Diagnostic Methods for Cirrhosis and Portal Hypertension

Book Preface

Cirrhosis is considered the end-stage of chronic liver disease of any etiology with a broad spectrum of clinical manifestations, from an entirely asymptomatic stage to a stage characterized by multiorgan failure. The clinical manifestations of cirrhosis are due mostly to portal hypertension and its hemodynamic consequences and/or to liver insufficiency.
Numerous prognostic studies over the years have indicated that the natural history of cirrhosis does not represent, as in most disease states, a continuum of a single entity but that cirrhosis is an entity that progresses across different stages, each with different prognosis, predictors of death and pathophysiological mechanisms.
A systematic review of 116 prognostic studies in cirrhosis had already demonstrated that cirrhosis is a heterogeneous disease with median survival times that ranged widely between 1–186 months [1]. This review also showed that, when patients are classified into two stages depending on the presence or absence of clinically evident liver-related events (specifically ascites, variceal hemorrhage, hepatic encephalopathy [HE] and/or jaundice), 1-year survival in patients without these events (compensated patients) is 95% (interquartile range 91–98%) while in those with any of these events (decompensated patients), it is 61% (interquartile range 56–70%) [1]. This systematic review also revealed that predictors of death are different in patients with compensated compared with those with decompensated cirrhosis [1].
From another perspective, analysis of individual patient data from two prospective Italian cohort studies including over 1600 patients demonstrated a median survival of greater than 12 years in patients with compensated cirrhosis, while patients with decompensated cirrhosis have a median survival of 1.8 years [1].
These results have been confirmed in a recent prospective study that analyzed a concurrent cohort of patients with cirrhosis (both compensated and decompensated) and showed that decompensation was, by far, the strongest predictor of death in cirrhosis. Furthermore, both stages have different predictors of death (age for compensated; Model for End-Stage Liver Disease [MELD] score for decompensated), and predictors that were common to both stages (albumin, platelet count) have different strengths of association [2].
Therefore, compensated cirrhosis and decompensated cirrhosis should be considered as two different disease entities, with different probabilities of death and different predictors of death and should be described, studied and managed separately.
Within these two main stages of cirrhosis, recent advances have provided further granularity that has allowed sub-staging of compensated and decompensated cirrhosis not only regarding prognosis but also regarding the predominant pathogenic mechanisms (Fig. 1.1). Before detailing this sub-staging, it is important to briefly summarize the pathophysiology of the complications of cirrhosis.