Hepatic Encephalopathy
Hepatic encephalopathy occurs when a damaged liver can no longer filter ammonia and other toxins from the blood. These substances accumulate and impair brain function, causing anything from mild confusion and forgetfulness to disorientation and, in severe cases, loss of consciousness. It is most common in people with cirrhosis, which remains a significant health burden due to high rates of hepatitis B and C and alcohol-related liver disease.
Key points
- Ammonia that a failing liver cannot convert to urea crosses into the brain and disrupts normal neural signalling.
- Identifying and resolving the event that triggered an episode, such as an infection or bleeding, matters just as much as treating the confusion.
- A gut-targeted antibiotic lowers ammonia by reducing the bacteria that produce it, helping prevent further episodes.
What drives the confusion
The liver normally converts ammonia, a by-product of protein digestion, into urea for excretion. When liver function is severely compromised, ammonia builds up in the bloodstream and crosses into the brain, disrupting normal neural signalling. Common triggers include gastrointestinal bleeding, infection, constipation, dehydration, or certain medications. Identifying and treating the trigger is as important as managing the encephalopathy itself.
Reducing ammonia with targeted treatment
The main goal of treatment is lowering ammonia levels and preventing episodes from recurring. Rifaximin, a minimally absorbed antibiotic that acts within the gut, reduces the ammonia-producing bacteria responsible for much of the toxic load. It is widely used to help prevent repeat episodes in people who have already had one.
Persistent or worsening confusion, inability to stay awake, or any rapid change in mental state warrants urgent medical attention.