Management of Compensated Liver Cirrhosis
For patients with compensated liver cirrhosis and no significant comorbidities, the primary medication strategy is treating the underlying etiology—particularly viral hepatitis with entecavir or tenofovir if HBV DNA ≥2,000 IU/mL—combined with diuretics (spironolactone with or without furosemide) if ascites develops, while avoiding NSAIDs and hepatotoxic medications. 1, 2, 3
Primary Treatment Strategy: Address the Underlying Cause
The management paradigm has fundamentally shifted from merely treating complications as they arise to preventing disease progression while patients remain compensated. 3, 4 This approach can potentially reverse early cirrhosis, prevent decompensation, and improve survival. 3, 4
For Viral Hepatitis B-Related Cirrhosis
- Initiate antiviral therapy if HBV DNA ≥2,000 IU/mL regardless of ALT levels using entecavir or tenofovir as first-line monotherapy due to their potent antiviral efficacy and high genetic barrier to resistance. 1, 3
- Long-term therapy is generally required, with monitoring every 3 months during treatment. 1
- Prolonged suppression of HBV DNA can prevent disease progression and even achieve reversal of cirrhosis with long-term entecavir or tenofovir therapy. 1
- Avoid lamivudine in cirrhotic patients due to high resistance risk that could result in clinical decompensation. 1
- Peginterferon alfa may be used with careful monitoring in patients with well-compensated cirrhosis and preserved liver function, though it carries risk of acute exacerbation. 1
For Viral Hepatitis C-Related Cirrhosis
- Patients with compensated cirrhosis should be treated with direct-acting antivirals in the absence of contraindications to prevent short to mid-term complications. 1
- Treatment improves liver function and reduces portal hypertension in many patients. 3, 4
- Continue HCC surveillance every 6 months regardless of achieving sustained virologic response (SVR), as risk persists even after viral eradication. 1, 3
Management of Ascites (If Present)
First-Line Diuretic Therapy
- Sodium restriction to less than 5 g/day plus spironolactone (starting dose 50-100 mg/day, maximum 400 mg/day) with or without furosemide (starting dose 20-40 mg/day, maximum 160 mg/day) is the first-line treatment for ascites. 2, 3, 4, 5
- Fluid restriction is unnecessary unless serum sodium drops below 120-125 mmol/L. 2, 3, 4
- For tense ascites, perform initial therapeutic paracentesis followed by sodium restriction and diuretic therapy. 4
Important Monitoring Considerations
- Initiate spironolactone in the hospital for patients with hepatic cirrhosis and ascites, as sudden alterations of fluid and electrolyte balance may precipitate hepatic encephalopathy and coma. 5
- Start with the lowest initial dose and titrate slowly in cirrhotic patients, as clearance of spironolactone and its metabolites is reduced. 5
- Monitor renal function closely, particularly in elderly patients and those with multiple risk factors for renal impairment. 1, 5
Prevention of First Decompensation
Non-Selective Beta-Blockers
- Consider non-selective beta-blockers (propranolol) for patients with clinically significant portal hypertension (HVPG ≥10 mmHg) to prevent decompensation by reducing portal pressure. 3, 4, 6, 7
- In responders, propranolol decreases risk of ascites, hepatorenal syndrome, spontaneous bacterial peritonitis, and hepatic encephalopathy beyond variceal bleeding prevention. 2, 3
- Use with caution in patients with severe or refractory ascites. 4
Variceal Screening
- Perform screening endoscopy to assess for varices requiring prophylaxis. 4
- Surveillance intervals: every 2 years for patients without varices, every 1 year for patients with small varices. 3
Critical Medications to Avoid
NSAIDs are absolutely contraindicated in patients with cirrhosis, as they can reduce urinary sodium excretion, precipitate renal dysfunction, and convert diuretic-sensitive ascites to refractory ascites. 3, 4, 8
- Discontinue ACE inhibitors and angiotensin receptor blockers. 4
- Avoid nephrotoxic agents and hepatotoxic drugs. 3, 4
- Screen all medications for safety in cirrhosis, as altered pharmacokinetics and increased susceptibility to toxicological effects occur. 9, 10
Addressing Aggravating Factors
- Complete and permanent cessation of alcohol consumption is mandatory for alcoholic cirrhosis, as this may lead to "re-compensation" and excellent long-term outcomes. 3, 4
- Manage obesity, diabetes, and dyslipidemia aggressively. 3, 11
- Ensure vaccination against hepatitis A and B if not immune. 1
Monitoring Strategy
- Liver function tests every 2-6 months. 1
- HBV DNA by real-time PCR every 2-6 months if viral hepatitis present. 1
- HCC surveillance with MRI (preferred), CT, AFP, or ultrasound every 6 months in high-risk patients. 1, 3
- Assess for development of complications at each visit. 4
Common Pitfalls to Avoid
- Do not delay treatment of underlying etiology—early intervention is critical before decompensation occurs, as median survival drops from 10-12 years in compensated cirrhosis to only 1-2 years after first decompensation. 11, 7
- Do not use interferon-based therapies in decompensated cirrhosis—they are absolutely contraindicated due to risk of serious infections and hepatic failure. 1, 3
- Do not prescribe excessive bed rest—this may cause muscle atrophy; patients can be managed outpatient unless complicated by bleeding, encephalopathy, infection, or hypotension. 4
- Do not use HbA1c for diabetes monitoring in cirrhotic patients; insulin is the only evidence-based option for type 2 diabetes in this population. 3