance intervals are informed by the endoscopic findings and activity of the patient's liver disease (algorithm 1). (See 'Surveillance intervals' above.)

General measures – General measures to prevent the first episode of variceal bleeding include:

Manage underlying liver disease – Patients with cirrhosis are evaluated for interventions that will slow or reverse the progression of liver disease (eg, avoiding alcohol) and prevent additional insults to the liver (eg, adjusting medications). (See "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'General management'.)

Referral for liver transplantation evaluation – We refer patients with decompensated cirrhosis for liver transplantation evaluation because transplantation is effective long-term therapy for preventing variceal bleeding and other complications of portal hypertension. (See "Liver transplantation in adults: Patient selection and pretransplantation evaluation".)

Specific preventive strategies – For patients with cirrhosis and esophageal varices at high risk for bleeding, we recommend prophylaxis with a nonselective beta blocker rather than no pharmacologic intervention because evidence suggests that beta blockers resulted in lower risk of mortality (Grade 1B). (See 'Pharmacologic prophylaxis' above.)

Patients with compensated cirrhosis – For patients with compensated cirrhosis, we typically initiate carvedilol at a low dose (3.125 mg orally twice daily) and gradually increase the dose while maintaining mean arterial pressure (MAP) >82 mmHg (calculator 1), with a target resting heart rate ranging from 55 to 60 beats per minute. The maximum carvedilol dose is 6.25 mg twice daily.

Patients with decompensated cirrhosis – For patients with decompensated cirrhosis, we typically begin a nonselective beta blocker such as nadolol or propranolol at low dose (eg, nadolol 20 mg, orally, once daily). We titrate the dose to a target resting heart rate ranging from 55 to 60 beats per minute, provided that the MAP is >82 mmHg.

Patients who cannot take beta blockers – For patients who have a contraindication to or cannot tolerate beta blockers, we suggest endoscopic variceal ligation (EVL) rather than no intervention because evidence suggests that EVL resulted in lower risk of variceal bleeding and mortality (Grade 2B). (See 'Endoscopic variceal ligation' above.)

Monitoring

Patients on beta blocker prophylaxis We continue nonselective beta blocker indefinitely while monitoring for adverse effects (ie, hypotension, shortness of breath, fatigue) (see "Major side effects of beta blockers"). Surveillance endoscopy is not necessary for patients on long-term beta blocker prophylaxis.

Patients who had EVL – For patients in whom esophageal varices have been eradicated with EVL, we perform surveillance upper endoscopy every three to six months for one year and then once annually thereafter.

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Topic 1245 Version 36.0

References

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