What is the treatment approach for patients with decompensated cirrhosis?

Treatment Approach for Decompensated Cirrhosis

The cornerstone of managing decompensated cirrhosis is removing the underlying etiological factor (particularly alcohol, hepatitis B, or hepatitis C) combined with targeted treatment of specific complications, as this dual approach reduces mortality and prevents further decompensation. 1

Primary Treatment Strategy: Address the Underlying Cause

Etiological treatment must be initiated immediately as this is associated with decreased risk of further decompensation and increased survival, though effectiveness varies based on disease severity at treatment initiation. 1

For Viral Hepatitis-Related Decompensated Cirrhosis

• Hepatitis B: Initiate entecavir (1 mg daily for decompensated patients) or tenofovir monotherapy regardless of HBV DNA level, as these agents have potent antiviral efficacy and high genetic barrier to resistance. 1, 2
• Interferon-α is absolutely contraindicated in decompensated cirrhosis due to risk of serious complications including infection and hepatic failure. 1, 2
• Monitor renal function every 1-3 months when using these agents, particularly in patients with multiple risk factors for renal impairment. 1
• Hepatitis C: Direct-acting antivirals improve liver function and portal hypertension in decompensated cirrhosis. 1, 3

For Alcoholic Cirrhosis

• Complete and permanent cessation of alcohol consumption is essential, as this may lead to "re-compensation" and improved outcomes in some patients, though not universally. 1, 3

Management of Specific Complications

Ascites Management

First-line treatment consists of sodium restriction plus spironolactone with or without furosemide. 2

• Initiate spironolactone in hospital setting for cirrhotic patients with ascites, starting at 100 mg daily (range 25-200 mg), administered for at least 5 days before dose escalation. 4
• Combination therapy with aldosterone antagonists plus loop diuretics is superior to sequential initiation, resolving ascites in 76% versus 56% of patients with lower hyperkalemia rates (4% vs 18%). 5
• Fluid restriction is unnecessary unless serum sodium drops below 120-125 mmol/L. 2
• For tense ascites: Perform initial therapeutic paracentesis followed by sodium restriction and diuretic therapy. 2
• Avoid NSAIDs completely as they reduce urinary sodium excretion and convert diuretic-sensitive ascites to refractory ascites. 2

Hepatic Encephalopathy

• Lactulose is first-line therapy, reducing mortality (8.5% vs 14% with placebo) and recurrent overt hepatic encephalopathy (25.5% vs 46.8%). 3, 5
• Rifaximin reduces risk of multiple cirrhosis complications beyond hepatic encephalopathy, though prospective randomized data are limited. 1

Variceal Bleeding Prevention and Management

• Initiate vasoactive drugs immediately upon suspicion of variceal bleeding, even before endoscopic confirmation. 2
• Antibiotic prophylaxis is mandatory: Use ceftriaxone 1 g/24h for up to 7 days in decompensated cirrhosis or quinolone-resistant settings; use oral norfloxacin 400 mg twice daily in remaining patients. 3, 2
• Endoscopic band ligation within 12 hours of admission once hemodynamic stability is achieved. 2
• Restrictive transfusion strategy: Maintain hemoglobin threshold of 7 g/dL with target range 7-9 g/dL. 3, 2
• After variceal bleeding: 60.3% of patients should receive nonselective beta-blockers for secondary prophylaxis. 6

Spontaneous Bacterial Peritonitis (SBP)

• Norfloxacin prophylaxis reduces risk of SBP and hepatorenal syndrome, though use is limited by potential for resistant bacteria. 1
• After SBP episode, 48% of patients should receive antibiotic prophylaxis to prevent recurrence. 6

Hepatorenal Syndrome

• Terlipressin improves reversal rate from 18% to 39% in hepatorenal syndrome. 5
• Avoid nephrotoxic drugs, large volume paracentesis without albumin, and beta-blockers during acute bleeding. 3, 2

Emerging Strategies to Prevent Disease Progression

While requiring further validation, several approaches show promise: 1, 3

• Enoxaparin (12-month course) may delay hepatic decompensation and improve survival in patients with Child-Pugh scores 7-10 by preventing portal vein thrombosis. 3
• Statins reduce portal hypertension and improve survival through pleiotropic effects, though validation studies are needed. 1
• Propranolol in responders decreases risk of ascites, hepatorenal syndrome, SBP, and hepatic encephalopathy beyond variceal bleeding prevention. 1, 3
• Long-term albumin administration shows contradictory findings in recent trials and requires further study. 1

Critical Monitoring and Referral

• Early referral for liver transplantation evaluation is essential for appropriate candidates, as decompensation significantly worsens prognosis (5-year survival drops from 80% in compensated to 30% in decompensated cirrhosis). 1, 3
• Monitor for hepatocellular carcinoma development (1-4% annual incidence) with imaging surveillance. 5
• Mean pulmonary arterial pressure ≥45 mmHg is an absolute contraindication to liver transplantation. 3

Common Pitfalls to Avoid

• Medication non-adherence is widespread: Only 4.5-17.3% of patients have enough medication to cover >50% of follow-up days for indicated therapies. 6
• Potentially inappropriate medication use is common: 53.2% fill opiates, 46% proton pump inhibitors, 14.2% benzodiazepines, and 10.1% NSAIDs—all potentially harmful in decompensated cirrhosis. 6
• Spironolactone can cause sudden alterations in fluid and electrolyte balance, precipitating worsening hepatic encephalopathy and coma; therefore, initiate in hospital setting with slow titration. 4