Management of Decompensated Non-Alcoholic Liver Cirrhosis
Immediately address the underlying etiology while simultaneously managing life-threatening complications—this dual approach is the cornerstone of treatment and directly impacts survival. 1, 2
Immediate Etiological Treatment (Priority #1)
Removing the causative factor is associated with decreased risk of further decompensation and increased survival, though effectiveness depends on disease severity at treatment initiation. 1, 2
For non-alcoholic cirrhosis, specific interventions include:
- Metabolic dysfunction-associated steatotic liver disease (MASLD): Implement aggressive weight loss (7-10% body weight), optimize diabetes control, and treat dyslipidemia 3
- Autoimmune hepatitis: Initiate or optimize immunosuppression with corticosteroids and azathioprine 1
- Hemochromatosis: Begin therapeutic phlebotomy 3
- Wilson's disease: Start chelation therapy 3
Management of Decompensating Events
Ascites (Most Common First Decompensation)
Perform diagnostic paracentesis immediately in all patients with new or worsening ascites to exclude spontaneous bacterial peritonitis (SBP)—neutrophil count >250 cells/µL requires immediate empirical antibiotics. 1, 2, 4
First-line treatment consists of sodium restriction (<5 g/day) plus spironolactone with or without furosemide. 1, 2, 5
Specific dosing protocol:
- Initiate spironolactone 100 mg daily in hospitalized patients, titrating slowly 6
- Add furosemide 40 mg daily if needed, maintaining 100:40 mg ratio (spironolactone:furosemide) 1
- Maximum doses: spironolactone 400 mg/day, furosemide 160 mg/day 1, 6
- Fluid restriction is unnecessary unless serum sodium drops below 120-125 mmol/L 2
Critical pitfall: In cirrhotic patients, initiate diuretic therapy in hospital setting with slow titration to avoid precipitating hepatic encephalopathy or renal failure 6, 7
Hepatic Encephalopathy
Identify and aggressively treat precipitating factors—up to 90% of patients recover from episodic overt hepatic encephalopathy by correcting precipitants alone. 1
Common precipitants to address:
- Infections (perform diagnostic paracentesis, blood/urine cultures) 1
- Gastrointestinal bleeding (check hemoglobin, initiate vasoactive drugs if suspected) 1
- Constipation (rapid resolution improves recovery) 1
- Electrolyte disturbances (check sodium, potassium) 1
- Nephrotoxic drugs or dehydration 5
Lactulose is first-line therapy, reducing mortality and recurrent episodes—dose to achieve 2-3 soft bowel movements daily. 1, 2, 5
Rifaximin 550 mg twice daily can be added to lactulose for recurrent episodes. 1
Grade 3-4 hepatic encephalopathy requires ICU admission due to aspiration risk. 1
Variceal Bleeding Prevention
Initiate non-selective beta-blockers (propranolol or carvedilol) for primary or secondary prophylaxis in patients with varices, as responders experience decreased risk of ascites, hepatorenal syndrome, SBP, and hepatic encephalopathy beyond bleeding prevention. 1, 2
If acute variceal bleeding is suspected, start vasoactive drugs immediately before endoscopic confirmation. 2
Antibiotic prophylaxis is mandatory: use ceftriaxone 1 g/24h for up to 7 days in decompensated cirrhosis; use oral norfloxacin 400 mg twice daily in compensated patients. 2
Spontaneous Bacterial Peritonitis (SBP)
Norfloxacin prophylaxis (400 mg daily) reduces risk of SBP and hepatorenal syndrome in high-risk patients (ascitic protein <1.5 g/dL, prior SBP, or variceal bleeding), though bacterial resistance is a concern. 1, 2
When SBP is diagnosed (ascitic neutrophils >250 cells/µL), start empirical third-generation cephalosporin immediately without awaiting culture results. 1, 5
Medications to Avoid
Strictly avoid nephrotoxic agents and medications that worsen portal hypertension or precipitate complications: 5, 8
- NSAIDs (precipitate renal failure) 5
- Aminoglycosides (nephrotoxic and ototoxic with furosemide) 5, 7
- Benzodiazepines (precipitate hepatic encephalopathy) 5, 8
- Opiates (worsen encephalopathy, though commonly prescribed inappropriately) 8
- Proton pump inhibitors (increase SBP risk, yet 46% of patients receive them) 8
Emerging Disease-Modifying Strategies
Statins may reduce portal hypertension and improve survival through pleiotropic anti-inflammatory effects, though validation studies are needed before routine recommendation. 1, 2
Rifaximin beyond hepatic encephalopathy may reduce other cirrhosis complications by improving gut-liver axis, though prospective randomized data are lacking. 1
Long-term albumin administration shows potential benefit by improving circulatory dysfunction, but requires further study. 1
Critical Monitoring and Transplant Evaluation
Refer for liver transplantation evaluation immediately upon first decompensation, as five-year survival drops from 80% in compensated cirrhosis to 30% in decompensated disease. 1, 2, 4
Calculate MELD score (bilirubin, creatinine, INR) to predict 3-month mortality and guide transplant prioritization. 4
Screen for hepatocellular carcinoma with ultrasound every 6 months, as annual incidence is 2-3% in cirrhotic patients. 1, 4
Mean pulmonary arterial pressure ≥45 mmHg is an absolute contraindication to transplantation—screen with echocardiography. 2
Common Pitfalls
Do not attribute all altered mental status to hepatic encephalopathy—perform brain imaging for first episode, seizures, focal signs, or inadequate treatment response. 4
Serum creatinine underestimates renal dysfunction in cirrhosis—measured GFR through exogenous marker clearance is the reference standard. 4
Most patients with decompensated cirrhosis do not fill indicated medications as recommended (only 4.5-17.3% have >50% days covered), while simultaneously receiving potentially harmful medications—review and reconcile medications at every visit. 8
Sudden alterations in fluid and electrolyte balance can precipitate hepatic coma—strict observation is necessary during diuresis, with supplemental potassium and aldosterone antagonist to prevent hypokalemia. 7