Conditions · Gastroenterology and hepatology
Hepatic encephalopathy !
A reversible brain dysfunction caused by liver failure, when toxins such as ammonia reach the brain. It ranges from subtle confusion to coma.
Updated 2026-11-01
Structures involved
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In the clinical exam
- Mental status: orientation, attention and screening tests
- Portal hypertension and the signs of chronic liver disease
Why it happens
- Functions of the liver
- Splanchnic and portal circulation
- Urea cycle
- Ammonia (ammonium)
- Glutamine synthetase
What it is
A spectrum of neuropsychiatric changes caused by liver insufficiency or portosystemic shunting, after other brain causes are excluded. It is a common reason for hospital admission in cirrhosis.
Who gets it
Overt encephalopathy affects a large share of people with cirrhosis during their illness, and minimal (covert) encephalopathy is even more frequent. In Colombia and Latin America the main underlying causes are alcohol-related liver disease, metabolic dysfunction-associated steatotic liver disease and chronic viral hepatitis.
Causes
- Cirrhosis with portal hypertension (most cases)
- Acute liver failure
- Portosystemic shunts, including after TIPS placement
- Precipitants: GI bleeding, infection (including spontaneous bacterial peritonitis), constipation, dehydration, hypokalaemia and alkalosis, sedatives and opioids, kidney injury
Risk factors
- Advanced cirrhosis (Child-Pugh B or C)
- Previous episode of encephalopathy
- TIPS or large spontaneous shunts
- Overuse of diuretics, hyponatraemia
- Use of benzodiazepines or other sedatives
Pathophysiology
Ammonia made by gut bacteria and intestinal glutamine metabolism normally reaches the liver through the portal vein and is cleared in the urea cycle. When liver function fails or blood bypasses the liver, ammonia reaches the brain, where astrocytes convert it to glutamine and swell. Inflammation, altered neurotransmission (increased GABA-ergic tone) and manganese deposition in the basal ganglia add to the dysfunction.
Classification
- West Haven grade 1: mild confusion, short attention span, sleep inversion
- Grade 2: lethargy, disorientation to time, inappropriate behaviour, asterixis
- Grade 3: somnolence but rousable, marked confusion, gross disorientation
- Grade 4: coma
- Covert (minimal and grade 1) versus overt (grades 2 to 4); episodic, recurrent or persistent
Symptoms and signs
- Day-night sleep reversal, forgetfulness and poor concentration
- Personality change, irritability or inappropriate behaviour
- Confusion and disorientation
- Asterixis (flapping tremor of the outstretched hands)
- Slurred speech, drowsiness and, in severe cases, coma
- Fetor hepaticus (sweet, musty breath)
Diagnosis
- Clinical
- A clinical diagnosis in a person with liver disease: mental status, West Haven grading, asterixis, and a search for precipitants (bleeding, infection, constipation, drugs, electrolytes). Other causes of altered mental status must be excluded.
- Tests
- Glucose, electrolytes, kidney function, blood count, cultures and diagnostic paracentesis when ascites is present. A raised ammonia supports the diagnosis but a normal value makes it unlikely; ammonia does not grade severity. Psychometric tests detect covert encephalopathy.
- Imaging
- Head CT when there are focal signs, trauma, a first episode or no response to treatment, to exclude haemorrhage. MRI may show pallidal hyperintensity on T1.
Differential diagnosis
- Hypoglycaemia and other metabolic encephalopathies (uraemia, hyponatraemia)
- Intracranial bleeding (subdural haematoma after falls)
- Wernicke encephalopathy and alcohol withdrawal
- Drug intoxication (sedatives, opioids, alcohol)
- Sepsis-associated encephalopathy or CNS infection
Goal of treatment
Identify and correct the precipitating factor, lower gut ammonia production and absorption, protect the airway in deep encephalopathy, and prevent recurrence.
Treatment
- Acute
- Treat the precipitant: control bleeding, treat infection, correct dehydration and electrolytes, stop sedatives and diuretics if needed; airway protection and ICU care in grade 3 or 4.
- Medical
- Non-absorbable disaccharides (lactulose) are first line, titrated to two or three soft stools per day; rifaximin is added to prevent recurrence. Lactulose enemas are used when oral intake is not possible.
- Lifestyle
- Adequate protein and energy intake with small frequent meals and a late-evening snack; protein restriction is no longer advised.
- Follow-up
- Nursing care: neurological checks and grading, stool count, fluid balance and electrolytes, aspiration and fall precautions, and avoiding sedatives.
- Surgical
- Liver transplantation is considered in recurrent or persistent encephalopathy with advanced liver disease.
Drugs for this condition
Complications
- Aspiration pneumonia
- Falls and injuries
- Recurrent episodes and loss of independence
- Cerebral oedema with raised intracranial pressure (mainly in acute liver failure)
- Impaired driving and work performance in covert encephalopathy
Prognosis
Episodes are usually reversible when the trigger is treated, but overt encephalopathy marks advanced liver disease and predicts poor survival without transplantation.
Prevention
- Secondary prophylaxis with lactulose, plus rifaximin after recurrence
- Avoiding constipation, dehydration, sedatives and excessive diuretics
- Early treatment of infections and GI bleeding in cirrhosis
Test yourself
Think of the answer, then tap the question to see it.
What is the key toxin implicated in hepatic encephalopathy?
Ammonia from the gut, which bypasses or escapes a failing liver and is converted to glutamine in astrocytes, causing swelling.
What classic sign is seen in grade 2 hepatic encephalopathy?
Asterixis: a flapping tremor of the outstretched, dorsiflexed hands, with lethargy and disorientation.
What are three common precipitants of hepatic encephalopathy?
GI bleeding, infection (such as spontaneous bacterial peritonitis), constipation; also dehydration, hypokalaemia and sedatives.
What is the first-line drug treatment and its nursing target?
Lactulose, adjusted to two or three soft bowel movements per day; rifaximin is added to prevent recurrence.
Is a normal blood ammonia useful in a confused patient with cirrhosis?
Yes: a normal ammonia makes hepatic encephalopathy unlikely and should prompt a search for another cause.
Related conditions
- Cirrhosis
- Portal hypertension
- Acute liver failure
- Ascites and spontaneous bacterial peritonitis
- Upper gastrointestinal bleeding
- Alcoholic liver disease (biochemistry)
- Wernicke encephalopathy (thiamine deficiency)
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Loss of brain function - liver disease: MedlinePlus Medical Encyclopedia (MedlinePlus (U.S. National Library of Medicine), 2025).
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