Elderly liver cirrhosis

　　There are many causes of liver cirrhosis, in China, liver cirrhosis caused by viral hepatitis is the main cause, and in foreign countries, alcoholism is more common, and the common causes are as follows:

　　1. Viral hepatitis: mainly due to overlapping infection of hepatitis B, C, and D viruses;

　　2. Alcoholism: long-term and excessive alcohol consumption, with an intake of 80g of ethanol per day for more than 10 years can lead to liver cirrhosis;

　　3. Bile stasis;

　　4. Circulatory disorders;

　　5. Industrial toxins or drugs: long-term exposure to carbon tetrachloride, phosphorus, arsenic, or the use of drugs such as methyldopa and tetracycline;

　　6. Metabolic disorders, including hepatolenticular degeneration, hemochromatosis, α1-antitrypsin deficiency disease, and galactosemia;

　　7. Nutritional disorders;

　　8. Immune disorder;

　　9. Schistosomiasis infection;

　　10. Those with unknown causes are called cryptogenic liver cirrhosis.

　　Liver cirrhosis in the elderly often dies due to complications. There are many complications of liver cirrhosis, among which the most common are as follows:
　　1. Hepatic encephalopathy
　　2. Upper gastrointestinal hemorrhage
　　Upper gastrointestinal bleeding in liver cirrhosis is most often due to the rupture of esophageal and gastric fundus varices, but it should be considered whether there are complications such as peptic ulcer, acute erosive gastritis, or cardialysis syndrome. The bleeding from varices is often caused by rough, hard, or angular foods that cause trauma, erosion of the esophagus by gastric acid reflux, or severe vomiting, resulting in vomiting blood and black stools. If the amount of bleeding is not large, only black stools may occur. Large amounts of bleeding can cause shock. Under conditions of ischemia and hypoxia in the liver, liver function often deteriorates. The loss of plasma protein due to bleeding can lead to the formation of ascites. After the blood is decomposed by bacteria in the intestines, ammonia is absorbed by the intestinal mucosa, which can induce hepatic encephalopathy and even lead to death. After bleeding, the enlarged spleen may shrink or become inapparent.
　　3. Infection
　　Due to the decline in immune function of the body, hyperactivity of the spleen, and the establishment of collateral circulation between the portal and systemic veins, there is an increased opportunity for pathogenic microorganisms to enter the systemic circulation, making it prone to various infections such as bronchitis, pneumonia, tuberculous peritonitis, primary peritonitis, biliary tract infection, and sepsis caused by Gram-negative bacilli. Primary peritonitis refers to an acute inflammatory condition of the peritoneum in patients with liver cirrhosis without organ perforation in the abdominal cavity, with an incidence rate of 3% to 10%. It often occurs in patients with a large amount of ascites and is usually caused by Escherichia coli. The cause is that the phagocytic function of phagocytes is weakened during liver cirrhosis, abnormal proliferation of bacteria in the intestines, and entry into the peritoneal cavity through the intestinal wall. Additionally, due to changes in the vascular structure inside and outside the liver, bacteria can also cause sepsis or the leakage of bacteremic lymph into the peritoneal cavity from under the liver capsule or the portal lymph nodes, leading to infection. Clinical manifestations include fever, abdominal pain, distension, tenderness and rebound pain on the abdominal wall, increased ascites, elevated white blood cell count, cloudy ascites, and exudative fluid or fluid between exudative and transudative. Ascites culture may show bacterial growth. A few patients with liver cirrhosis may not have abdominal pain or fever, but instead present with hypotension or shock, refractory ascites, and progressive liver function failure.
　　4. Hepatorenal syndrome
　　When liver cirrhosis complicated with refractory ascites is not treated appropriately or the efficacy is poor, it is easy to develop hepatorenal syndrome. Its characteristics are oliguria or anuria, hyponatremia and low urinary sodium, without organic changes in the kidneys, so it is also called functional renal failure. The pathogenesis is not fully understood. Hepatorenal syndrome occurs in decompensated liver cirrhosis and is often accompanied by hypoproteinemia, portal hypertension, and severe ascites, severe sodium retention, often accompanied by jaundice. It often occurs after the extensive use of diuretics or gastrointestinal bleeding, as well as after paracentesis. Patients with low sodium, low potassium, and hepatic encephalopathy are more prone to develop it. Liver cirrhosis patients can develop oliguria or anuria without any nephritis or pyelonephritis. Urinalysis shows almost no abnormalities. Urinary concentration function is normal, and there is no sodium in the urine. Water loading test often has difficulty in urination. Azotemia may occur due to anuria, and ultimately die of uremia.
　　5. Ascites
　　In normal people, there is a small amount of fluid in the abdominal cavity, about 50ml. When the fluid volume exceeds 200ml, it is called ascites. Ascites is a common complication of decompensated liver cirrhosis.
　　6. Primary liver cancer
　　Liver cirrhosis is prone to complications of liver cancer, especially after hepatitis cirrhosis. In recent years, it has been proven that hepatitis B virus is one of the direct causes of liver cancer, with an incidence rate of 9.9% to 39.2%. About two-thirds of liver cancers occur on the basis of liver cirrhosis. If clinical symptoms such as progressive liver enlargement, especially localized enlargement and rapid onset of a large amount of ascites or blood-containing ascites, acute deterioration of the condition, jaundice, and severe pain in the liver area appear, alpha-fetoprotein (α-FP) should be tested, and a suspicion of liver cancer should be raised if the level is greater than 200ng/ml. It should be observed dynamically, and a diagnosis can be made if the level gradually increases and the condition does not improve. Alpha-FP can also be elevated during active hepatitis, but it can decrease with improvement in the condition. Liver radionuclide scanning, ultrasound, CT, and other methods are helpful for the diagnosis of liver cancer. The most reliable diagnostic basis is the pathological finding of liver cancer cells in liver biopsy.

　　The onset and progression of liver cirrhosis are generally slow, but may remain latent for several years (on average 2-5 years). Many patients are diagnosed only during physical examination, or when they suddenly vomit blood due to esophageal varices, or during laparotomy for other diseases, or even at autopsy.
　　First, General symptoms
　　Fatigue and weakness are one of the early symptoms, which are related to the activity degree of liver disease. The reasons for easy fatigue and weakness are related to insufficient calorie intake due to loss of appetite, as well as intermediate metabolic disorders of carbohydrates, proteins, fats, and insufficient energy production. In addition, due to liver damage or poor bile excretion, the decrease in blood cholinesterase affects the normal physiological function of the neuromuscular system and the reduction in the conversion of lactic acid to glycogen in the liver, resulting in excessive accumulation of lactic acid after muscle activity; weight loss is also a common symptom, mainly due to decreased appetite, impaired gastrointestinal digestion and absorption, and reduced synthesis of albumin in the body; the cause of low fever may be liver cell necrosis, inflammation activity, or due to endotoxins produced by intestinal bacteria and other endothermic substances entering the systemic circulation through collateral circulation without being inactivated by the liver. In addition, the liver cannot inactivate endothermic hormones such as reduced urinary testosterone, etc., can also be found.
　　Second, Gastrointestinal symptoms
　　There are often symptoms such as loss of appetite, accompanied by nausea, vomiting, abdominal distension, and diarrhea. These are caused by liver dysfunction and portal hypertension, which lead to obstructive congestion of the gastrointestinal tract and a disorder of secretion and absorption. In the late stage, ascites or gastrointestinal bleeding may occur.
　　1, Esophageal-gastric fundus varices, hemorrhoidal varices: Both can cause massive hemorrhage, among which massive hemorrhage due to esophageal variceal rupture is more common. It is manifested by vomiting a large amount of bright red blood and black stools. The hemorrhage is often rapid, and the patient may fall into shock or even die. Blood stools may be excreted when massive hemorrhage occurs. Hemorrhoidal hemorrhage is fresh stools, but it is less common.
　　2, Gastric mucosal lesions: They are often complications of liver cirrhosis. The condition caused by portal hypertension is called portal hypertension-related gastritis. Portal hypertension causes general expansion and distortion of the gastric mucosal and submucosal blood vessels (including capillaries, small arteries, and small veins), forming arteriovenous shunts and angiomas, and submucosal venous arteriolarization. The characteristic manifestations under endoscopy are hyperemic macules, 'mosaic sign' or 'snake skin sign'. Generally, scattered red spots appear on the basis of diffuse congestion and edema, with the center being obviously red and the periphery gradually fading, with a significant contrast between red and white areas, and clear boundaries. Some show obvious spider nevus-like changes, often accompanied by scattered or even diffuse erosion, hemorrhage, or small ulcers. It can cause upper gastrointestinal hemorrhage, the bleeding of which is milder than that from esophageal variceal rupture, and can have vomiting of coffee-colored matter and black stools.
　　3, Peptic ulcer: It is more common in patients with liver cirrhosis than in normal people. According to reports, the incidence is 18.6% and 17.7% respectively in clinical autopsies, with duodenal ulcers more common than gastric ulcers. The pathogenesis may be:
　　4, Reflux esophagitis: Due to increased abdominal pressure in patients with ascites, gastric juice refluxes into the esophagus, erodes the esophageal mucosa and causes inflammation, leading to the rupture of esophageal varices and massive hemorrhage.
　　5, Diarrhea: It is quite common, mostly with unformed stools.
　　6, Biliary infection and gallstones: The incidence of this condition in patients with liver cirrhosis is higher than in those without liver cirrhosis. Biliary infection is mostly chronic viral infection. The cause of gallstones is due to the formation of bilirubin calcium stones due to chronic hemolysis, splenic secretion of hemolysin, and biliary infection.
　　Third, manifestations of malnutrition
　　Weight loss, anemia, and various vitamin deficiencies. Such as night blindness, rough skin, follicular keratosis, smooth tongue, cheilitis, scrotal inflammation, seborrheic dermatitis. Pale or spoon-shaped nails, polyneuritis, etc.
　　Fourth, hematological manifestations
　　Hemorrhagic tendency is common, caused by a lack of coagulation factors and thrombocytopenia due to splenic hyperfunction, leading to bleeding spots or ecchymosis on the skin and mucous membranes, nosebleeds, and gum bleeding. Women often have menorrhagia. When splenic hyperfunction occurs, it inhibits the production of blood cells and increases the destruction of blood cells, resulting in a decrease in red and white blood cells and platelets. Anemia can be caused by a lack of iron, folic acid, and vitamin B12. Hemolytic anemia can be caused by splenic hyperfunction, with mild symptoms and difficult to identify clinically. Post-hepatitis liver cirrhosis can also be complicated with aplastic anemia and hematological diseases (thrombocytosis, acute myeloid leukemia, chronic myeloid leukemia, chronic lymphocytic leukemia, and Evans syndrome).
　　Bone marrow examination is helpful in distinguishing various anemias. There may be an increase in plasma cells during hypergammaglobulinemia, and the bone marrow is hyperactive during chronic liver failure. Hemochromatosis patients may have excessive hemosiderin in the bone marrow. Rare cases may appear with spherocytic anemia.
　　Fifth, nervous and mental symptoms
　　If symptoms such as drowsiness, excitement, and rigidity occur, one should be vigilant about the occurrence of hepatic encephalopathy.
　　Liver cirrhosis can be divided into compensated and decompensated phases according to clinical manifestations and liver function status.
　　The formation and development process of liver cirrhosis is usually slow (except for acute severe type and sub-severe type hepatitis, which can develop into liver cirrhosis in a short period of time), the liver has a strong regeneration ability, has a large compensatory capacity, and often has a relatively long compensatory period. If liver cirrhosis in the compensatory period is detected in time and the progression of the disease is controlled, it may be possible to keep the patient in the compensatory stage for a long time.
　　

　　Elderly liver cirrhosis should strengthen the three-level prevention measures.

　　1.一级预防

　　It should prevent the cause through health education to achieve the goal of no disease prevention. It should actively prevent viral hepatitis, improve living standards, have a reasonable diet, adjust drugs that affect liver function, reduce alcohol consumption, etc.

　　2.二级预防

　　This means early diagnosis and early treatment, and it should actively organize effective physical examinations for the elderly, promptly discover asymptomatic patients with liver cirrhosis, monitor the liver structure and functional status, prevent the occurrence of severe complications, and take appropriate health care measures to delay the aging of the body.

　　3.三级预防

　　That is, to establish a diagnosis and through reasonable treatment, reduce the damage of liver cirrhosis to the body, reduce the harm of complications to the body, and establish timely contact with secondary and tertiary hospitals through community services to improve the health status and quality of life of the elderly.

　　The diagnosis of decompensated liver cirrhosis in the elderly is not difficult, as symptoms, signs, and laboratory tests all show significant manifestations; early diagnosis of liver cirrhosis is more difficult, and it requires the integration of multiple examination results for a definitive diagnosis. The routine examination methods for elderly liver cirrhosis are as follows:
　　Firstly, laboratory examinations
　　1. Blood routine
　　In the case of splenic hyperfunction, there is a decrease in the total blood count. Leukopenia is often at 4.0×10⁹/L (4,000) below. Platelets are usually below 50×10⁹/L (50,000) below. Most cases present with normal cellular anemia, and a few cases of liver cirrhosis may be macrocytic anemia.
　　2. Urinalysis
　　Urine examination shows jaundice when bilirubin/urobilinogen in urine is positive.
　　3. Routine examination of ascites
　　Ascites is transudative fluid, with a density below 1.018, negative Lee's test, and a cell count of 100/mm³Below, the protein quantification is less than 25g/L.
　　4. Liver function tests
　　Liver function is very complex. There are many clinical testing methods, but it is still difficult to reflect the whole functional state. Various laboratory results need to be combined with clinical manifestations and other examinations for comprehensive analysis.
　　Secondly, auxiliary examinations
　　1. Ultrasound examination
　　During liver cirrhosis, due to the proliferation of fibrous tissue, ultrasound shows uniform, diffused dense dot-like echoes, and the echoes are enhanced in the late stage. The liver volume may decrease. If there is portal hypertension, the portal vein may widen, and the spleen may thicken.
　　2. Liver biopsy
　　This method can determine the diagnosis and understand the histological type of liver cirrhosis and the degree of liver cell damage and connective tissue formation. However, if the amount of tissue taken is too little, there may be false-negative results. Currently, the rapid puncture method is often used, which is simple to operate, has few complications, and is safe.
　　3. Laparoscopy
　　It is one of the reliable methods for diagnosing liver cirrhosis, which can directly observe the liver surface. In typical cases, nodular liver surface, varices on the abdominal wall, and splenomegaly can be seen. Liver biopsy can also be performed under direct vision. For cases that cannot be diagnosed clinically, this examination can confirm the diagnosis and can also find early lesions.
　　4. Esophageal X-ray barium meal examination
　　When there are varices in the esophagus, the varices are higher than the mucosa, and the contrast agent is unevenly distributed on the mucosa, resulting in worm-eaten or earthworm-like filling defects, and the longitudinal mucosal folds become wider. When there are varices in the fundus of the stomach, the contrast agent appears in a chrysanthemum-like filling defect.
　　5. Esophagogastroduodenoscopy or gastroscopy
　　It can directly observe whether there is varices in the esophagus and stomach, and understand the degree and range of varices, which is helpful for the differential diagnosis of upper gastrointestinal bleeding. The accuracy of gastroscopy in detecting varices is higher than that of esophageal X-ray barium meal examination.
　　6. Radionuclide scanning
　　Colloid 198 Au or other radionuclides are used for liver scanning, and in patients with liver cirrhosis, the liver area can be seen to have a general sparse, uneven, or spotted reduction in radioactivity. Scanning with 99mTc and 113In can show the size and shape of the spleen. During liver cirrhosis, in the compensatory stage, the liver shadow may increase, and in the late stage, the liver shadow may decrease, and the spleen shadow may increase.
　　7. Computerized X-ray tomography (CT)
　　It has little diagnostic value for liver cirrhosis. In the early stage, the liver is enlarged and has low density. In the late stage, the liver shrinks, the density is often increased, accompanied by splenomegaly and ascites. Some people believe that the ratio of the width of the lingula to the right lobe can be used to diagnose liver cirrhosis, and the ratio is greater than 65%, indicating a very high possibility of liver cirrhosis; less than 6% indicates a low possibility.
　　8. Selective hepatic artery angiography
　　It can reflect the degree, scope, and type of liver cirrhosis, and has certain significance for distinguishing it from primary liver cancer.
　　9. Percutaneous splenic vein angiography
　　It can observe the images of splenic vein, portal vein, and collateral veins, differentiate whether the portal hypertension is caused by intraportal or extraportal obstruction, and understand the degree and blood flow direction of collateral circulation, providing data for shunting surgery.
　　10. Liver venous catheterization
　　Liver venous pressure can be measured to understand the changes in portal vein pressure.

　　Dietary recommendations for elderly liver cirrhosis patients:

　　1. Reasonable protein intake

　　Protein is the main raw material for the repair and regeneration of liver tissue cells. Therefore, the supply of protein must be sufficient, with 1.5-2 grams per kilogram of body weight per day, with a total protein intake of about 100-120 grams per day. It is advisable to eat more high-quality protein-rich foods such as milk, eggs, lean meat, fish, shrimp, and soy products.

　　2. High caloric intake

　　High caloric intake can ensure that the protein provided in the diet is fully utilized by the body to synthesize its own protein, repair denatured and necrotic liver cells, and also provide sufficient energy for the liver.

　　3. High carbohydrates

　　Adequate carbohydrates can provide energy, synthesize glycogen, protect liver cells, and prevent toxins from damaging liver cells.

　　4. Adequate vitamins

　　Vitamin B group is a coenzyme that catalyzes biochemical reactions in the body. The need for vitamin B group in the body increases when consuming high-carbohydrate foods. Vitamin C can protect liver cells and enhance resistance.

　　5. Moderate fat

　　When liver function decreases, the synthesis and secretion of bile汁 decrease, affecting fat metabolism. Eating too much fat is easy to deposit in liver cells, causing liver cell damage.

　　6. Limit salt

　　When liver cirrhosis in the late stage appears edema and ascites, the intake of salt should be restricted, and low-salt, sodium-free, or low-sodium diet should be adopted according to the condition.

　　7. Avoid刺激性 foods and various spicy foods

　　Such as green onions, garlic, pepper, chili, etc.

　　8. Eat less and more often

　　The amount of food consumed per meal should not be excessive, and the frequency of meals can be appropriately increased.

　　There is no special treatment for elderly liver cirrhosis, the key is early diagnosis, targeted treatment for the cause and strengthening general treatment, so as to alleviate the condition and extend the compensation period. For patients in the decompensation period, the main treatment is symptomatic treatment, improving liver function, and rescuing complications.

　　First, treatment

　　1. Routine treatment

　　(1) General treatment:

　　Rest: Patients with compensated liver function can participate in light work and pay attention to the combination of work and rest, and have regular follow-up. Patients with decompensated liver function or complications need rest or hospital treatment.

　　Diet: It is advisable to consume high-calorie, high-protein, vitamin-rich and easily digestible foods. The daily caloric requirement is 125.5 to 167.4 J/kg (30 to 40 Cal/kg), with the distribution of calories from carbohydrates and fats each accounting for 40%, and protein 20%. It is strictly forbidden to drink alcohol, and the intake of animal fats should not be excessive. Patients with hepatic encephalopathy should strictly limit protein-rich foods. Those with ascites should be on a low-sodium or sodium-free diet. Patients with esophageal varices should avoid rough and hard foods.

　　(2) Elimination of the cause: When liver damage is caused by drug intoxication, medication should be stopped. For liver damage secondary to other diseases, treatment of the primary disease should be given first. For liver damage caused by parasitic infection, treatment of the parasitic disease should be given. For liver damage caused by malnutrition, nutrition should be supplemented. For liver damage caused by bacterial infection, antibiotic treatment should be given. When there is active chronic hepatitis, control of hepatitis should be carried out, and antiviral and immunomodulatory treatment, such as interferon, arabinoside, etc., should be given if necessary.

　　(3) Antifibrotic treatment: Clinically proven drugs include prednisone (prednisone), lycorine, colchicine, penicillamine (D-penicillamine). Traditional Chinese medicine includes cucurbitin, B papain, salvia miltiorrhiza, Cordyceps sinensis, sparganium, etc., and free radical scavengers have a significant antifibrotic effect.

　　(4) Vitamin supplementation: Vitamin deficiency is manifested in liver cirrhosis, and appropriate supplementation of vitamin B1, B2, C, B6, niacin, folic acid, B12, A, D, and K is recommended.

　　(5) Protection of liver cells, prevention and treatment of liver cell necrosis, and promotion of liver cell regeneration with the drug glucuronic acid (glucuronolactone), which can have the effect of releasing liver toxins. In addition, there are inosine, coenzyme A, which all have the function of protecting the liver cell membrane, and energy preparations, protein anabolic agents, etc., which all have the function of promoting liver cell regeneration. Recent research has proven that liver cell growth factors, dinoprost (prostaglandin E2), thiol compounds (glutathione, cysteine), vitamin E, etc., have the effects of anti-liver cell necrosis and promoting liver cell regeneration.

　　(6) Treatment of ascites:

　　①Limiting sodium and water intake: Daily intake of sodium salt should be limited to 500-800mg (sodium chloride 1.2-2.0g), and water intake should be limited to about 1000ml/day. If there is significant hyponatremia, it should be limited to 500ml or less. Approximately 15% of patients can produce spontaneous diuresis through the limitation of sodium and water intake, leading to the reduction of ascites.

　　②Diuretics: The combination of potassium-sparing diuretics and potassium-wasting diuretics is mainly used, with intermittent application. If potassium-wasting diuretics are used alone, attention should be paid to potassium supplementation. The diuretic treatment should aim to reduce body weight by no more than 0.5kg per day, and the dose should not be supplemented excessively. The speed of diuretics should not be too rapid to avoid triggering hepatic encephalopathy,肝肾 syndrome, and other complications. Moreover, elderly patients using diuretics should pay attention to changes in blood pressure due to body position, and they have poor internal environment stability, which is prone to disorders of water and electrolyte metabolism and glucose metabolism. Regular monitoring of electrolytes is recommended.

　　③Drainage of ascites combined with injection of human serum albumin: Drain ascites 3 times a day or a week, each time 4000-6000ml, or 10000ml at a time, and simultaneously intravenously inject 40g of human serum albumin. This is better than the therapeutic effect of large-dose diuretics, can shorten the hospital stay, and has fewer complications.

　　④To improve plasma colloid osmotic pressure: Regular, small, multiple intravenous infusions of fresh blood or human serum albumin per week are helpful for improving the general condition of the body, restoring liver function, increasing plasma osmotic pressure, and promoting the regression of ascites.

　　⑤ Ascites Concentration and Reinfusion: 5000-10000ml of ascites can be drained, processed or 500ml, and then reinfused intravenously. In addition to clearing part of the retained sodium and water, it can increase the plasma protein concentration and effective blood volume, improve renal blood circulation, thereby reducing or eliminating ascites.

　　⑥ Abdominal-Cervical Venous Drainage, also known as LeVeen Drainage Method.

　　⑦ Transjugular Intrahepatic Portosystemic Shunt (TIPSS): It is a method of establishing a shunt channel between the main branches of the portal vein and the hepatic vein in the liver using interventional radiology.

　　(7) Treatment of Complications:

　　① Upper Gastrointestinal Bleeding: The bleeding caused by the rupture of esophageal and gastric varices is the most severe, posing a serious threat to the patient's life.

　　② Hepatic Encephalopathy: There is currently no specific treatment, and comprehensive measures should be taken for treatment.

　　③ Treatment of Hepatorenal Syndrome

　　④ Spontaneous Peritonitis: After the occurrence of spontaneous peritonitis and sepsis, liver damage often worsens rapidly, so it is necessary to actively strengthen supportive treatment and the application of antibacterial drug treatment, emphasizing early treatment, combined use of antibiotics, and immediate treatment upon diagnosis, without waiting for the report of abdominal fluid (or blood) bacterial culture before starting treatment. Antibiotics mainly targeting Gram-negative bacilli and considering Gram-positive cocci should be selected. Due to the high recurrence rate of the disease, the duration of medication should not be less than two weeks. In the elderly, due to less body water and poor renal function, attention should be paid to the high drug concentration and toxic reactions caused by the same dose as young people.

　　(8) Liver Transplantation: Since the first human liver transplantation in 1963, due to the advancement of surgical techniques, the improvement of organ procurement and preservation methods, especially the introduction of the new immunosuppressive agent cyclosporin A, liver transplantation has moved from the experimental stage to a new era of clinical application, becoming an effective method to save severe liver disease patients.

　　2. Optimal Scheme

　　Liver cirrhosis patients should strengthen etiological treatment. Liver-protecting drugs can be used with silybin (Yiganling). For patients with liver cirrhosis caused by hepatitis B and C, antiviral treatment can be applied, using lamivudine (Hepadine) and interferon. Antifibrotic treatment, colchicine is the first choice. In the early stage of liver cirrhosis, the compound Danshen and huanghua injection each 20ml should be administered intravenously in 250ml of 5% glucose. The clinical efficacy is good. The compound 861 mixture (consisting of huanghua Danshen, chongxue藤, and other 10 herbs), has a significant therapeutic effect on chronic hepatitis and liver cirrhosis. For the treatment of ascites, diuretics should be used in combination with potassium-sparing diuretics and potassium-wasting diuretics, intermittently and alternately.原则上，firstly use spironolactone, and add furosemide or hydrochlorothiazide if ineffective. Measure the ratio of urine sodium to potassium, if this value is 1, use furosemide or spironolactone in combination. Initially, use spironolactone 20mg, 4 times a day, and increase by 80ml/d every 5 days according to the diuretic response. If the effect is still not significant, add furosemide, 40-60mg/d. For patients with esophageal and gastric varices rupture and upper gastrointestinal bleeding, endoscopic sclerotherapy and drug treatment to reduce portal vein pressure should be the first choice. If the above treatment is ineffective and bleeding recurs, if the patient's liver function is good, surgical treatment can be considered.

　　3. Rehabilitation Treatment

　　Patients with liver cirrhosis should strengthen reasonable nutrition, minimize the use of drugs that affect liver function, and regularly review liver function and conduct liver ultrasound and other imaging examinations. For patients with esophageal varices and gastroesophageal varices, attention should be paid to avoid spicy, rough foods, and minimize alcohol consumption. It is necessary to avoid activities that increase abdominal pressure, such as forceful defecation and severe coughing, and to regularly review gastroscopy. If there is a red sign, it should be timely to inject sclerosing agents to prevent rebleeding. For patients with liver cirrhosis complicated with splenomegaly and hypersplenism, consideration can be given to scheduled splenic embolization or splenectomy. For patients with hepatic encephalopathy, attention should be paid to avoid high-protein diets and keep the bowels通畅. For patients with liver cirrhosis complicated with ascites, regular infusion of human serum albumin should be considered. Through the above treatments, efforts should be made to minimize the damage to liver cirrhosis patients from complications and improve the quality of life.

　　II. Prognosis

　　Early cirrhosis of the liver can be stabilized and symptoms improved with appropriate treatment, maintaining the ability to work, and partial reversal of liver pathological changes. If the etiology continues to act, the liver inflammation and necrosis are in an active state, the condition will continue to develop, from the compensation period to the decompensation period.