Evaluation and Management of Esophageal and Gastric Varices in Patients with Cirrhosis

Types of gastro-esophageal varices

Esophageal varices are the most common type of gastro-esophageal varices, with a prevalence of 50–60% among patients with cirrhosis, up to 85% in patients with decompensated cirrhosis. Gastric varices are present in about 20% of patients with cirrhosis and they can be of different types¹. Sarin’s classification² is the most commonly used to define the type of gastric varices (Figure 1): GOV type 1 (GOV1) are esophageal varices extending below the cardia into the lesser curvature and are the most common (75% of gastric varices). GOV type 2 (GOV2) are esophageal varices extending into the fundus. Isolated GV type 1 (IGV1) are located in the fundus (IGV1). Isolated GV type 2 (IGV2) are located elsewhere in the stomach, but are very rare.

Figure 1.

Classification of gastroesophageal varices

Esophageal varices and GOV1 will be considered together as gastro-esophageal varices (GEV) because their management is the same. GOV2 and IGV1 will be referred to as fundal varices and their specific therapeutic approach will be discussed separate from GEV.

In order to make an impact on the natural history of varices and improve clinical outcomes, specific interventions are recommended and will be discussed throughout this review. Variceal screening, surveillance and prophylaxis of variceal bleeding are usually addressed in an outpatient setting, while acute variceal bleeding requires inpatient care and sometimes transfer to a tertiary center. Among the cirrhosis quality metrics developed by AASLD³, seven measures are applicable to the management of varices (Table 1). These measures aim to prevent variceal bleeding, but based on emerging data the paradigm may change, with a focus on treating clinically significant portal hypertension rather than high-risk varices, and preventing any decompensations (variceal bleeding, ascites, hepatic encephalopathy) rather than just variceal bleeding (Figure 2).

Table 1.

AASLD cirrhosis quality metrics regarding gastroesophageal varices

Variceal screening	• Patients with cirrhosis, with platelet count < 150,000/mm3 or liver stiffness measurement > 20 kPa, and no documentation of previous GI bleeding, should have EGD to screen for varices within 12 months of cirrhosis diagnosis  • Patients with decompensated cirrhosis and no documented history of previous GI bleeding should have EGD to screen for varices within 3 months of cirrhosis diagnosis
Primary prophylaxis of variceal bleeding	• Patients with cirrhosis, no documented history of previous GI bleeding, and medium/large varices on endoscopy should receive either NSBB or EVL within 1 month of varices diagnosis
Variceal bleeding	• Patients who are admitted with or develop GI bleeding should receive antibiotics within 24 hours of admission or presentation. Antibiotics should be continued for at least 5 days  • Patients with cirrhosis who present with upper GI bleeding should have EGD within 12 hours of presentation  • Patients with cirrhosis who are found to have bleeding esophageal varices should receive EVL or sclerotherapy at the time of index endoscopy
Secondary prophylaxis of variceal bleeding	• Patients with cirrhosis who survive an episode of acute variceal hemorrhage should receive a combination of EVL and NSBB

Figure 2.

Management of varices and points of intervention

This new paradigm is based on a large randomized controlled trial (PREDESCI trial)⁴ showing that non-selective beta-blockers (NSBB) prevent decompensation (not only variceal hemorrhage, but mainly ascites) in patients with compensated cirrhosis and clinically significant portal hypertension (CSPH). In this trial, CSPH was diagnosed using invasive measures: hepatic venous pressure gradient (HVPG) of 10 mm Hg or higher. However, CSPH can be diagnosed non-invasively by liver stiffness measurement/platelet count, presence of gastroesophageal varices (any size) and/or presence of large collaterals on cross-sectional imaging. Therefore, in patients with compensated cirrhosis and varices, NSBB would be preferred over endoscopic variceal ligation (EVL). In a patient that has obvious collaterals on imaging, EGD may not even be necessary.

Outpatient management of GEV

The most common scenario in outpatient setting requiring gastroenterologists to think about GEV is when a patient presents for management of cirrhosis. A practical three-pronged approach includes: 1) establishing the stage of cirrhosis, 2) deciding if/when to proceed with upper endoscopy, and 3) determining if/what type of treatment is necessary.

1. The first step in the assessment of GEV is establishing the stage of cirrhosis: compensated or decompensated. Patients can transition from one stage to another, and the stage of cirrhosis is essential when deciding the management of GEV. When using Child–Turcotte–Pugh (CTP) classification, patients in CTP-A class are compensated, and patients in CTP-B/C class are mostly decompensated.

   Compensated cirrhosis is asymptomatic and its diagnosis is based on:

   • Clinical findings (firm and/or enlarged left liver lobe, splenomegaly, spider angioma, palmar erythema)

   • Laboratory data (thrombocytopenia, liver synthetic dysfunction with abnormal albumin, INR, bilirubin)

   • Imaging (nodular liver, with or without portal hypertension suggested by recanalized umbilical vein, portosystemic collaterals, splenomegaly)

   • Liver elastography, if available (based on Baveno VI consensus⁵, patients with two separate liver stiffness measurements (LSM) >15kPa on transient elastography (TE) have severe fibrosis or compensated cirrhosis and are at risk to develop GEV)

   • Liver biopsy, when data is discordant

   Decompensated cirrhosis is easier to diagnose, as it is defined by the presence of any overt complications of cirrhosis such as ascites, hepatic encephalopathy, and/or variceal hemorrhage. In addition to the suggestive history and physical exam, laboratory and imaging data confirm the diagnosis and liver biopsy is rarely needed.

2. The next step is to determine if and when an upper endoscopy is indicated.

   In patients with compensated cirrhosis, the severity of portal hypertension correlates with the development of GEV and risk of variceal bleeding⁶. Patients with compensated cirrhosis and without clinically significant portal hypertension (CSPH) are at a very low risk of having or developing varices in the next 5 years. GEV usually occur once patients develop CSPH, and patients with CSPH not only have a higher risk of developing varices but also have a higher risk of decompensation⁷. The presence or absence of CSPH is determined by measuring the hepatic venous pressure gradient through transjugular hepatic vein catheterization, and is very useful in research but is impractical in routine clinical care. Noninvasive tests such as imaging showing portosystemic collaterals or recanalized umbilical vein or reversal of portal flow, liver stiffness measurement, platelet count, and spleen diameter can help identify patients with a high risk of CSPH across cohorts of patients with different etiology of cirrhosis or post hepatitis C eradication^8–16.

   In compensated cirrhosis:

   • No EGD in patients with LSM >20–25 kPa by TE or recanalized umbilical vein/portosystemic collaterals on imaging. These patients are very likely to have CSPH and they benefit from NSBB, with the goal of preventing decompensation (based on PREDESCI trial⁴, they should receive carvedilol or propranolol).

   • EGD in patients with compensated cirrhosis with likely CSPH but who cannot tolerate or have contraindications to NSBB. These patients need to be monitored for development of large varices which would benefit from EVL

   In decompensated cirrhosis:

   • Screening EGD in patients with decompensated cirrhosis is still recommended to be performed at the time of diagnosis of cirrhosis decompensation, followed by annual surveillance EGD if no varices were seen on prior EGD.

   • Given the presence of decompensation, all these patients have CSPH. Turco et al showed in a meta-analysis including patients with and without ascites that those who respond to treatment with NSBB (based on reduction of HVPG) have a reduced risk of events, death, or liver transplantation¹⁷. This data suggests that patients with decompensated cirrhosis have additional benefits from NSBB regardless of presence of varices at high-risk of bleeding, and EGD may not be required in the future to initiate NSBB.

   Of note, for patients already on NSBB, either for primary prophylaxis of variceal bleeding or for other indications, as long as their heart rate is 55–60 beats/min (on nadolol or propranolol) or carvedilol is dosed at least 12.5 mg/day regardless of heart rate, screening or surveillance EGD is NO longer required as it will not change their current regimen based on EGD findings. For patients in whom endoscopic variceal ligation is used for primary prophylaxis for variceal bleeding, EGD interval is discussed below. If TIPS (transjugular intrahepatic portosystemic shunt) was inserted for ascites having obtained a portosystemic gradient less than 12 mm Hg and TIPS has remained patent, EGD for screening or surveillance of varices is not necessary, as the pressure reduction achieved by TIPS is sufficient to make variceal bleed unlikely or even to make varices disappear. Importantly, TIPS should not be placed with the purpose of preventing first variceal hemorrhage, as this porto-systemic shunting has been associated with a higher mortality in this setting.

3. Ultimately, clinicians need to determine if non-selective beta-blocker (NSBB) and/or endoscopic variceal ligation (EVL) are indicated.

In patients without prior variceal bleeding, the current recommendations address solely the prevention of the first variceal bleeding in patients with high-risk varices (HRV) considered to have a high risk of bleeding (>15% per year): patients with medium or large varices (which constitute the largest group), patients with small varices with red wale marks, or CTP-class C patients with any size varices. Studies on primary prophylaxis of variceal bleeding, spanning almost 3 decades, have reported on the benefits of NSBBs such as propranolol, nadolol, and more recently carvedilol^18–24. The other therapy with a proven beneficial effect in preventing first variceal bleeding in patients with HRV is EVL. Either one or the other should be used (Table 2), as combination therapy has no advantages and can increase side effects. Shared-decision making considering patients’ preference when choosing between NSBB and EVL should be strongly considered, to ensure patients’ adherence.

Table 2.

For patients with cirrhosis and no prior variceal bleeding: NSBB or EVL (also see Figure 3)

Therapy	No ascites	Ascites	Goal
Propranolol	20–160 mg BID	20–80 mg BID	Titrate to HR 55–60 or SBP <90
Nadolol	20–160 mg daily	20–80 mg daily	Titrate to HR 55–60 or SBP <90
Carvedilol	3.125 – 12.5 mg daily	Avoid	Titrate to 12.5-25 mg/day or SBP<90
EVL	EGD q 2–8 weeks until EV eradication → repeat EGD at 3–6 months → EGD q6–12 months if no large varices		Variceal eradication; if recurrent large varices → resume banding q2–8 weeks

In the PREDESCI trial, patients with compensated cirrhosis and CSPH but without HRV, treated with propranolol (titrated to 160 mg bid or maximum dose tolerated) or carvedilol (titrated to 25 mg/day or maximum dose tolerated) had an increased decompensation-free survival, especially a delayed development of ascites⁴. Of note, this effect was seen after two years of follow up, and the majority of patients had untreated chronic hepatitis C.

Based on PREDESCI trial, the new paradigm will aim to prevent any decompensation in patients with CSPH, not just the first variceal bleeding in patients with HRV. As such, in patients with compensated cirrhosis, NSBB will be initiated earlier without the requirement of finding HRV on EGD, as the decision will be based on non-invasive testing suggestive of CSPH. In patients with decompensated cirrhosis, recommendations may change as well to favor initiation of NSBB without EGD, given the high prevalence of small varices in these patients, the difficulty to perform EVL for small varices, and possible additional benefits from NSBB¹⁷. EGD may be reserved for patients who cannot tolerate NSBB, with the goal to perform EVL if large varices are detected.

After initiating NSBB, patients need to be carefully monitored for side effects while titrating the dose to goal (Table 2) or to the maximally tolerated dose. For propranolol and nadolol, the treatment goal is to achieve a resting heart rate of 55–60 beats/min, in the absence of hypotension or side effects. For carvedilol, a dose of 12.5 mg/day was found to prevent first variceal bleed, without a specific heart rate goal^{25, 26}. NSBBs have the advantage of decreasing portal pressure and therefore have the potential of reducing not only variceal hemorrhage, but other complications of cirrhosis.

Safety concerns have been raised regarding the use of NSBBs in patients with decompensated cirrhosis, particularly in patients with refractory ascites or after an episode of spontaneous bacterial peritonitis^{27, 28}. These earlier reports finding increased kidney dysfunction and mortality secondary to NSBBs have been challenged by subsequent studies^{29, 30}. It seems that the harmful effect is dose-dependent and related to a low mean arterial pressure³¹. Therefore, NSBBs are not contraindicated in patients with ascites, but they require careful use or interruption if severe circulatory dysfunction (hypotension, hyponatremia, hepatorenal syndrome); avoid high doses (not to exceed 80 mg propranolol orally twice a day or 80 mg nadolol orally daily); avoid carvedilol given its additional vasodilating effect and therefore higher likelihood to decrease blood pressure; titrate NSBBs to avoid systolic BP<90 mm Hg; temporarily discontinue NSBBs in the setting of bleeding, infection, or kidney dysfunction¹.

EVL is a local therapy without an effect on portal pressure and carries the risk of bleeding from ligation-induced ulcers^{32, 33}. Additionally, EVL is not recommended in patients with high-risk small varices because small varices are difficult to ligate. Importantly, if NSBB are chosen as primary prophylactic therapy, there is no need for surveillance endoscopies. If EVL is chosen, endoscopy is done every 2 to 8 weeks if varices are large enough for band ligation; once variceal eradication is achieved, repeat endoscopy for surveillance is indicated at 3–6 months, followed by EGD every 6–12 months until large varices are detected and band ligation is required again¹.

Special considerations regarding primary prophylaxis of bleeding from fundal varices

There is no specific approach regarding primary prophylaxis of variceal bleeding from fundal varices, given limited data in these patients¹. The use of NSBB or endoscopic obliteration with cyanoacrylate glue was evaluated in patients with large fundal varices (GOV2 or IGV1) and no prior bleeding³⁴. There was a lower bleeding rate observed with endoscopic obliteration, but the small number of patients could support a firm recommendation. AASLD guidance suggests that NSBB can be used for primary prophylaxis of bleeding from GOV2/IGV1, as this is the least invasive treatment and it could also prevent decompensation of cirrhosis¹. As discussed for esophageal varices, the issues regarding preventing decompensation in patients with compensated cirrhosis with fundal varices would favor the use of NSBB.

Secondary prophylaxis of variceal bleeding: NSBB AND EVL

In patients who have bled from varices, the 1-year risk of recurrent variceal bleeding can be as high as 60% in the absence of secondary prophylaxis. The recommended treatment to prevent recurrent hemorrhage consists of combination therapy NSBB plus EVL:

1. NSBB used for secondary prophylaxis of variceal bleeding are nadolol or propranolol (dose and goals as per Table 2). In this setting, there is not enough data to recommend carvedilol as there are no randomized controlled trials and patients may have more severe liver disease and more prone to be more vasodilated. NSBB should be started during hospitalization, once octreotide is discontinued, to allow monitoring of blood pressure, heart rate, and occurrence of any clinical side effects prior to discharge.

2. EVL every 2–8 weeks until varices are eradicated, followed by surveillance endoscopy at 3–6 months post variceal eradication, and every 6–12 months indefinitely. When large varices recur, EVL is resumed every 2–8 weeks until variceal eradication.

The key element of combination therapy is NSBB, particularly in CTP-B/C class patients in whom a higher mortality has been shown when patients are on EVL alone compared to combination therapy NSBB + EVL³⁵.

Patients who had TIPS placed during the episode of acute variceal bleeding should not receive NSBB or EVL as the shunt resolves portal hypertension and varices. However, they will require Doppler ultrasound of the TIPS every 6 months (at the time of HCC surveillance) to assess TIPS patency.

Special considerations regarding secondary prophylaxis of bleeding from fundal varices

If the initial bleeding resolved or it was controlled with cyanoacrylate glue obliteration, strategies to decrease the risk of rebleeding from fundal varices include repeat cyanoacrylate glue, TIPS, or intravascular obliteration with sclerosant (Balloon-occluded Retrograde Transvenous Obliteration or BRTO) ^36–39. To allow retrograde access to the fundal varices, BRTO requires the presence of a spontaneous gastrorenal or splenorenal shunt, which actually occur in 60–80% of patients with fundal varices. Because it does not divert the portal blood flow from the liver but actually increases it, BRTO does not cause hepatic encephalopathy but it may cause worsening ascites or bleeding from esophageal varices. TIPS and BRTO are recommended by AASLD as first line treatments to prevent rebleeding, reserving the use of cyanoacrylate glue injections for situations when TIPS or BRTO are not feasible¹.

Figure 3 presents a stepwise approach for the outpatient management of patients with cirrhosis to appropriately use NSBB, EVL, and other interventions targeting gastro-esophageal varices.

Figure 3.

NSBB, EVL, and other interventions targeting gastro-esophageal varices in the outpatient management of patients with cirrhosis.

Inpatient management of GEV

Treatment of acute variceal bleeding is the most important aspect of inpatient management of GEV, but it is important to note that most hospital admissions for patients with cirrhosis are complications not related to variceal bleeding. These hospitalizations are opportunities to evaluate that patients receive appropriate management of GEV, as detailed above.

Acute variceal bleeding

Advances in the management of acute variceal bleeding are associated with improved survival, but the 6-week mortality rate remains high, up to 20%^{40, 41}. Several therapies, including vasoactive medications, antibiotics, endoscopic methods (EBL or sclerotherapy, glue injection, balloon tamponade, esophageal stent, hemostatic powder), and interventional radiology treatments (TIPS, coil embolization, balloon-occluded retrograde transvenous obliteration) are currently used to treat acute variceal bleeding. Figure 4 summarizes the inpatient management of GEV, including interventions recommended by AASLD as quality metrics in cirrhosis care.

Figure 4.

Inpatient management of varices (*measures included in AASLD quality metrics)

General management should focus on:

• Resuscitation (iv access, Airway/Breathing/Circulation); orotracheal intubation especially if patient with massive hematemesis or mental status changes

• Restrictive transfusion of packed red blood cells - transfuse when hemoglobin is below <7 g/dL with the goal of 7–9 g/dL⁴²

• Avoid unnecessary “correction of coagulopathy”, as there is no evidence that correcting platelet count or INR are of benefit in variceal hemorrhage¹

• Discontinue outpatient medications (diuretics, NSBB) if low blood pressure in the setting of bleeding; of note, NSBB could blunt the sympathetic response to hemorrhage

Specific pharmacologic therapy for acute variceal hemorrhage should be initiated as soon as diagnosis is suspected and while planning for an urgent upper endoscopy. This includes:

• Vasoactive therapy causes splanchnic vasoconstriction and reduction in portal pressure - octreotide, terlipressin or somatostatin, with similar efficacy⁴³, or vasopressin which is less commonly used

  • Octreotide: IV bolus of 50 mcg followed by a continuous infusion of 50 mcg/hour (2–5 days)
  • Terlipressin: 2 mg IV every 4 hours (initial 48 hours), followed by 1 mg IV every 4 hours (2–5 days)
  • Somatostatin: IV bolus of 250 mcg followed by a continuous infusion of 250–500 mcg/hour (2–5 days)
• Antibiotic prophylaxis to decrease the variceal rebleeding rate and mortality by decreasing the risk of bacterial infection (in particular spontaneous bacterial peritonitis)⁴⁴

  • IV ceftriaxone 1 gm/24h, 5–7 days (stop once off vasoactive therapy, or at the time of discharge)

Proton pump inhibitors (PPI) have no effect on variceal bleeding. While it is reasonable to start iv PPI while awaiting EGD, it should be discontinued once variceal bleeding is confirmed. If used briefly to help with post-banding ulcer, although the evidence is limited, PPI should not be continued post-discharge.

EGD needs to be performed within 12 hours of admission, with EVL if a diagnosis of variceal hemorrhage is established based on the following criteria¹:

• active bleeding from a varix

• stigmata of recent hemorrhage are observed on a varix (clot, white nipple)

• only non-bleeding varices are seen and there is no other source of bleeding.

For patients in whom bleeding is brisk and banding cannot be performed, or if refractory bleeding not controlled with medical and endoscopic therapy, several temporizing measures may help. Balloon tamponade involves using a tube with an esophageal and a gastric balloon. It requires training and following a specific protocol, to avoid complications. It is effective in controlling bleeding temporarily, as a bridge to TIPS or, less likely, liver transplantation. It can cause lethal complications such as aspiration, esophageal ulceration and perforation. Recently, self-expandable esophageal stents were found to have greater efficacy and less complications than balloon tamponade in the control of EVH in treatment failures⁴⁵. Early application of hemostatic powder was also evaluated for acute variceal bleeding⁴⁶, but it requires follow up EGD for EVL after 24 hours and more data is needed to establish its role. Balloon tamponade and esophageal stents are temporary, bridge therapies, as ultimately, patients with refractory bleeding require TIPS placement (rescue TIPS). Because patients who rebleed despite standard therapy and require rescue TIPS are mostly Child C patients, the mortality post rescue TIPS is high.

Pre-emptive (“early”) TIPS (pTIPS) placement is a strategy that anticipates treatment failure and death by pre-emptively placing TIPS soon after therapeutic EVL in patients at high risk of failing standard therapy. In a randomized trial including patients with a CTP score of 10–13 (excluding those with score 14 or 15) and CTB-B patients with active bleeding at endoscopy, pTIPS was associated with a 25% absolute risk reduction in mortality⁴⁷. Subsequent studies have confirmed lower mortality with pTIPS in CTB-C (10–13 points)^48–50, despite which pTIPS is unfortunately placed in only a minority of these patients⁵¹. The indication for pTIPS in CTP-B patients still requires further investigation. Interestingly, when using MELD score, pTIPS was found to be associated with improved survival in patients with MELD ≥19, with no survival benefit if MELD<12⁵².

Other considerations in patients with acute VH to help plan for further treatment if necessary:

• Diagnostic paracentesis to evaluate for spontaneous bacterial peritonitis which could have precipitated variceal bleeding, should be performed before starting antibiotics

• Doppler ultrasound to assess the presence of hepatocellular carcinoma and portal vein patency should be performed prior to TIPS. Portal vein thrombosis can further increase portal pressure and anticoagulation is of benefit to prevent recurrent variceal hemorrhage, but should not be initiated in the setting of active or recent hemorrhage. In fact, a recent trial showed that TIPS placement was more effective thank EVL plus propranolol in preventing variceal rebleeding in patients with cirrhosis and PVT occluding >50% of the lumen⁴⁹

• For patients with GEV requiring enteral feeding, there is reluctance to insert nasogastric or enteric tubes especially early post endoscopic treatment, out of fear that it may precipitate variceal (re)bleeding. While the mere presence of varices is not considered a contraindication, most hepatology/gastroenterology providers wait 24–48 hours post endoscopic treatment, although there is limited data in this regard. A recent retrospective chart review on patients requiring enteric feeding, with known EV but no recent bleeding or endoscopic treatment, reported that 14% of patients developed hematemesis, bloody nasogastric aspirate, or melena within 48 hours from tube placement⁵³, but it does not offer details regarding the source of bleeding. A small randomized study⁵⁴ looked at enteral feeding vs. no feeding after variceal hemorrhage and found no differences in outcomes, including gastrointestinal hemorrhage, however the study was underpowered to detect a statistically significant difference

• Risk stratification of early rebleeding or death using CTP score and MELD score is essential, as it modifies the therapeutic strategy for high-risk patients

TIPS considerations:

• Adjunctive embolization of esophageal and/or gastric collaterals at the time of TIPS placement is routinely performed by many interventional radiologists, as it was shown to decrease short-term rebleeding rate^{55, 56}

• Discontinue vasoactive medication (once TIPS is in place, octreotide or other vasoactive medication is of no benefit, as pressure reduction achieved by TIPS is much greater than reduction with pharmacological therapy)

• Secondary prophylaxis with NSBB and EVL is not recommended as long as TIPS remains patent with a gradient less than 12 mm Hg (the threshold associated with complications secondary to portal hypertension)

• TIPS will need evaluation with ultrasound Doppler every 6 months to check for patency. If suspicion for stenosis, TIPS interrogation/revision is necessary to make sure the gradient remains less than 12 mm Hg

Acute variceal bleeding from fundal varices

While the general management is similar, endoscopic treatment of bleeding fundal varices does not rely upon EVL as complete suction of the varix into the ligator is difficult (fundal varices are usually larger than esophageal varices and the gastric mucosa is thicker), and post banding ulcers can lead to severe hemorrhage¹. More efficient endoscopic methods to control bleeding from GOV2/IGV1 include obliteration with cyanoacrylate glue or endoscopic ultrasound with combined coil insertion and cyanoacrylate or other adjuncts such as Gelfoam^57–62, although not approved in the United States and currently used off-label. Interventional radiology treatments include TIPS and BRTO^63–66. TIPS has more than 90% success rate in achieving initial hemostasis⁶⁷ and it is recommended by the AASLD as the treatment of choice for bleeding from fundal varices¹. As fundal varices may bleed at lower porto-systemic pressure gradient than esophageal varices and may persist post-TIPS, BRTO is an attractive alternative in patients with a patent gastro or spleno-renal shunt. Furthermore, combining TIPS and BRTO may be an effective approach in selected patients with bleeding gastric varices.^{68, 69} Given the complexity of care and the high expertise required for optimal treatment, patients with bleeding fundal varices should be treated in a tertiary center by a multidisciplinary team.

In conclusion, several interventions are currently recommended for the outpatient and inpatient management of esophageal and gastric varices. Although a select group of patients is best served by a multidisciplinary portal hypertension treatment team in a tertiary center, most patients can and should receive optimal treatment from practicing gastroenterologists.

KEY POINTS.

1. Gastroesophageal varices can be seen endoscopically in patients with cirrhosis in both the compensated and the decompensated stages but are more common in decompensated patients.

2. In patients with compensated cirrhosis, the presence of gastroesophageal varices on endoscopy is indicative of the presence of clinically significant portal hypertension, the main predictor of decompensation.

3. In patients with varices that have never ruptured, the use of non-selective beta-blockers are preferred as they will not only prevent the first episode of variceal hemorrhage but will also prevent the development of other decompensating events.

4. Acute variceal bleeding is a life-threatening complication of cirrhosis, but the mortality associated with it has decreased with current management based on careful blood transfusion, vasoactive medications, antibiotics, endoscopic and pre-emptive transjugular intrahepatic porto-systemic shunt.

5. Prevention of recurrent variceal hemorrhage is based on the combination of non-selective beta-blockers and endoscopic variceal ligation.

SYNOPSIS.

Variceal bleeding is one of the complications of cirrhosis that defines decompensation and, when associated with another complication such as ascites, it carries a high mortality. Important advances in the management of gastro-esophageal varices have led to a significant decrease in the morbidity and mortality associated with variceal bleeding. Achieving these results in clinical practice is contingent on clinicians applying the best practice strategies and appropriate referral to a tertiary center. Several quality metrics were developed by the American Association for the Study of Liver Diseases to define high-value cirrhosis care as it relates to the management of gastro-esophageal varices. This review addresses the needs of the busy gastroenterologists aiming to update their outpatient and inpatient strategies to include the latest recommendations on variceal screening and surveillance, primary and secondary prophylaxis of variceal bleeding, and therapy for patients with acute variceal bleeding.