Baveno VII — Personalized Care for Portal Hypertension

Key Thresholds from Baveno VII

Portal hypertension — elevated blood pressure in the veins feeding the liver — is the main driver of serious cirrhosis complications, including fluid buildup (ascites), bleeding from enlarged veins (varices), and confusion from toxin buildup (hepatic encephalopathy). ref 1 In October 2021, an international panel of liver experts convened the Baveno VII consensus workshop — building on 35 years of meetings dating back to 1986 — to update recommendations on diagnosing and managing these complications. ref 2

Understanding Your Disease Stage

Baveno VII emphasizes that patients with chronic liver disease move through distinct prognostic stages, each carrying different risks and requiring different care. Understanding where you sit is essential for choosing the right monitoring and treatment plan.

Compensated vs. Decompensated Cirrhosis

Compensated cirrhosis means you have never had a major complication from your liver disease. ref 31 Once a complication occurs — the transition to decompensated cirrhosis — mortality risk increases substantially. ref 31

The events that define decompensation are: obvious fluid buildup (overt ascites), significant confusion or altered consciousness (hepatic encephalopathy, West Haven grade ≥II), and bleeding from varices. ref 33

The Role of CSPH

Even within compensated cirrhosis, there are two sub-stages based on whether you have clinically significant portal hypertension (CSPH). ref 32 CSPH is formally defined by a hepatic venous pressure gradient (HVPG) of 10 mmHg or greater. ref 4 HVPG above 5 mmHg indicates some degree of portal hypertension. ref 3

Patients with CSPH face higher risk of developing their first complication. CSPH also matters for surgery: it is associated with higher decompensation risk after liver cancer resection ref 5, and an HVPG of 16 mmHg or above increases short-term mortality risk after non-liver abdominal surgery. ref 6

Compensated Advanced Chronic Liver Disease (cACLD)

Baveno VII uses the term cACLD — compensated advanced chronic liver disease — to reflect the continuum from severe fibrosis to cirrhosis. It is a practical, non-invasive way to identify patients at risk, using FibroScan (transient elastography) rather than requiring a liver biopsy. ref 8

Non-Invasive Diagnosis: The Rule of 5

One of Baveno VII's most important contributions is a simple stiffness-based framework — the "Rule of 5" — that uses FibroScan thresholds at 10, 15, 20, and 25 kPa to guide clinical decisions. ref 11 These thresholds apply regardless of the underlying cause of your liver disease.

FibroScan can produce false positive results, so an initial reading of 10 kPa or above should be repeated under fasting conditions or confirmed with a blood-based fibrosis marker. ref 13 The liver stiffness thresholds also hold prognostic value during follow-up — meaning serial measurements over time help predict your trajectory. ref 7

Ruling CSPH In and Out Non-Invasively

You do not necessarily need an HVPG measurement (an invasive catheter procedure) to assess CSPH. Non-invasive tests are sufficiently accurate for clinical practice. ref 16

Rule out CSPH: FibroScan below 15 kPa plus platelet count above 150×10⁹/L excludes CSPH with over 90% sensitivity and negative predictive value. ref 17

Rule in CSPH: FibroScan of 25 kPa or above is sufficient to confirm CSPH (specificity and positive predictive value over 90%) in patients with virus-related, alcohol-related, or non-obese NASH-related cACLD. ref 18

Grey zone (15–25 kPa): The ANTICIPATE model combines liver stiffness and platelet count to estimate CSPH probability. Patients with stiffness of 20–25 kPa and platelets below 150, or stiffness of 15–20 kPa and platelets below 110, have at least a 60% chance of CSPH. ref 19

In viral hepatitis specifically, spleen stiffness can also help: values below 21 kPa by TE rule out CSPH, while values above 50 kPa rule it in. ref 22

When You Can Avoid Endoscopy

Many patients dread the upper endoscopy (camera exam) used to check for varices. Baveno VII provides clear rules for when it can be safely skipped.

If you are already taking a beta-blocker (NSBB) to prevent decompensation: No screening endoscopy is needed, because finding varices would not change your treatment — you are already on the recommended therapy. ref 36

If you are NOT on a beta-blocker (due to contraindications or intolerance): Endoscopy is needed when your FibroScan is 20 kPa or above, or your platelet count is 150×10⁹/L or below. ref 20

If neither threshold is met: You can be followed up with yearly FibroScan and platelet count. If liver stiffness rises to 20 kPa or above, or platelets drop below 150, then endoscopy becomes necessary. ref 21

Preventing Your First Complication (Decompensation)

For patients with compensated cirrhosis and CSPH, the primary goal is to prevent that first complication — whether it is ascites, variceal bleeding, or encephalopathy.

Beta-Blockers: Carvedilol Is Preferred

Non-selective beta-blockers (NSBBs) — propranolol, nadolol, or carvedilol — should be considered for preventing decompensation in patients with CSPH. ref 34 Baveno VII identifies carvedilol as the preferred choice because it is more effective at reducing portal pressure, tends to be better tolerated, and has been shown to improve survival compared to no active treatment. ref 35

There is no role for NSBBs in patients who do not have CSPH. ref 37 For compensated patients with high-risk varices who cannot tolerate beta-blockers, endoscopic band ligation is the recommended alternative. ref 38

Addressing Co-Factors

Non-hepatic comorbidities are common in compensated cirrhosis and can worsen your prognosis — they should be actively managed. ref 70 Superimposed liver injuries (alcoholic hepatitis, acute viral hepatitis, drug-induced liver injury) can trigger decompensation. ref 71

Treating the Underlying Cause

Removing or suppressing the underlying cause of your liver disease leads to meaningful drops in portal pressure and substantially reduces the risk of decompensation. ref 23 If CSPH resolves after successful treatment, decompensation is effectively prevented. ref 72 However, obesity, diabetes, and alcohol remain important contributors to disease progression even after the primary cause is addressed. ref 60

For hepatitis C patients who achieve sustained virological response (SVR): if your FibroScan drops below 12 kPa and platelets rise above 150×10⁹/L, you can be discharged from portal hypertension surveillance (including endoscopy), though HCC screening should continue. ref 24

Supportive Therapies (Beyond Treating the Cause)

Baveno VII includes several notable recommendations about common medications that can benefit cirrhosis patients beyond their usual indications.

Statins

If you have an existing reason to be on a statin (such as high cholesterol), Baveno VII says the medication should be encouraged in cirrhosis — not avoided. Statins may lower portal pressure and improve overall survival. ref 25 In more advanced disease (Child-Pugh B/C), lower doses should be used (simvastatin max 20 mg/day) with close monitoring for muscle and liver side effects. ref 26

Aspirin

Similarly, aspirin should not be discouraged if you have an approved reason to take it. It may reduce the risk of liver cancer (HCC), liver-related complications, and death. ref 27

Anticoagulants (Blood Thinners)

Anticoagulation should not be avoided in cirrhosis patients who need it for other conditions — it may actually reduce liver-related outcomes and improve overall survival. ref 29 Direct-acting oral anticoagulants (DOACs) are as safe and effective in Child-Pugh A/B cirrhosis as in patients without cirrhosis. ref 30 DOACs are not recommended in Child-Pugh C cirrhosis outside clinical trials.

Albumin, Antibiotics, and Rifaximin

Short-term albumin infusion is indicated in several specific situations: spontaneous bacterial peritonitis (SBP), acute kidney injury beyond stage 1A, large-volume paracentesis (drainage of ascites fluid), and combined with terlipressin for hepatorenal syndrome. ref 28 Preventive antibiotics are recommended for high-risk SBP patients (those with GI bleeding or Child-Pugh C with low-protein ascites). ref 74 Rifaximin is indicated for preventing recurrent hepatic encephalopathy. ref 66

Managing Acute Variceal Bleeding

Variceal bleeding is a medical emergency and one of the most feared complications of portal hypertension. Baveno VII provides a detailed treatment framework.

Immediate Management

Blood transfusions should be conservative, targeting a haemoglobin of 7–8 g/dl. ref 39 Vasoactive drugs (terlipressin, somatostatin, or octreotide) should be started as soon as variceal bleeding is suspected and continued for 2–5 days. ref 40 Antibiotic prophylaxis is mandatory from the point of admission. ref 41

Endoscopy and Procedures

Upper endoscopy should be performed within 12 hours of presentation. ref 42 Band ligation is the standard endoscopic treatment for oesophageal variceal bleeding. ref 43

For high-risk patients, pre-emptive TIPS (a procedure that creates a shunt to reduce portal pressure) should be performed within 72 hours, ideally within 24 hours. High-risk criteria include: Child-Pugh C cirrhosis (score below 14), Child-Pugh B (score above 7) with active bleeding at endoscopy, or HVPG above 20 mmHg. ref 44 After TIPS, reducing the portal pressure gradient to below 12 mmHg provides near-complete protection from further portal hypertensive bleeding. ref 45

If bleeding cannot be controlled, self-expandable metal stents (SEMS) are recommended as bridge therapy before TIPS. They are as effective as balloon tamponade but safer. ref 75 The key outcome measure in variceal bleeding studies is survival at 6 weeks after the episode. ref 48

Preventing Further Decompensation

Once a first complication has occurred, preventing further decompensation becomes critical. Further decompensation carries even higher mortality than the first episode. ref 49

All patients with decompensated cirrhosis should be evaluated for liver transplantation. ref 50

After Variceal Bleeding

First-line prevention of recurrent bleeding is the combination of a beta-blocker (NSBB or carvedilol) plus endoscopic band ligation. ref 52 If rebleeding occurs despite this, TIPS is the treatment of choice. In patients with ascites and high-risk varices, NSBBs or carvedilol are preferred over band ligation alone for preventing first bleeding. ref 73

Recurrent Ascites

TIPS should be considered if you require 3 or more large-volume paracenteses (ascites drainages) within one year, regardless of whether you also have varices. ref 51

Beta-Blocker Safety in Decompensated Patients

Beta-blockers should be dose-reduced or temporarily stopped if your systolic blood pressure drops below 90 mmHg (or mean arterial pressure below 65 mmHg), or if hepatorenal syndrome develops. They can be restarted once blood pressure recovers. ref 53

Infections, Nutrition, and Sarcopenia

Bacterial infections are common in decompensated cirrhosis and can trigger further decompensation. All hospitalized patients should be screened for infections. ref 54 Frailty, malnutrition, and muscle wasting (sarcopenia) worsen survival and should be formally assessed. ref 55 Every patient with decompensated cirrhosis should receive nutrition counseling and be encouraged to exercise. ref 56

Recompensation — When Things Improve

Baveno VII formally defines "recompensation" for the first time — acknowledging that cirrhosis can partially reverse. To qualify, all three of the following must be met: ref 57

1. The underlying cause is treated — hepatitis C cured (SVR), hepatitis B suppressed, or sustained alcohol abstinence achieved.

2. Complications have resolved without medications — no ascites (off diuretics), no encephalopathy (off lactulose/rifaximin), and no recurrent variceal bleeding for at least 12 months.

3. Liver function tests show stable improvement — albumin, INR, and bilirubin are trending in the right direction.

Even after recompensation, CSPH may persist. Therefore, beta-blockers should not be stopped unless CSPH is confirmed to have resolved. ref 58

Vascular Disorders of the Liver

Baveno VII also addresses three important vascular conditions beyond typical cirrhotic portal hypertension.

Portal Vein Thrombosis (PVT)

Blood clots in the portal vein can occur with or without cirrhosis. Screening for PVT is recommended in all potential liver transplant candidates. ref 61 In non-cirrhotic patients, recent PVT rarely resolves on its own, so anticoagulation (blood thinners) should be started immediately at full therapeutic dose. ref 62 Treatment should continue for at least 6 months. ref 63

Budd-Chiari Syndrome (BCS)

BCS involves blockage of the veins draining the liver. Management follows a stepwise approach: first anticoagulation, then angioplasty or stenting if needed, then TIPS, and finally liver transplantation in refractory cases. ref 68 All patients with primary BCS should receive long-term anticoagulation. ref 69

Porto-Sinusoidal Vascular Disorder (PSVD)

PSVD is a broad condition that can cause portal hypertension without true cirrhosis, encompassing entities previously called non-cirrhotic portal fibrosis or nodular regenerative hyperplasia. ref 64 Importantly, in NASH-related cirrhosis, a small proportion of patients may show clinical signs of portal hypertension even with HVPG below 10 mmHg — PSVD should be considered in such cases. ref 67

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