Definition of Compensated advanced chronic liver disease (cACLD)
The use of elastography in clinical practice has enabled the early identification of patients with untreated/active chronic liver disease at risk of having CSPH and consequently, at risk of decompensation and liver-related death.
The term “compensated advanced chronic liver disease (cACLD)” had been proposed to reflect the continuum of severe fibrosis and cirrhosis in patients with ongoing chronic liver disease. A pragmatic definition of cACLD based on liver stiffness measurement (LSM) is aimed at stratifying the risk of CSPH and decompensation at point of care, irrespective of histological stage or the ability of LSM to identify these stages.
Currently, both terms “cACLD” and “compensated cirrhosis” are acceptable, but not interchangeable.
Criteria to identify cACLD
LSM values by transient elastography (TE) <10 kPa in the absence of other known clinical/imaging signs rule out cACLD; values between 10 and 15 kPa are suggestive of cACLD; values >15 kPa are highly suggestive of cACLD.
Patients with chronic liver disease and an LSM <10 kPa by TE have a negligible 3-year risk (≤1%) of decompensation and liver-related death.
Patients with cACLD should be referred to a liver disease specialist for further work-up.
Invasive methods (liver biopsy, HVPG) can be used for further work-up in an individualised manner at referral centres.
Outcome and prognosis
LSM (irrespective of the technique used for its measurement) holds prognostic information in cACLD, both at index investigation and during follow-up.
A rule of 5 for LSM by TE (10-15-20-25 kPa) should be used to denote progressively higher relative risks of decompensation and liver-related death independently of the aetiology of chronic liver disease.
How to monitor
Patients with LSM values 7-10 kPa and ongoing liver injury should be monitored on a case-by-case basis for changes indicating progression to cACLD.
TE can lead to false positive results, therefore an index LSM ≥10 kPa should be repeated in fasting conditions as soon as feasible or complemented with an established serum marker of fibrosis (fibrosis-4 ≥2.67, enhance liver fibrosis test ≥9.8, FibroTest ≥0.58 for alcohol-related/viral liver disease, FibroTest ≥0.48 for non-alcoholic fatty liver disease).
In patients with cACLD, LSM could be repeated every 12 months to monitor changes.
A clinically significant decrease in LSM, which is associated with substantially reduced risk of decompensation and liver-related death, can be defined as a decrease in LSM of ≥20% associated with LSM <20 kPa or any decrease to a LSM <10 kPa.
Corrigendum to ‘Baveno VII – Renewing consensus in portal hypertension’ [J Hepatol (2022) 959-974] Journal of Hepatology, Vol. 77, Issue 2