Management of Decompensated Liver Cirrhosis
Immediate Priority: Treat the Underlying Cause
The single most important intervention is immediate initiation of etiological treatment, as this is directly associated with decreased risk of further decompensation and increased survival. 1
Etiology-Specific Treatment Approaches
For alcoholic cirrhosis:
- Complete and permanent cessation of alcohol consumption is mandatory, as this can lead to "re-compensation" and excellent long-term outcomes in some patients, though progression may continue in others despite abstinence 2, 1
For hepatitis B-related decompensated cirrhosis:
- Initiate antiviral therapy immediately regardless of HBV DNA level 3
- Use entecavir (1 mg/day) or tenofovir as first-line agents due to their potent antiviral efficacy and high genetic barrier to resistance 3
- Interferon-α is absolutely contraindicated in decompensated cirrhosis due to risk of serious complications including infection and hepatic failure 3
- Entecavir demonstrates superior HBV DNA suppression (57% vs 20% undetectability at week 48 compared to adefovir) and improves Child-Pugh scores in almost half of treatment-naïve patients 3
For hepatitis C-related decompensated cirrhosis:
- Direct-acting antivirals improve liver function and portal hypertension, though benefits are not universal across all treated patients 2, 1
For autoimmune hepatitis:
- Immunosuppressive therapy may provide beneficial effects on removing the responsible factor 2
Management of Specific Complications
Ascites Management
First-line treatment consists of sodium restriction (less than 5 g/day) plus spironolactone with or without furosemide. 1, 3
Diuretic dosing strategy:
- Start spironolactone at 50-100 mg/day, with maximum dose of 400 mg/day 3
- Add furosemide 20-40 mg/day if needed, with maximum dose of 160 mg/day 3
- Spironolactone (aldosterone antagonist) is the mainstay of treatment 3
Fluid restriction is unnecessary unless serum sodium drops below 120-125 mmol/L 1, 3
For grade 3 (tense) ascites:
- Perform initial therapeutic paracentesis followed by sodium restriction and diuretic therapy 3
Critical medications to avoid:
- NSAIDs must be discontinued as they reduce urinary sodium excretion and can convert diuretic-sensitive ascites to refractory ascites 3
- ACE inhibitors and angiotensin receptor blockers should be discontinued 3
Common pitfall: Bed rest is not recommended, as excessive bed rest causes muscle atrophy; patients can be managed outpatient unless complicated by bleeding, encephalopathy, infection, hypotension, or liver cancer 3
Hepatic Encephalopathy
Lactulose is first-line therapy, as it reduces mortality and prevents recurrent overt hepatic encephalopathy. 1
For screening and diagnosis:
- Use the animal naming test for rapid bedside screening (requires only 60 seconds, no equipment needed) 2
- Screen for mild hepatic encephalopathy using easily accessible tests, as this may identify those at risk of progression to overt encephalopathy 2
- Overt hepatic encephalopathy should be diagnosed when at least temporal disorientation (3 mistakes out of 5 questions exploring orientation to time) and/or flapping tremor are present 2
Ammonia-lowering strategies may help clinch a diagnosis in those with high functional capacity 2
Variceal Bleeding
Initiate vasoactive drugs immediately upon suspicion of variceal bleeding, even before endoscopic confirmation. 1, 3
Antibiotic prophylaxis is mandatory:
- Use ceftriaxone 1 g/24h for up to 7 days in decompensated cirrhosis or quinolone-resistant settings 1, 3
- Use oral norfloxacin 400 mg twice daily in remaining patients 1, 3
Transfusion strategy:
- Use a restrictive transfusion strategy with hemoglobin threshold of 7 g/dL, targeting 7-9 g/dL 3, 4
- Overuse of blood products may worsen portal hypertension 4
Endoscopic management:
- 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
- TIPS should be used as rescue therapy for persistent bleeding or early rebleeding 3
Critical medications to avoid during acute variceal hemorrhage:
- Avoid nephrotoxic drugs, large volume paracentesis without albumin, beta-blockers, and other hypotensive drugs 3, 4
Spontaneous Bacterial Peritonitis (SBP)
Perform diagnostic paracentesis without delay in all cirrhotic patients with ascites on hospital admission. 3
Diagnostic criteria:
- Ascitic neutrophil count >250/mm³ is the gold standard for diagnosis 3
Treatment:
- Initiate immediate empirical antibiotic therapy, determined by context, severity, and local resistance patterns 3
- For patients with GI bleeding and ascites, provide prophylactic antibiotics such as cefotaxime or based on local data 3
Strategies to Prevent Disease Progression
Non-Selective Beta-Blockers
Propranolol in responders decreases risk of ascites, hepatorenal syndrome, SBP, and hepatic encephalopathy beyond variceal bleeding prevention. 1, 4
- These effects occur specifically in patients who respond to propranolol treatment by markedly decreasing portal pressure 2
- Use with caution in patients with severe or refractory ascites 3
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, 4
Pentoxifylline
Pentoxifylline can reduce liver-related complications (infections, renal failure, encephalopathy) by preventing intestinal bacterial translocation. 2, 4
Nutritional Management
Perform rapid nutritional screening in all patients, assuming high risk for malnutrition if BMI <18.5 kg/m² or Child-Pugh C. 3
Assess for sarcopenia using CT scan, anthropometry, DEXA, or BIA 3
Evaluate muscle function with handgrip strength and/or short physical performance battery 3
Sodium restriction should be less than 5 g/day for controlling ascites, but greater restriction is not recommended as it may worsen malnutrition 3
Management of Type 2 Diabetes in Decompensated Cirrhosis
Insulin therapy is the only evidence-based option for treating type 2 diabetes in decompensated cirrhosis. 2
Key considerations:
- HbA1c should not be used for diagnosis or assessing glycemic control 2
- Insulin should be initiated in hospital due to high variations in glucose levels and risks of hypoglycemia, which may be confused with hepatic encephalopathy 2
- Optimal fasting blood glucose levels should not exceed 10 mmol/L to avoid hyperglycemic complications 2
- Metformin increases the risk of lactic acidosis and should not be used 2
- Other oral agents (thiazolidinediones, insulin secretagogues, alpha-glucosidase inhibitors, DPP-4 inhibitors, GLP-1 receptor agonists) are not recommended as most are eliminated by liver or kidney 2
Liver Transplantation Considerations
Early referral for liver transplantation evaluation is essential for appropriate candidates, as decompensation significantly worsens prognosis. 1, 5
Absolute contraindication:
- Mean pulmonary arterial pressure ≥45 mmHg is an absolute contraindication to liver transplantation 1, 4
Important considerations for low MELD scores:
- Patients with grade 3 ascites or overt hepatic encephalopathy have significant mortality and should be considered for transplantation despite low MELD 5
- Current evidence demonstrates a mortality reduction of approximately 40% with liver transplantation in patients with low MELD 5
- Living donor liver transplant has demonstrated significant survival benefit in patients even at MELD-Na scores as low as 11 5
Monitoring and Follow-up
Use telemedicine and remote monitoring technologies (Bluetooth-linked weighing scales, smartphone apps) to enable early detection of complications and reduce hospital readmissions. 3, 4
Heart rate variability monitoring may identify patients at risk of decompensation 3, 4