Gastrointestinal · PANCE / PANRE

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 Variable1 point2 points3 points
Bilirubin (mg/dL)<22-3>3
Albumin (g/dL)>3.52.8-3.5<2.8
INR<1.71.7-2.3>2.3
AscitesNoneMild (diuretic responsive)Moderate-severe (refractory)
EncephalopathyNoneGrade 1-2Grade 3-4
Class A5-6 points; 1-yr survival ~100%
Class B7-9 points; 1-yr survival ~80%
Class C10-15 points; 1-yr survival ~45%
Child-Pugh score for cirrhosis severity. MELD-Na is used for transplant allocation but Child-Pugh remains useful clinically.

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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