Treatment of Hepatic Encephalopathy, December 15, 1988

Treatment of Hepatic Encephalopathy, December 15, 1988

Hepatic encephalopathy, also known as hepatic coma, occurs when severe liver dysfunction prevents the detoxification of metabolic byproducts, particularly those resulting from protein metabolism, such as amino acids and phenylalanine breakdown products. Some of these nitrogen-containing metabolites cross the blood-brain barrier, leading to brain toxicity. Clinical manifestations include agitation, somnolence, coma, flapping tremor or shaking, halitosis, and pathological reflexes.

1. Contributing Factors
   (1) Massive upper gastrointestinal bleeding: ① increases intestinal ammonia production; ② circulatory failure reduces ammonia and urea excretion.
   (2) Infection with high fever promotes protein breakdown.
   (3) Diuretics cause potassium loss; when the liver is severely damaged, it becomes extremely sensitive to potassium deficiency.

2. Clinical Manifestations of Hepatic Encephalopathy
   Altered consciousness, increased muscle tone, flapping tremor, halitosis (mild cases smell like apples, severe cases like ammonia), and the appearance of pathological reflexes.

3. Treatment
   (1) Treat the underlying disease: protect the liver with benzbromarone, 25mg orally three times daily, which effectively lowers enzyme levels. Vitamin C, vitamin B, 10% glucose, thymosin, interferon, mushroom preparations, and poria polysaccharides can also be used; opinions differ on whether hormones should be employed. Insulin therapy can promote hepatocyte regeneration and is therefore applicable.
   (2) Anti-infection: ampicillin is the best choice; for the intestines, neomycin 4–8g can be administered via enema to inhibit intestinal bacteria, thereby reducing ammonia production and absorption.
   (3) Maintain intestinal acidity: pH below 6.0; add a small amount of dilute hydrochloric acid or vinegar to tap water for retention enemas. After ingesting 20–30mL of lactulose orally, it breaks down into lactic acid and acetic acid, and acidophilic lactic acid bacteria further produce lactic acid in the gut. Lactobacillus 1.0g, taken orally three times daily.
   (4) Keep the intestines clear: take 30mL of 50% magnesium sulfate orally or drink a decoction of rhubarb.
   (5) Supplement potassium: patients with hepatic encephalopathy are extremely sensitive to potassium deficiency.
   (6) Reduce blood ammonia: sodium glutamate + NH4^+^ = glutamine (non-toxic); arginine + NH^+^4= urea.
   (7) Vitamins B, E, K, ATP, and Co-A.
   (8) Levodopa is a precursor to dopamine, a neurotransmitter in the brain; when taken orally, it competitively blocks the intestinal absorption of aromatic amino acids such as methionine, phenylalanine, and tyrosine, thereby inhibiting ammonia formation.
   (9) Use mannitol for cerebral edema.