# Esophageal Varices

Use noninvasive portal-hypertension assessment to identify patients who need endoscopy or preventive therapy, recognize acute variceal hemorrhage early, and combine vasoactive treatment, antibiotics, endoscopic therapy, and timely TIPS referral to reduce failure and recurrent bleeding.

**Clinical question:** How should physicians diagnose, prevent, treat, and monitor esophageal varices in patients with portal hypertension?

Updated: 2026-09-16T00:53:30.392447+00:00

## What matters in practice
- Clinical decompensation, gastroesophageal varices, portosystemic collaterals, or hepatofugal portal flow establishes clinically significant portal hypertension (CSPH). [1]
- In compensated advanced chronic liver disease, liver stiffness measurement (LSM) of 25 kPa or greater rules in CSPH; LSM of 15 kPa or less with platelets of at least 150 × 10^9/L rules it out with at least 90% sensitivity and negative predictive value. [1]
- For suspected acute variceal hemorrhage, begin vasoactive therapy, antimicrobial prophylaxis, conservative transfusion, and arrange endoscopy within 12 hours. [13]
- Recommend preemptive TIPS within 72 hours, ideally within 24 hours of index endoscopy, for Child-Turcotte-Pugh class B with score greater than 7 plus active bleeding or class C with score 10-13, absent absolute contraindications. [13]
- After an acute esophageal variceal bleed without TIPS, use indefinite nonselective beta-blocker therapy plus repeated endoscopic variceal ligation every 2-6 weeks for secondary prevention. [13][24]

## Identify CSPH before deciding on endoscopy or preventive therapy

Use objective portal-hypertension evidence rather than cirrhosis alone to direct screening and prophylaxis.

Diagnose CSPH when any overt portal-hypertension manifestation is present: hepatic decompensation, gastroesophageal varices on endoscopy, portosystemic collaterals on imaging, or hepatofugal portal-vein flow. These findings move the patient directly to portal-hypertension management; an invasive pressure measurement is not required for that decision. [1]

For compensated advanced chronic liver disease without overt portal-hypertension manifestations, combine vibration-controlled transient elastography (VCTE) LSM with platelet count. CSPH is diagnosed by the rule-of-five thresholds: LSM at least 25 kPa regardless of platelets; LSM 20-24.9 kPa with platelets below 150 × 10^9/L; or LSM 15-19.9 kPa with platelets below 110 × 10^9/L. [1]

Rule out CSPH when LSM is 15 kPa or less and platelets are at least 150 × 10^9/L; this combination has sensitivity and negative predictive value of at least 90%. Do not use an isolated LSM as a variceal-screening substitute: published LSM thresholds for predicting varices have variable specificity, including 43% specificity at 17.6 kPa in hepatitis C-associated cirrhosis. [1][3]
- If VCTE/platelet findings are indeterminate, perform upper endoscopy to determine whether varices are present and thereby confirm or exclude CSPH. [1]
- If endoscopy is declined in an indeterminate patient without detected varices, repeat VCTE and platelet count in 1 year; this is particularly reasonable when underlying liver disease is inactive. [1]
- HVPG of 10 mm Hg or greater is the threshold associated with variceal formation; values of 12 mm Hg or greater are associated with increased bleeding risk. [4]

*Noninvasive CSPH interpretation in compensated advanced chronic liver disease. [1]*

| VCTE LSM | Platelet count | Interpretation | Next step |
| --- | --- | --- | --- |
| ≤15 kPa | ≥150 × 10^9/L | CSPH ruled out with ≥90% sensitivity and negative predictive value. [1] | Do not use this result alone to diagnose varices; continue liver-disease assessment and reassess if clinical status changes. [1] |
| 15-19.9 kPa | <110 × 10^9/L | CSPH diagnosed. [1] | Manage as CSPH; assess for varices and preventive strategy. [1] |
| 20-24.9 kPa | <150 × 10^9/L | CSPH diagnosed. [1] | Manage as CSPH; assess for varices and preventive strategy. [1] |
| ≥25 kPa | Any count | CSPH diagnosed. [1] | Manage as CSPH; assess for varices and preventive strategy. [1] |
| Other combinations | Other combinations | Indeterminate rule-of-five result. [1] | Perform endoscopy; if negative, repeat LSM and platelet count in 1 year. [1] |

## Use endoscopy to define bleeding risk and select primary prevention

Variceal size, red wale marks, and liver dysfunction determine hemorrhage risk.

Endoscopy remains the definitive test for visualizing esophageal varices and identifying red wale marks. The highest-risk pattern combines larger varices, red wale marks, and advanced hepatic dysfunction; Child-Pugh B/C status and red wale marks independently predict first hemorrhage. [2][8]

If endoscopy in a patient with indeterminate noninvasive CSPH criteria identifies varices, initiate a nonselective beta-blocker (NSBB). This approach treats the presence of CSPH rather than waiting for a first hemorrhage. [1]

In compensated cirrhosis with gastric varices, NSBBs should be considered as primary prophylaxis because gastric varices indicate CSPH; the same portal-pressure strategy is relevant when gastroesophageal varices coexist. [16]
- Avoid applying VCTE/platelet criteria designed for cirrhosis to suspected porto-sinusoidal vascular disorder (PSVD); patients with PSVD require EGD for variceal screening. [17]
- For PSVD, manage detected esophageal varices with an NSBB or endoscopic variceal ligation (EVL), similarly to cirrhosis-associated varices. [17]
- In PSVD with portal-hypertension features, obtain Doppler ultrasonography every 6 months to detect portal-vein thrombosis; the yearly probability of portal-vein thrombosis is approximately 9%. [17]

*Endoscopic and clinical features that increase first-bleed risk. [2][8]*

| Finding | Clinical interpretation | Management implication |
| --- | --- | --- |
| Large varices | A major predictor of variceal hemorrhage. [8] | Use primary-prevention therapy rather than observation alone. [1][8] |
| Red wale marks | Predict increased first-bleed risk. [2][8] | Treat as a high-risk endoscopic feature. [2][8] |
| Child-Pugh B/C cirrhosis | Predicts hemorrhage risk, especially with high-risk endoscopic findings. [2] | Escalate preventive planning and reassess promptly with decompensation. [2] |

## Treat suspected acute variceal hemorrhage before endoscopic confirmation

Control portal pressure and procedure-ready bleeding risk while arranging urgent endoscopy.

For acute upper gastrointestinal bleeding in a patient with portal hypertension or known varices, manage as acute variceal hemorrhage while diagnostic endoscopy is arranged. Initial management includes conservative transfusion, antimicrobial prophylaxis, vasoactive therapy, and endoscopic evaluation within 12 hours. [13]

Start a vasoactive agent promptly and continue it for 2-5 days. Octreotide and terlipressin are established adjuncts to endoscopic therapy; in a randomized trial of 324 patients receiving endoscopic band ligation, control of bleeding was 92.6% with terlipressin and 95.6% with octreotide, with no significant difference in in-hospital mortality. [5][12]

Perform EVL as the preferred endoscopic method for esophageal variceal hemostasis. If band ligation is technically difficult, endoscopic injection sclerotherapy is an alternative. Combined endoscopic and pharmacologic treatment is superior to EVL alone for acute variceal bleeding. [5][18]
- Do not defer vasoactive therapy until endoscopy when acute variceal bleeding is suspected. [5][13]
- Apply the same initial bundle to bleeding gastric or ectopic varices: vasoactive therapy, antimicrobials, conservative transfusion, and endoscopy within 12 hours. [13]
- If active bleeding cannot be controlled, use a covered expandable esophageal stent where available or balloon tamponade only as a bridge to TIPS. [13]

### Escalate early to preemptive TIPS

Recommend preemptive TIPS for Child-Turcotte-Pugh class B with score greater than 7 and active bleeding at endoscopy, or class C with score 10-13. Create TIPS within 72 hours and ideally within 24 hours of initial upper endoscopy; transfer to a TIPS-capable center when local access would delay intervention. [13]
- Use bridge therapy rather than repeated temporizing endoscopy alone when hemorrhage remains uncontrolled and TIPS is planned. [13]

*Acute variceal hemorrhage sequence and escalation thresholds. [5][13]*

| Clinical point | Action | Timing or threshold |
| --- | --- | --- |
| Suspected acute variceal hemorrhage | Begin conservative transfusion, antimicrobial prophylaxis, and vasoactive therapy; arrange upper endoscopy. [13] | Endoscopy within 12 hours. [13] |
| Endoscopic hemostasis | Perform EVL; use injection sclerotherapy if ligation is technically difficult. [5] | At index endoscopy. [5] |
| High risk of treatment failure | Recommend preemptive TIPS if CTP B >7 with active bleeding or CTP C 10-13. [13] | Within 72 hours, ideally within 24 hours of index endoscopy. [13] |
| Uncontrolled bleeding | Use covered esophageal stent or balloon tamponade as bridge to TIPS. [13] | Immediate rescue bridge. [13] |

## Prevent recurrent hemorrhage with NSBB plus serial ligation

The default post-bleed strategy is combined portal-pressure reduction and variceal eradication.

For patients who recover from acute variceal hemorrhage without TIPS, initiate an NSBB when vasoactive therapy is discontinued. Use the NSBB indefinitely and combine it with EVL every 2-6 weeks for prevention of recurrent hemorrhage. [13][24]

Do not substitute EVL alone for combined secondary prevention when an NSBB can be used: adding an NSBB to EVL reduces rebleeding after an acute esophageal variceal bleed. [18]

After variceal eradication, continue surveillance endoscopy. In patients without varices on an initial endoscopy, a follow-up examination at 2-3 years is described, with a 2-year interval when liver function deteriorates; a change in hepatic function should therefore shorten reassessment rather than waiting for a fixed long interval. [9]
- If a patient with prior acute variceal hemorrhage receives TIPS, coordinate follow-up through the portal-hypertension/TIPS program rather than automatically applying the non-TIPS secondary-prevention sequence. [13]
- For PSVD, do not give prophylactic anticoagulation solely to prevent portal-vein thrombosis; treat portal-vein thrombosis according to cirrhosis portal-vein thrombosis management principles if it develops. [17]

*Post-hemorrhage prevention by TIPS status. [13][24]*

| Patient group | Secondary-prevention strategy | Monitoring trigger |
| --- | --- | --- |
| Acute variceal hemorrhage without TIPS | Start NSBB at vasoactive-therapy discontinuation; continue indefinitely plus EVL every 2-6 weeks. [13][24] | Repeat EVL sessions until eradication and continue endoscopic surveillance. [24] |
| Preemptive-TIPS eligible patient | TIPS within 72 hours, ideally within 24 hours, after initial endoscopy. [13] | Transfer promptly if TIPS is not locally available. [13] |
| No varices on initial endoscopy | Continue surveillance rather than prophylactic eradication therapy. [9] | Repeat at 2-3 years; use 2 years if liver function deteriorates. [9] |

## Recognize gastric-varix anatomy and noncirrhotic portal hypertension

Anatomic subtype and portal-hypertension cause alter procedural planning and surveillance.

Do not assume all gastroesophageal varices have identical anatomy. GOV2 and isolated gastric varices type 1 (IGV1) involve the fundus and are considered cardiofundal varices; they are associated with portal hypertension from cirrhosis, hepatocellular carcinoma, or portal-vein thrombosis. IGV1 may also arise with splenic-vein thrombosis and splenomegaly. [16]

Cardiofundal varices account for about 20% of gastric varices and carry higher bleeding risk. Persistent gastric varices after endoscopic management should prompt repeat cross-sectional imaging to guide subsequent therapy; EUS-guided coil therapy is one advanced-endoscopic option used for secondary prophylaxis in multidisciplinary practice. [16]

When portal hypertension and varices occur without cirrhosis, evaluate for PSVD and associated immunologic disease, prothrombotic or genetic disorders, and drug or toxin exposures. Preserved liver function does not eliminate variceal or portal-vein thrombosis risk, so EGD screening and serial Doppler surveillance remain indicated. [17]
- Manage bleeding gastric or ectopic varices initially with the same stabilization bundle as esophageal varices. [13]
- For ectopic-varix rebleeding, endoscopic treatment and endovascular embolization of the feeding vessel with or without TIPS are reported options, but data are limited largely to small retrospective cohorts. [13]

*Branches that should change the usual esophageal-varix pathway. [13][16][17]*

| Branch | Discriminator | Action |
| --- | --- | --- |
| Cardiofundal gastric varices | GOV2 or IGV1 in the gastric fundus. [16] | Consider NSBB primary prophylaxis in compensated cirrhosis; obtain repeat cross-sectional imaging for persistent varices to guide therapy. [16] |
| Splenic-vein thrombosis pattern | IGV1 with splenomegaly can reflect splenic-vein thrombosis. [16] | Define vascular anatomy before choosing endoscopic or endovascular therapy. [16] |
| PSVD/noncirrhotic portal hypertension | Portal hypertension with absence of cirrhosis. [17] | Perform EGD rather than applying Baveno noninvasive criteria; screen associated causes and obtain Doppler ultrasound every 6 months. [17] |
| Ectopic variceal bleeding | Varices outside esophagus or proximal stomach. [13] | Use the acute bleeding bundle, then consider endoscopic therapy or feeding-vessel embolization with or without TIPS. [13] |

## References
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## Editorial note

Prepared from cited clinical literature using Astra's research workflow. Verify recommendations against current guidance and patient-specific factors.