Liver failure: acute, chronic and acute-on-chronic
- Topic
When most of the liver stops working, toxins build up, blood stops clotting, the brain clouds and the kidneys may fail.
What it is
Liver failure is the loss of most hepatic function. It can be acute (in a person without prior liver disease, with encephalopathy and coagulopathy within weeks), chronic (the end of cirrhosis), or acute-on-chronic (a sudden insult on top of cirrhosis, with multiorgan failure). The clinical picture comes from the functions the liver no longer performs: clearing bilirubin, ammonia and hormones, and making albumin and clotting factors.
Step by step
- Massive hepatocyte loss (acute) or scar replacing most parenchyma (chronic) removes functional mass.
- Bilirubin, ammonia and estrogens are no longer cleared: jaundice, encephalopathy, signs of hyperestrogenemia.
- Synthesis falls: low albumin (edema, ascites) and low clotting factors (bleeding, raised INR).
- Splanchnic vasodilation lowers effective blood volume; the kidneys vasoconstrict: hepatorenal syndrome.
- Gut bacteria and endotoxins pass the failing liver: infections and spontaneous bacterial peritonitis.
- A trigger on cirrhosis (infection, alcohol, bleeding) can tip it into acute-on-chronic liver failure with multiorgan failure.
The three forms of liver failure
| Form | Setting | Typical causes | Liver at pathology |
|---|---|---|---|
| Acute liver failure | No prior liver disease; encephalopathy within weeks | Acetaminophen, idiosyncratic drugs, viral hepatitis A, B, E, autoimmune hepatitis, ischemia, Wilson disease | Massive or submassive necrosis (or microvesicular steatosis) |
| Chronic liver failure | End stage of chronic disease | Viral hepatitis, alcohol, MASLD, biliary and metabolic disease | Cirrhosis |
| Acute-on-chronic liver failure | Sudden decompensation of known cirrhosis | Infection, alcoholic hepatitis, bleeding, flare of hepatitis B | Cirrhosis plus new injury |
Clinical notes
- Jaundice, ascites, edema, bruising, confusion, fetor hepaticus.
- Liver transplantation is the definitive treatment of irreversible failure.
In the lab
- Prothrombin time/INR and bilirubin rise; albumin falls; ammonia may rise.
- Very high aminotransferases suggest acute necrosis (toxic, viral, ischemic); they may be near normal in end-stage cirrhosis.
Test yourself
Think of the answer, then tap the question to see it.
What two features define acute liver failure?
Hepatic encephalopathy and coagulopathy developing within weeks of onset in a person with no previous liver disease.
Why do kidneys fail in hepatorenal syndrome if they look normal?
Splanchnic vasodilation lowers effective blood volume and the renal arteries constrict intensely; the failure is functional, not structural.
Why do men with cirrhosis develop gynecomastia and spider angiomas?
The failing liver clears estrogens poorly, so estrogen levels rise relative to androgens.
What is the most common cause of acute liver failure in many high-income countries?
Acetaminophen toxicity, a dose-dependent hepatotoxin.
Elsewhere in DurgiPedia
- Functions of the liver
- Liver function tests: reading the pattern
- Ammonia (ammonium)
- Urea cycle
- Serum albumin as a lab test
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Loss of brain function - liver disease: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Hepatorenal syndrome: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026).
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Representative model, for educational purposes only.