Ammonia toxicity is an important pathogenesis of hepatic encephalopathy, especially portal shunt hepatic encephalopathy. Patients with hepatic encephalopathy should reasonably restrict protein intake. Protein metabolism in the digestive tract produces ammonia, which is diffused into the blood through the intestinal mucosa. With poor liver function and portal shunt surgery, blood ammonia is elevated, and ammonia in the blood can cross the blood-brain barrier and interfere with brain function in many ways. Patients with hepatic encephalopathy should ensure the supply of calories as much as possible to avoid hypoglycemia; supplement all kinds of vitamins; transfuse plasma or clear protein as appropriate. Protein is forbidden for several days after acute onset of the disease (stage 1~2 hepatic encephalopathy can be limited to less than 20g/d). After portosystemic shunt, those who are intolerant to protein should avoid a large protein diet, but should still maintain a small amount of protein supplementation continuously. In addition, patients with hepatic encephalopathy should pay attention to preventing and controlling infections, preventing constipation, and using sedative-hypnotic drugs and drugs that impair liver function with caution to avoid aggravating the condition. When diagnosed with hepatic encephalopathy, the treatment should be standardized under the guidance of doctors.