Cirrhosis of the liver: definition, stages, causes, symptoms, diagnosis and treatment
DEFINITION AND STAGES
Cirrhosis is diffuse hepatic fibrosis with regenerative nodules and distortion of normal architecture, producing portal hypertension and impaired synthetic, metabolic and detoxifying function. It is the end stage of many chronic liver diseases, although fibrosis may partially regress when the cause is removed. Clinically, patients are described as compensated or decompensated. Decompensation is marked by ascites, variceal haemorrhage, hepatic encephalopathy or jaundice. Severity is commonly assessed with Child–Pugh and MELD-Na scores.
CAUSES AND PATHOGENESIS
Causes include chronic HBV/HCV, alcohol-related liver disease, metabolic dysfunction-associated steatotic liver disease, autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis, haemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency, drugs and chronic biliary obstruction. Persistent hepatocyte injury activates Kupffer cells and hepatic stellate cells, leading to collagen deposition, bridging fibrosis and regenerative nodules. Vascular resistance rises, portal pressure increases and effective circulating volume falls. Splanchnic vasodilatation activates RAAS and ADH, promoting sodium and water retention and ascites.
CLINICAL FEATURES
Early disease may be silent. Symptoms include fatigue, anorexia, weight loss, nausea and pruritus. Signs include jaundice, spider naevi, palmar erythema, muscle wasting, parotid enlargement, testicular atrophy, gynaecomastia, caput medusae, splenomegaly, ascites, peripheral oedema and asterixis. Decompensation presents with tense ascites, spontaneous bacterial peritonitis, variceal bleeding, encephalopathy, hepatorenal syndrome or severe jaundice.
INVESTIGATIONS
CBC may show thrombocytopenia from hypersplenism; liver tests may show raised bilirubin, AST/ALT and ALP, while albumin and prothrombin time/INR reflect synthetic function. Evaluate renal function, sodium and aetiology-specific tests (viral serology, autoimmune markers, iron studies, caeruloplasmin, etc.). Ultrasound with Doppler assesses liver morphology, spleen, ascites and portal/hepatic vessels. Elastography estimates fibrosis; CT/MRI are used for focal lesions or complications. Endoscopy assesses varices according to risk and local guidance. Diagnostic paracentesis is required for new-onset or worsening ascites and suspected infection. Liver biopsy is reserved for uncertain diagnosis when it changes management.