16-11: Cirrhosis

GENERAL CONSIDERATIONS

Cirrhosis, the eleventh leading cause of death globally and eighth leading cause of death in the United States with a prevalence rate of 0.27%, is the result of hepatocellular injury that leads to both fibrosis and regenerative nodules throughout the liver. Hospitalization rates for cirrhosis and portal hypertension are rising in the United States, and patients with chronic liver disease have longer hospital stays, more readmissions, and less access to post-acute care than patients with other chronic diseases. Causes include chronic viral hepatitis; alcohol; drug toxicity; autoimmune and metabolic liver diseases, including NAFLD; and miscellaneous disorders. Celiac disease appears to be associated with an increased risk of cirrhosis. Many patients have more than one risk factor (eg, chronic hepatitis and alcohol use) and likely genetic predisposition. Mexican Americans and African Americans have a higher frequency of cirrhosis than whites because of a higher rate of risk factors. In persons at increased risk for liver injury (eg, heavy alcohol use, obesity, iron overload), higher coffee and tea consumption and statin use reduce the risk of cirrhosis. The risk of hospitalization or death due to cirrhosis has been reported to correlate with protein and cholesterol consumption and with hyperuricemia and inversely with carbohydrate consumption.

The most common histologic classification divides cirrhosis into micronodular, macronodular, and mixed forms. These are descriptive terms rather than separate diseases, and each form may be seen in the same patient at different stages of the disease. In micronodular cirrhosis—typical of alcohol-associated liver disease (Laennec cirrhosis)—the regenerative nodules (eFigure 16–17) are no larger than the original lobules, ie, approximately 1 mm in diameter or less. Macronodular cirrhosis is characterized by larger nodules, which can measure several centimeters in diameter and may contain central veins (eFigure 16–18). This form corresponds more or less to postnecrotic (posthepatitic) cirrhosis but does not necessarily follow episodes of massive necrosis and stromal collapse. Clinically, cirrhosis is considered to progress through three stages that correlate with the thickness of fibrous septa: compensated, compensated with varices, and decompensated (ascites, variceal bleeding, encephalopathy, or jaundice). A diagnosis of acute-on-chronic liver failure should be made in a patient with cirrhosis and acute decompensation (new or worsening ascites, gastrointestinal hemorrhage, overt encephalopathy, worsening nonobstructive jaundice, or bacterial infection associated with other organ failure). Precipitating factors include infections, hemodynamic instability, heavy alcohol use, and drug hepatotoxicity.