Author information

• ¹Gastroenterology Unit, Ospedale V. Cervello, Clinica La Maddalena, Palermo, Italy. Electronic address: pangeli@unipd.it.
• ²Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.
• ³Department of Medicine, Unit of Internal Medicine and Hepatology (UIMH), University of Padova, Italy. Electronic address: pangeli@unipd.it.

Abstract

There is a universal agreement on the fact that the occurrence of clinical complications, such as ascites, hepatic encephalopathy, gastrointestinal bleeding, and jaundice mark the transition from the compensated to the decompensated stage of liver cirrhosis. Decompensation is associated with a substantial worsening of patient prognosis, and is therefore considered the most important stratification variable for the risk of death. However, this classification sounds as an oversimplification, as it does not discriminate between the prognostic subgroups that characterize the course of decompensation, which depends on the type and number of decompensating events. A deeper insight into the clinical course of decompensated cirrhosis is provided by observational studies characterizing acute decompensation (AD) which occurs mostly in patients who have already experienced decompensating events. Decompensation presents as AD in a portion of patients while in many others it presents as a slow development of ascites or mild hepatic encephalopathy grade 1 or 2, or jaundice, not requiring hospitalization. Thus, we propose that decompensation of cirrhosis occurs through two distinguished pathways: a non-acute (NAD) and an acute one (AD, which includes ACLF). Moreover, while NAD is the most frequent pathway of the first decompensation, AD mostly represents further decompensation.