Table of Contents · 11 sections
In a nutshell. Cirrhosis is the end-stage of chronic liver diseases characterized by diffuse fibrosis and nodular regeneration. Severity is assessed using the Child-Pugh score (A/B/C: bilirubin, albumin, PT, ascites, encephalopathy) and the MELD score (bilirubin, INR, creatinine, Na), which form the basis of the transplantation waiting list. Four key complications: variceal bleeding, ascites, hepatic encephalopathy, and SBP. Transplantation is the only radical treatment for decompensation.
1. Etiology
- Viral hepatitis B and C (60% in Russia).
- Alcohol-related liver disease.
- Non-alcoholic fatty liver disease (NAFLD/MASLD) — an increasingly prevalent cause.
- Autoimmune: autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis.
- Inherited: hemochromatosis, Wilson's disease, α1-antitrypsin deficiency.
- Cardiogenic ("nutmeg liver") in chronic right-sided heart failure.
- Drug-induced (methotrexate, amiodarone, nitrofurans).
2. Pathogenesis
Repeated hepatocyte injury → activation of hepatic stellate cells (Ito cells) → collagen synthesis → formation of septa connecting portal tracts and central veins → disrupted lobular architecture, nodular regeneration. Consequences: ↓ synthetic function (albumin, clotting factors), ↓ detoxification (ammonia → encephalopathy), ↑ resistance to portal blood flow → portal hypertension.
3. Clinical presentation
Compensated cirrhosis
- Often asymptomatic.
- Asthenia, dyspepsia, flatulence.
- "Minor" hepatic signs: spider angiomas, palmar erythema, gynecomastia, Dupuytren's contracture.
Decompensated cirrhosis
- Jaundice, pruritus.
- Ascites, edema.
- Bleeding (esophageal varices, skin hematomas).
- Hepatic encephalopathy (somnolence, tremor, asterixis, coma).
- Splenomegaly, portosystemic anastomoses ("caput medusae").
4. Diagnosis
- Biochemistry: ↑ ALT/AST, ↑ GGT and ALP, ↑ bilirubin, ↓ albumin, ↑ INR, thrombocytopenia.
- Etiological workup: HBsAg, anti-HCV, iron/ferritin, ceruloplasmin, AMA, ANA, ASMA, IgG.
- Ultrasound + Doppler: nodular contours, heterogeneity, ↑ portal vein diameter > 13 mm, reversal of flow.
- Elastography (FibroScan) — non-invasive assessment of fibrosis; > 12–14 kPa indicates cirrhosis.
- CT/MRI — assessment of volume, HCC lesions.
- EGD — screening for esophageal varices — mandatory for all patients with cirrhosis.
- Liver biopsy — for unclear etiology or fibrosis assessment; the gold standard, though increasingly replaced by elastography.
5. Child-Pugh classification
| Sign | 1 point | 2 points | 3 points |
|---|---|---|---|
| Encephalopathy | No | I–II | III–IV |
| Ascites | No | Moderate | Tense |
| Bilirubin, µmol/L | < 34 | 34–50 | > 50 |
| Albumin, g/L | > 35 | 28–35 | < 28 |
| PT (seconds prolongation) or INR | < 4 / < 1,7 | 4–6 / 1,7–2,3 | > 6 / > 2,3 |
Total score: 5–6 — Class A (1-year survival ~100%); 7–9 — Class B (~80%); 10–15 — Class C (~45%).
6. MELD score
MELD = 3.78 × ln(bilirubin) + 11.2 × ln(INR) + 9.57 × ln(creatinine) + 6.43. Range 6–40. Used for liver transplant allocation. Addition of Na (MELD-Na) improves prognostic accuracy in hyponatremia.
7. Complications
Portal hypertension and esophageal varices
- Hepatic venous pressure gradient > 10 mmHg — clinically significant; > 12 mmHg — bleeding risk.
- Primary prophylaxis: non-selective β-blockers (carvedilol, propranolol, nadolol) or endoscopic band ligation.
- Acute bleeding: vasoactive drugs (terlipressin, octreotide) + endoscopic band ligation + antibiotics (ceftriaxone for 5–7 days).
- Recurrent bleeding — TIPS (transjugular intrahepatic portosystemic shunt).
Ascites
- Diagnostic paracentesis: rule out SBP (neutrophils > 250/µL).
- Sodium restriction to 2 g/day, fluid restriction if Na < 125 mmol/L.
- Spironolactone 100 mg + furosemide 40 mg (100:40 ratio), titrating up to 400:160 mg.
- Refractory ascites — large-volume paracentesis with albumin 8 g per 1 L of removed fluid, TIPS, transplantation.
Hepatic encephalopathy
- West Haven criteria grades I–IV.
- Triggers: infections, gastrointestinal bleeding, constipation, electrolyte imbalances, sedatives.
- Treatment: lactulose (target — 2–3 soft bowel movements per day), rifaximin 550 mg BID for secondary prophylaxis.
- L-ornithine L-aspartate (LOLA), branched-chain amino acids — as adjunctive therapy.
Spontaneous bacterial peritonitis (SBP)
- Diagnosis: neutrophils > 250/µL in ascetic fluid.
- Flora: usually monomicrobial (E. coli, Klebsiella, S. pneumoniae).
- Treatment: ceftriaxone 2 g/day for 5–7 days + albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 (↓ hepatorenal syndrome).
- Secondary prophylaxis: norfloxacin or rifaximin.
Hepatorenal syndrome
- Functional renal failure associated with cirrhosis.
- Type 1 — rapid GFR decline; type 2 — slow.
- Treatment: terlipressin + albumin; radical treatment — liver transplantation.
HCC
- Screening: ultrasound + AFP every 6 months.
- Diagnosis using LI-RADS on contrast-enhanced MRI/CT.
- BCLC staging determines tactics: resection, ablation, TACE, lenvatinib/atezolizumab + bevacizumab, transplantation (Milan criteria).
8. Etiology-based treatment
- HBV — tenofovir, entecavir lifelong.
- HCV — direct-acting antivirals (sofosbuvir + velpatasvir, etc.) — SVR > 95%.
- Alcohol — complete abstinence; corticosteroids in severe alcoholic hepatitis (Maddrey > 32).
- PBC — ursodeoxycholic acid 13–15 mg/kg/day; obeticholic acid if response < 40%.
- AIH — prednisone + azathioprine.
- Hemochromatosis — phlebotomies; Wilson's disease — D-penicillamine, zinc.
9. Liver transplantation
- Indications: Child-Pugh C, MELD ≥ 15, refractory complications, HCC within Milan criteria.
- Contraindications: uncorrectable HIV, active extrahepatic malignancies, severe cardiopulmonary disease, active substance abuse.
- 5-year survival — 70–75%.
10. Management of compensated cirrhosis
- EGD at diagnosis; if no esophageal varices — repeat in 2–3 years.
- Ultrasound + AFP every 6 months.
- Vaccination: HAV, HBV, influenza, pneumococcus.
- Avoid NSAIDs, aminoglycosides, benzodiazepines.
- Nutritional support, protein 1.2–1.5 g/kg, late evening snack.
11. FAQ
Is cirrhosis reversible?
Fibrosis and early cirrhosis may partially regress upon elimination of the cause (HCV eradication, alcohol cessation). Advanced cirrhosis is irreversible.
Which β-blockers are preferred for esophageal varices?
Carvedilol — lowers the pressure gradient more effectively than propranolol and does not cause tachyphylaxis.
Are NSAIDs allowed in cirrhosis?
No — they impair renal blood flow, precipitate acute kidney injury, and trigger variceal bleeding. Paracetamol up to 2 g/day is preferred.
When is TIPS indicated versus a surgical shunt?
TIPS — for refractory ascites and recurrent bleeding; surgical shunts are outdated and rarely used.
How to differentiate transudate from exudate in ascites?
Serum-ascites albumin gradient (SAAG): ≥ 11 g/L — portal hypertension; < 11 — inflammation, carcinomatosis, tuberculosis.
See also: IBD · GERD · Viral hepatitis · Diuretics · Gastroenterology catalog · Clinical scales