18-11: Cirrhosis

ESSENTIALS OF DIAGNOSIS

GENERAL CONSIDERATIONS

Cirrhosis is the result of hepatocellular injury with inflammation that leads to both fibrosis and regenerative nodules throughout the liver. The prevalence is 0.27%, with an estimated 1.5 billion persons having chronic liver disease and 2.14 million liver-related deaths worldwide (11th leading cause). 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 alcohol; MASLD; chronic viral hepatitis; drug toxicity; autoimmune and metabolic liver diseases; 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 American and Black persons have a higher frequency of cirrhosis than White persons 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 18–17) 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 18–18). 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 ...