Hepatic encephalopathy is not scary! Uncover the causes and find ways to deal with it

Author: Wang Xiangxiang, The Fifth Medical Center, PLA General Hospital

Reviewer: Jin Bo, Chief Physician, Fifth Medical Center, PLA General Hospital

Hepatic encephalopathy is a neuropsychiatric syndrome of varying severity based on metabolic disorders, caused by acute or chronic severe liver dysfunction or various portal vein-systemic shunt (hereinafter referred to as "portal-systemic shunt") abnormalities. It is also called "hepatic coma." In short, hepatic encephalopathy is a complex syndrome in which brain function is impaired due to the accumulation of toxins when liver disease develops to a serious stage. Faced with this disease, the public often panics due to lack of understanding, as if they are in a fog and don't know what to do. Today, we will explore in depth the causes and treatments of hepatic encephalopathy, and strive to help everyone face hepatic encephalopathy with a scientific attitude, and jointly protect the health and tranquility of life.

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1. What are the causes of hepatic encephalopathy?

1. The most direct cause: Diffuse damage to the liver parenchyma can cause hepatic encephalopathy, such as cirrhosis, severe hepatitis and liver cancer.

2. The most common cause: infection, including abdominal, intestinal, urinary and respiratory tract infections, especially abdominal infection.

3. Other causes: gastrointestinal bleeding, electrolyte and acid-base imbalance, large-scale ascites, high-protein diet, hypovolemia, diuresis, diarrhea, vomiting, constipation, transjugular intrahepatic portosystemic shunt, and the use of hypnotic sedatives, anesthetics, etc.

2. What are the common treatments for hepatic encephalopathy?

Early identification and timely treatment are the key to improving the prognosis of hepatic encephalopathy.

1. Remove the trigger

(1) Infection is the most common triggering factor. The source of infection should be actively sought and sensitive antimicrobial drugs should be used for treatment as early as possible.

(2) Hepatic encephalopathy is likely to occur on the day of gastrointestinal bleeding or a few days thereafter. Bleeding should be stopped as soon as possible and blood accumulated in the gastrointestinal tract should be cleared.

(3) Excessive diuresis can cause hypovolaemic alkalosis and electrolyte imbalance, which can induce hepatic encephalopathy. Diuretics should be discontinued, and fluids and albumin should be supplemented to correct electrolyte imbalance.

(4) Patients with hypovolemic hyponatremia (especially blood sodium ≤110 mmol/L) should be given sodium chloride solution of appropriate concentration as prescribed by the doctor.

(5) In case of constipation, enema or catharsis can be performed. The first choice is 0.9% sodium chloride solution cleansing enema, or 100 ml lactulose retention enema. Weak acid solution (such as dilute acetic acid solution) can also be used for enema. Soap water enema is prohibited.

2. Medication

(1) Deamination treatment: Hyperammonia is an important factor in the occurrence of hepatic encephalopathy. Therefore, it is very important to reduce the production and absorption of ammonia. Commonly used deamination drugs include: ① Lactulose, which can lower intestinal pH, inhibit intestinal bacterial growth, reduce intestinal bacterial ammonia production, and reduce ammonia absorption, promoting the excretion of ammonia in the blood from the intestine. The usual dose is 15-30 ml per oral administration, 2-3 times a day (adjust the dose according to the patient's response), and 2-3 soft stools a day are appropriate. ② Ornithine aspartate, which reduces ammonia levels by promoting liver ornithine circulation and glutamine synthesis, and can significantly reduce fasting blood ammonia and postprandial blood ammonia in patients. The dose is generally 10-40 g per day by intravenous drip. ③ Other ammonia-lowering drugs, such as arginine and glutamine.

(2) Sedatives: Suitable for patients with severe mental disorders during hepatic encephalopathy, such as mania, endangering the safety of themselves or others, and unable to cooperate with doctors' diagnosis and treatment.

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3. Dietary nutritional support

(1) Energy intake: The ideal daily energy intake is 35-40 kcal/kg (including at least 50 g of complex carbohydrates). Patients are encouraged to eat small meals frequently, evenly distribute small meals throughout the day, and have a snack before bedtime. Daytime fasting time should not exceed 3-6 hours.

(2) Protein intake: Generally, patients with cirrhosis need to take in 1.2-1.5 g/kg of protein per day to maintain nitrogen balance. Obese or overweight patients with cirrhosis should maintain a daily dietary protein intake of 2 g/kg. Protein supplementation for patients with hepatic encephalopathy should follow the following principles: patients with grade 3 or 4 hepatic encephalopathy should not supplement protein from the intestine; patients with mild hepatic encephalopathy or grade 1 or 2 hepatic encephalopathy should limit their protein intake to 20 g per day for the first few days. As symptoms improve, 10-20 g of protein can be added every 2-3 days. Plant protein is preferred, such as beans (preferably soybeans), cereals, rice, potatoes, and dried fruits. Patients with chronic hepatic encephalopathy are encouraged to eat small meals frequently, and protein intake should be individualized to gradually increase the total amount of protein. The protein content of common foods is shown in the figure below.

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(3) Eat more foods that are good for bowel movements and rich in vitamins, such as bananas, honey, oats, yogurt, fresh vegetables, fruits, soy products, and whole grain products, to keep bowel movements smooth. Chew slowly when eating and avoid eating greasy or fried foods.

4. Artificial liver treatment: It can remove some inflammatory factors, endotoxins, blood ammonia and bilirubin to a certain extent, and can improve hepatic encephalopathy.

5. Liver transplantation.