Okay. So I was just told by my hepatologist's assistant I'm being put on Lactulose to assist in my memory loss and falling, as in ending up in the ER falling. My doctors feel that my advanced cirrhosis is the cause of the falling and impaired memory, because just about every test was run on my blood, etc. and thus we end up with the liver being the problem, which I was guessing anyway.
Ahem. No one ever told me I have cirrhosis, much less advanced cirrhosis. I'm being put on Lactulose. I have an appointment with brilliant hepatologist 4/16 after having an ultrasound at the same hospital right before I see doctor. I also was told I'm fortunate that despite the advanced cirrhosis, my liver is well-compensated and the Lactulose will continue to protect my liver, and that the oral-only trial meds won't be out for another year. I can't take interferon as it caused retinal hemorrhaging in 2005, the last time I treated.
A few hurrahs might make me feel better, because at this point I'm only thinking of not being able to watch my 10-month-old grandson grow up.I know many people have been worse off than me. I'm just really bummed.
I am so sorry for your situation. However the fact that you are well compensated is good news as is the news that you are seeing a good Hepatologist.
Cirrhosis is a very serious disease but not necessarily fatal. There are many of us with compensated cirrhosis and we are doing fine.
You should be able to treat within a few years and once you are free from the virus you will be on the mend.
I was very close to ESLD according to my Hepa and since TX I am feeling so much better and my labs are terrific. In time some of the fibrosis will regress.
Cirrhosis is not a death sentence.
Eat well, take your approved vitamins, drink lots of water and keep exercising. There is hope.
Thank you, thank you. Thank you! You were correct in putting into words that cirrhosis for me, what I have, is not a death sentence. It just really feels discouraging since I remember when I was first diagnosed in 1992, that that was a death sentence. Three failed treatments since then, but still feeing pretty good most of the time. So did you SVR your last time on treatment? I'm glad that you feel better, beat the treatment or just still feeling good since TX?
I was in a clinical trial with GS 7977 and Ribavirin and I have SVR now.
I initially felt better after being undetected but I had a lot of extrahepatic manifestations that really became apparent when I was cirrhotic. The extreme fatigue, bleeding and itching stopped, but it wasn't until very recently that I feel like my body is making a comeback.
I really thought I would die, but the liver is such an amazing organ, always working to heal itself. Now it really has that opportunity and I expect to be better than ever in time. Day by day the healing continues.
It will be that way for you too. :)
Lactulose is the first line of treatment for hepatic encephalopathy. HE is common in patient with cirrhosis and hepatitis C. HE is caused by cirrhosis and portal hypertension and can appear in compensated patients. Since you apparently do have ascites, internal bleeding and other signs of decompensation and its symptoms you do NOT have advanced cirrhosis. Compensated cirrhosis is not advanced cirrhosis. For many but not all patients who are compensated, they may be no symptoms of complications from their cirrhosis. It is only when a patient becomes decompensated the complications of cirrhosis appear.
Hepatic encephalopathy (HE) is defined as mental or neuromotor dysfunction in a patient with acute or chronic liver disease. HE may be clinically apparent in as many as one third of cirrhotic patients and, if rigorously tested, up to two thirds have some degree of mild or subclinical HE.
The exact cause of how HE develops is largely unknown. The premise of most pathophysiologic theories involves the accumulation of ammonia in the central nervous system, producing alterations of neurotransmission that affect consciousness and behavior. Ammonia interferes with brain function at many sites. Ammonia crosses the blood-brain barrier and directly depresses the central nervous system. In patients with progressive HE, there is a gradual decrease in level of consciousness, intellectual capacity, and logical behavior, along with the development of specific neurologic deficits.
Because the toxins believed to be responsible for HE arise in the gastrointestinal tract, removal of the nitrogenous load is the mainstay of therapy. Various pharmacologic agents may be used, but the nondigestable disaccharide known as Lactulose is currently the first-line therapy. After consumption, lactulose passes through the small bowel completely undigested. Once in the colon, lactulose is metabolized by colonic bacteria and the pH is lowered. As a result, peripheral ammonia levels are reduced.
Rifaximin (550 mg 2x per day) is also used with Lactulose and doesn't have the unpleasant side effects of Lactulose.
Common precipitants that may trigger an episode of hepatic encephalopathy in patients with otherwise stable liver disease include:
Eating red meats. Patients with HE should get their protein from chicken, fish and vegetables.
• Infection: Although infection involving almost any site, including the urinary tract and lungs, many trigger hepatic encephalopathy in patients with advanced cirrhosis, infection of ascites (abdominal fluid) - called spontaneous bacterial peritonitis (SBP) - is one of the most frequent triggers of encephalopathy. Sampling ascites fluid using a needle, a procedure called paracentesis, is required to determine if SBP is present.
• Gastrointestinal bleeding: Patients with cirrhosis frequently suffer from bleeding in the digestive tract, usually from dilated veins in the esophagus (esophageal varices). Digested blood represents a large protein load in the gut which can lead to higher levels of ammonia and other toxins and, not surprisingly, hepatic encephalopathy is frequent in this setting.
• Medications: Drugs that suppress the central nervous system, particularly opiate pain medications (e.g., codeine) and benzodiazepines (e.g. diazepam, lorazepam), may trigger hepatic encephalopathy.
• Electrolyte problems: Low serum sodium (hyponatremia) and potassium (hypokalemia) are common in cirrhotic patients treated with diuretics and both can worsen hepatic encephalopathy. Hypokalemia appears to exacerbate encephalopathy in part by stimulating ammonia production from the kidneys.
• Constipation: Slow transit of stool through the gut appears to increase the time for bacteria digest foodstuffs and make ammonia and other toxins, potentially triggering hepatic encephalopathy.
• Kidney failure: Dehydration from diuretic therapy and diarrhea, infection, some medications, and progression of liver disease can all lead to kidney failure, which in turn leads to decreased clearance of urea, ammonia, and other toxins that can contribute to encephalopathy.
• Other factors: A rise of blood pH (alkalosis), which often results from diuretics and resulting dehydration, may facilitate entry of ammonia into the brain and exacerbate encephalopathy.
Patients suffering hepatic encephalopathy may come to the doctor with a spectrum of symptoms. In mild cases, called minimal hepatic encephalopathy, the patient may have no symptoms but have cognitive deficits revealed by formal neuropsychiatric testing (e.g., number connection tests, etc.). With more advanced hepatic encephalopathy, fatigue, and at least mild deficits of memory, concentration, and coordination may become apparent. At this stage, common complaints by the patient include:
- “I feel like my head is in the clouds.”
- “I’ll walk into a room and forget why I am there.”
- “I am always tired…but I can’t sleep.”
- “I often forget what to say in mid-sentence.”
- “My memory is poor.”
- “My coordination is poor.”
- “My boss is telling me that my work is slipping.”
- “My handwriting has changed to scribble,”
- “My hands shake so much, I can’t hold my coffee cup without spilling it.”
Nighttime insomnia is a very common and troublesome symptom associated with hepatic encephalopathy. In fact, patients with encephalopathy may ultimately sleep more during the day, with fitful naps, than at night, and this “day-night reversal” is a hallmark of more advanced hepatic encephalopathy. Family and friends frequently notice a deterioration of the patient’s cognitive function as well as a change in the patient’s personality—with frequent irritability, bouts of anger, and loss of social graces. They may also witness firsthand deterioration of the patient’s driving skills (“He would have run off the road if I hadn’t grabbed the wheel!”).
People with chronic HE should NOT drive.
Two of the most common physical (as opposed to subjective) manifestations of hepatic encephalopathy are asterixis and fetor hepaticus. Asterixis is a non-synchronous and coarse tremor– known colloquially as a “liver flap” – that is best elicited by asking the patient to outstretch the hands with straight elbows, wrists cocked at 90 degrees, and fingers spread apart, instructions easily communicated with the command, “Stop traffic!” Although such a tremor is not specific for hepatic encephalopathy (it can also be seen with renal failure and other conditions), it certainly suggests the diagnosis in patients with liver disease. Fetor hepaticus is a musty sweet odor that is usually evident by casually sniffing the patient’s breath.
When symptoms of hepatic encephalopathy progress, the patient may slip into a stupor or even comatose state and be virtually unarousable. Such situations are medical emergencies, and the patient should be brought to medical attention immediately! Go to the ER!
Good luck with your hepatologist. They know all this and will treat you accordingly.
" No one ever told me I have cirrhosis, much less advanced cirrhosis. I'm being put on Lactulose ... " Now can you see why I'm confused? When I questioned my GP doctor about the Lactulose, she said it was to clear up my intermittent problems with constipation and that it would be good for my liver as well. She had apparently just gotten off the phone with GURU doctor. The first thng I did when I got home was look up Lactulose. It still seemed like "over-kill" for treating HepC. I didn't even know there was such a drug. Then I got on here and started researching Lactulose and became quite panicked, to put it mildly, that it was for the HepC. I called the hospital, and the research assistant that works with my GURU doc explained it was for the HepC and that my doctor was going to talk to be about it at my appointment but to go head with taking the medicine.
When I asked what Lactulose had to do with HepC, she said they always treat their cirrhotic patients this way. When I became upset, she was surprised no one had told me about my having cirrhosis, but said it's not uncommon for patients to get them confused, because Stage 3 HCV, much less Stage IV, kind of blended together with cirrhosis, that it's not that cut and dried. She was very reassuring and if I had questions, to be sure to call.
Combine this with my memory loss, I'm surprised I remember any of it. Oh, yeah. I was diagnosed with a mild stroke in June 2009, Hypokalemia June 2012 (last year) and my GP doctor and I think I had a second stroke a couple of weeks ago. Never dull around here.
I am so happy for you! I've tried to find out what percentage of patients who used Lactulose went on to clear. I had no idea when it was prescribed (the Lactulose) that it had anything to do with HepC.
Also 3-4 weeks ago or so I had another stroke, which is what started all this testing, to see if certain drugs I'm on or a combination of them could be causing these symptoms. It's the HepC. Tuesday I see my GURU hepatologist and an appointment with GURU doctor right after the ultrasound. I'll post the results here.
Okay. My viral load is over 10,000,000, but I'm not worried about that because the number doesn't necessariy correlate with the condition of your liver. Doctor wants to treat this fall after the dugs get FDA, and we'll keep monitor my eyes carefully. He said the reason people are e saying "cirrhotic" in reference to the HelpC is is they are pro-actively treating me as though I had cirrhosis, but I don't have cirrhosis. I have a 6x5x4 mm hypoechoic nodule adjacent to the gall bladder and is most likely a hepatic cyst. Gall bladder is in every way normal except 5 mm polyp in the fundus. "No ascites is seen." Spleen is fine, pancreas showing slight 2.5 mm in diameter but not pathologcally, kidneys are fine. So here they are: 1) 6x5x4 hypoechoic nodule near gallbladder fundus is probably a hepatic cyst. "Mildly echogenic liver compatible with mild hepatic steatosis. Other advanced forms of liver disease including significant hepatic fibrosis, cirrhosis or hepatitis cannot be excluded on this study. Liver biopsy May 20, and he wants to put me in treatment this fall. And so, oh wise ones, I await your interpretation.
Lactulose. It does the work the liver can no longer do, extracting bad cells and sending them to the colon for elimination. Second, I feel silly asking this,but ifI can't wear my clothes anywhere because I look like I'm 8 months pregnant, I asked my doctor if it was fluid collecting in my adbomen, my liver starting to fail, or too many chocolate bars. He said it was too many cholocate bars. I mean if I going into treatment I'm going to lost some weight there. I just really can't stand this weight. Any ideas?
Hi. I sent a quick note about weight gain/loss, HepC or something else? Now I remember why I was so concerned about this. I was diagnosed with an umbilical hernia in December, and cautioned by HepC doc not to do anything too strenuous, plus at Stag3/4 in the HepC picture. My usual exercise regime wasn't working, no matter what I did, diet, exercise, blah blah blah. I figured it out. Clothes are fitting differently, as in my sweat pants the waist was so tight tight they dig into my waist line to the point they hurt, and then I'm worried that it's the hernia causing the swelling.. Anyway, as I said, silly question on my part.
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