1, the metabolic characteristics of patients with hepatic insufficiency liver is the central organ of nutrient metabolism, with the progress of chronic liver disease, protein energy malnutrition gradually aggravated, the incidence of liver function in the compensated period 20%, and in liver disease in the decompensated period the incidence of 60%. Malnutrition increases the incidence of ascites, hemorrhage, infection and hepatic encephalopathy in patients with liver disease, and affects liver function and accelerates the disease process. Proper nutritional intervention can slow down the further development of systemic failure and improve hepatocyte metabolism. The role of the liver in carbohydrate metabolism is to store glycogen and perform gluconeogenesis. In hepatic insufficiency, hepatic glycogen storage decreases, and glucose oxidation is impaired due to increased glucagon and insulin resistance, which makes the body less tolerant to glucose and prone to glucose disorders. The role of liver in fat metabolism is fat, carnitine, ketone body synthesis and fatty acid oxidation. In patients with hepatic insufficiency, bile secretion is reduced, resulting in impaired fat absorption, lack of essential fatty acids (linoleic acid and -linolenic acid), and increased proportion of fat oxidation for energy supply and body fat depletion, the extent of which is related to the severity of malnutrition and the severity of liver disease. The role of the liver in protein metabolism is to synthesize proteins, break down aromatic amino acids and convert ammonia into urea. In patients with hepatic insufficiency, protein synthesis is reduced and catabolism is increased, leading to hypoproteinemia, resulting in organ dysfunction, decreased immunity and increased ascites, which accelerates the progression of hepatic insufficiency. When hepatic insufficiency progresses to hepatic encephalopathy, the amino acid metabolite ammonia conversion in the liver is impaired, leading to an increase in blood ammonia concentration, and the breakdown of aromatic amino acids (phenylalanine, tyrosine, tryptophan) in the liver is impaired, and the breakdown of branched-chain amino acids (leucine, isoleucine, valine) outside the liver is increased, resulting in an imbalance in the ratio of branched-chain amino acids/aromatic amino acids in the blood, which promotes the development of hepatic encephalopathy. The decrease in appetite and digestive malabsorption in hepatic insufficiency make vitamin absorption impaired, and the decrease in bile salt secretion makes the absorption of fat-soluble vitamins impaired even more obvious, and VitA, D, E and K deficiency is likely to occur. 2, the principles of nutritional support for patients with hepatic insufficiency (1) nutrient supply: about 15-20% of patients with cirrhosis show an increased metabolic rate, 25-30% of patients show a decreased metabolic rate, their energy consumption measured value of individual differences, and Harris-Benedict (H-B) formula prediction value correlation is poor. If there is no condition to measure energy consumption, the energy supply of patients with cirrhosis is 104.6-146.4 kJ/(kg?d) [25-35 kcal/(kg?d)] during the compensatory period, which can be increased when combined with malnutrition, and should be reduced when combined with hepatic encephalopathy. Because of impaired sugar utilization and increased fat oxidation, the proportion of calories provided by carbohydrates should be reduced, with about 60%-70% of calories provided by carbohydrates and 30%-40% of calories provided by fats. Medium-chain fat emulsions do not require carnitine participation and can enter mitochondrial oxidative metabolism directly, which has little effect on liver function and immune function. Excessive carbohydrates or fats will increase the burden on the liver, leading to or aggravating xanthogranuloma and increased transaminases and glucose, impaired blood ester profile, and decreased immune function. In patients with early cirrhosis, protein catabolism increases and hypoproteinemia accelerates the progression of hepatocellular damage and hepatic insufficiency. At this time, protein supplementation (amino acids) can promote positive nitrogen balance without causing hepatic encephalopathy, and 1.3-1.5g/(kg?d) of protein can be given according to liver function compensation. In the end stage of liver disease, increased protein intake may lead to increased blood ammonia and accelerate the development of hepatic encephalopathy, protein intake can be reduced to 0.5-1.0g/(kg?d). For children, even if they have hepatic encephalopathy, protein intake does not need to be restricted too much, because of catabolic hyperactivity and the need for protein for growth and development, protein intake can be 2.5-3.og/(kg?d). Amino acid solution rich in branched-chain amino acids can correct the imbalance of plasma branched-chain amino acids/aromatic amino acids ratio in patients with liver failure, and there is evidence that supplementation of branched-chain amino acids can improve hepatic protein synthesis, reduce catabolism and alleviate hepatic encephalopathy. When hepatic insufficiency is combined with a large amount of ascites, sodium intake should be restricted and caloric intake density should be increased to reduce water retention in the body. Special attention should be paid to the supplementation of fat-soluble vitamins and trace elements. (2) Nutritional pathway selection: Patients with hepatic insufficiency can tolerate normal diet in the early stage, but when combined with moderate to severe malnutrition, enteral nutrition should be strengthened by oral or tube feeding, and the number of times of feeding can be increased to 4-7 times per day to reduce nutritional intolerance and the occurrence of hypoglycemia, but in hepatic insufficiency combined with esophageal variceal bleeding, attention should be paid to the damage of esophageal mucosa and induced However, in the case of hepatic insufficiency combined with esophageal variceal bleeding, the placement of enteral nutrition tube should pay attention to the damage of esophageal mucosa and induce digestive bleeding, but it is not absolutely contraindicated. Open gastrojejunostomy placement in patients with cirrhotic ascites may lead to peritonitis and ascites leakage, so caution should be exercised. When patients with liver dysfunction have decreased appetite and impaired digestion and absorption, resulting in severe malnutrition, energy and amino acids, microbiotics and trace elements can be supplemented through parenteral nutrition. Recommendation: 1. In critically ill patients with combined hepatic insufficiency, nutritional support should increase the supply of branched-chain amino acids and reduce the proportion of aromatic amino acids (level C). 2. In critically ill patients with combined hepatic insufficiency, non-protein calories should be supplied with dual energy sources of sugar and fat, of which fat supplementation is appropriate with medium and long chain fat emulsions (level C).