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Effects of Amonia Levels in the Liver
Are the effects of elevated amonia levels reversible? After the the levels have been brought back down and other complications due to the levels will a person not be confused and unresponsive? Someone I love dearly had ulcers the were bleeding in the lower part of her esophagus. That and the history of a liver disease caused the amonia levels to get high enough that she was comatose. They got the levels down and removed her ventillator but she still has a blank stare and is not responsive. Are there cases where people don't regain their mental capacity or is it completley reversible?
Have your friend discuss the drug, ‘Rifaximin’ (xifaxan) with her care providers:
http://www.hivandhepatitis.com/hep_c/news/2010/040610_a.html
“SUMMARY: The U.S. Food and Drug Administration (FDA) recently announced the approval of a new indication for the antibiotic rifaximin (Xifaxan) as a therapy to prevent recurrence of hepatic encephalopathy, a type of brain impairment associated with advanced liver dysfunction, as can occur in people with chronic hepatitis B or C. A recently published study showed that rifaximin performed better than placebo at maintaining remission in patients who had experienced at least 2 episodes of hepatic encephalopathy during the prior 6 months”
Ultimately, though, the cause of the disease will need to be remedied; her elevated ammonia level is a symptom, and not a cause.
Good luck to you and your friend-
Bill
http://www.hivandhepatitis.com/hep_c/news/2010/040610_a.html
“SUMMARY: The U.S. Food and Drug Administration (FDA) recently announced the approval of a new indication for the antibiotic rifaximin (Xifaxan) as a therapy to prevent recurrence of hepatic encephalopathy, a type of brain impairment associated with advanced liver dysfunction, as can occur in people with chronic hepatitis B or C. A recently published study showed that rifaximin performed better than placebo at maintaining remission in patients who had experienced at least 2 episodes of hepatic encephalopathy during the prior 6 months”
Ultimately, though, the cause of the disease will need to be remedied; her elevated ammonia level is a symptom, and not a cause.
Good luck to you and your friend-
Bill
how can you get them down so they will not go up again. My good friend has a high amonia level and I would like to know what she can do besides lactolose that the dr is giving her. she lives in the nursing home and we are like sisters. can anyone help me understand this problem so I can help her too. Her liver does not work properly and maybe this is the cause and we can't do anything about it. she never drank so that can't be the problem. She has been on lactolose for 4 weeks now and it went up 2 points. How can this be?
WILL IT EVER GO DOWN...PLEASE HELP THANKS
WILL IT EVER GO DOWN...PLEASE HELP THANKS
yes, reversible, I got mine down to 1/5 of it's original level.
diet is key, probiotics, and sometime lactulose, though I believe diet and probiotics are safer and should be tried first unless yours is very high.
search for ammonia levels in this forum and read the threads.
Mainly lower protein intake to 2-3 oz. per meal... and increase bowel movements by increasing fiber and focusing on a healthy colon.
If you add yogurt, veggies and fruits, fiber tablets etc and get to 1-3 evacuations pr. day you should be able to get along without lactulose until well into ESLD.
mb
diet is key, probiotics, and sometime lactulose, though I believe diet and probiotics are safer and should be tried first unless yours is very high.
search for ammonia levels in this forum and read the threads.
Mainly lower protein intake to 2-3 oz. per meal... and increase bowel movements by increasing fiber and focusing on a healthy colon.
If you add yogurt, veggies and fruits, fiber tablets etc and get to 1-3 evacuations pr. day you should be able to get along without lactulose until well into ESLD.
mb
Dear Hector, thank you so much for posting, I have learned much from you and do appreciate
Happy Holidays
Dorene
Happy Holidays
Dorene
More info on hepatic encephalopathy including causes (such as upper GI bleeding), coma and HE and stages of HE.
Common Precipitants of Hepatic Encephalopathy
Some patients with a history of hepatic encephalopathy may have normal mental status while under treatment. Others have chronic memory impairment in spite of medical management. Both groups of patients are subject to episodes of worsened encephalopathy. One of the common precipitating factors is:
... * Gastrointestinal bleeding: The presence of blood in the upper gastrointestinal tract results in increased ammonia and nitrogen absorption from the gut. Bleeding may predispose to kidney hypoperfusion and impaired renal function. Blood transfusions may result in mild hemolysis, with resulting elevated blood ammonia levels.
**** So the bleeding from ulcers could trigger an episode of hepatic encephalopathy (HE) in a patient with cirrhosis and HE to begin with.***
Management of Hepatic Encephalopathy
Approach Considerations The approach to the patient with hepatic encephalopathy depends upon the severity of mental status changes and upon the certainty of the diagnosis. As an example, a patient with known cirrhosis and mild complaints of decreased concentration might be served best by an empiric trial of rifaximin or lactulose and a follow-up office visit to check its effect.
**** However, the patient presenting in hepatic coma requires a different approach. General management recommendations include the following:
* Patients with severe encephalopathy (ie, grade 3 or 4) who are at risk for aspiration should undergo prophylactic endotracheal intubation. They are optimally managed in the intensive care unit.
* Precipitants of hepatic encephalopathy, such as metabolic disturbances, gastrointestinal bleeding, infection, and constipation, should be corrected.
* Exclude nonhepatic causes of altered mental function.
* Consider checking an arterial ammonia level in the initial assessment of a hospitalized patient with cirrhosis and with impaired mental function. Ammonia levels have less use in a stable outpatient.
* Precipitants of hepatic encephalopathy, such as metabolic disturbances, gastrointestinal bleeding, infection, and constipation, should be corrected.
* Avoid medications that depress central nervous system function, especially benzodiazepines. Patients with severe agitation and hepatic encephalopathy may receive haloperidol as a sedative. Treating patients who present with coexisting alcohol withdrawal and hepatic encephalopathy is particularly challenging. These patients may require therapy with benzodiazepines in conjunction with lactulose and other medical therapies for hepatic encephalopathy.
* Fanelli et al investigated the efficacy of using an hourglass-shaped expanded polytetrafluoroethylene (ePTFE) stent-graft to treat patients whose hepatic encephalopathy was refractory to conventional medical therapy.22 In the study, 12 patients who, subsequent to receiving a transjugular intrahepatic portosystemic shunt, had developed refractory hepatic encephalopathy underwent shunt reduction with the stent-graft.
* The reduction procedure immediately produced a portosystemic gradient increase in the above study's patients, who, within 18-26 hours after insertion of the stent-graft, no longer exhibited symptoms of hepatic encephalopathy. The condition did not recur over a mean follow-up period of 74 weeks. Over the course of the study, 4 patients died of cardiovascular failure, another underwent orthotopic liver transplantation, and 2 more were lost to follow-up. The 5 remaining patients finished the study in good clinical condition. The authors concluded that hourglass-shaped ePTFE stent-grafts appear to effectively reduce shunt flow and quickly improve patients’ clinical conditions.
Most current therapies are designed to treat the hyperammonemia that is a hallmark of most cases of hepatic encephalopathy.
***So it appears that the correct treatment is being giving.
Clinical Features of Hepatic Encephalopathy
Grading of the symptoms of hepatic encephalopathy is performed according to the so-called West Haven classification system:
* Grade 0 - Minimal hepatic encephalopathy (previously known as subclinical hepatic encephalopathy). Lack of detectable changes in personality or behavior. Minimal changes in memory, concentration, intellectual function, and coordination. Asterixis is absent.
* Grade 1 - Trivial lack of awareness. Shortened attention span. Impaired addition or subtraction. Hypersomnia, insomnia, or inversion of sleep pattern. Euphoria, depression, or irritability. Mild confusion. Slowing of ability to perform mental tasks. Asterixis can be detected.
* Grade 2 - Lethargy or apathy. Disorientation. Inappropriate behavior. Slurred speech. Obvious asterixis. Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, and intermittent disorientation, usually regarding time.
* Grade 3 - Somnolent but can be aroused, unable to perform mental tasks, disorientation about time and place, marked confusion, amnesia, occasional fits of rage, present but incomprehensible speech
* Grade 4 - Coma with or without response to painful stimuli
***Ask the doctor questions about what you do not understand.
***Find out what the prognosis is.
***Write your questions down on paper before you visit.
Best of luck to you!!!
hectorsf
Common Precipitants of Hepatic Encephalopathy
Some patients with a history of hepatic encephalopathy may have normal mental status while under treatment. Others have chronic memory impairment in spite of medical management. Both groups of patients are subject to episodes of worsened encephalopathy. One of the common precipitating factors is:
... * Gastrointestinal bleeding: The presence of blood in the upper gastrointestinal tract results in increased ammonia and nitrogen absorption from the gut. Bleeding may predispose to kidney hypoperfusion and impaired renal function. Blood transfusions may result in mild hemolysis, with resulting elevated blood ammonia levels.
**** So the bleeding from ulcers could trigger an episode of hepatic encephalopathy (HE) in a patient with cirrhosis and HE to begin with.***
Management of Hepatic Encephalopathy
Approach Considerations The approach to the patient with hepatic encephalopathy depends upon the severity of mental status changes and upon the certainty of the diagnosis. As an example, a patient with known cirrhosis and mild complaints of decreased concentration might be served best by an empiric trial of rifaximin or lactulose and a follow-up office visit to check its effect.
**** However, the patient presenting in hepatic coma requires a different approach. General management recommendations include the following:
* Patients with severe encephalopathy (ie, grade 3 or 4) who are at risk for aspiration should undergo prophylactic endotracheal intubation. They are optimally managed in the intensive care unit.
* Precipitants of hepatic encephalopathy, such as metabolic disturbances, gastrointestinal bleeding, infection, and constipation, should be corrected.
* Exclude nonhepatic causes of altered mental function.
* Consider checking an arterial ammonia level in the initial assessment of a hospitalized patient with cirrhosis and with impaired mental function. Ammonia levels have less use in a stable outpatient.
* Precipitants of hepatic encephalopathy, such as metabolic disturbances, gastrointestinal bleeding, infection, and constipation, should be corrected.
* Avoid medications that depress central nervous system function, especially benzodiazepines. Patients with severe agitation and hepatic encephalopathy may receive haloperidol as a sedative. Treating patients who present with coexisting alcohol withdrawal and hepatic encephalopathy is particularly challenging. These patients may require therapy with benzodiazepines in conjunction with lactulose and other medical therapies for hepatic encephalopathy.
* Fanelli et al investigated the efficacy of using an hourglass-shaped expanded polytetrafluoroethylene (ePTFE) stent-graft to treat patients whose hepatic encephalopathy was refractory to conventional medical therapy.22 In the study, 12 patients who, subsequent to receiving a transjugular intrahepatic portosystemic shunt, had developed refractory hepatic encephalopathy underwent shunt reduction with the stent-graft.
* The reduction procedure immediately produced a portosystemic gradient increase in the above study's patients, who, within 18-26 hours after insertion of the stent-graft, no longer exhibited symptoms of hepatic encephalopathy. The condition did not recur over a mean follow-up period of 74 weeks. Over the course of the study, 4 patients died of cardiovascular failure, another underwent orthotopic liver transplantation, and 2 more were lost to follow-up. The 5 remaining patients finished the study in good clinical condition. The authors concluded that hourglass-shaped ePTFE stent-grafts appear to effectively reduce shunt flow and quickly improve patients’ clinical conditions.
Most current therapies are designed to treat the hyperammonemia that is a hallmark of most cases of hepatic encephalopathy.
***So it appears that the correct treatment is being giving.
Clinical Features of Hepatic Encephalopathy
Grading of the symptoms of hepatic encephalopathy is performed according to the so-called West Haven classification system:
* Grade 0 - Minimal hepatic encephalopathy (previously known as subclinical hepatic encephalopathy). Lack of detectable changes in personality or behavior. Minimal changes in memory, concentration, intellectual function, and coordination. Asterixis is absent.
* Grade 1 - Trivial lack of awareness. Shortened attention span. Impaired addition or subtraction. Hypersomnia, insomnia, or inversion of sleep pattern. Euphoria, depression, or irritability. Mild confusion. Slowing of ability to perform mental tasks. Asterixis can be detected.
* Grade 2 - Lethargy or apathy. Disorientation. Inappropriate behavior. Slurred speech. Obvious asterixis. Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, and intermittent disorientation, usually regarding time.
* Grade 3 - Somnolent but can be aroused, unable to perform mental tasks, disorientation about time and place, marked confusion, amnesia, occasional fits of rage, present but incomprehensible speech
* Grade 4 - Coma with or without response to painful stimuli
***Ask the doctor questions about what you do not understand.
***Find out what the prognosis is.
***Write your questions down on paper before you visit.
Best of luck to you!!!
hectorsf
The Doctor said that he would get her on transplant list because the serosis along with the hep is what is causing so many problems. The ICU nurses aren't being very helpful with giving us information. They pulled her vent today and she is no longer sedated but she is non responsive. I will try to find out more tomorrow when I go up to the Hospital. Thank you for responding I really appreciate it.
Hepatic encephalopathy is totally reversible. It is caused by toxins that are not filtered out of the blood do to the liver being very damaged. By using lactulose and rifaximin in the proper amounts the levels of ammonia and other toxins are reduced. The ammonia is created when food such as animal protein is not being digested properly. The rifaximin modifies the breakdown of food in the intestine. Lactulose keeps the digested food from staying in the intestines and creating ammonia and other toxins. I have had various levels of HE and when my mind is clear I can think as well as ever. Many friends have been comatose from HE. After their transplants they are fully recovered.
Also ammonia levels do not exactly correlate with the degree of encephalopathy.
What does her doctor say about this?
Hectorsf
Also ammonia levels do not exactly correlate with the degree of encephalopathy.
What does her doctor say about this?
Hectorsf
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