Liver Cirrhosis — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Liver cirrhosis is the final stage of progressive hepatic fibrosis — the replacement of functional liver tissue by fibrous scar tissue (collagen), disrupting normal liver architecture and blood flow. It results from repeated cycles of liver injury and regeneration in response to a chronic insult (alcohol, viral hepatitis, or metabolic liver disease). Cirrhosis affects over 100 million people globally and causes approximately 1.32 million deaths annually — accounting for 2.4% of all global deaths. Cirrhosis is classified as compensated (liver still adequately performs its functions — patients may be asymptomatic) or decompensated (liver can no longer maintain adequate function — clinically manifest with ascites, variceal haemorrhage, hepatic encephalopathy, or jaundice). The transition from compensated to decompensated cirrhosis represents a major clinical milestone — 5-year survival falls from approximately 80% in compensated cirrhosis to 20-50% after the first decompensation. Hepatocellular carcinoma (HCC) develops in approximately 2-4% of patients with cirrhosis per year — 6-monthly surveillance ultrasound is required.

Alcohol-related liver disease (ARLD): the leading cause in Europe and North America — approximately 50% of cirrhosis cases in the UK. Progressive stages: fatty liver (alcoholic steatosis — reversible), alcoholic hepatitis (acute inflammatory injury), and cirrhosis. The risk threshold is approximately 80g/day (8 UK units) in men and 40g/day (4 UK units) in women — but individual susceptibility varies. Hepatitis C (HCV): the most common cause in the USA and parts of Asia — 10-20% of people with chronic HCV develop cirrhosis over 20-30 years; now largely curable with direct-acting antivirals (DAAs). Hepatitis B (HBV): a major cause in Asia and sub-Saharan Africa; largely preventable by vaccination; antiviral therapy prevents cirrhosis progression. Metabolic dysfunction-associated steatotic liver disease (MASLD — previously NAFLD/NASH): the most rapidly growing cause globally; strongly associated with obesity, type 2 diabetes, and metabolic syndrome; approximately 10-25% of those with MASH (metabolic-associated steatohepatitis) develop cirrhosis over decades. Other causes: primary biliary cholangitis (PBC — autoimmune bile duct destruction in women), primary sclerosing cholangitis (PSC — associated with IBD), autoimmune hepatitis (AIH), haemochromatosis (iron overload), Wilson's disease (copper accumulation), alpha-1-antitrypsin deficiency, and drug-induced liver injury (methotrexate, amiodarone, isoniazid).

Compensated cirrhosis: often asymptomatic for years — discovered incidentally on ultrasound, blood tests, or during investigation of another condition. Non-specific symptoms: fatigue, weakness, malaise, and decreased appetite. Clinical signs on examination: spider naevi (dilated dermal arterioles — 5 or more clinically significant), palmar erythema (redness of the palms), leukonychia (white nails — hypoalbuminaemia), clubbing, parotid enlargement, caput medusae (prominent periumbilical veins), gynaecomastia and testicular atrophy in men (oestrogen excess due to impaired hepatic metabolism), and moderate splenomegaly. Decompensated cirrhosis: Ascites — abdominal distension from peritoneal fluid accumulation (portal hypertension and hypoalbuminaemia); the most common first decompensation. Spontaneous bacterial peritonitis (SBP) — infection of ascitic fluid; presents with fever, abdominal pain, and encephalopathy — 20-30% in-hospital mortality. Variceal haemorrhage — bleeding from oesophageal, gastric, or anorectal varices (dilated veins due to portal hypertension); presents with haematemesis (vomiting blood) or melaena (black tarry stools) — life-threatening. Hepatic encephalopathy — neuropsychiatric dysfunction from failure to clear nitrogenous waste; ranges from subtle cognitive impairment to coma; precipitants include infection, constipation, GI bleed, and dehydration. Hepatorenal syndrome — renal failure as a complication of advanced cirrhosis with ascites — a pre-terminal complication. Jaundice — yellow discolouration of skin and sclerae from failure of bilirubin processing.

Liver function tests: elevated bilirubin, low albumin (hepatic synthetic function), elevated ALT/AST (hepatocellular injury), and elevated GGT (cholestasis or alcohol). Coagulation: prolonged prothrombin time/INR indicates impaired clotting factor synthesis (prognostic). FBC: thrombocytopenia (splenomegaly trapping platelets — portal hypertension), anaemia, and leucopenia (hypersplenism). Non-invasive fibrosis assessment: FIB-4 index (age × AST / platelet count × ALT^0.5) — easily calculated from routine blood tests; liver elastography (FibroScan) measures liver stiffness in kilopascals — greater than 12.5-15 kPa suggests cirrhosis. Liver ultrasound: nodular liver surface, heterogeneous echotexture, splenomegaly, portal hypertension features (enlarged portal vein, ascites) — initial imaging for liver assessment. CT or MRI abdomen: characterises liver morphology, assesses for HCC, portal venous anatomy, and varices (CT with portal venous phase). Upper GI endoscopy (OGD): mandatory at diagnosis of cirrhosis — identifies and grades oesophageal and gastric varices (risk of haemorrhage determines prophylactic treatment). Liver biopsy: previously the gold standard for staging fibrosis; now largely replaced by non-invasive methods — still used when aetiology is uncertain or when concurrent hepatic pathology is suspected. Child-Pugh score and MELD (Model for End-Stage Liver Disease) score: prognostic scoring systems used to assess severity and prioritise liver transplant listing.

Treat the underlying cause — this is the most important intervention to halt or reverse fibrosis (early-stage fibrosis can partially reverse when the causative injury is removed): complete alcohol cessation (ARLD — most important intervention; alcohol abstinence can stabilise or improve compensated cirrhosis and reduce portal hypertension), HBV antiviral therapy (tenofovir, entecavir — dramatically reduces progression), HCV cure with direct-acting antivirals (HCV elimination reduces portal hypertension, reverses some fibrosis, and reduces HCC risk), weight loss and metabolic management for MASLD, and immune-suppression for autoimmune hepatitis (prednisolone and azathioprine). Portal hypertension management: non-selective beta-blockers (propranolol, carvedilol) — reduce portal pressure and prevent first variceal bleed (primary prophylaxis) and recurrent bleeding (secondary prophylaxis — combined with endoscopic variceal band ligation); transjugular intrahepatic portosystemic shunt (TIPSS) — a radiological procedure placing a metal stent between portal and hepatic veins to decompress the portal circulation — used for refractory variceal haemorrhage and refractory ascites. Acute variceal haemorrhage: terlipressin (vasoconstrictor — reduces portal pressure), broad-spectrum antibiotics (norfloxacin or ceftriaxone — reduces SBP risk and mortality), urgent endoscopy and variceal band ligation, blood product transfusion (target Hb 70-80 g/L), and balloon tamponade (Sengstaken tube) as a bridge to definitive treatment. Ascites management: dietary sodium restriction (below 88 mmol/day), spironolactone (100mg — first-line diuretic), furosemide (40mg — added if needed). Paracentesis (drainage of ascitic fluid) with albumin infusion (8g per litre removed) for tense or refractory ascites. Prophylactic antibiotics (primary norfloxacin or ciprofloxacin) for SBP prophylaxis in high-risk patients. Hepatic encephalopathy management: lactulose (laxative — reduces ammonia absorption), rifaximin (non-absorbable antibiotic — reduces gut ammonia-producing bacteria, reduces recurrence risk), protein intake should not be restricted (adequate nutrition is essential). Hepatorenal syndrome (HRS): terlipressin and albumin infusion (type 1 HRS — acute, potentially reversible). Liver transplantation: definitive treatment for end-stage liver disease — indicated for MELD score above 15-17, intractable decompensation, or HCC within Milan criteria (single lesion 2-5 cm or up to 3 nodules each under 3 cm). Excellent outcomes: 5-year survival 70-80% after transplant.

Cirrhosis is the final common pathway of chronic liver injury and generates life-threatening portal hypertension complications. Variceal haemorrhage — from rupture of oesophageal or gastric varices — presents with haematemesis or melaena and carries 15-20% per-episode mortality; rebleeding occurs in 70% without prophylaxis (propranolol or endoscopic band ligation). Ascites — fluid accumulation from portal hypertension and hypoalbuminaemia — affects 50% of cirrhotic patients within 10 years and carries 50% 2-year mortality; refractory ascites requiring large-volume paracentesis or TIPS (transjugular intrahepatic portosystemic shunt) has even worse prognosis. Spontaneous bacterial peritonitis (SBP) — infection of ascitic fluid (most commonly E. coli, Klebsiella) — carries 30% in-hospital mortality per episode; long-term norfloxacin prophylaxis is indicated after a first episode. Hepatic encephalopathy — ammonia-driven cerebral dysfunction causing confusion, asterixis, and coma — is graded I-IV (West Haven criteria) and may be covert, impairing driving ability and employment. Hepatorenal syndrome — functional acute kidney injury from severe splanchnic vasodilation and renal vasoconstriction — has two types: Type 1 (rapid, creatinine doubling to above 226 mcmol/L within 2 weeks — 90% 2-week mortality without liver transplantation) and Type 2 (slower, associated with refractory ascites). Hepatocellular carcinoma develops in 1-5% of cirrhotic patients annually and is a leading indication for liver transplantation.

Alcohol: the most important preventable cause of cirrhosis in the West. UK guidelines recommend a maximum of 14 units per week for men and women, with several alcohol-free days. For anyone with established liver disease, complete abstinence is recommended. Hepatitis B vaccination: prevents HBV acquisition and therefore HBV-related cirrhosis — a universal infant and adolescent vaccine programme prevents the majority of HBV-related cirrhosis. HCV treatment: all patients with chronic HCV should be offered curative direct-acting antiviral treatment — this prevents cirrhosis in those with early disease and slows progression and reduces HCC risk in those with established cirrhosis. MASLD prevention: healthy weight, regular exercise (150 minutes moderate intensity per week), low glycaemic diet, and treatment of metabolic risk factors (diabetes, hypertension, dyslipidaemia). Avoid unnecessary hepatotoxic medications: check with a pharmacist or doctor before taking herbal remedies, supplements, and medications metabolised by the liver. HCC surveillance: all patients with cirrhosis should have 6-monthly liver ultrasound (plus or minus AFP) for early detection of hepatocellular carcinoma — when detected early, HCC is potentially curable by resection, ablation, or liver transplant.

See a GP if you have risk factors for liver disease (heavy alcohol use, known hepatitis B or C, obesity with diabetes) and symptoms such as fatigue, abdominal bloating, or jaundice — liver function tests and a liver ultrasound may detect liver disease before cirrhosis develops. Seek immediate emergency care for: vomiting blood or passing black tarry stools (variceal haemorrhage — call 999 immediately, a life-threatening emergency), confusion or drowsiness in a patient with known liver disease (hepatic encephalopathy), fever with abdominal pain and ascites (suspected SBP — sepsis from infected ascitic fluid), and jaundice developing suddenly in a patient with cirrhosis. If you have established cirrhosis: maintain 6-monthly HCC surveillance appointments, attend gastroenterology clinics regularly, and seek immediate review for new onset confusion, fever, abdominal pain, leg swelling, or darkening urine — these may indicate the first decompensation. Liver transplant assessment should be sought early — waiting lists can be long.