Synopsis
Recognise overt hepatic encephalopathy, protect the deteriorating patient, identify reversible precipitants, and prevent recurrence without mistaking a clinical syndrome for an ammonia result.
- Hepatic encephalopathy is a clinical neuropsychiatric syndrome caused by liver insufficiency or portosystemic shunting after competing explanations have been considered.
- Asterixis supports metabolic encephalopathy but is neither specific to liver disease nor reliably present in deep coma.
- Search actively for infection, gastrointestinal bleeding, constipation, dehydration, acute kidney injury, electrolyte disturbance and medicines that depress cognition.
Key red flags
Disorientation to time or place, inappropriate behaviour, lethargy and asterixis suggest overt encephalopathy, but fever, focal signs, head injury or meningism should redirect urgent investigation.
Investigation priorities
Detect immediately reversible coma and quantify acute physiological compromise.
Management branches
A person with cirrhosis or portosystemic shunting develops new disorientation, somnolence or coma.
- Perform ABCDE assessment, check glucose, record Glasgow Coma Scale and West Haven features, obtain intravenous access, and call for senior help if airway protection is doubtful.
- Stop or withhold non-essential sedatives and nephrotoxic or volume-depleting medicines while assessing bleeding, sepsis, renal injury, electrolyte imbalance and recent alcohol or drug exposure.
Key medicines
Lactulose oral solutionInitially 30–45 mL three or four times daily for hepatic encephalopathy, then adjust to produce two or three soft stools daily; follow the current SmPC and local acute pathway.
Rifaximin 550 mg tabletsTake 550 mg twice daily when prescribed by the specialist service to reduce recurrence of overt hepatic encephalopathy; review continued need and adherence according to the local pathway.