What is the recommended management for a patient with decompensated chronic liver disease (cirrhosis)?

Management of Decompensated Chronic Liver Disease

Immediately initiate treatment of the underlying liver disease etiology while simultaneously managing acute complications—this dual approach is the single most important intervention to reduce further decompensation and improve survival. 1, 2

Immediate Etiological Treatment (Priority #1)

The management paradigm has shifted from reactive treatment of complications to aggressive early treatment of the underlying cause, which directly impacts mortality and morbidity. 1, 2

Viral Hepatitis B

• Start antiviral therapy immediately if HBV DNA is detectable by PCR, regardless of ALT levels or HBV DNA quantity. 1
• Use entecavir 1 mg daily (not 0.5 mg) or tenofovir monotherapy as first-line agents due to potent antiviral efficacy and high genetic barrier to resistance. 1
• Entecavir demonstrates superior HBV DNA suppression (57% undetectability at week 48) compared to adefovir (20%) and improves Child-Pugh scores in nearly half of treatment-naïve patients. 1
• Peginterferon-α is absolutely contraindicated due to risk of hepatic failure, infection, and death. 1
• Clinical improvement typically requires 3–6 months of antiviral therapy; some patients may progress to hepatic failure despite treatment. 1

Viral Hepatitis C

• Initiate direct-acting antivirals immediately—they improve liver function, reduce portal hypertension, and likely improve survival. 2

Alcoholic Cirrhosis

• Mandate complete and permanent alcohol cessation—this can lead to "re-compensation" with excellent long-term outcomes in some patients, though progression may continue in others despite abstinence. 1, 2

Autoimmune Hepatitis

• Start immunosuppressive therapy, which shows clear beneficial effects even in decompensated disease. 1, 2

Concurrent Management of Specific Complications

Ascites Management

Initial approach:

• Restrict dietary sodium to <5 g/day (88 mmol/day)—more stringent restriction worsens malnutrition and is not recommended. 1, 3, 2
• Fluid restriction is unnecessary unless serum sodium falls below 120–125 mmol/L. 1, 3

Diuretic therapy algorithm:

• Grade 2 ascites (moderate, visible): Start spironolactone 100 mg once daily as monotherapy. 3, 2
• If weight loss is <2 kg/week: Increase spironolactone by 100 mg every 72 hours, up to maximum 400 mg/day. 3, 2
• Add furosemide 40 mg/day when spironolactone alone is insufficient or serum potassium >5.5 mmol/L; titrate in 40-mg increments to maximum 160 mg/day. 3, 2
• Grade 3 ascites (massive/tense): Perform therapeutic paracentesis first, then initiate sodium restriction and diuretics. 1, 3, 2
• Monitor serum creatinine, sodium, and potassium at least weekly during the first month of diuretic therapy. 3

Large-volume paracentesis:

• Administer 8 g albumin per liter of ascites removed (approximately 100 mL of 20% albumin for every 3 L) when removing ≥5 L. 3
• For <5 L removed, synthetic plasma expanders (150–200 mL gelofusine or Haemaccel) are sufficient. 3

Hyponatremia management:

• Serum sodium 126–135 mmol/L: Continue diuretics with close monitoring. 3
• Serum sodium 121–125 mmol/L with normal creatinine: Stop diuretics or use cautiously. 3
• Serum sodium 121–125 mmol/L with elevated/rising creatinine: Stop diuretics and give volume expansion. 3
• **Serum sodium <120 mmol/L:** Stop diuretics and perform volume expansion with colloid or saline, avoiding sodium increase >12 mmol/L per 24 hours. 3

Spontaneous Bacterial Peritonitis (SBP)

• Perform diagnostic paracentesis without delay in all cirrhotic patients with ascites on hospital admission or with any clinical deterioration (fever, abdominal pain, altered mental status, new encephalopathy, renal impairment, unexplained leukocytosis). 1, 3, 2
• Inoculate ≥10 mL ascitic fluid into blood-culture bottles at bedside to improve pathogen detection. 3
• Ascitic neutrophil count >250 cells/mm³ confirms SBP. 1, 3
• Administer albumin 1.5 g/kg within 6 hours of diagnosis, followed by 1 g/kg on day 3, especially when serum creatinine is rising or elevated. 3
• After SBP recovery, prescribe continuous oral norfloxacin 400 mg daily (or ciprofloxacin 500 mg daily) for secondary prophylaxis. 3

Variceal Bleeding

• Initiate vasoactive drugs immediately upon suspicion of variceal bleeding, even before endoscopic confirmation. 4, 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. 4
• Perform endoscopic band ligation within 12 hours once hemodynamic stability is achieved. 3
• Use restrictive transfusion strategy: Hemoglobin threshold of 7 g/dL, target 7–9 g/dL. 3

Hepatic Encephalopathy (HE)

• Identify and treat precipitating factors: GI bleeding, infection, dehydration, constipation, electrolyte disturbances. 3
• Serum sodium <130 mmol/L is an independent risk factor for HE and predicts poor response to lactulose. 3
• Discontinue benzodiazepines immediately—they are contraindicated in decompensated cirrhosis. 3
• Limit proton-pump inhibitor use to validated indications only. 3
• Initiate lactulose as first-line therapy—it reduces mortality and prevents recurrent overt HE. 4, 2
• Add rifaximin for persistent or recurrent HE episodes. 3
• Blood ammonia measurement is only useful when HE diagnosis is uncertain: Normal value argues against HE, but elevated value does not confirm it. 3

Prevention of Further Decompensation

Non-Selective Beta-Blockers (NSBBs)

• In patients with clinically significant portal hypertension (HVPG ≥10 mmHg) without high-risk varices, NSBBs reduce decompensation or death from 27% to 16%. 3
• Propranolol in responders decreases risk of ascites, hepatorenal syndrome, SBP, and hepatic encephalopathy beyond variceal bleeding prevention. 4, 2
• Use carvedilol or propranolol titrated to target heart-rate response. 3
• In refractory ascites, continue NSBBs with close monitoring—not an absolute contraindication—but reduce or stop if mean arterial pressure falls <65 mmHg or acute/progressive renal dysfunction develops. 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. 4, 2

Medications to Absolutely Avoid

• NSAIDs are absolutely contraindicated—they reduce urinary sodium excretion, precipitate renal dysfunction, and convert diuretic-responsive ascites to refractory ascites. 1, 3, 2
• Metformin is contraindicated due to lactic acidosis risk. 3
• Sulfonylureas should be avoided due to hypoglycemia risk. 3
• ACE inhibitors and angiotensin receptor blockers must be discontinued. 3

Diabetes Management in Decompensated Cirrhosis

• Insulin therapy is the only evidence-based option for treating type 2 diabetes in decompensated cirrhosis. 4, 2
• Do not use HbA1c for diagnosis or monitoring glycemic control in decompensated cirrhosis. 4

Nutritional Assessment

• Perform rapid nutritional screening in all patients—assume high risk for malnutrition if BMI <18.5 kg/m² or Child-Pugh C. 4, 2
• Assess sarcopenia using CT scan, anthropometry, DEXA, or BIA. 3
• Evaluate muscle function with handgrip strength and/or short physical performance battery. 3
• Bed rest is discouraged—prolonged inactivity causes muscle atrophy and sarcopenia. 3

Liver Transplantation Evaluation

• Refer all patients with decompensated cirrhosis for liver transplantation evaluation immediately—this is the definitive treatment and decompensation significantly worsens prognosis. 1, 4, 3, 2
• Early referral is critical in acute-on-chronic liver failure (ACLF) because delayed referral may render transplantation impossible due to rapid disease progression. 4
• Mean pulmonary arterial pressure ≥45 mmHg is an absolute contraindication to liver transplantation. 4, 2
• In patients with ≥4 organ failures or CLIF-C ACLF score >64 at days 3–7 after ACLF-3 diagnosis, intensive organ support should be discontinued as futile when transplantation is contraindicated or unavailable. 4

Monitoring Schedule

• Liver function tests every 1–3 months. 1
• Serum HBV DNA by real-time PCR plus HBeAg status every 2–6 months (if HBV-related). 1
• Serum creatinine, sodium, and potassium at least weekly during first month of diuretic therapy. 3
• Consider telemedicine and remote monitoring technologies (Bluetooth-linked weighing scales, smartphone apps) to enable early detection of complications and reduce hospital readmissions. 4, 2

Extracorporeal Liver Support Systems

• Extracorporeal liver support systems (MARS, Prometheus) are NOT recommended for routine use—large RCTs show no survival benefit in ACLF. 4
• A sub-analysis suggested potential benefit in patients with MELD >30, but this requires prospective validation before clinical adoption. 4

Common Pitfalls to Avoid

• Do not delay antiviral therapy in HBV-related decompensation—prompt treatment is required even though clinical improvement takes 3–6 months, and some patients progress despite therapy. 1
• Do not use peginterferon in decompensated cirrhosis—it causes serious complications including hepatic failure. 1
• Do not impose routine fluid restriction—only restrict when serum sodium is severely low (<120–125 mmol/L). 1, 3
• Do not rely on ammonia levels to diagnose or monitor HE—HE remains a clinical diagnosis of exclusion. 3
• Do not prescribe bed rest—it worsens sarcopenia; patients can be managed outpatient unless complicated by bleeding, encephalopathy, infection, hypotension, or liver cancer. 3