Gastroenterology
AKT · Gastroenterology/Liver

Cirrhosis & chronic liver disease

Irreversible hepatic fibrosis/nodular regeneration → portal hypertension + liver failure

Overview

End-stage fibrosis and nodular regeneration of the liver from chronic injury (alcohol, MASLD, viral hepatitis B/C, autoimmune, haemochromatosis/Wilson, PBC/PSC). Compensated cirrhosis may be silent; DECOMPENSATION brings the complications of portal hypertension and liver failure: ascites/SBP, variceal bleeding, hepatic encephalopathy, jaundice, coagulopathy and HCC. Managed by treating the cause, preventing/treating complications, and surveillance.

Recognise

  • Stigmata: jaundice, spider naevi, palmar erythema, gynaecomastia, Dupuytren, clubbing, caput medusae, splenomegaly, leukonychia
  • Decompensation: ASCITES (± SBP), variceal BLEEDING, hepatic ENCEPHALOPATHY (asterixis, confusion), jaundice, coagulopathy
  • Synthetic failure: low albumin, raised INR; thrombocytopenia (hypersplenism)

Red flags

  • Decompensation (ascites/SBP, variceal bleed, encephalopathy) → admit/treat
  • HCC (rising AFP/new lesion); hepatorenal/hepatopulmonary syndrome

Differentials & how to tell them apart

Acute liver failureacute, no pre-existing chronic liver disease, rapid coagulopathy/encephalopathy
Other causes of ascitescardiac, malignant, nephrotic — SAAG distinguishes portal hypertension
Right heart failure / Budd-Chiarihepatic congestion — different vascular cause
Decompensated cirrhosis — gross ascites with distended abdomen (and caput medusae)

Decompensated cirrhosis — gross ascites with distended abdomen (and caput medusae)

James Heilman, MD / CC BY-SA 3.0 — Wikimedia Commons

Investigations

LFTs, albumin, INR (synthetic function), FBC (low platelets), U&Es; USS + fibroscan; identify the cause (viral serology, autoantibodies, ferritin/caeruloplasmin); ENDOSCOPY (varices); USS ± AFP 6-monthly (HCC); ascitic tap (SBP).

Management

Treat the cause + prevent/treat complications + HCC/variceal surveillance

  1. 1Treat the underlying cause and stop alcohol; nutritional support; vaccinate (A/B, pneumococcal/flu). Surveillance: HCC (USS ± AFP 6-monthly) and oesophageal varices (endoscopy at diagnosis, then 3-yearly unless on a non-selective beta-blocker).Gate: Avoid drugs that precipitate decompensation — opioids/benzodiazepines/constipation precipitate encephalopathy; NSAIDs worsen renal function/ascites; aminoglycosides are nephrotoxic in the cirrhotic
  2. 2Complication-specific: ascites → salt restriction + spironolactone±furosemide (± SBP prophylaxis/tap); varices → NSBB/banding; encephalopathy → lactulose ± rifaximin; HCC → treat; transplant for end-stage disease.
Treat the cause + stop alcohol + nutritionantivirals (B/C), abstinence, weight loss; avoid hepatotoxins
Non-selective beta-blocker (propranolol/carvedilol)primary prevention of variceal bleeding/decompensation
Spironolactone (± furosemide) for ascites; lactulose ± rifaximin for encephalopathycomplication-specific
HCC + variceal surveillanceUSS±AFP 6-monthly; endoscopy at diagnosis/every 3 years (unless on NSBB)

Key points

Stigmata + synthetic failure (low albumin, high INR, low platelets) = cirrhosis. Decompensation = ascites/SBP, variceal bleed, encephalopathy. Surveillance (HCC USS±AFP 6-monthly; varices). Don't prescribe sedatives/opioids/NSAIDs carelessly.

Monitor & prognosis

Synthetic function; surveillance; decompensation.

Compensated can be stable for years; decompensation is poor (Child-Pugh/MELD).

Source: NICE NG50; BSG; CKS Cirrhosis