Management of Chronic Liver Disease (Cirrhosis)
The cornerstone of cirrhosis management is aggressive treatment of the underlying etiology combined with systematic prevention and management of complications through sodium restriction, diuretic therapy, variceal surveillance, and regular monitoring for hepatocellular carcinoma. 1, 2, 3
Treat the Underlying Cause First
This is the single most important intervention that directly impacts mortality and prevents decompensation. 2, 3
Alcoholic Cirrhosis
- Complete and permanent cessation of alcohol consumption is mandatory. 1, 3 Patients with Child-Pugh class C cirrhosis who stop drinking have approximately 75% 3-year survival, while those who continue drinking have 0% survival at 3 years. 1
- This can lead to "re-compensation" of cirrhosis with dramatic improvement in reversible components of liver disease. 1, 3
Viral Hepatitis B
- Initiate antiviral therapy if HBV DNA ≥2,000 IU/mL regardless of ALT levels using entecavir or tenofovir as first-line agents due to their potent antiviral efficacy and high genetic barrier to resistance. 3
- All patients with decompensated cirrhosis should receive treatment regardless of HBV DNA level. 3
- Interferon-α is absolutely contraindicated in decompensated cirrhosis due to risk of serious complications including infection and hepatic failure. 3
- Entecavir (1 mg/day) demonstrates superior HBV DNA suppression compared to adefovir (57% vs 20% undetectability at week 48) and improves Child-Pugh scores in almost half of treatment-naïve patients. 3
Viral Hepatitis C
- Direct-acting antivirals improve liver function and reduce portal hypertension. 3
- Continue hepatological follow-up despite successful antiviral therapy, as patients remain at risk for HCC and portal hypertension complications. 4
Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)
- Lifestyle modification including weight loss, dietary changes, and physical exercise. 4
- Optimal management of comorbidities including use of incretin-based therapies (semaglutide, tirzepatide) for type 2 diabetes or obesity if indicated. 4
- Bariatric surgery is an option in individuals with MASLD and obesity. 4
- For non-cirrhotic MASH with significant fibrosis (stage ≥2), consider resmetirom if locally approved. 4
Autoimmune Hepatitis
- Immunosuppressive therapy shows beneficial effects even in decompensated cirrhosis. 3
Nutritional Management
Sodium Restriction
- Restrict dietary sodium to <5 g/day (2000 mg/day or 88 mmol/day) for ascites control. 1, 2, 3 Greater restriction is not recommended as it may worsen malnutrition. 3
- Fluid restriction is unnecessary unless serum sodium drops below 120-125 mmol/L. 2, 3
Caloric and Protein Intake
- Carbohydrate: 2-3 g/kg/day 1
- Protein: 1.2-1.5 g/kg/day 1
- Total caloric intake: 35-40 kcal/kg/day 1
- Rapid nutritional screening should be performed in all patients, assuming high risk for malnutrition if BMI <18.5 kg/m² or Child-Pugh C. 3
Sarcopenia Assessment
- Evaluate using CT scan, anthropometry, DEXA, or BIA. 3
- Assess muscle function with handgrip strength and/or short physical performance battery. 3
Management of Ascites
Grade 1 Ascites (Mild)
- Sodium restriction 3
- Treatment of underlying disease 3
- Discontinue NSAIDs, ACE inhibitors, or angiotensin receptor blockers 3
- Nutritional treatment and education 3
Grade 2 Ascites (Moderate)
- Sodium restriction plus oral diuretics 2, 3
- Start spironolactone 50-100 mg/day (maximum 400 mg/day) as the mainstay of diuretic treatment 3
- Add furosemide 20-40 mg/day (maximum 160 mg/day) if needed for rapid onset of action 3
- Treatment of underlying disease 3
- Discontinue NSAIDs, ACE inhibitors, or angiotensin receptor blockers 3
Grade 3 Ascites (Tense)
Refractory Ascites
- Options include serial large-volume paracentesis (LVP) with albumin replacement, transjugular intrahepatic portosystemic stent-shunt (TIPS), liver transplantation, peritoneovenous shunt, or experimental medical therapy. 1, 3
- Patients requiring paracenteses more frequently than every 2 weeks likely have poor dietary compliance. 3
- Refer to gastroenterology for refractory ascites not responding to maximum diuretic therapy. 3
- Offer palliative care referral to patients with refractory ascites who are not transplant candidates. 3
Prevention and Management of Variceal Bleeding
Primary Prophylaxis
- Perform screening endoscopy to assess for varices requiring prophylaxis. 3
- Prophylactic band ligation is standard of care for varices. 3
- Consider non-selective beta-blockers (propranolol) for prevention, which also decrease the risk of ascites, hepatorenal syndrome, spontaneous bacterial peritonitis, and hepatic encephalopathy beyond variceal bleeding prevention. 2, 3
- Use beta-blockers with caution in patients with severe or refractory ascites. 3
Acute Variceal Bleeding Management
- Initiate vasoactive drugs immediately upon suspicion, even before endoscopic confirmation. 2, 3
- Antibiotic prophylaxis is mandatory: 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. 3
- Use a restrictive transfusion strategy with hemoglobin threshold of 7 g/dL, target 7-9 g/dL. 3
- Administer erythromycin 250 mg IV 30-120 minutes before endoscopy to improve visibility, unless QT prolongation is present. 3
- Perform endoscopic band ligation within 12 hours of admission once hemodynamic stability is achieved. 3
- Use TIPS as rescue therapy for persistent bleeding or early rebleeding. 3
- Avoid nephrotoxic drugs, large volume paracentesis, and hypotensive drugs during acute variceal hemorrhage. 3
Management of Spontaneous Bacterial Peritonitis (SBP)
- Perform diagnostic paracentesis without delay in all cirrhotic patients with ascites on hospital admission. 3
- Ascitic neutrophil count >250/mm³ is the gold standard for diagnosis. 3
- Initiate immediate empirical antibiotic therapy determined by context, severity, and local resistance patterns. 3
- Patients with GI bleeding and ascites should receive prophylactic antibiotics such as cefotaxime or based on local data. 3
- Provide antibiotic prophylaxis for SBP when indicated. 3
Management of Hepatic Encephalopathy
- Lactulose is first-line therapy as it reduces mortality and prevents recurrent overt hepatic encephalopathy. 2
- Oral non-absorbable disaccharides may prevent the development of hepatic encephalopathy. 3
- Rifaximin can be added for refractory cases. 5
- The use of osmotic laxatives or non-absorbable antibiotics to lower ammonia levels is not recommended in acute liver failure. 4
Hepatocellular Carcinoma (HCC) Surveillance
- Perform ultrasound screening every 6 months for all patients with cirrhosis. 5, 6
- Continue surveillance even after achieving sustained virologic response in viral hepatitis. 3
Medications to Avoid
- NSAIDs are absolutely contraindicated as they can reduce urinary sodium excretion, precipitate renal dysfunction, and convert diuretic-sensitive ascites to refractory ascites. 3
- Discontinue ACE inhibitors and angiotensin receptor blockers. 3
- Avoid anabolic steroids as they can cause abnormal liver biochemistry. 4
- Avoid drugs with potential for hepatotoxicity. 6
Monitoring and Follow-Up
- Clinical assessment with laboratory tests and calculation of Child-Pugh and MELD scores should occur every 6 months. 6
- Use FIB-4 score and transient elastography (FibroScan) for non-invasive assessment of fibrosis progression. 4
- FibroScan value ≥15 kPa is highly suggestive of compensated advanced chronic liver disease (cACLD). 4
- Consider telemedicine and remote monitoring technologies including Bluetooth-linked weighing scales and smartphone apps to enable early intervention for weight changes, potentially improving outcomes and reducing hospital readmissions. 1, 3
- Heart rate variability monitoring may identify patients at risk of decompensation. 2, 3
Indications for Gastroenterology Referral
- Development of any decompensation events such as ascites, variceal bleeding, or hepatic encephalopathy. 3
- Refractory ascites not responding to maximum diuretic therapy. 3
- Need for TIPS placement for refractory ascites or recurrent variceal bleeding. 3
- Need for evaluation for liver transplantation. 3
Liver Transplantation
- Evaluation for liver transplantation is indicated for patients with MELD score ≥15, complications of cirrhosis, or hepatocellular carcinoma. 6
- Liver transplantation is potentially optimal therapy for small-size, otherwise resectable HCC in patients with moderate to severe cirrhosis (Child-Pugh class B or C). 1
- Mean pulmonary arterial pressure ≥45 mmHg is an absolute contraindication to liver transplantation. 2
- Management of MASH-related cirrhosis includes adaptations of metabolic drugs, nutritional counselling, surveillance for portal hypertension and HCC, as well as liver transplantation in decompensated cirrhosis. 4
Emerging Preventive Strategies
- Anticoagulation with 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. 2
- Statins show promise in reducing portal hypertension and improving survival in patients with advanced cirrhosis, though these effects require validation in future studies. 3
Common Pitfalls
- Bed rest is not recommended as excessive bed rest may cause muscle atrophy; patients can be managed on an outpatient basis unless complicated by bleeding, encephalopathy, infection, hypotension, or liver cancer. 3
- Only 10-30% of patients initially presenting with HCC will be eligible for surgery, and surgery in patients with underlying cirrhosis can be associated with substantial morbidity and mortality (30-50% in Child-Pugh class B or C, but only 5-10% in Child-Pugh class A). 1
- Patients with MELD score <9 have significantly lower mortality rates when undergoing resection of HCC. 1
- Do not use HbA1c for diagnosis or monitoring glycemic control in patients with decompensated cirrhosis. 3
- Metformin is contraindicated in decompensated cirrhosis due to lactic acidosis risk; insulin therapy is the only evidence-based option for treating type 2 diabetes in decompensated cirrhosis. 3