Upon completion of the chapter, the reader will be able to:
Explain the pathophysiology of cirrhosis and portal hypertension.
Identify signs and symptoms of cirrhosis.
Identify laboratory abnormalities that result from liver disease and describe the associated pathophysiology.
Describe the consequences associated with cirrhosis and decreased hepatic function.
Identify treatment goals for a patient with complications of cirrhosis.
Recommend a specific treatment regimen for a patient with cirrhosis that includes lifestyle changes, nonpharmacologic measures, and pharmacologic therapy.
Cirrhosis involves replacement of normal hepatic architecture with fibrous scar tissue. Scarring is accompanied by the loss of viable hepatocytes (the functional cells of the liver) and alterations in hepatic blood flow. Cirrhosis is characterized by progressive damage and deterioration of liver function, but even with extensive scarring, some patients remain asymptomatic. Advanced cirrhosis is irreversible and leads to portal hypertension, which in turn is responsible for the complications that define decompensated cirrhosis. Complications of cirrhosis include ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy (HE), hepatorenal syndrome (HRS), and variceal bleeding.1 These complications carry high mortality rates and indicate disease progression. The only cure for cirrhosis is liver transplantation.
EPIDEMIOLOGY AND ETIOLOGY
Overall, cirrhosis is the 11th leading cause of death in the United States. Rates vary by age, gender, race, and ethnicity, but cirrhosis places an enormous burden on society from hospitalizations, lost wages, decreased productivity, and emotional strain on patients and their families.
Cirrhosis results from long-term insult to the liver, but damage usually doesn’t become clinically evident until the fourth decade of life. Infection with one or more strains of viral hepatitis causes acute, potentially reversible hepatic inflammation, whereas chronic infection with hepatitis B (HBV) or C (HCV) often leads to cirrhosis. Globally, viral hepatitis and alcoholic and nonalcoholic liver disease are the most common causes of cirrhosis. Alcohol and HCV are the most common causes of cirrhosis in the United States, whereas HBV accounts for the majority of cases worldwide.2 Newer HCV therapies provide sustained virologic response (SVR) and are expected to dramatically decrease new cases of HCV cirrhosis. Even patients who have already developed HCV cirrhosis benefit from antiviral therapy, and recent guidelines recommend treatment for nearly all patients (see Chapter 25, Viral Hepatitis, for more details).3
Nonalcoholic fatty liver disease (NAFLD) begins with asymptomatic fatty liver but can progress to cirrhosis; it is the leading cause of chronic liver disease worldwide. NAFLD is a diagnosis of exclusion; viral, genetic, and environmental causes must be ruled out. NAFLD is so closely associated with diabetes mellitus, dyslipidemia, obesity, insulin resistance, and other conditions associated with increased hepatic fat that an international consensus recently recommended a change in nomenclature to metabolic dysfunction–associated fatty liver disease (MAFLD).4
Alcoholic cirrhosis usually develops after decades of heavy drinking. It develops ...