Hepatic encephalopathy is the most serious complication of cirrhosis, but the manifestation of its condition is often overlooked. Mild hepatic encephalopathy, which is treated as normal due to the absence of obvious clinical manifestations, may show abnormalities in personality and behavior when participating in normal social activities, such as suddenly showing agitation and aggressiveness, or indifference and selfishness recently, or being prone to dangerous accidents when driving transportation. If hepatic encephalopathy is not recognized and treated in a timely manner, further development of the disease may show cognitive impairment of time, place, and loved ones. If the disease progresses further, it can manifest itself as lethargy or even a coma with no consciousness at all, which can be life-threatening. Common causes of hepatic encephalopathy in patients with cirrhosis include: 1. eating a high-protein diet: resulting in increased ammonia production in the intestine; 2. constipation: preventing the timely discharge of toxic substances such as ammonia and mercaptans from the intestine; 3. infection: increasing the decomposition of tissues, resulting in increased ammonia production; 4. gastrointestinal bleeding: the accumulation of blood in the intestine leads to increased ammonia production, and the ischemia and shock caused by bleeding reduces the tolerance of brain cells to toxic substances, and the tolerance of brain cells to toxic substances. 5, alkalosis: vomiting, diarrhea, or eating too little, can cause hypokalemic alkalosis, and alkalosis accelerates the formation of ammonia, and easy to enter the brain; 6, sedation, hypnosis: barbiturates, Valium and other sedative drugs, can directly inhibit the brain nerve conduction function of patients with cirrhosis, thus inducing hepatic encephalopathy. In response to the above causes of hepatic encephalopathy, patients with cirrhosis decompensated stage should pay attention to and choose in their daily regimen and supplements. Firstly, avoid eating a high protein diet, so as not to cause a sudden increase in ammonia production in the human intestinal tract. Second, in particular, do not eat large amounts of animal protein. In addition to increased ammonia production, the metabolites of animal protein contain more aromatic amino acids, which can also inhibit brain nerve conduction and induce hepatic coma in cirrhosis, which is one of the reasons why Auntie Li’s coma occurred with a large amount of chicken and turtle soup. Thirdly, patients in the decompensated stage of cirrhosis should consume a small amount of vegetable protein because there are fewer aromatic amino acids in vegetable protein but more branched-chain amino acids, which can antagonize the blockage of brain nerve function by some toxic substances. Fourthly, bananas and other fruits can be consumed to keep the bowels open, 1-2 times a day, always maintaining the timely removal of ammonia production in the intestine. Fifthly, when appetite decreases, or when vomiting or diarrhea is present, timely potassium supplementation is required, such as quoting fresh cucumber juice and apple juice, to avoid hypokalemic alkalosis leading to hepatic encephalopathy. Sixthly, appropriate supplementation of vitamins and probiotics, such as vitamin C, vitamin B2, vitamin K and Lactobacillus acidophilus, etc., to stabilize the internal environment of the body. Seventh Avoid taking nutrients or minerals containing iron preparations in general cirrhotic patients unless there is obvious anemia after bleeding, because iron has the effect of aggravating liver sclerosis. Eighthly, try to avoid the use of sedative and sleeping drugs to avoid the liver coma directly caused by this. Ninthly, for those who have esophageal varices, food should be made fine and soft, avoid too coarse food, forbid to eat hard and thorny food, such as fish with thorns, chicken with bones and nuts, etc., to prevent the upper gastrointestinal bleeding caused by the rough and hard food scratching the varices of esophageal veins or gastric fundic veins.