Cirrhosis !
Cirrhosis is the late stage of chronic liver damage, when scar tissue replaces normal liver; it leads to portal hypertension and liver failure.
Updated 2026-10-30
Structures involved
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In biochemistry
- Ammonia (ammonium)
- Alanine aminotransferase (ALT, GPT)
- Aspartate aminotransferase (AST, GOT)
- Glutamine synthetase
- Cori cycle
- Glucose–alanine cycle
- LCAT (lecithin–cholesterol acyltransferase)
- Bile acid synthesis
- Liver function tests: reading the pattern
- Aminotransferases (ALT and AST) as lab tests
- Gamma-glutamyl transferase (GGT) as a lab test
- Urea and blood urea nitrogen (BUN) as lab tests
- Serum albumin as a lab test
- Alpha-fetoprotein (AFP)
- Carcinoembryonic antigen (CEA)
- CA-125
- Nitrogen balance
- α-Amanitin
- Plasma proteins and electrophoresis
- Albumin
- α1-antitrypsin
- Vitamin K (phylloquinone)
Microorganisms that cause it
In histology
In embryology
In the clinical exam
- Abdominal inspection
- Abdominal percussion: liver span and tympany
- Ascites: shifting dullness and fluid wave
- Palpation of the liver and spleen
- Edema: pitting, grading and distribution
- Digital clubbing and nail signs
- Portal hypertension and the signs of chronic liver disease
- Jaundice: prehepatic, hepatic and posthepatic
- Dehydration and fluid overload
In physiology
- The coagulation cascade
- Coagulation tests: PT/INR, aPTT and platelets
- Thrombosis and bleeding: Virchow's triad and hemostatic defects
- Starling forces at the capillary
- How edema forms
- How the lymphatic system works
- Splanchnic and portal circulation
- Functions of the liver
- Sodium and extracellular volume regulation (with natriuretic peptides)
- Where and how diuretics act
- Mixed acid–base disorders
- Dehydration and fluid overload
- Pleural fluid: formation and drainage
Why it happens
- Alcohol: how it injures the liver, brain, heart and fetus
- Fibrosis in organs: TGF-β and the myofibroblast
- Liver regeneration
- Edema and effusions: the four mechanisms
- Tissue repair: regeneration or scar; labile, stable and permanent cells
- Precancerous conditions: when chronic inflammation, metaplasia or hyperplasia raise the risk
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What it is
The late stage of chronic liver injury, in which diffuse fibrosis and regenerative nodules replace normal liver structure, leading to portal hypertension and liver failure.
Who gets it
A major cause of death from liver disease worldwide. In Latin America, alcohol, metabolic dysfunction-associated steatotic liver disease (MASLD, rising with obesity and diabetes) and hepatitis B and C are the main causes. In Peru, cirrhosis-related morbidity rose from 52.3 to 117.9 per 100,000 (2004 to 2016) and mortality from 13.6 to 16.8 per 100,000 (2004–05 to 2015–16).
Causes
- Alcohol-related liver disease
- Chronic hepatitis B and C (hepatitis D with B)
- Metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD)
- Autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis
- Haemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency
- Budd-Chiari syndrome, chronic heart failure, drugs
Risk factors
- Harmful alcohol use
- Obesity, type 2 diabetes and metabolic syndrome
- Unsafe injections, transfusion before screening, sexual or perinatal hepatitis B exposure
- Family history of inherited liver disease
Pathophysiology
Repeated injury activates hepatic stellate cells, which lay down collagen; fibrous septa and nodules distort the sinusoids. Resistance to portal flow plus splanchnic vasodilation cause portal hypertension, with collaterals (oesophageal varices), splenomegaly and ascites. Loss of hepatocyte function reduces albumin and clotting factors and impairs ammonia and bilirubin clearance.
Classification
- Compensated vs decompensated (ascites, variceal bleeding, encephalopathy or jaundice)
- Child-Pugh class A, B or C: bilirubin, albumin, INR, ascites and encephalopathy
- MELD (or MELD-Na) score: bilirubin, INR, creatinine (and sodium), used for prognosis and transplant priority
Symptoms and signs
- Often silent while compensated
- Fatigue, weakness, loss of appetite and muscle wasting
- Jaundice and itching
- Abdominal swelling (ascites), leg oedema
- Spider angiomas, palmar erythema, gynaecomastia, testicular atrophy
- Easy bruising; caput medusae and splenomegaly from portal hypertension
- Confusion, sleep inversion and flapping tremor (asterixis) in hepatic encephalopathy
Diagnosis
- Clinical
- History of alcohol, hepatitis risk and metabolic disease; signs of chronic liver disease and portal hypertension. Assessment of decompensation and severity with Child-Pugh and MELD.
- Tests
- Liver tests, bilirubin, albumin, INR, platelet count (low with hypersplenism), creatinine and sodium. Cause work-up: hepatitis B and C serology, autoantibodies, ferritin and transferrin saturation, ceruloplasmin, alpha-1 antitrypsin. Non-invasive fibrosis scores (FIB-4, APRI); diagnostic paracentesis for ascites. Biopsy if the cause is unclear.
- Imaging
- Ultrasound with Doppler: nodular liver surface, splenomegaly, ascites, portal vein flow and thrombosis, and screening for liver masses. Transient elastography measures stiffness. CT or MRI to characterise nodules. Upper endoscopy looks for varices.
Differential diagnosis
- Non-cirrhotic portal hypertension (e.g., portal vein thrombosis, schistosomiasis)
- Acute hepatitis or acute liver failure
- Heart failure or constrictive pericarditis (congestive hepatopathy)
- Peritoneal carcinomatosis or tuberculous peritonitis (ascites)
- Nephrotic syndrome
Goal of treatment
Remove or control the cause, prevent and treat the complications of portal hypertension and liver failure, detect liver cancer early and refer suitable patients for transplantation.
Treatment
- Medical
- Treat the cause: alcohol abstinence with support, antivirals for hepatitis B and C, weight loss and metabolic control in MASLD, immunosuppressants in autoimmune hepatitis.
- Medical
- Non-selective beta-blockers to lower portal pressure and prevent variceal bleeding; diuretics (an aldosterone antagonist, often with a loop diuretic) and sodium restriction for ascites.
- Procedure
- Large-volume paracentesis with intravenous albumin for tense or refractory ascites; endoscopic band ligation for varices.
- Medical
- Acute variceal bleeding: resuscitation, vasoactive drugs (somatostatin analogues or vasopressin analogues), antibiotic prophylaxis and urgent endoscopy. Lactulose, with rifaximin if needed, for encephalopathy; antibiotics for spontaneous bacterial peritonitis.
- Procedure
- TIPS (transjugular intrahepatic portosystemic shunt) for refractory ascites or recurrent or uncontrolled variceal bleeding in selected patients.
- Follow-up
- Surveillance for hepatocellular carcinoma with ultrasound about every six months (with or without alpha-fetoprotein), endoscopic screening for varices, and regular review of nutrition and kidney function.
- Surgical
- Liver transplantation for decompensated cirrhosis or limited liver cancer, prioritised by the MELD score.
- Lifestyle
- Adequate protein and calorie intake, avoidance of alcohol and of hepatotoxic or nephrotoxic drugs (e.g., NSAIDs), and vaccination against hepatitis A and B, pneumococcus and influenza.
Drugs for this condition
- Rifaximin
- Ribavirin
- Sofosbuvir + velpatasvir
- Terlipressin
- Lactulose
- Human albumin
- Furosemide
- Spironolactone
- Bumetanide
- Chlorothiazide
Complications
- Ascites and spontaneous bacterial peritonitis
- Variceal bleeding (oesophageal or gastric)
- Hepatic encephalopathy
- Hepatorenal syndrome and hyponatraemia
- Hepatocellular carcinoma
- Portal vein thrombosis, hepatopulmonary syndrome, portopulmonary hypertension
- Malnutrition, sarcopenia and infections
Prognosis
Compensated cirrhosis can stay stable for years, especially if the cause is removed. Once decompensation occurs, survival falls markedly without transplantation; Child-Pugh and MELD scores estimate the risk.
Prevention
- Limiting alcohol use
- Hepatitis B vaccination and screening and treatment of hepatitis B and C
- Prevention and treatment of obesity and diabetes
- Safe injection and transfusion practices
Test yourself
Think of the answer, then tap the question to see it.
Which variables make up the Child-Pugh score?
Bilirubin, albumin, INR (or prothrombin time), ascites and hepatic encephalopathy.
Which laboratory values are used in the MELD score?
Bilirubin, INR and creatinine; MELD-Na also adds serum sodium.
Which drug class is used to prevent first variceal bleeding in cirrhosis?
Non-selective beta-blockers; endoscopic band ligation is the alternative or complement.
What finding on diagnostic paracentesis defines spontaneous bacterial peritonitis?
An ascitic fluid neutrophil count of 250 cells/mm³ or more, without a surgical source of infection.
Why do patients with cirrhosis need ultrasound surveillance about every six months?
To detect hepatocellular carcinoma early, when curative treatment is still possible.
Related conditions
- Upper gastrointestinal bleeding
- Portal hypertension
- Viral hepatitis
- Hepatocellular carcinoma
- Heart failure
- Umbilical hernia
- Peritonitis
- Haemorrhoids
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Hepatic Cirrhosis (StatPearls (NCBI Bookshelf), 2022); Morbimortality Associated with Liver Cirrhosis in Peru: An Ecological Analysis for the Period of 2004-2016 (International journal of environmental research and public health, 2022) · adapted, CC BY 4.0.
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Representative model, for educational purposes only.
