What is the treatment for cirrhosis in a patient?

Treatment of Cirrhosis

The cornerstone of cirrhosis treatment is immediate initiation of etiological therapy to address the underlying cause, as this is the single most important intervention associated with decreased risk of further decompensation and increased survival. 1

Primary Treatment Strategy: Address the Underlying Cause

The management paradigm has shifted from merely treating complications as they arise to preventing disease progression while patients remain compensated. 2 Treatment effectiveness varies based on disease severity at intervention, making early action critical. 2

Specific Etiological Treatments

Alcoholic Cirrhosis:

• Complete and permanent alcohol cessation is mandatory and can lead to dramatic "re-compensation" in some patients. 2, 3
• Patients with Child-Pugh class C who stop drinking have approximately 75% 3-year survival, while those who continue drinking have 0% survival at 3 years. 3

Viral Hepatitis B:

• Initiate antiviral therapy if HBV DNA ≥2,000 IU/mL regardless of ALT levels. 4
• Use entecavir or tenofovir as first-line agents due to potent antiviral efficacy and high genetic barrier to resistance. 4
• In decompensated cirrhosis (Child-Pugh B or C), treat all patients regardless of HBV DNA level with entecavir, tenofovir, or combination therapy with tenofovir plus lamivudine. 4
• Critical caveat: Interferon-α is absolutely contraindicated in decompensated cirrhosis due to risk of serious complications including infection and hepatic failure. 4

Viral Hepatitis C:

• Direct antiviral agents improve liver function and portal hypertension, though effects are not universal. 2

Autoimmune Hepatitis:

• Immunosuppressive therapy shows beneficial effects in decompensated cirrhosis. 2

Management of Compensated Cirrhosis

Ascites Management (First Episode or Mild)

First-line therapy consists of: 1, 4

• Sodium restriction to <5 g/day (88 mmol/day or 2000 mg/day). 4, 3
• Spironolactone 50-100 mg/day initially, titrated up to maximum 400 mg/day. 4, 5
• Add furosemide 20-40 mg/day if needed, maximum 160 mg/day. 4, 6

Important management points:

• Fluid restriction is unnecessary unless serum sodium drops below 120-125 mmol/L. 1, 4
• In cirrhotic patients, initiate diuretic therapy in a hospital setting and titrate slowly due to risk of precipitating hepatic coma with sudden fluid shifts. 5, 6
• Administer spironolactone for at least 5 days before increasing dose when used as sole diuretic. 5
• Avoid NSAIDs, ACE inhibitors, and angiotensin receptor blockers as they reduce urinary sodium excretion and can convert diuretic-sensitive to refractory ascites. 4

Tense Ascites (Grade 3)

• Perform initial therapeutic paracentesis followed by sodium restriction and diuretic therapy. 4
• For large-volume paracentesis, albumin replacement is recommended. 3

Prevention of Variceal Bleeding

Non-selective beta-blockers (propranolol):

• In responders, propranolol decreases risk of ascites, hepatorenal syndrome, spontaneous bacterial peritonitis, and hepatic encephalopathy beyond variceal bleeding prevention. 1
• Use with caution in patients with severe or refractory ascites. 4
• Prophylactic endoscopic band ligation is standard of care for varices. 4

Emerging Preventive Strategies

Anticoagulation:

• Enoxaparin may delay hepatic decompensation and improve survival in patients with Child-Pugh scores 7-10 by preventing portal vein thrombosis and reducing intestinal barrier damage. 1

Management of Decompensated Cirrhosis

Acute Variceal Bleeding

Immediate interventions (before endoscopy):

• Initiate vasoactive drugs immediately upon suspicion, even before endoscopic confirmation. 1, 4
• Start antibiotic prophylaxis: ceftriaxone 1 g/24h for up to 7 days in decompensated cirrhosis or quinolone-resistant settings; oral norfloxacin 400 mg twice daily in remaining patients. 1, 4
• Use restrictive transfusion strategy with hemoglobin threshold of 7 g/dL, target 7-9 g/dL. 4
• Administer erythromycin 250 mg IV 30-120 minutes before endoscopy to improve visibility, unless QT prolongation is present. 4

Endoscopic management:

• Perform endoscopic band ligation within 12 hours of admission once hemodynamic stability is achieved. 4
• TIPS should be used as rescue therapy for persistent bleeding or early rebleeding. 4

Hepatic Encephalopathy

• Lactulose is first-line therapy, reducing mortality and recurrent overt hepatic encephalopathy. 1
• Oral non-absorbable disaccharides may prevent development of hepatic encephalopathy. 4

Spontaneous Bacterial Peritonitis

• Perform diagnostic paracentesis without delay in all cirrhotic patients with ascites on hospital admission. 4
• Ascitic neutrophil count >250/mm³ is diagnostic. 4
• Initiate immediate empirical antibiotic therapy based on context, severity, and local resistance patterns. 4
• Patients with GI bleeding and ascites require prophylactic antibiotics such as cefotaxime. 4

Refractory Ascites

Options include: 4

• Serial large-volume paracentesis with albumin replacement
• Transjugular intrahepatic portosystemic stent-shunt (TIPS)
• Liver transplantation evaluation
• Patients requiring paracenteses more frequently than every 2 weeks likely have poor dietary compliance. 4

Diabetes Management in Decompensated Cirrhosis

• Screen all patients with decompensated cirrhosis for diabetes given high prevalence. 2
• Do not use HbA1c for diagnosis or monitoring glycemic control. 2
• Insulin therapy is the only evidence-based option for treating type 2 diabetes in decompensated cirrhosis. 2
• Initiate insulin in hospital due to high glucose variability and hypoglycemia risk, which can mimic hepatic encephalopathy. 2
• Metformin is contraindicated due to lactic acidosis risk. 2
• Optimal fasting blood glucose should not exceed 10 mmol/L. 2

Nutritional Management

• Sodium restriction to <5 g/day, but avoid excessive restriction that worsens malnutrition. 4, 3
• Nutritional intake targets: carbohydrate 2-3 g/kg/day, protein 1.2-1.5 g/kg/day, caloric intake 35-40 kcal/kg/day. 3
• Perform rapid nutritional screening in all patients, assuming high malnutrition risk if BMI <18.5 kg/m² or Child-Pugh C. 4
• Assess sarcopenia using CT scan, anthropometry, DEXA, or bioelectrical impedance analysis. 4
• Evaluate muscle function with handgrip strength and/or short physical performance battery. 4
• Avoid excessive bed rest as it causes muscle atrophy; manage patients outpatient unless complicated by bleeding, encephalopathy, infection, hypotension, or liver cancer. 4

Liver Transplantation

• Early referral for liver transplantation evaluation is essential for appropriate candidates, as decompensation significantly worsens prognosis. 1
• Mean pulmonary arterial pressure ≥45 mmHg is an absolute contraindication to liver transplantation. 1
• Liver transplantation is potentially optimal therapy for small hepatocellular carcinoma in patients with moderate to severe cirrhosis (Child-Pugh class B or C). 3

Monitoring and Follow-up

• Consider telemedicine and remote monitoring technologies (Bluetooth-linked weighing scales, smartphone apps) to enable early intervention for weight changes, improving outcomes and reducing hospital readmissions. 4, 3
• Heart rate variability monitoring may identify patients at risk of decompensation. 4
• Continuous monitoring for cirrhosis-related complications and hepatocellular carcinoma is needed even after achieving sustained virologic response in viral hepatitis. 2

Common Pitfalls to Avoid

• Never initiate diuretics in outpatient setting for cirrhotic patients with ascites - hospitalization required for initial therapy and titration. 5, 6
• Avoid nephrotoxic drugs, large volume paracentesis without albumin, and hypotensive drugs during acute variceal hemorrhage. 4
• Do not use interferon in decompensated cirrhosis. 4
• Recognize that only 10-30% of patients with hepatocellular carcinoma will be eligible for surgery, with substantial morbidity and mortality (30-50% in Child-Pugh class B or C, but only 5-10% in Child-Pugh class A). 3