Sign of end-End Stage Liver Disease

First, its nice to meet you'all. Just sorry we all seem to be facing this horrible disease.

My father was diagnosed in February 2009 with liver cancer, hep c & cirrosis. He was given 3-6 months then.

What I'm needing to know is...without further treatment how long does he have? We aren't wanting to speed up his passing but we are getting so tired and do not want to see him suffer longer.

He's not a transplant candidate, can't be resectioned & has had chemoemobolization. He is also on Nexavar & Laculose.

He is only eating sweets and drinking tea. Anything else makes him sick and those two things don't always stay down. He is starting to have severe pain in the liver area now.

Thanks for all replies. We just want to know what to expect.

Dad has already been near coma level once because of his ammonia. The doctor put him on laculose that has helped. But now he has constant diareahha even without it.

It is so nice to have someone to talk to that is experiencing the same things.

God Bless everyone and have a wonderful Christmas.

Doglover1961, Welcome.

Having just been through this process with my father the journey ahead may be a rough one. My father was told he had 12 months to 3 years. He passed away after 14 months.

My father also had numerous encephalopathy turns and significant mood changes.

In a similar fashion to Pink Grandma my father slipped into a coma and passed away in less than 48 hours.

I did a lot of reading on end stage liver disease and found this forum to be fantastic support. Even from the perspective of knowing there are others out there in the same position as you.

In terms of what to expect – that is a tricky one. If your fathers situation is not good then it is very difficult to know what to expect. Part of my battle was to understand what the liver actually did and what happens when it does not work properly.

I found the information below in explaining some of the issues of increased ammonia in the body:

Hepatic encephalopathy is a major neuropsychiatric complication of chronic liver disease that occurs when large amounts of ammonia accumulate within brain tissues. Ammonia is normally produced by the breakdown of protein in the bowel, and in healthy individuals it is metabolized by the liver to form urea. In patients with significant portal hypertension, blood cannot pass into the liver and the ammonia enters the systemic circulation where it enters brain tissues. Hepatic encephalopathy and its final stage, hepatic coma, occur in 4 stages.

• In the first stage, the patient may exhibit mild confusion, mood changes, inability to concentrate, sleep disturbances, and mild asterixis: rapid involuntary flapping of the wrists, also known as "liver flap."
• In stage two, the patient experiences confusion, apathy, aberrant behavior, asterixis and apraxia: problems in carrying out familiar, purposeful movements.
• Stage three is characterized by severe confusion, incoherence, diminished responsiveness to verbal stimuli, and hyperactive deep tendon reflexes.
• Hepatic coma occurs in the last stage: the patient has no reaction to painful stimuli, no corneal reflex, dilated pupils, and assumes the flexion or extension posture characteristic of severe brain damage.

Correcting pH and electrolyte disturbances, restricting dietary protein, preventing constipation, and preventing gastrointestinal bleeding are methods used to treat hepatic encephalopathy in its early stages. When bleeding occurs in the gastrointestinal tract, bacterial action creates increased ammonia. Sterilizing the bowel by giving neomycin, a drug that is poorly absorbed from the gastrointestinal tract, may prevent ammonia formation by decreasing bacterial counts. Lactulose may also be given to help contain ammonia in the gastrointestinal tract where it can be excreted in the feces.

I hope this information helps - Come back to the forum and ask as many questions as you like.