Cirrhosis of the liver is identified histologically based on the following three criteria: (1) diffuse disease, (2) the presence of fibrosis and (3) replacement of normal architecture by abnormal nodules. The progressive deposition of fibrous tissue creates islands of normal hepatocytes called “pseudolobules.” The size of these pseudolobules determines whether the defect is called micronodular cirrhosis (less than 3 cm) or macronodular cirrhosis (more than 3 cm). Unlike fibrosis, cirrhosis is not a reversible process. Anand reviewed the characteristics of liver cirrhosis and the challenges of management.
A complete diagnosis should include the cause of the liver disease (e.g., alcoholic or viral cirrhosis) and determine if the patient has decompensated liver disease. Laboratory tests determine the presence and severity of disease and help establish the etiology. An increase in aminotransferase suggests hepatocellular disease; a predominant increase in alkaline phosphatase indicates cholestatic or biliary tract problems. Imaging studies may reveal outflow obstruction. For a comprehensive review of additional diagnostic tests, see the accompanying table.
Clinical presentation varies widely, ranging from complete absence of symptoms to vague illness (i.e., fatigue, malaise and weight loss) to serious decompensated liver disease (i.e., edema, ascites, easy bruising, poor memory and other mental status changes). Physical signs, caused by hyperdynamic circulation and blood shunting around the liver, include tachycardia, a bounding pulse, warm extremities and breathlessness.
Management focuses primarily on treating complications. Dietary restrictions generally are not needed in uncomplicated cirrhosis, although patients with edema should avoid salt. Diuretics can help reduce fluid accumulation, but patients with resistant ascites are candidates for a shunt procedure or a liver transplant. Patients who have cirrhosis with ascites are prone to spontaneous bacterial peritonitis. Signs and symptoms of the latter include fever, abdominal pain and an ascitic fluid neutrophil count of more than 250 per mm3. Intravenous antibiotic therapy is appropriate.
Portal hypertension with bleeding varices is a serious complication of cirrhosis that can be treated surgically and with drug therapy. Patients with encephalopathy require a low-protein diet and enough lactulose to produce three or four bowel movements daily. Hepatorenal syndrome, defined as oliguric renal failure in a patient with advanced liver disease, is caused by reduced renal perfusion. Treatment is limited to placement of a shunt or liver transplant. Because cirrhosis is considered a premalignant condition with an enhanced risk of hepatocellular carcinoma, screening with alpha-fetoprotein determinations and ultrasonography every six months is appropriate.