Acute liver failure

　　The main causes of acute liver failure in China are hepatitis viruses (mainly hepatitis B virus), followed by drugs and hepatotoxic substances (such as alcohol, chemical agents, etc.). Acute liver failure in children can also be seen in hereditary metabolic diseases. Specifically, the main reasons include the following aspects:

　　One, hypoxic liver injury, such as liver congestion and hypoxia caused by chronic heart failure or shock for a certain period of time.

　　One, poisoning by toxins, such as mushroom poisoning, smelly rice flour poisoning, carbon tetrachloride poisoning, etc.

　　Three, various types of viral hepatitis, such as hepatitis A, B, C, D, and E. It can also be caused by mixed or overlapping infection of two or more hepatitis viruses affecting the liver.

　　Four, other diseases such as acute Wilson's disease.

　　Acute liver failure can easily lead to hepatic coma: hepatic coma can occur when liver function is severely impaired. Normally, the liver metabolizes protein amino acids as follows: protein → amino acids → deamination → ammonia → urea. In the late stage of acute liver failure, due to severe liver dysfunction, deamination is poor, ammonia cannot be further synthesized into urea, the concentration of ammonia in the blood increases, and it poisons the central nervous system. Initially, patients may be restless, delirious, and spasmodic, and later may become drowsy and comatose. At the same time, due to hypoxia, ischemia, and necrosis of liver cells, as well as the anaerobic metabolism of cell tissues that produce a large amount of toxic substances, the central nervous system is also poisoned, further aggravating hepatic coma. When liver function fails, the decomposition of glycogen is weakened, blood sugar decreases, which can also cause hepatic coma. In addition, when liver cirrhosis leads to liver failure, the three major metabolic disorders in the liver cause the biochemical processes of blood and various tissues and organs in the body, especially brain tissue cells, to become disordered, resulting in cerebral blood flow disorders and hypoxia, as well as the liver's inability to process and detoxify a large amount of metabolic products in the body. These are all important factors leading to hepatic coma.

　　(1) Severe fatigue, with明显 obvious anorexia, vomiting, and abdominal distension, and other serious gastrointestinal symptoms.

　　(2) Jaundice progressively deepens (serum total bilirubin ≥ 171μmol/L or daily increase ≥ 17.1μmol/L).

　　(3) Tendency to hemorrhage, 30%.

　　(4) Marked tendency to hemorrhage (petechiae or ecchymosis), and 20%.

　　(5) The occurrence of grade II or less hepatic encephalopathy and/or significant ascites.

　　The mortality rate of acute liver failure is high, and efforts should be made to prevent its occurrence. Clinically, attention should be paid to the adverse effects on the liver when taking medication. For example, when treating tuberculosis with rifampicin, isoniazid, or pyrazinamide, blood transaminases and bilirubin should be checked. If changes in liver function are found, the medication should be changed in a timely manner. Before major surgical procedures, particular attention should be paid to the patient's liver function, especially for those with pre-existing liver cirrhosis, hepatitis, jaundice, hypoproteinemia, and other conditions. Adequate preparation is required. Anesthesia should avoid hepatotoxic drugs. During and after surgery, it is necessary to prevent hypoxia, hypotension, or shock, infection, etc., to avoid damage to liver cells. After surgery, liver function should be continuously monitored according to the condition, maintaining good respiration and circulation, anti-infection, and maintaining nutritional metabolism, which is beneficial to the liver.

　　(1) Transaminases may increase, but they may not increase when diffuse liver necrosis occurs.

　　(2) Blood bilirubin levels may increase.

　　(3) Platelets are often reduced; white blood cells are often increased.

　　(4) Blood creatinine or blood urea nitrogen may increase (due to reduced renal function).

　　(5) Disordered blood electrolytes such as hyponatremia, hyperkalemia, or hypokalemia, hypomagnesemia, etc.

　　(6) Acid-base imbalance, mostly metabolic acidosis, early may have respiratory or metabolic (hypoxia, hypokalemia, etc.) alkalosis.

　　(7) When DIC occurs, the coagulation time, prothrombin time, or partial thromboplastin time may be prolonged, fibrinogen may decrease, and its degradation products (FDP) may increase. Erythrocyte sedimentation rate tests may be positive.

　　(1) The diet of patients with acute liver failure should avoid hard, spicy, hot, and fast food. The food should be light, fresh, and easy to digest, with a focus on liquid and semi-liquid diets; strictly limit the intake of tobacco and alcohol.

　　(2) In the early stage of the disease, parenteral nutrition is the main method, with oral nutrition as a supplement. In the recovery period, oral nutrition is the main method, with parenteral nutrition as a supplement. Some critically ill patients can be treated with nasogastric duodenal feeding tubes to infuse nutritional fluids. If there is no diabetes, the method of eating less and more often can be chosen. During parenteral nutrition support therapy, the nutritional fluid should include a comprehensive supplement of glucose, medium and long-chain fatty emulsion, amino acids, as well as various vitamins, electrolytes, trace elements, and other nutrients. It is recommended to infuse slowly and continuously through the vein.

　　(3) Yogurt contains a lot of lactic acid bacteria, which can inhibit the growth of harmful bacteria in the intestines and promote the absorption of calcium, phosphorus, and iron, and it is recommended to take it between meals.

　　(4) Ensure a total calorie intake of more than 1500 kcal per day (depending on the severity of the condition), and for patients with hepatic encephalopathy, the intake of protein should be restricted, and amino acid preparations can be taken.

　　(5) In addition to normal meals during the day, it is emphasized that a bedtime snack (200-300 kcal) is necessary. Studies have shown that a bedtime snack helps improve the body's 'starvation state' and ultimately improve the patient's metabolic state.

　　(6) For patients with a large amount of ascites or edema, appropriate control of salt and water intake should be exercised. The daily sodium intake should be 500-800mg (sodium chloride 1.2-2.0g), and the water intake should be limited to about 1000ml. If there is severe hyponatremia, adjustments should be made under the guidance of a doctor.

　　1. Pathogen in the 分Qi

　　The main symptoms of acute liver failure at this time are sudden onset, yellowing of the body and eyes, gradually deepening, deep yellow urine, high fever and thirst, rough breathing, irritability and restlessness, or confusion and delirium, nausea and vomiting, dry mouth and bitter taste, abdominal distension and rib pain, constipation, deep red tongue, yellow greasy fur, and wiry slippery and rapid pulse. The modified recipe of Yin Chen Hao Decoction: The main herbs are Yin Chen Hua, Gardenia, and Dahuang, which can be added with Antelope Horn, Da Qing Ye, Tu Hu茯苓, Pu Gong Ying, and Jin Yin Hua.

　　If the pathogenic heat is intense and the fever does not subside, add raw gypsum and Anemarrhena to clear heat and relieve fire; if the pathogenic heat blocks the heart orifices and causes confusion, take Anju Huangwan Wan to open the窍and醒神. For those with upward-moving stomach Qi and vomiting, add bamboo shoots and Coptis to harmonize the stomach and relieve vomiting; for those with pain in the right rib, it is due to damp-heat accumulation and blood stasis, add Bupleurum, Yuanhu, and Yujin to soothe the liver and benefit the gallbladder, remove blood stasis and relieve pain; for those with abdominal distension and stuffiness, it is due to the blockage of Qi in the bowels, add Atractylodes and Magnolia to promote Qi and unblock the bowels.

　　2. Pathogen entering the营blood

　　The main symptoms of acute liver failure at this time are severe fever at night, yellowish skin and eyes like gold, scanty urine, deep yellow urine color, swelling and pain in the ribs, confusion and delirium, drowsiness and confusion, or twitching and convulsions, or nosebleeds, vomiting blood, urine, and feces, or macules on the skin, or abdominal distension with fluid, red and purple tongue, yellow and dry fur, and wiry and thin pulse. The treatment drugs are rhinoceros horn (replaced by water buffalo horn), Coptis, Cimicifuga, Gardenia, Artemisia, Rehmannia, Moutan Cortex, and White Peony Root.