Overview
In an estimated 20 to 30% of persons with hepatitis C virus (HCV) infection, chronic viremia results in inflammation, followed by fibrosis and cirrhosis.[1,2,3] Advanced fibrosis and cirrhosis—at their early stages—are not usually clinically detectable or symptomatic.[4] As individuals develop more extensive hepatic fibrosis, physiologic complications can develop, such as increased pressure within the portal system, disruption in bilirubin metabolism, and reduced production of coagulation factor proteins.[5,6]
Defining Compensated and Decompensated Cirrhosis
Once it has been established that an individual has cirrhosis, it becomes very important to determine whether they have compensated or decompensated cirrhosis.[7] Persons with compensated cirrhosis often do not have signs or symptoms related to their cirrhosis, although they may have evidence of portal hypertension, such as esophageal or gastric varices.[8,9,10] In contrast, persons with decompensated cirrhosis often have symptomatic complications related to cirrhosis, including those related to hepatic insufficiency (jaundice or hepatic encephalopathy), and those related to portal hypertension (ascites or variceal hemorrhage).[11]
Distinguishing Compensated versus Decompensated Cirrhosis
Prognosis and survival are markedly better in persons with compensated cirrhosis than in those with decompensated cirrhosis (Figure 1) and (Figure 2).[12,13] In addition, the presence of decompensated cirrhosis can have major implications regarding management and prevention of cirrhosis-related complications, as well as the potential need for a referral for liver transplantation evaluation.[14] In general, any person with decompensated cirrhosis should receive evaluation and medical care by a hepatologist or liver diseases specialist.[7] Some experts have proposed a 4-stage cirrhosis classification system that risk stratifies individuals according to the presence of ascites, esophageal varices, and variceal bleeding to differentiate and stage compensated and decompensated disease (Figure 3).[15,16]