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Hepatology›Condition·Updated Jul 11, 2026·v1

Cirrhosis

Cirrhosis is a diffuse process of advanced hepatic fibrosis and nodular regeneration representing the common end-stage of chronic liver disease. It affects 1.3% globally, with steep mortality after decompensation. Management pivots on etiologic cure, prevention of decompensation with NSBB in CSPH, complication-specific protocols (variceal bleeding, SBP, HE, HRS-AKI), and early transplant referral. Recompensation is increasingly achievable with sustained etiologic control.

High Evidence554 references·9,508 words·39 min read·v1
cirrhosisportal hypertensiondecompensationascitesvariceal hemorrhagehepatic encephalopathyhepatorenal syndromeMELDliver transplantationMASLDalcohol-associated liver diseasehepatitis Bhepatitis C

Quick Reference

RxDrug of choiceFor primary prevention of decompensation in CSPH: carvedilol 6.25-12.5 mg daily. For acute variceal hemorrhage: terlipressin 2 mg IV bolus then 1-2 mg q4-6h + ceftriaxone 1 g IV daily + endoscopic band ligation.
AltAlternativesPropranolol 20-160 mg BID for NSBB; octreotide 50 mcg bolus then 50 mcg/h for variceal hemorrhage; norepinephrine 0.5-3 mg/h for HRS-AKI; rifaximin 550 mg BID for HE; norfloxacin 400 mg daily for SBP prophylaxis (if available).
⊘AvoidAvoid NSAIDs, non-dihydropyridine CCBs, and aggressive diuresis in decompensated cirrhosis. Avoid terlipressin in HRS-AKI with ACLF grade 3 or baseline SpO₂ <90%.
DxTest of choiceFirst-line: FIB-4 (calculate from age, AST, ALT, platelets). If ≥1.3, follow with VCTE (>12.1 kPa cirrhosis). For etiologic workup: HBsAg, anti-HCV, alcohol history with PEth, TSAT/ferritin, AMA, ANA/anti-smooth muscle, IgG.
ScKey scoreMELD-Na (bilirubin, INR, creatinine, sodium) predicts 90-day mortality and drives transplant allocation. CTP (bilirubin, albumin, INR, ascites, encephalopathy) for surgical risk and variceal bleeding.
→When to referRefer to hepatology at first decompensation event (ascites, variceal bleed, HE, jaundice) or when MELD-Na >15. Refer for liver transplantation evaluation at first decompensation; early LT evaluation improves access.
Cirrhosis is a staged disease: prevent first decompensation with NSBB in CSPH; treat underlying etiology (antivirals, abstinence, MASH therapy); manage complications with targeted protocols (vasoactive drugs, antibiotics, lactulose, terlipressin); refer early for transplantation.
Cirrhosis is the end-stage of chronic liver disease, defined by advanced fibrosis, architectural distortion, and regenerative nodules. It is the 11th leading cause of death globally, with a pooled prevalence of 1.3%. The natural history is dichotomized into compensated (median survival >15 years) and decompensated (median survival ~2 years) phases. Prevention of first decompensation, primarily with non-selective beta-blockers in patients with clinically significant portal hypertension, is the central therapeutic goal. Management focuses on etiologic therapy, complication control, and early transplant referral.

Overview and Recommendations

Background

  • •Cirrhosis is the common end-stage of any chronic liver disease, characterized by diffuse fibrosis, architectural distortion, and regenerative nodules that replace functional parenchyma. It affects approximately 1.3% of the global population, with advanced fibrosis affecting 3.3%, and accounts for two million deaths annually, 4% of all deaths worldwide.
  • •The natural history bifurcates into compensated cirrhosis (asymptomatic, median survival >15 years) and decompensated cirrhosis (defined by ascites, variceal hemorrhage, hepatic encephalopathy, or jaundice; median survival ~2 years). This transition is the single most powerful prognostic milestone and drives all management decisions.
  • •Clinically significant portal hypertension (CSPH), defined by a hepatic venous pressure gradient ≥10 mmHg, is the key hemodynamic milestone in compensated disease that predicts decompensation. Non-selective beta-blockers (NSBB) reduce the risk of first decompensation by 49% (PREDESCI trial; NNT=9).
  • •Etiologically, cirrhosis is driven by chronic viral hepatitis (HBV, HCV), alcohol-associated liver disease (ALD), and metabolic dysfunction-associated steatotic liver disease (MASLD), the latter now the leading cause in high-income countries. Other causes include cholestatic diseases (PBC, PSC), autoimmune hepatitis, and genetic disorders (hemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency).
  • •Recompensation, resolution of ascites, encephalopathy, and jaundice with stable liver function off specific therapy, occurs in approximately 35% of decompensated patients who achieve sustained etiologic control, highest in HBV (49%) and lowest in ALD (19%). Recompensation is associated with significantly reduced HCC (OR 0.55) and mortality (OR 0.33).

Evaluation

  • •Suspect cirrhosis in any patient with exertional dyspnea, unexplained fatigue, abdominal distension, or confusion, especially with a history of chronic liver disease risk factors (viral hepatitis, alcohol use, metabolic syndrome, family history of liver disease).
  • •Ask about alcohol consumption (quantity, frequency, pattern) and corroborate with serum phosphatidylethanol (PEth), a sensitive biomarker for recent alcohol use. In cryptogenic cases, screen for metabolic risk factors (diabetes, obesity, dyslipidemia) and consider MASLD.
  • •Examine for physical stigmata of chronic liver disease: spider angiomata (>5 on upper trunk), palmar erythema, gynecomastia, testicular atrophy, Dupuytren contracture, splenomegaly, and abdominal wall collaterals. In decompensated disease, look for ascites (bulging flanks, shifting dullness), hepatic encephalopathy (asterixis, disorientation), and jaundice.
  • •Order first-line non-invasive testing with the Fibrosis-4 Index (FIB-4), calculated from age, AST, ALT, and platelet count. A FIB-4 <1.3 rules out advanced fibrosis with NPV >90%; a score ≥2.67 rules in cirrhosis with 80% PPV and 96% specificity. Intermediate values (1.3-2.67) require further testing.
  • •Perform vibration-controlled transient elastography (VCTE) if FIB-4 is ≥1.3. Liver stiffness measurement (LSM) >12.1 kPa confirms cirrhosis with 90% specificity and AUROC 0.93. A cutoff of 6.5 kPa excludes advanced fibrosis with NPV 0.91. Magnetic resonance elastography (MRE) is the most accurate non-invasive method (AUROC 0.96) and may be used when VCTE is unavailable or discordant.
  • •In patients with intermediate FIB-4 (1.3-2.67) and VCTE 8-12 kPa, consider enhanced liver fibrosis (ELF) testing or proceed directly to MRE. If still indeterminate or if autoimmune/cholestatic disease is suspected, perform liver biopsy (gold standard, invasive with 0.5% major bleeding risk).
  • •Order etiologic serologies in all patients with established cirrhosis: HBsAg and anti-HCV (with HCV RNA if positive), transferrin saturation and ferritin for hemochromatosis (TSAT >45% women, >50% men), antimitochondrial antibody (AMA) for PBC, ANA/anti-smooth muscle antibody and IgG for autoimmune hepatitis, and tissue transglutaminase IgA for celiac disease in cryptogenic cases (pooled prevalence 4.6%).
  • •Calculate severity scores at diagnosis: Child-Turcotte-Pugh (CTP) class A (5-6), B (7-9), C (10-15) predicts 1-year survival (95%, 80%, 50% respectively). The MELD score (bilirubin, INR, creatinine) and MELD-Na (adding sodium) predict 90-day mortality and drive transplant allocation. MELD >20 defines severe alcohol-associated hepatitis.
  • •Screen for complications at baseline: esophagogastroduodenoscopy for varices (if LSM <20 kPa and platelets >150,000/mm³, varices can be safely excluded per Baveno VII criteria), abdominal ultrasound with alpha-fetoprotein (AFP) every 6 months for HCC surveillance, and diagnostic paracentesis in any patient with new or worsening ascites to rule out spontaneous bacterial peritonitis (SBP; neutrophil count >250 cells/mm³).
  • •Also consider evaluating for extrahepatic manifestations: hepatopulmonary syndrome (orthodeoxia, platypnea), portopulmonary hypertension (dyspnea, elevated right heart pressures on echo), cirrhotic cardiomyopathy (prolonged QT, diastolic dysfunction), and sarcopenia/frailty (grip strength, chair stands, balance). Assess nutritional status, as malnutrition affects >60% of patients.

Management

  • •Initiate etiology-directed therapy as the foundation of management. For HBV with detectable DNA, start entecavir 0.5 mg daily or tenofovir disoproxil fumarate 300 mg daily indefinitely. For HCV, prescribe pangenotypic direct-acting antiviral (DAA) therapy (e.g., sofosbuvir/velpatasvir 400/100 mg daily for 12 weeks) achieving SVR >95% even in decompensated disease.
  • •For alcohol-associated liver disease, recommend complete abstinence. Offer multidisciplinary integrated care including hepatology, addiction medicine, and social work. Consider pharmacotherapy for alcohol use disorder (e.g., baclofen 5-10 mg TID, naltrexone 50 mg daily). Abstinence halves decompensation risk (HR 0.61) and improves survival.
  • •For MASLD with F2-F3 fibrosis, start resmetirom 80 mg PO daily (FDA-approved) or semaglutide 2.4 mg SC weekly (accelerated approval August 2025). Both agents improve NASH resolution and fibrosis but are not approved for compensated cirrhosis (F4). For nondiabetic MASH, vitamin E 800 IU daily may be used.
  • •In compensated cirrhosis with clinically significant portal hypertension (HVPG ≥10 mmHg), initiate non-selective beta-blocker (NSBB) therapy to prevent first decompensation regardless of variceal status. Start carvedilol 6.25 mg once daily, titrate to 12.5 mg once daily (target HR 55-65 bpm). Alternatively, propranolol 20 mg BID, up to 160 mg BID. Avoid in asthma, bradycardia <50 bpm, or SBP <90 mmHg.
  • •For primary prophylaxis of variceal bleeding in patients with high-risk varices (medium/large, red signs, or Child C), combine carvedilol with variceal band ligation (VBL), the CAVARLY trial showed combination therapy reduced first bleed by 62.9% vs VBL alone (HR 0.37) and 69.3% vs carvedilol alone (HR 0.31), with 6.3% 1-year mortality in the combination arm.
  • •Manage acute variceal hemorrhage with immediate vasoactive therapy: terlipressin 2 mg IV bolus then 1-2 mg IV q4-6h (or octreotide 50 mcg IV bolus then 50 mcg/h infusion). Perform endoscopic band ligation within 12 hours. Give antibiotic prophylaxis: ceftriaxone 1 g IV daily for 5-7 days. Consider pre-emptive TIPS within 72 hours in high-risk patients (Child-Pugh 10-13 or Child B 8-9 with active bleeding) to improve 1-year survival (86% vs 61%).
  • •For spontaneous bacterial peritonitis (SBP), perform diagnostic paracentesis in any cirrhotic patient with new ascites or clinical deterioration. Start empiric antibiotics: cefotaxime 2 g IV q8h or ceftriaxone 2 g IV daily. Give intravenous albumin: 1.5 g/kg at diagnosis, then 1 g/kg on day 3. After resolution, start secondary prophylaxis with norfloxacin 400 mg PO daily or trimethoprim-sulfamethoxazole 1 DS tab PO daily.
  • •For hepatic encephalopathy (HE), identify and treat precipitants (infection, GI bleed, electrolyte disturbance). Start lactulose 25 mL PO q1-2h until 2-3 soft stools, then titrate to 2-3 bowel movements daily. If no improvement after 24-48 hours, add rifaximin 550 mg PO BID. For severe HE, consider L-ornithine L-aspartate (LOLA) 30 g/day continuous IV added to lactulose+rifaximin. For secondary prophylaxis, maintain lactulose plus rifaximin (HR 0.42 for recurrence; NNT=4).
  • •For hepatorenal syndrome-AKI (HRS-AKI), first exclude other causes: discontinue diuretics, hold nephrotoxins, volume expand with albumin 1 g/kg/day IV for 2 days. If creatinine does not decrease by ≥0.3 mg/dL, start vasoconstrictor: terlipressin 0.5-1 mg IV q4-6h (or continuous infusion 2 mg/day) plus albumin 20-40 g/day. Alternative: norepinephrine 0.5-3 mg/h IV. Monitor for respiratory failure with terlipressin (11% vs 2% placebo). Definitive therapy is liver transplantation.
  • •Provide nutritional support: small frequent meals with a nighttime snack, protein intake 1.2-1.5 g/kg/day (do not restrict protein in HE), two or more cups of coffee daily. For sarcopenia, encourage exercise and ensure adequate caloric intake. Avoid NSAIDs, excessive diuresis, and large-volume paracentesis without albumin replacement (6-8 g of 20-25% albumin per liter removed for volumes >5 L).
  • •Refer for liver transplantation evaluation at the first decompensation event (ascites, bleeding, encephalopathy, jaundice) or when MELD-Na >15. One-year survival post-transplant is ~90%. Patients who achieve recompensation may be considered for delisting if stable off specific therapy for ascites and HE with improved liver function.

Board Review — High Yield

  • •Compensated vs decompensated survival, Median survival >15 years in compensated cirrhosis, ~2 years after first decompensation, ~9 months with further decompensation.
  • •CSPH threshold, HVPG ≥10 mmHg defines clinically significant portal hypertension; predicts decompensation and guides NSBB therapy.
  • •PREDESCI trial, NSBB (carvedilol/propranolol) reduced first decompensation or death by 49% (HR 0.51) in compensated CSPH; NNT=9.
  • •CAVARLY trial, Carvedilol + VBL reduced first variceal bleed by 62.9% vs VBL alone in Child B/C; 1-year mortality 6.3% in combination arm.
  • •Terlipressin caution, Avoid in HRS-AKI with ACLF grade 3 or SpO₂ <90% due to respiratory failure risk (11% vs 2%).
  • •Recompensation rates, Occurs in ~35% overall; highest in HBV (49%) and lowest in ALD (19%); associated with reduced HCC (OR 0.55) and death (OR 0.33).
  • •FIB-4 cutoffs, <1.3 rules out advanced fibrosis; ≥2.67 rules in cirrhosis (PPV 80%, specificity 96%). Intermediate values require VCTE or MRE.
  • •HCC surveillance, Ultrasound + AFP every 6 months in all cirrhosis; ultrasound alone sensitivity 47%, adding AFP improves to 63%.
  • •MELD-Na ≤28 in AIH decompensation, Identifies patients likely to benefit from immunosuppression; 4-week MELD-Na drop ≥11 has 100% NPV for death/transplant.
  • •Variceal screening, Endoscopy at cirrhosis diagnosis; Baveno VII: if LSM <20 kPa and platelets >150,000, endoscopy can be safely avoided.

Deep Dive — Evidence Details

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