Cirrhosis: Diagnosis and Treatment

Diagnosis

History and physical examination should include a special focus on alcohol use, exposure to toxins, intravenous drug abuse, blood transfusion, history of viral infections, the presence of tattoos, and the characteristic presentation of cirrhosis. Additional investigations are described below. 

Abdominal CT scan and ultrasound can provide evidence of abnormal liver architecture to define the extent of cirrhosis. They can also identify ascites and other hepatic and abdominal pathology, such as hepatocellular carcinoma and portal hypertension.

Percutaneous liver biopsy is diagnostic and may suggest the underlying cause of cirrhosis. However, biopsy may not be necessary when the diagnosis is clearly established by clinical, laboratory, and radiologic findings.

Liver function tests can be normal early in the disease, but become abnormal as the liver is destroyed. Transaminase levels reflect hepatocellular injury; alkaline phosphatase reflects cholestasis; and albumin reflects hepatic synthetic activity.

Metabolic and electrolyte abnormalities are common, including hypoalbuminemia, hypocholesterolemia, decreased coagulation factors, decreased nitrogen, elevated ammonia, anemia, thrombocytopenia, and leukopenia.

Upper gastrointestinal (GI) endoscopy may be used to diagnose esophageal varices.

Treatment

Treatment is aimed at slowing or reversing disease progression (if the underlying disease is treatable), preventing and treating complications, and, if possible, providing a cure through liver transplantation.

It is essential to address the underlying etiology. Required measures include avoiding alcohol and hepatotoxic medications, treating viral hepatitis with appropriate antiviral regimens (eg, alpha interferon plus ribavirin), and treating autoimmune hepatitis or severe alcoholic hepatitis with steroids or immunosuppressive agents.

Also critical are prevention and treatment of cirrhosis complications. Esophageal varices can be treated with a beta–blocker to decrease the risk of bleeding. Bleeding varices can be treated with endoscopic rubber banding, sclerotherapy, intravenous vasopressin or somatostatin, or balloon tamponade.

Lactulose decreases ammonia absorption from the gut, thereby decreasing the risk of hepatic encephalopathy.

Ascites can be managed with sodium restriction and diuretics. For severe or recurrent symptomatic ascites, slow removal of ascitic fluid via paracentesis is indicated. Ascites complicated by bacterial infection (spontaneous bacterial peritonitis) requires intravenous antibiotics.

Patients can be screened for the development of hepatocellular carcinoma by serum α–fetoprotein (AFP) concentration and right–upper–quadrant ultrasound.

Ultimately, liver transplantation is the only potential cure. Transplantation is an option for appropriate patients with advanced disease and severe complications, including variceal hemorrhage, hepatic encephalopathy, and hepatorenal syndrome. Transplantation is contraindicated in patients who continue to use alcohol or drugs. It is also contraindicated in patients who are unsuitable for surgery due to cardiopulmonary disease.