Blood ammonia of 285

[JimiWitter]

I have ESLD and have had hidden hep c for 25 years. Never have consumed alcohol, but did smoke pot. My bili levels were at 5.4, INR 2.1, my ammonia level is currently 286, have some cloudiness, blurred vision, etc. I have had up to 7 litres of ascitic fluid per week. I'm on IV infused ulbumin, because of a lab value of 2. It seems over the winter months everything gets worse and I spend summer recovering. My albumin level is at 3.9 now, my liver function values have drastically improved and my meld went from 26 to 15. I'm on Xifaxin 550 PID and lactulose. But my ammonia stays high. The last blood draw, the blood looked like a purplish bloody marry. Any ideas as to why the blood discoloration and high ammonia. I'm also on my own low sodium/low protein diet. Thanks for your consideration in this matter.

[HectorSF]

Wow. Looks like you are in good hands. Which is super important.
Looks like we eat about the same foods. Your HE sounds like mine. Mostly minimal HE with a few flairs now and then. Have you ever experienced "Asterixis" (flapping tremor)? a tremor of the wrist when your wrists are extended like to stop a car? I never have as yet. It is amazing your ammonia is so high yet you have minimal HE symptoms. But it is a good thing.

It sounds like a good plan your docs have.

Thanks for mentioning "blurred vision". I have that too. Some days I can see anything. It's crazy. Everything it a blur. Of course I don't tell anyone. They'd think I was nuts. Their probably right too.
"turn of the switch temper and attitude" Great saying. Oh don't I know it. One minute I am having one of my "melt downs" crying uncontrollably creating rivers of tear drops then I'm laughing hysterically about a joke a saw. Looney tunes time. Tweetie Pie - "You'd be puny too if all you ate was birdseed!" Sometimes noises sound so loud it hurts my head just hearing it. I figure I should at least get a laugh out of this disease. There is plenty of pain, misery, fear, etc. to go around

That is great your docs are willing to have you try treatment. That is extremely rare since technically you are decompensated. The new meds are available now so you should try to treat when you are relatively healthy. Do you know if they will transfuse you to raise your platelet count? It will be tough but if you can either avoid or delay transplant it is well worth it. I was going to do the same treatment here at UCSF. I was completing my last time before starting treatment and boom, I was diagnosed with liver cancer (HCC) June 1st. So "the save my liver option" is no longer an option for me. (The only cure for HCC is transplant).

Hang in there. I think it is great that you have a reduced MELD now. Some where around 20 I found I felt so much worse then now. My MELD is only 12. Which is great cause I can function quite will most of the time. So it is now the cancer that will kill me way before my liver fails.

Best -
Hector

[JimiWitter]

Thanks so much for the info. I was taken off the transplant list, because in Charlotte if the meld drops below 18 with improved liver enzyme function, you are removed. I am working with Chapel Hill now and things look promising. The lactulose does work, but only 2 to 3 loose stools a day. I have several spinal fusions with serious nerve damage, and on 120 mgs of oxycontin a day, have been at same amount for 7 years. This leads to come constipation. Diet is chicken/fish/white meat pork. Steamed varied veggies and lots of fruit. Little to none processed foods. Beverages are skim milk,no sugar added natural fruit juices, filtered water, some coffee. I really don't feel that bad. A little fuzzy in the head, some memory issues, mild motor function manipulation, turn of the switch temper and attitude. Small things are more aggravating than usual. I have an excellent hepatology team in my corner. My Dr. For now wants just to maintain an even keel, he hopes for treatment cures to become available for geno type 1. He feels even with the severity of advancement my hep c has shown, that I am still quite strong and the healthiest terminally I'll patient he has ever encountered. He thinks I may be able to avoid transplant. Other than portal hypertension, splenomegaly and my back and neck issues, I'm pretty healthy. Not overweight, no heart concerne's, lungs great, the ammonia is the stubborn one. Guess I'll just keep on keeping on, lol. Thanks again for the info and link, very much appreciated.
JimiWitter

[HectorSF]

Here is a link to a good current article on HE and ammonia.

http://www.medscape.com/viewarticle/722010

Treatment Options for Hepatic Encephalopathy - Thomas D. Schiano, M.D.

Excerpts:

Abstract

Few formal treatment guidelines exist for managing hepatic encephalopathy. The nonabsorbable disaccharide, lactulose, is considered the first-line therapeutic agent for treating hepatic encephalopathy. Acidification of the gastrointestinal tract is the principal mechanism by which the drug inhibits production of ammonia by coliform bacteria.

Elevated ammonia levels are seen in more than 80% of patients with hepatic encephalopathy. Systemic antibiotics, primarily neomycin, have also been employed to reduce bacterial production of ammonia, but associated adverse events limit their use in patients with hepatic encephalopathy. The semisynthetic, nonsystemic antibiotic, rifaximin, was approved in March 2010 by the United States Food and Drug Administration for the treatment of overt hepatic encephalopathy. Rifaximin decreases intestinal production and absorption of ammonia by altering gastrointestinal flora and is almost completely excreted unchanged in the feces. Rifaximin has been effective in improving behavioral, laboratory, mental, and intellectual abnormalities in patients with hepatic encephalopathy. The drug was compared with lactulose in well-designed clinical studies in patients with hepatic encephalopathy. Rifaximin was generally found to be equal or superior to lactulose in these studies. Although dosages have varied, most medical centers use a dosage of rifaximin 400 mg 3 times/day for hepatic encephalopathy. Recent clinical trials have used 550 mg twice/day in order to improve patient compliance. Additional clinical trials are being undertaken to further define the efficacy and safety of rifaximin in hepatic encephalopathy.

Introduction

Initial treatment protocols, going as far back as the 1970s, lacked a formal definition of hepatic encephalopathy, grading scales for the disease, and results from placebo-controlled clinical studies. These deficiencies have limited the formation of treatment guidelines, particularly when measuring the effects of newer therapies. Published studies over the last 10 years have exploded in number, further underlying the need for evidence-based reviews of treatment strategies for hepatic encephalopathy. Such reviews, however, would go far beyond the scope of this brief overview of currently available treatment options.

Therapy that reduces ammonia levels has received a great amount of attention because elevated levels are seen in more than 80% of patients with hepatic encephalopathy. Although removal of ammonia appears to be important in the treatment of hepatic encephalopathy, the relationship between ammonia levels and the pathogenesis of the disease has yet to be confirmed. On the other hand, an elevated ammonia level above 250 μmol/L in an individual with fulminant hepatic failure is a key issue and bodes for an extremely poor prognosis. However, the disease pathophysiology in patients with fulminant hepatic failure is different from that of patients with hepatic encephalopathy.

Treatment for hepatic encephalopathy includes ruling out nonhepatic causes of diminished mental function; providing specialized nursing care that includes frequent neurological checks; treating precipitating factors, such as sepsis and electrolyte disturbances; initiating therapy based on the ammonia hypothesis; and managing severe hepatic encephalopathy in the intensive care unit (ICU), if possible. This article will review several treatment modalities available for hepatic encephalopathy, with particular emphasis on rifaximin dosed twice/day.....

Conclusion

Lactulose remains the first-line agent for both acute episodic and persistent hepatic encephalopathy. Rifaximin is the second-line agent, either when used alone or in combination with lactulose. Results of several clinical studies suggest that rifaximin 400 mg 3 times/day or 550 mg twice/day is suitable for the treatment of hepatic encephalopathy, is very well tolerated, and is at least as effective as other commonly used agents such as lactulose or neomycin. More data are needed to assess the effects of rifaximin alone versus rifaximin combined with lactulose, particularly in patients with MHE. Additional well-controlled clinical trials are being conducted to further define the efficacy and safety of rifaximin for hepatic encephalopathy.

Hector