Liver cirrhosis - emergency‑medicine revision (Hepatitis B → Cirrhosis)
Overview
Cirrhosis is the end result of chronic liver injury in which regenerative nodules and fibrous septa distort hepatic architecture, producing portal hypertension and progressive loss of synthetic, metabolic and excretory liver function.
Cirrhosis may be compensated (relatively preserved function) or decompensated (overt complications such as jaundice, ascites, variceal haemorrhage, hepatic encephalopathy).
Chronic hepatitis B is a key cause of progressive fibrosis and cirrhosis; patients with HBV and significant fibrosis or cirrhosis need specialist follow‑up, consideration of antiviral therapy and hepatocellular carcinoma (HCC) surveillance (NICE CG165; GOV.UK Hepatitis B guidance).
Use in the ED: recognise decompensation, rapidly stabilise (ABCs), perform targeted investigations (bloods, bedside ultrasound, paracentesis), start empiric therapies for spontaneous bacterial peritonitis (SBP) or variceal bleeding, and contact hepatology/gastroenterology early (NICE NG50).
Pathophysiology
Repeated hepatocellular injury leads to inflammation and extracellular matrix deposition, producing bridging fibrosis and regenerative nodules. Architectural distortion increases intrahepatic resistance and causes portal hypertension, which underlies ascites, varices and splenomegaly. Progressive hepatocyte loss causes hypoalbuminaemia, coagulopathy and impaired detoxification (for example, ammonia accumulation).
Common causes and risk factors
- Chronic viral hepatitis: hepatitis B virus (HBV) and hepatitis C virus (HCV).
- Alcohol misuse.
- Metabolic disease: non‑alcoholic fatty liver disease (NAFLD) associated with obesity and type 2 diabetes.