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Unifying Concepts

Baveno VI Criteria for Compensated Advanced Chronic Liver Disease (cACLD)

Portal hypertension is the haemodynamic abnormality associated with the most severe complications of cirrhosis, including ascites, hepatic encephalopathy and bleeding from gastroesophageal varices. Variceal bleeding is a medical emergency associated with a mortality that, in spite of recent progress, is still in the order of 10–20% at 6 weeks. The evaluation of diagnostic tools and the design and conduct of good clinical trials for the treatment of portal hypertension have always been difficult.

Definition of compensated advanced chronic liver disease

  • The introduction of transient elastography (TE) in clinical practice has allowed the early identification of patients with chronic liver disease (CLD) at risk of developing clinically significant portal hypertension (CSPH).
  • For these patients, the alternative term ‘‘compensated advanced chronic liver disease (cACLD)’’ has been proposed to better reflect that the spectrum of severe fibrosis and cirrhosis is a continuum in asymptomatic patients, and that distinguishing between the two is often not possible on clinical grounds.
  • Currently, both terms: ‘‘cACLD’’ and ‘‘compensated cirrhosis’’ are acceptable.
  • Patients with suspicion of cACLD should be referred to a liver disease specialist for confirmation, follow-up and treatment.

Criteria to suspect cACLD

  • Liver stiffness by TE is sufficient to suspect cACLD in asymptomatic subjects with known causes of CLD.
  • TE often has false positive results; hence two measurements on different days are recommended in fasting conditions.
  • TE values <10 kPa in the absence of other known clinical signs rule out cACLD; values between 10 and 15 kPa are suggestive of cACLD but need further test for confirmation; values >15 kPa are highly suggestive of cACLD.

Criteria to confirm cACLD

  • Invasive methods are employed in referral centres in a stepwise approach when the diagnosis is in doubt or as
    confirmatory tests Methods and findings that confirm the diagnosis of cACLD are:

    • Liver biopsy showing severe fibrosis or established cirrhosis.
    • Collagen proportionate area (CPA) measurement on histology provides quantitative data on the amount of fibrosis and holds prognostic value and its assessment is recommended.
    • Upper GI endoscopy showing gastroesophageal varices.
    • Hepatic venous pressure gradient (HVPG) measurement; values >5 mmHg indicate sinusoidal portal hypertension.

Diagnosis of CSPH in patients with cACLD

  • HVPG measurement is the gold-standard method to assess the presence of CSPH, which is defined as HVPG ≥10 mmHg.
  • By definition, patients without CSPH have no gastro-oesophageal varices, and have a low five year risk of developing them.
  • In patients with virus related cACLD non-invasive methods are sufficient to rule-in CSPH, defining the group of patients at risk of having endoscopic signs of PH. The following can be used:
    • Liver stiffness by TE (≥20–25 kPa; at least two measurements on different days in fasting condition; caution should be paid to flares of ALT; refer to EASL guidelines for correct interpretation criteria), alone or combined to platelets and spleen size.
  • The diagnostic value of TE for CSPH in other aetiologies remains to be ascertained.
  • Imaging showing collateral circulation is sufficient to rule-in CSPH in patients with cACLD of all aetiologies.

Identification of patients with cACLD who can safely avoid screening endoscopy

  • Patients with a liver stiffness <20 kPa and with a platelet count >150,000 have a very low risk of having varices requiring treatment, and can avoid screening endoscopy.
  • These patients can be followed up by yearly repetition of TE and platelet count.
  • If liver stiffness increases or platelet count declines, these patients should undergo screening esophagogastroduodenoscopy.

Surveillance of oesophageal varices

  • In compensated patients with no varices at screening endoscopy and with ongoing liver injury (e.g. active drinking in alcoholics, lack of SVR in HCV), surveillance endoscopy should be repeated at 2 year intervals.
  • In compensated patients with small varices and with ongoing liver injury (e.g. active drinking in alcoholics,
    lack of SVR in HCV), surveillance endoscopy should be repeated at one year intervals.
  • In compensated patients with no varices at screening endoscopy in whom the aetiological factor has been
    removed (e.g. achievement of SVR in HCV; long-lasting abstinence in alcoholics) and who have no co-factors
    (e.g. obesity), surveillance endoscopy should be repeated at three year intervals.
  • In compensated patients with small varices at screening endoscopy in whom the aetiological factor has been
    removed (e.g. achievement of SVR in HCV; long-lasting abstinence in alcoholics) and who have no co-factors
    (e.g. obesity), surveillance endoscopy should be repeated at two year intervals.

Abbreviations: Sustained Virologic Response (SVR), Hepatitis C Virus (HCV).

 

References:

  1. de Franchis R; Baveno VI Faculty. Expanding consensus in portal hypertension: Report of the Baveno VI Consensus Workshop: Stratifying risk and individualizing care for portal hypertension. J Hepatol. 2015 Sep;63(3):743-52. [Medline]
  2. Vuille-Lessard É, Rodrigues SG, Berzigotti A. Noninvasive Detection of Clinically Significant Portal Hypertension in Compensated Advanced Chronic Liver Disease. Clin Liver Dis. 2021 May;25(2):253-289. [Medline]
  3. Podrug K, Trkulja V, Zelenika M, Bokun T, Madir A, Kanizaj TF, O’Beirne J, Grgurevic I. Validation of the New Diagnostic Criteria for Clinically Significant Portal Hypertension by Platelets and Elastography. Dig Dis Sci. 2021 Nov 5:1–6. [Medline]

 

Created Nov 09, 2021.

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