One of the conditions that occurs with advanced liver disease caused by chronic alcohol abuse is hepatic encephalopathy. Hepatic encephalopathy is different from Wernicke-Korsakoff syndrome, another condition associated with long-term alcohol abuse that is caused by a severe thiamine (B1) deficiency. However, the two conditions may coexist and lead to alcohol-related dementia.

If liver disease is caught in time – a state in which the liver is fatty (too much fat is in the liver, which means the liver has to work harder to do its job), but not permanently scarred and damaged – and thiamine supplementation (usually intravenously) is given, many of the symptoms of Wernike-Karsokoff syndrome can be reversed. These include balance problems and weakness. However, memory loss (short-term) associated with Wernike-Karsokoff syndrome cannot be reversed.

To recover from fatty liver disease, all alcohol use must be completely stopped for the rest of the person’s life. The liver, over time, will heal, but other chronic conditions associated with long-term alcohol abuse may not be resolved completely or at all.

Once liver disease advances past the fatty liver stage, the damage to the liver cannot be reversed. As the liver stops functioning properly due to extensive scarring, it is likely that hepatic encephalopathy will occur.

Symptoms of extensive liver damage may not appear until liver disease is advanced beyond the point of no return. Symptoms of hepatic encephalopathy may be mild at first. They may include unexplained muscle weakness in the arms and legs, random tripping and falling while doing routine things, sporadic slurring of speech, slower thinking, difficulty finding common words, occasional confusion, less executive control (making more frequent bad judgment calls), and being more tired than usual.

As hepatic encephalopathy progresses, confusion increases, drowsiness or a lack of energy is prevalent, personality changes are severe, motor skills further decline, and fatigue is constant. Frequent seizures and severe anxiety may also occur.

All of these symptoms are related to how the liver and the brain work together, and they indicate that relationship has been severely disrupted.

As liver function deteriorates, the liver is not able to remove toxins from the system, so they get into the bloodstream and eventually travel to the brain, where they accumulate, and just like the buildup of the toxic proteins tau and beta amyloid that cause Alzheimer’s disease, they cause damage to the brain.

The key toxin that is associated with hepatic encephalopathy is ammonia. A blood test is all that’s required to see high levels of ammonia in the body. Ammonia is normally eliminated through the digestive system when the liver is functioning normally, but when liver function diminishes, ammonia stays in the digestive system and is then carried by blood throughout the rest of the body, including the brain.

Hepatic encephalopathy has five stages. In Stage 0, symptoms are minor. In Stage 1, symptoms are relatively mild, with only sleep pattern and attention span changes being noticeable. In Stage 2, symptoms are moderate, with the key changes being continual lethargy and times of being disoriented. In Stage 3, the ability to do basic tasks has disappeared. Severe personality changes develop and confusion increases. Stage 4, the last stage, is going into a coma, which will lead to death.

Hepatic encephalopathy can be managed with medication and its advancement can be halted with a combination of medication (lactulose, a laxative that keeps the digestive system clear, and rifaximin, an antibiotic which can help limit brain damage from severe liver disease) and total abstinence from alcohol, which will stop the progression of liver damage.

However, even when the medications are used to treat high ammonia levels in the bloodstream, hepatic encephalopathy will continue to worsen if alcohol is still be used. At this point, any amount of alcohol consumption is dangerous, because the liver is already so severely compromised.

The prognosis for survival of hepatic encephalopathy with continued alcohol use is very poor. Only 34% of people who have hepatic encephalopathy and continue to use alcohol will live a full year after diagnosis of the condition is made. Survival rates past one year after diagnosis plummet dramatically.

If you’ve abused alcohol for a long time, now is the time to work with a medical professional to stop drinking (suddenly stopping long-term alcohol abuse on your own is dangerous and can cause death within days of quitting because the body can’t handle the shock) and have your blood tested for ammonia buildup.

Honesty about your use of alcohol is extremely important. Underreporting the level of your alcohol use can delay getting the help and treatment you need, which can lead to further liver damage. 

Have your primary care physician get a nutritionist on board to develop a hepatic encephalopathy diet, which in part limits animal proteins, but includes a lot of vegetable and dairy proteins, to help with ammonia levels in the bloodstream.

Find support that works for you, but also keeps you accountable. Alcoholics Anonymous (AA) is a great place to start, but it may not be the best fit for you.

If AA is not a good fit, then have your primary care physician do a referral to a licensed therapist who specializes in alcohol addiction, because while alcoholism is a disease, with predisposition often being genetic, there are usually underlying traumas that led to the overuse of alcohol in the first place.

Don’t wait until it’s too late.