Cirrhosis (Ascites, Varices, Encephalopathy)
End-stage liver fibrosis with portal hypertension; ascites, varices, and encephalopathy define decompensation.
Also known as: cirrhosis, decompensated cirrhosis, ascites, hepatic encephalopathy, portal hypertension
Overview
Diffuse hepatic fibrosis with regenerative nodules, representing the end stage of chronic liver injury from any cause. Compensated cirrhosis is asymptomatic; decompensated cirrhosis is defined by ascites, variceal bleeding, hepatic encephalopathy, or jaundice.
Epidemiology
Affects ~600,000 US adults; 12th leading cause of death. Common etiologies in US: MASLD/MASH, alcohol-associated liver disease, chronic HCV (declining with DAAs), chronic HBV. Mortality dependent on Child-Pugh and MELD scores; 1-yr mortality 1-3% compensated, 20-60% decompensated.
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Risk factors
- Chronic alcohol use
- Chronic viral hepatitis B and C
- Metabolic-associated steatohepatitis (MASH/NASH) — obesity, diabetes, metabolic syndrome
- Autoimmune hepatitis
- Primary biliary cholangitis (PBC)
- Primary sclerosing cholangitis (PSC) — associated with IBD
- Hemochromatosis (HFE mutation)
- Wilson disease (ATP7B mutation)
- Alpha-1 antitrypsin deficiency
- Drug-induced (methotrexate, amiodarone, isoniazid)
- Vascular (Budd-Chiari, cardiac cirrhosis, congestive hepatopathy)
- Cryptogenic
Pathophysiology
Repeated hepatocellular injury triggers hepatic stellate cell activation, collagen deposition, and architectural disruption. Fibrosis and nodular regeneration distort vascular flow → increased intrahepatic resistance and splanchnic vasodilation → portal hypertension. Portosystemic shunting bypasses hepatic detoxification → encephalopathy. Splanchnic vasodilation activates RAAS and ADH → sodium and water retention → ascites. Hepatocellular dysfunction → coagulopathy, hypoalbuminemia, jaundice.
Clinical presentation
Symptoms
- Compensated: often asymptomatic; fatigue, vague RUQ discomfort, decreased exercise tolerance
- Decompensated: jaundice, abdominal distension (ascites), confusion (encephalopathy), GI bleeding (varices)
- Pruritus (cholestasis)
- Easy bruising, bleeding (coagulopathy)
- Anorexia, weight loss, muscle wasting (sarcopenia)
- Loss of libido, impotence, amenorrhea
Signs / physical exam
- Stigmata of chronic liver disease: spider angiomata, palmar erythema, gynecomastia, testicular atrophy, Dupuytren contracture, caput medusae, parotid enlargement
- Jaundice, scleral icterus
- Ascites: shifting dullness, fluid wave, bulging flanks
- Splenomegaly
- Asterixis (encephalopathy)
- Fetor hepaticus (sweet, musty breath)
- Clubbing
- Muscle wasting, temporal hollowing
Classic findings
Decompensation triad: jaundice, ascites, encephalopathy. Stigmata of chronic liver disease on exam.
Differential diagnosis
- Acute hepatitis with marked transaminitis — ALT/AST in thousands, distinct etiology (viral, ischemic, toxic); imaging without nodularity
- Constrictive pericarditis / right heart failure (cardiac cirrhosis) — JVD, Kussmaul sign, pericardial calcification or thickening; right-sided pressures elevated
- Budd-Chiari syndrome — Acute or subacute ascites and hepatomegaly; hepatic venous outflow obstruction on Doppler
- Nephrotic syndrome — Edema, proteinuria; urinalysis
- Hypothyroidism / myxedema — Generalized edema, fatigue; TSH
- Peritoneal carcinomatosis or TB peritonitis — Ascites with elevated SAAG <1.1; cytology, ADA, AFB
- Protein-losing enteropathy — Hypoalbuminemia without liver dysfunction; alpha-1 antitrypsin clearance
Diagnostic workup
Diagnostic criteria
Histologic gold standard but rarely needed; clinical, biochemical, and imaging features are usually sufficient. Compensated vs decompensated cirrhosis based on presence of ascites, variceal bleeding, hepatic encephalopathy, or jaundice.
Labs
- LFTs — AST/ALT often mildly elevated or even normal; AST > ALT and AST:ALT >2:1 suggests alcohol; alk phos and GGT cholestatic
- Bilirubin, albumin, INR (synthetic function — used for Child-Pugh and MELD)
- CBC — thrombocytopenia (hypersplenism, decreased thrombopoietin), anemia, leukopenia
- BMP — hyponatremia (dilutional), AKI (hepatorenal syndrome)
- Ammonia (limited utility; correlates poorly with severity of encephalopathy)
- Etiologic workup: hepatitis serologies, autoimmune panel (ANA, ASMA, AMA, anti-LKM, IgG), ferritin/transferrin saturation, ceruloplasmin/24-h urine copper, A1AT level and phenotype, HFE genotype, alpha-fetoprotein
- Ascitic fluid analysis (diagnostic paracentesis): cell count and differential (PMN ≥250 = SBP), albumin (SAAG ≥1.1 = portal hypertension), culture, cytology, total protein, glucose
Imaging
- Abdominal ultrasound with Doppler — nodular liver contour, splenomegaly, ascites, portal vein patency and flow direction
- Transient elastography (FibroScan) — fibrosis staging
- Triphasic CT or MRI with contrast for HCC surveillance and characterization
- Upper endoscopy at diagnosis to screen for varices (or non-invasive criteria — Baveno VI/VII: liver stiffness <20 kPa + platelets >150,000 allows deferral)
- MELD/Child-Pugh scoring for prognostication and transplant evaluation
Diagnostic algorithm
| Child-Pugh Variable | 1 point | 2 points | 3 points |
|---|---|---|---|
| Bilirubin (mg/dL) | <2 | 2-3 | >3 |
| Albumin (g/dL) | >3.5 | 2.8-3.5 | <2.8 |
| INR | <1.7 | 1.7-2.3 | >2.3 |
| Ascites | None | Mild (diuretic responsive) | Moderate-severe (refractory) |
| Encephalopathy | None | Grade 1-2 | Grade 3-4 |
| Class A | 5-6 points; 1-yr survival ~100% | ||
| Class B | 7-9 points; 1-yr survival ~80% | ||
| Class C | 10-15 points; 1-yr survival ~45% |
Treatment
First-line
- Treat underlying cause: alcohol cessation, antiviral therapy (HBV nucleoside analogues, HCV DAAs), weight loss for MASH, immunosuppression for autoimmune hepatitis, phlebotomy for hemochromatosis, chelation for Wilson
- Vaccinate against HAV, HBV, pneumococcus, influenza, COVID-19
- Avoid hepatotoxins: alcohol, acetaminophen >2 g/day, NSAIDs, herbal supplements
- Nutritional support — late-evening snack to reduce muscle catabolism; protein 1.2-1.5 g/kg/day; supplementation of B12, folate, thiamine, vitamin D
- HCC surveillance: ultrasound ± AFP every 6 months
- Variceal screening EGD (or non-invasive criteria)
Ascites
- Sodium restriction <2 g/day
- Diuretics: spironolactone (start 100 mg) + furosemide (start 40 mg) in 100:40 ratio; titrate to maintain ratio
- Therapeutic large-volume paracentesis (>5 L) — give albumin 6-8 g/L removed
- Refractory ascites: TIPS (avoid in encephalopathy, EF<60%, advanced age, decompensated MELD); serial paracenteses; liver transplantation
- SBP prophylaxis: norfloxacin or ciprofloxacin daily if ascitic protein <1.5 g/dL plus poor liver function or prior SBP
- SBP treatment: ceftriaxone 2 g/day × 5-7 days + albumin 1.5 g/kg day 1, 1 g/kg day 3 (reduces hepatorenal syndrome and mortality)
Esophageal varices
- Primary prophylaxis for medium/large varices: non-selective beta-blocker (propranolol, nadolol, carvedilol) titrated to HR 55-60 OR serial EVL (band ligation)
- Acute variceal bleed: octreotide infusion + ceftriaxone 1 g + EGD with EVL within 12 h + restrictive transfusion (Hgb ~7); early TIPS for high-risk patients
- Secondary prophylaxis after bleed: NSBB + serial EVL until eradication
Hepatic encephalopathy
- Identify and treat precipitants: GI bleed, infection (SBP, UTI, pneumonia), electrolyte imbalance (hypokalemia, hyponatremia, alkalosis), constipation, dehydration, medications (sedatives, opioids), TIPS, hepatocellular carcinoma
- Lactulose 30-45 mL PO q1-2h until 3-4 soft bowel movements, then maintenance
- Rifaximin 550 mg BID — add for recurrent or refractory encephalopathy (Bass NM, NEJM 2010 RFHE3001 trial)
- Avoid sedatives, opioids, benzodiazepines
- Adequate protein intake — DO NOT restrict (worsens sarcopenia)
Second-line / adjunct
- TIPS (transjugular intrahepatic portosystemic shunt) for refractory ascites, refractory variceal bleeding, or hepatic hydrothorax — risks include precipitating encephalopathy
- Liver transplantation — definitive treatment for decompensated cirrhosis; allocation by MELD-Na score; consider when MELD ≥15 or decompensation event
- Hepatorenal syndrome: terlipressin (now FDA-approved) + albumin OR norepinephrine + albumin; bridge to transplant
- Treat extrahepatic complications: hepatopulmonary syndrome, portopulmonary hypertension, cirrhotic cardiomyopathy
Complications
- Ascites and spontaneous bacterial peritonitis (SBP)
- Variceal hemorrhage
- Hepatic encephalopathy
- Hepatorenal syndrome (HRS-AKI, HRS-CKD)
- Hepatopulmonary syndrome (intrapulmonary vascular dilation, hypoxia, orthodeoxia)
- Portopulmonary hypertension
- Hepatocellular carcinoma
- Coagulopathy (decreased synthesis of factors; balanced — not as protective as INR suggests; balance rebalances toward thrombosis with portal vein thrombosis risk)
- Sarcopenia, malnutrition
- Sepsis, immune dysfunction
- Cardiopulmonary: cirrhotic cardiomyopathy
- Endocrine: hypogonadism, glucose intolerance
PANCE pearls
- SAAG (serum-ascites albumin gradient) ≥1.1 g/dL = portal hypertension as cause of ascites; <1.1 = other (carcinomatosis, TB, pancreatic, nephrotic).
- Spontaneous bacterial peritonitis: ascitic PMN ≥250/mm³ regardless of culture — start empiric ceftriaxone and albumin immediately.
- Albumin in SBP (1.5 g/kg day 1, 1 g/kg day 3) reduces hepatorenal syndrome and mortality (Sort, NEJM 1999).
- Restrictive transfusion (Hgb ~7) in variceal bleed reduces rebleed and mortality vs liberal (Villanueva, NEJM 2013).
- Early TIPS within 72 h of variceal bleed for high-risk patients (Child-Pugh C <14, or B with active bleed at EGD) reduces mortality (García-Pagán, NEJM 2010).
- Lactulose first-line for hepatic encephalopathy; add rifaximin for recurrence (Bass NM, NEJM 2010 RFHE3001 trial).
- Do NOT restrict protein in cirrhosis — worsens sarcopenia and outcomes.
- INR overestimates bleeding risk in cirrhosis; coagulopathy is REBALANCED — thrombosis risk is real.
- MELD-Na is the standard score for transplant allocation; Child-Pugh remains useful at the bedside.
- Acute kidney injury in cirrhosis differential: pre-renal (volume depletion, response to albumin), HRS (no response to albumin, no other cause), ATN, drug-induced — albumin challenge differentiates.
- Avoid NSAIDs (renal failure), aminoglycosides, ACEi/ARBs in advanced cirrhosis.
References
- AASLD 2021 Ascites — Biggins SW et al. Diagnosis, Evaluation, and Management of Ascites, Spontaneous Bacterial Peritonitis and Hepatorenal Syndrome: 2021 Practice Guidance by the AASLD. Hepatology 2021;74:1014-1048
- AASLD 2014 HE — Vilstrup H et al. Hepatic Encephalopathy in Chronic Liver Disease: 2014 Practice Guideline by AASLD and EASL. Hepatology 2014;60:715-735
- Baveno VII — de Franchis R et al. Baveno VII — Renewing consensus in portal hypertension. J Hepatol 2022;76:959-974
- RFHE3001 (Rifaximin HE) — Bass NM et al. Rifaximin Treatment in Hepatic Encephalopathy. NEJM 2010;362:1071-1081
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