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

Liver cirrhosis is the irreversible replacement of normal liver tissue with fibrous scar tissue, causing progressive loss of hepatic function. Affecting over 112 million people globally, it is the final common pathway for many chronic liver diseases and a major cause of morbidity and liver-related mortality.Liver cirrhosis is irreversible replacement of functional liver tissue with fibrous scar tissue (fibrosis), causing progressive loss of hepatic synthetic function, portal hypertension, and ultimately liver failure. It affects an estimated 112 million people globally and is the 11th leading cause of death worldwide, responsible for approximately 1.3 million deaths annually. Cirrhosis is classified as compensated (liver maintains near-normal function despite fibrosis — often asymptomatic for years) or decompensated (loss of hepatic compensation causing life-threatening complications). The Child-Pugh score (5–15, incorporating albumin, bilirubin, INR, ascites, and encephalopathy) and the MELD score (Model for End-Stage Liver Disease — based on bilirubin, creatinine, INR) stratify severity and prioritize liver transplant allocation. Decompensated cirrhosis has a 2-year mortality of approximately 50%, highlighting the need for early diagnosis and treatment of the underlying cause before irreversible decompensation occurs.

Chronic alcohol use disorder accounts for 40-50% of cases in Western countries. Chronic hepatitis B and C infection are the leading global causes. Non-alcoholic steatohepatitis (NASH) related to obesity and metabolic syndrome is rapidly increasing. Other causes include autoimmune hepatitis, primary biliary cholangitis, and hemochromatosis.Alcohol-related liver disease (ArLD) — the hepatotoxic threshold is approximately 14–21 units/week for women and 21 units/week for men, though genetic susceptibility varies widely. ArLD progresses through fatty liver (steatosis — reversible) → alcoholic hepatitis (steatohepatitis — partially reversible) → cirrhosis (irreversible). Severe alcoholic hepatitis (Maddrey Discriminant Function above 32 — indicating 35% 28-day mortality) requires prednisolone 40 mg/day for 28 days. Hepatitis B virus (HBV) — the leading cause of cirrhosis and hepatocellular carcinoma globally, particularly in East Asia and Sub-Saharan Africa — causes cirrhosis through immune-mediated hepatocyte destruction during periods of immune reactivation; antiviral therapy (tenofovir, entecavir) halts progression and in some cases allows fibrosis regression. Hepatitis C virus (HCV) — 20–30% of untreated chronically infected patients develop cirrhosis within 20–30 years; fibrosis regression occurs in 35–40% of patients achieving SVR with DAA therapy, including those with established cirrhosis. Non-alcoholic steatohepatitis (NASH) — the hepatic manifestation of metabolic syndrome (obesity, type 2 diabetes, dyslipidaemia, hypertension) — is the most rapidly growing cause of cirrhosis in the Western world and the leading indication for liver transplantation in some centres; weight loss of 7–10% of body weight significantly reduces NASH activity and fibrosis. Other causes: autoimmune hepatitis (ANA, anti-smooth muscle antibody, elevated IgG — treated with azathioprine and prednisolone); primary biliary cholangitis (PBC — anti-mitochondrial antibody, predominantly women; treated with ursodeoxycholic acid and obeticholic acid); primary sclerosing cholangitis (PSC — strongly associated with IBD; no effective medical therapy; liver transplantation); Wilson's disease (autosomal recessive copper metabolism disorder — Kayser-Fleischer rings, low caeruloplasmin; treated with D-penicillamine or trientine); haemochromatosis (HFE gene mutation — iron overload; treated with venesection).

Compensated cirrhosis may be asymptomatic. Decompensation presents with jaundice, ascites, peripheral edema, hepatic encephalopathy (confusion, asterixis), variceal bleeding, and spontaneous bacterial peritonitis. Spider angiomas, palmar erythema, gynaecomastia, and caput medusae are characteristic signs.Compensated cirrhosis may be entirely asymptomatic — discovered incidentally on imaging or routine blood tests showing thrombocytopenia (from hypersplenism), mildly elevated liver enzymes, and prolonged INR. Clinical signs detectable in compensated cirrhosis include hepatomegaly (initially; the liver may shrink as cirrhosis advances), splenomegaly, spider naevi (dilated superficial arterioles on the upper trunk and face — more than 5 is clinically significant), palmar erythema, leukonychia (white nails — from hypoalbuminaemia), terry's nails (proximal white, distal red-brown), Dupuytren's contracture, parotid enlargement, and gynaecomastia (in alcohol-related cirrhosis). Decompensation events: ascites (most common decompensation event, fluid accumulation in the peritoneal cavity from portal hypertension and reduced oncotic pressure); variceal bleeding (haematemesis from gastro-oesophageal varices — occurs in 30–40% of cirrhotic patients and carries 15–25% mortality per episode); hepatic encephalopathy (spectrum from mild cognitive impairment to deep coma — precipitated by constipation, gastrointestinal bleeding, infection, dietary protein excess, diuretics); jaundice (failure of bilirubin excretion indicating hepatic decompensation); and spontaneous bacterial peritonitis (SBP — infection of ascitic fluid with Gram-negative organisms from gut bacterial translocation — 20–30% in-hospital mortality).

Liver function tests, coagulation profile (INR), albumin, and platelet count reveal hepatic dysfunction. Liver ultrasound with Doppler assesses portal hypertension. Transient elastography (FibroScan) noninvasively measures liver stiffness. Liver biopsy remains the gold standard for staging fibrosis and confirming the etiology.Liver function tests (LFTs) in cirrhosis: elevated bilirubin (direct and indirect), elevated AST and ALT (though may be near-normal in 'burned out' cirrhosis), markedly reduced albumin (below 35 g/L), and prolonged INR (reduced prothrombin time from synthetic dysfunction). Serum albumin and INR provide the most sensitive markers of hepatic synthetic function — deterioration signals decompensation. Platelet count: thrombocytopenia (below 150,000/µL) from hypersplenism (portal hypertension causes splenomegaly with platelet sequestration) is an early and sensitive marker of clinically significant portal hypertension. Liver ultrasound with Doppler: assesses liver morphology (heterogeneous echogenicity, nodular surface, caudate lobe hypertrophy — classic cirrhotic features), portal vein diameter and flow velocity (portal hypertension), splenomegaly, and ascites. FibroScan (transient elastography): measures liver stiffness in kilopascals — above 8–10 kPa suggests significant fibrosis; above 12–15 kPa suggests cirrhosis; above 20 kPa indicates clinically significant portal hypertension. FIB-4 index (age × AST / [platelet count × √ALT]) — above 3.25 suggests advanced fibrosis. Liver biopsy (percutaneous or transjugular in coagulopathic patients): the gold standard for staging fibrosis (Metavir F0–F4) and confirming aetiology — reserved for diagnostic uncertainty or when non-invasive tests are discordant. Upper GI endoscopy (OGD): screens for oesophageal and gastric varices — grade I (small), II (moderate), III (large varices) — guides beta-blocker prophylaxis and band ligation decisions. Hepatocellular carcinoma (HCC) surveillance: 6-monthly liver ultrasound ± AFP in all cirrhotic patients — EASL and AASLD recommend surveillance for all compensated cirrhotic patients.

Treat the underlying cause: abstinence from alcohol, antiviral therapy for hepatitis B or C, weight loss for NASH, or immunosuppressants for autoimmune hepatitis. Manage complications: diuretics for ascites, beta-blockers for portal hypertension, lactulose for encephalopathy, antibiotics for SBP. Liver transplantation for end-stage disease.Treating the underlying cause: alcohol abstinence (can partially reverse fibrosis and dramatically reduces decompensation risk), antiviral therapy for HBV (tenofovir alafenamide — TAF — or entecavir — long-term suppression reduces HCC risk by 50–80%) or HCV (DAA therapy — achieving SVR reverses fibrosis in 35% and reduces liver-related mortality by 70%), weight loss for NASH (bariatric surgery in selected patients), immunosuppression for autoimmune hepatitis (prednisolone + azathioprine), ursodeoxycholic acid (UDCA) for PBC. Ascites management: low-sodium diet (below 5 g NaCl/day — 2 g sodium); diuretics — spironolactone 100–400 mg/day (aldosterone antagonist, first-line) + furosemide 40–160 mg/day; large-volume paracentesis (LVP) for tense refractory ascites with concomitant IV albumin 8 g/L of ascites drained (prevents post-paracentesis circulatory dysfunction); transjugular intrahepatic portosystemic shunt (TIPS) for refractory ascites or recurrent variceal bleeding — reduces portal pressure by creating a shunt between portal and hepatic veins. Variceal bleeding management: acute haemostasis — endoscopic band ligation (EBL) of oesophageal varices within 12 hours of presentation + terlipressin (vasopressin analogue, 2 mg IV every 6 hours for 5 days) or octreotide to reduce portal pressure; ceftriaxone 1 g IV daily for 7 days (prophylaxis against bacterial infection — reduces mortality); secondary prophylaxis — carvedilol or non-selective beta-blockers (propranolol) to prevent rebleeding; EBL at 2–4 weekly intervals until variceal eradication. Hepatic encephalopathy: identify and treat precipitant; lactulose (30–60 mL 2–4 times daily) as first-line — achieves 2–3 soft stools daily; rifaximin (550 mg twice daily) as second-line or add-on — reduces encephalopathy recurrence by 58% (NEJM, 2010); dietary protein not restricted in modern practice (protein reduces sarcopenia, which worsens prognosis). SBP: IV cefotaxime 2 g every 8 hours for 5 days; IV albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 (prevents hepatorenal syndrome — reduces mortality from 30% to 10%); long-term prophylaxis with norfloxacin 400 mg/day after the first SBP episode. Liver transplantation: indicated for decompensated cirrhosis with MELD score above 15–20 or MELD-Na above 11 points; contraindications include active alcohol use (most centres require 6 months abstinence), active malignancy outside Milan criteria, severe cardiopulmonary disease, and multi-organ failure. 5-year post-transplant survival exceeds 75–80%. Recurrence of underlying disease (HCV — eliminated with DAAs pre/post-transplant; NASH from obesity; ALD from ongoing alcohol use) must be prevented.

Portal hypertension leads to gastroesophageal varices (risk of life-threatening bleeding), ascites, and hepatorenal syndrome. Spontaneous bacterial peritonitis, hepatic encephalopathy, hepatopulmonary syndrome, and hepatocellular carcinoma (annual incidence 1-4% in cirrhosis) are major complications requiring close monitoring.Portal hypertension — defined as a hepatic venous pressure gradient (HVPG) above 10 mmHg — is the primary driver of cirrhosis complications. Gastro-oesophageal varices develop in 30–40% of compensated cirrhotics and carry a bleeding risk of 15–25% per year for large varices. Each variceal bleeding episode carries 15–25% in-hospital mortality — surviving patients have a 60–70% risk of rebleeding without secondary prophylaxis. Ascites — the most common complication (50% of cirrhotics develop ascites within 10 years) — impairs quality of life, increases infection risk, and indicates 2-year mortality of 40–50% without transplant. Spontaneous bacterial peritonitis (SBP) — neutrophil count above 250 cells/mm³ in ascitic fluid — occurs in 15–30% of hospitalised cirrhotics annually; polymicrobial SBP suggests secondary peritonitis from bowel perforation requiring urgent surgical assessment. Hepatorenal syndrome (HRS) — functional acute kidney failure from splanchnic vasodilation and renal vasoconstriction — occurs in 10% of cirrhotics and carries high short-term mortality without terlipressin + albumin treatment. Type 1 HRS (acute, rapidly progressive) has median survival of 2 weeks without treatment; Type 2 HRS is more gradual, associated with refractory ascites. Hepatocellular carcinoma (HCC): annual incidence 1–4% in cirrhotic patients — risk highest in HBV and HCV-related cirrhosis, NASH, and alcohol-related cirrhosis. HCC is amenable to curative resection (Child-Pugh A, solitary lesion below 2 cm) or locoregional therapy (TACE, radiofrequency ablation) in early stages; sorafenib or lenvatinib for advanced HCC. Hepatopulmonary syndrome (HPS) — intrapulmonary vascular dilatation causing hypoxaemia — and portopulmonary hypertension (PPH — elevated pulmonary artery pressure from portal hypertension) are specific complications affecting transplant candidacy.

Avoid excessive alcohol consumption and maintain a healthy weight to prevent NAFLD. Vaccinate against hepatitis A and B. Treat chronic hepatitis B or C infection early before cirrhosis develops. Regular surveillance with 6-monthly liver ultrasound and AFP for HCC detection is essential for all cirrhotic patients.Alcohol abstinence or strict limitation (below 14 units/week for women, 21 units/week for men) is the single most important modifiable risk factor for alcohol-related liver disease — complete abstinence is required once cirrhosis is established. Universal hepatitis B vaccination — three-dose schedule providing above 95% seroprotection — is the most effective strategy for preventing HBV-related cirrhosis; the global WHO target is 90% infant HCV vaccination coverage by 2030. Treat HCV infection with curative DAA therapy before cirrhosis develops — SVR eliminates HCV replication, prevents fibrosis progression, and substantially reverses established fibrosis. NASH prevention: maintain BMI below 25 kg/m², control type 2 diabetes (SGLT2 inhibitors and GLP-1 receptor agonists — semaglutide, liraglutide — reduce NASH activity and fibrosis), adopt Mediterranean diet, avoid fructose-rich beverages. Coffee consumption (4+ cups/day) is associated with 40% reduced cirrhosis risk across multiple cohort studies — mechanisms include antioxidant and anti-fibrotic properties of coffee polyphenols. HCC surveillance: 6-monthly liver ultrasound ± AFP for all cirrhotic patients — identifies HCC at resectable stage in 40–50% of surveilled patients versus 10–20% of unsurveilled patients.

Call 999 or go to A&E immediately for: vomiting blood (haematemesis) or passing black tarry stools (melaena) — signs of variceal or peptic ulcer bleeding, which is a life-threatening emergency requiring immediate endoscopy and resuscitation; sudden confusion, disorientation, or drowsiness in a patient with known cirrhosis (hepatic encephalopathy — may be triggered by infection, GI bleeding, constipation, or drugs); fever with abdominal pain and distension in a patient with known ascites (spontaneous bacterial peritonitis — SBP — requires immediate diagnostic paracentesis and IV antibiotics; untreated SBP has very high mortality); or rapidly increasing jaundice with systemic illness. See your hepatologist urgently for: rapidly accumulating ascites requiring repeated paracentesis, new confusion in a cirrhotic patient, or any abdominal mass or pain suggesting hepatocellular carcinoma. All patients with confirmed cirrhosis must attend regular hepatology follow-up for 6-monthly ultrasound and AFP (HCC screening), endoscopic variceal surveillance, and optimisation of prophylactic beta-blockers, lactulose, and rifaximin where indicated.