Liver failure

　　Currently in China, the main cause of liver failure is still hepatitis virus, followed by drugs or hepatotoxic substances such as alcohol, chemical agents, etc.; in Western countries, drugs are the main cause of acute subacute liver failure, while alcohol often leads to chronic liver failure. In addition, acute fatty liver of pregnancy, autoimmune liver disease, parasitic infection, etc., can also lead to the occurrence of liver failure.

　　The etiology of pediatric liver failure is often unknown. Zhu Shishu and others analyzed 120 cases of liver failure in children, and the etiology was unknown in both the infant group and the group over 1 year old, accounting for 40.6% and 30.7% respectively. The etiology of liver failure can be a single factor, such as infection with a certain hepatitis virus, alcohol intoxication, taking certain drugs, etc., or a combination of multiple factors, such as overlapping infection with other viruses on the basis of chronic hepatitis, or combined viral infection on the basis of chronic alcohol intoxication, etc.

　　(1) Hepatic encephalopathy:Liver failure can lead to various complications due to the comprehensive impairment of liver function, which can cause different degrees of nervous system disorders, mainly manifested as disturbance of consciousness, abnormal behavior, and coma, which can ultimately lead to death.

　　(2) Disruption of water, electrolyte, and acid-base balance:Due to the patient's severe gastrointestinal symptoms and the use of diuretics, hyponatremia, hypokalemia, hyperkalemia, and acid-base imbalance may occur.

　　(3) Renal insufficiency:Due to insufficient effective blood volume and endotoxins, functional renal insufficiency may occur, and if not corrected in a timely and effective manner, it can further lead to organic renal insufficiency and ultimately renal failure.

　　(4) Severe hospital-acquired infection:Due to the low immune function of the patient's body, unbalanced intestinal microecology, reduced intestinal mucosal barrier function, and a large number of invasive operations, various hospital-acquired infections can occur during the hospital stay, which can worsen the condition, including various fungi and bacteria, etc.

　　(5) Various hemorrhages caused by coagulation and energy supply disorders:Such as nosebleeds, ecchymosis of the mucosa, even internal hemorrhage, etc.

　　(6) Abnormal blood glucose metabolism:Poor appetite and metabolic disorders of glucose by the liver can lead to severe hypoglycemia.

　　Main common clinical symptoms: extreme fatigue, severe gastrointestinal symptoms (abdominal pain, distension, nausea, anorexia, vomiting), progressive deepening of jaundice of the skin and mucous membranes, progressive deepening of urine color, and severe coagulation dysfunction (skin and mucosal bleeding, nosebleeds, gum bleeding, gastrointestinal bleeding, urethral bleeding, etc.).

　　The specific clinical manifestations vary to some extent due to the different classifications of liver failure.

　　(1) Acute liver failure: Onset is acute, with grade II or higher hepatic encephalopathy occurring within 2 weeks. The manifestations include changes in personality, abnormal behavior, mental confusion, confusion, sleep disorders, reduced orientation and understanding ability, etc.

　　(2) Subacute liver failure: Onset is relatively acute, with a duration of 15 days to 26 weeks. In addition to the same characteristics of symptoms and signs as acute liver failure, jaundice deepens rapidly. Due to the prolonged course of the disease, the incidence of various complications increases, such as ascites, peritoneal infection, and hepatic encephalopathy. Patients may experience abdominal distension, edema, and disturbance of consciousness.

　　(3) Acute-on-chronic (subacute) liver failure: There are previous manifestations of chronic liver disease, and acute or subacute liver failure occurs within a short period of time, with clinical symptoms being more severe than those of acute hepatitis.

　　(4) Chronic liver failure: On the basis of liver cirrhosis, there is progressive deterioration and decompensation of liver function, coagulation dysfunction, and various complications such as ascites, gastrointestinal bleeding, and hepatic encephalopathy.

　　The prevention of liver failure emphasizes the prevention of etiology first:

　　(1) For patients with chronic hepatitis virus infection, regular annual examination of liver function and the status of hepatitis B virus replication should be conducted. If liver function abnormalities are found, effective treatment measures should be taken in a timely manner under the guidance of a specialist doctor. Once jaundice occurs in patients with chronic hepatitis, hospitalization should be timely and liver failure should be警惕.

　　(2) Patients who have been taking antiviral drugs orally should not discontinue medication arbitrarily. Discontinuation of medication can cause a large number of viral replicates, leading to an immune reaction that may result in acute liver failure. Regular复查 of liver function and hepatitis B virus quantification should be conducted to understand whether there is a virus mutation, and the treatment plan should be adjusted in a timely manner if any mutation occurs.

　　(3) For alcoholics, it is necessary to quit drinking and to persist in doing so.

　　(4) Drug use should be cautious, and common drug-induced liver failure should not be ignored. It is important to discard the idea that 'herbal medicine is harmless'.

　　First, serological examination

　　1. Serum bilirubin: The total serum bilirubin is generally over 171.0 μmol/L (10 mg/dl), with an average daily increase of 17.1 μmol/L (1 mg/dl) or more, mainly due to the rise of direct bilirubin.

　　2. Enzyme-bilirubin dissociation: In severe liver disease, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) significantly decrease, showing a dissociation phenomenon with the rise of bilirubin, known as 'enzyme-bilirubin dissociation'.

　　3. Blood amino acid measurement: When the ratio of branched/phenylalanine is normal, the molar ratio is 3:1 to 4:1. In severe hepatitis, it decreases to below 1:1 to 1.5:1. Free tryptophan is significantly increased, playing an important role in promoting the occurrence of hepatic encephalopathy.

　　4. Prealbumin measurement: Early response to liver failure. Liver failure affects protein synthesis, with a half-life of albumin in the body of about 20 days, and prealbumin is only 1.9 days. Therefore, its concentration in the blood of patients decreases earlier.

　　Second, pathogenetic detection

　　Enzyme-linked immunosorbent assay or radioimmunoassay is used to detect serum viral hepatitis-related antigens or antibodies, or DNA probe hybridization is used to detect viral nucleic acids to determine the pathogen. If necessary, virus antigens and viral nucleic acids can be detected by liver immunohistochemistry and in situ hybridization methods. Blood cultures and other examinations should be performed multiple times for concurrent bacterial or fungal infections.

　　B-ultrasound examination

　　It can monitor the size of organs such as liver, spleen, gallbladder, bile ducts, and ultrasonic images, as well as the presence of ascites, tumors, etc.

　　Electroencephalogram examination

　　In the early stage of hepatic encephalopathy, patients show abnormalities.

　　Liver living tissue examination

　　Using 1s needle aspiration negative pressure technology for liver living tissue examination, the operation is simple, safe, and has a high success rate. It can assist in the diagnosis of hepatitis and hereditary metabolic liver disease, or help judge the prognosis. Poor prognosis is seen in patients with extensive and severe necrosis of liver cells in viral hepatitis; better prognosis is seen in those with cell swelling.

　　Through the measurement of resting energy metabolism and dietary records of different liver failure patients, it was found that liver failure patients generally have insufficient dietary nutrition intake and imbalance in the metabolism of the three major nutrients. In combination with the clinical type of liver failure and the characteristics of different complications, the following points should be paid attention to in the diet of patients:

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

　　(2) In the early stage of the disease, intravenous nutrition should be the main method, with oral nutrition as a supplement. In the recovery period, oral nutrition should be the main method, with intravenous nutrition as a supplement.

　　(3) Ensure a daily total calorie intake of more than 1500 kcal, with specific calories determined by the severity of the condition. For patients with hepatic encephalopathy, protein intake should be restricted, and amino acid preparations can be taken.

　　(4) In addition to normal daytime meals, the necessity of adding a snack before bedtime (200-300 kcal) is emphasized. Studies show that adding a snack before bedtime (mainly 50g of carbohydrates) helps improve the body's 'starvation state' and improve the patient's metabolic state.

　　1. Basic supportive therapy

　　(1) Strict isolation: The child should stay in an isolation ward, which should be disinfected, and cared for by a dedicated nurse. Electroencephalogram, intracranial pressure, B-ultrasound, and other监护 should be conducted.

　　(2) Adjusting diet: For patients with significant digestive symptoms of hepatitis, protein intake should be restricted; for those with pre-coma signs, strict fasting should be implemented, and the duration should vary according to the condition, generally 3 to 5 days. After the coma condition improves, food intake should start with a small amount of carbohydrates, and protein intake should be gradually increased as the condition stabilizes.

　　(3) Regulation of Water and Electrolyte Balance: Those with low potassium, low calcium, or low magnesium levels should be corrected promptly. According to blood sodium measurements, if there is no significant hyp钠, it is not advisable to supplement sodium salts excessively, maintaining physiological needs is sufficient to prevent cerebral edema. During the period of fasting, the daily fluid intake should be strictly limited, and glucose solution should be administered to maintain nutrition and provide calories. When there is low calcium, 5-10ml of 10% calcium gluconate should be administered intravenously daily, and for every 200ml of citrate blood administered, an additional 1g of calcium should be supplemented. For patients with metabolic alkalosis, 20-60ml of 25% arginine should be administered intravenously. Hypokalemia is prone to metabolic alkalosis, which can induce or exacerbate hepatic encephalopathy. In cases where urine output is normal, potassium should be supplemented in a timely manner.

　　2. Promoting Liver Cell Regeneration

　　(1) Glucagon-Insulin Therapy (G-I Therapy): Prevents liver cell necrosis, promotes liver cell regeneration, improves hyperammonemia and adjusts amino acid metabolism balance. The two are used in appropriate proportions to produce a synergistic effect, and the dosage varies with age. The commonly used dosage of glucagon is 0.2-0.8mg, and insulin is 2-8U (in a ratio of 1:8 to 1:10), added to 100-200ml of 10% glucose solution for intravenous infusion, 1-2 times a day. The amount of glucose should be 4g per unit of insulin, and the course of treatment is generally 10-14 days.

　　(2) Human Serum Albumin or Plasma: When the liver fails and the liver's ability to synthesize albumin is impaired, the administration of human serum albumin helps in the regeneration of liver cells and can increase the colloid osmotic pressure of plasma, alleviate ascites and cerebral edema; albumin can also bind bilirubin, reduce hyperbilirubinemia. Fresh plasma can supplement regulators and complement, enhance the body's ability to resist infection. The dosage of human serum albumin is 0.5-1.0g/kg, and plasma is 25-100ml, administered alternately, once a day or every other day.

　　(3) Hepatocyte Growth Factor (HGF): The dosage is 40-80mg of HGF added to 100-200ml of 10% glucose solution, administered by intravenous infusion, once a day, for a course of 1-2 months.

　　3. Immune Regulatory Therapy

　　Thymosin can enhance the body's ability to resist diseases and reduce serious infections. It is administered intramuscularly or intravenously at a dose of 10-40mg daily, or 40-80mg, twice or thrice a week by intravenous infusion.