Primary prevention

Methods of primary prevention include:

  • Prevention strategies aimed at reducing excessive alcohol consumption, intravenous drug use, and unprotected intercourse

  • Vaccination programs for hepatitis B

  • Public health strategies to control the rising incidence of obesity and diabetes

  • Screening patients with risk factors for liver disease with noninvasive markers of liver fibrosis to identify liver disease before cirrhosis develops

  • Treatment of any underlying chronic liver disease to prevent the progression to cirrhosis

  • Appropriate screening of family members of patients with cirrhosis secondary to hemochromatosis or Wilson disease

  • Screening of blood donors and products for viral hepatitides.

Secondary prevention

The following secondary preventive strategies are aimed at minimizing the level of superimposed hepatic insult in an established cirrhotic liver:

  • Treatment of any underlying chronic liver disease

  • Avoidance of alcohol and other hepatotoxins such as nonsteroidal anti-inflammatory drugs and high doses of acetaminophen (>2-3 g/day)

  • Immunization against hepatitis A and B for susceptible patients.

    • In particular, the US Advisory Committee on Immunization Practices recommends that all patients with cirrhosis should be vaccinated against hepatitis A and B.[226]

There is some evidence to suggest that long-term treatment with beta-blockers (propranolol or carvedilol) increases decompensation-free survival, compared with placebo, in patients with compensated cirrhosis and clinically significant portal hypertension.[227][228] Nonselective beta-blockers such as carvedilol may be considered to prevent decompensation in patients with compensated advanced chronic liver disease with clinically significant portal hypertension, except in those with contraindications such as asthma, advanced heart block, and bradyarrhythmias.[2][229] The American Association for the Study of Liver Diseases recommends against the use of nonselective beta-blockers to prevent decompensation in patients with cirrhosis without clinically significant portal hypertension.[2]

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