From the Guidelines
The primary goal of lactulose therapy in hepatic encephalopathy is to reduce blood ammonia levels by trapping and eliminating ammonia through the gastrointestinal tract. Lactulose is typically administered orally at a dose of 20-30 g, 3-4 times per day, until the patient is having at least 2 bowel movements a day, then adjusted to achieve two to three soft stools per day 1. For acute episodes, lactulose can also be given as an enema (200 g mixed with 700 mL water) performed 3-4 times per day in severe cases. Lactulose works by creating an acidic environment in the colon that converts ammonia (NH3) to ammonium (NH4+), which cannot be reabsorbed into the bloodstream. Additionally, it acts as an osmotic laxative, accelerating intestinal transit and reducing the time for bacterial ammonia production. The acidic environment also alters gut flora, reducing ammonia-producing bacteria. Patients should be monitored for dehydration, electrolyte imbalances, and excessive diarrhea, with dosage adjustments made accordingly.
Some key points to consider when using lactulose for hepatic encephalopathy include:
- The dose should be titrated to achieve 2-3 soft bowel movements per day 1
- Lactulose can be administered via nasogastric tube if patients are unable to take medications orally 1
- Enema with lactulose may be performed in severe cases 1
- Patients should be monitored for potential side effects, such as dehydration and electrolyte imbalances 1
It's also important to note that lactulose is not the only treatment option for hepatic encephalopathy, and other medications such as rifaximin may be used in conjunction with lactulose 1. However, lactulose remains a first-line treatment option due to its efficacy and low cost 1.
Overall, lactulose is a effective treatment option for hepatic encephalopathy, and its use should be tailored to the individual patient's needs and response to treatment.
From the FDA Drug Label
For the prevention and treatment of portal-systemic encephalopathy, including the stages of hepatic pre-coma and coma. Controlled studies have shown that lactulose solution therapy reduces the blood ammonia levels by 25 to 50%; this is generally paralleled by the improvement in the patients’ mental state and by an improvement in EEG patterns.
The primary goal of lactulose therapy in hepatic encephalopathy is to:
- Prevent and treat portal-systemic encephalopathy
- Reduce blood ammonia levels
- Improve the patient's mental state and EEG patterns 2
From the Research
Primary Goal of Lactulose Therapy
The primary goal of lactulose therapy in hepatic encephalopathy is to reduce the production and absorption of ammonia in the gut, thereby decreasing its levels in the blood and brain. This is achieved through the acidification of the gastrointestinal tract, which inhibits the production of ammonia by coliform bacteria 3.
Mechanism of Action
Lactulose is a non-absorbable disaccharide that is catabolized by the bacterial flora to short-chain fatty acids, which lower the colonic pH and favor the formation of non-absorbable NH4+ from NH3, trapping NH4+ in the colon and reducing plasma ammonia concentrations 4.
Key Benefits
The key benefits of lactulose therapy in hepatic encephalopathy include:
- Reduction of ammonia levels in the blood and brain
- Improvement in neurological status and cognitive function
- Decrease in mortality rates
- Low risk of serious side effects
Comparison with Other Therapies
Studies have compared the efficacy of lactulose with other therapies, such as rifaximin, and found that lactulose is effective as a first-line treatment for hepatic encephalopathy 5, 6. However, the combination of lactulose and rifaximin may be more effective than lactulose alone in some cases 5.
Administration
Lactulose can be administered orally or rectally, and its therapy is considered a first-line treatment for hepatic encephalopathy 4. The administration of lactulose causes an increase in fecal nitrogen, but very little increase in ammonia nitrogen, and reduces the urea production rate consistent with a reduced entry of ammonia into portal blood 7.