I will share my husband's experience with you. He takes 30 ml lactulose twice a day and is also taking Xifaxin 550 mg twice a day. He has not had an HE episode in two months. Every patient is different with his/her own unique medical history. However, taking lactulose 4 times a day sounds excessive. Before starting back on Xifaxin, my husband was taking 30 ml three times a day. You will need to find out what dosage works for you. Having 2-3 BM's
Is the goal. Lactulose, as others have posted, is the recommended treatment for HE, for the reasons already explained.
Here are some helpful links to webinars on HE by the American Liver Foundation.
Good luck. Keeping your HE under control is very important.
Hi there, I once had the same question you have now. I believe that the lactulose reduces the ammonia in your gut and brain and that's why it is important to take, if the ammonia gets too high it can cause you to have problems thinking, driving, cooking etc. I am not as good as explaining things as Hector so I have taken one of his explanations and am pasting it here.
I also just read an explanation that the lactulose helps your body do the job the liver would do if it was working right. I hope this helps, I found it in the cirrhosis forum. Dee
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!
I found an article Treatment Basics about Lactulose & Hepatic Encephalopathy from the American Liver Foundation.
"Lactulose works by drawing water from your body into your colon, which softens stools and causes you to have more bowel movements. This helps lessen the absorption of toxins in your intestines and flush them out of your system. It also reduces the amount of ammonia in your blood by drawing the ammonia into the colon where it’s removed from the body via bowel movements."
I assume Lactulose is specifically ment to perform this action where OTC laxitives do not. The purpose of Lactulose is not as alaxative but to prevent episodes of HE. It does this by enabling the body to eliminate toxins normally removed by your liver through your intestinal tract.
Here are some medical definitions for lactulose that also describe its action.
Produces osmotic effect, which increases water content in colon and enhances peristalsis. Breakdown products in colon lead to acidification of colonic contents, softening of feces, and decreased ammonia absorption from colon to systemic circulation. These effects reduce blood ammonia level in portal-system encephalopathy.
If you're achieving 2-3 bowl movements a day, I believe you should stay hydrated and drink at least 8 glasses of water a day as I was told. My Cirrhosis was very advanced to the point I couldn't get out of bed due to weakness. I bought Bay Pharma brand at Walgreens. It comes in a dark brown plastic bottle. Tasted really good. I believe I was drinking 3 tablespoons daily. It did help. Good luck and remember to keep your head about you, it's a matter of time and you will be cured...
I forgot to add I would ask my doctor about the frequency of BM's if you are already having 2-3 a day. You definately don't want to get diarrhea and become dehydrated as that also can cause HE. But if you have been prescribed Lactulose for your HE then you need to be taking it to help prevent or reduce your HE episodes.
I have seen others say it is a balencing act to get the dosing of Lactulose correct so you can have the 2-3 loose BM's and not have it become diarrhea.
Lactulose was prescribed to you to treat your HE not for constipation although it can be used as a laxative for patients with constipation issues but that is not why you were prescribed it.Other laxatives don't help with HE symptoms.
Get clarification from your doctors office about dosing questions
Hi flyinlynn and Magnum gave you great advice.
The lactulose draws the ammonia into your intestines to be excreted which laxatives to not.
I remember having this same question a couple of years ago when I was taking lactulose