Overview:

Liver cirrhosis is a common chronic liver disease, which is caused by the long-term or repeated action of one or more causes, causing diffuse damage to the liver. Histopathologically, there is extensive hepatocyte degeneration, necrosis, regeneration and regenerative nodule formation, connective tissue proliferation and fibrous septa formation, leading to the structural destruction of liver lobules and the formation of false lobules. The liver gradually deforms, hardens and develops into cirrhosis. . Clinically, in the early stage, there may be no obvious symptoms due to the strong compensatory function of the liver; in the later stage, multiple systems are involved, with liver function damage and portal hypertension as the main manifestations, and gastrointestinal bleeding, hepatic encephalopathy, secondary infection, and Cancer and other serious complications.

Cause:

(1) Viral hepatitis is mainly hepatitis B and C (formerly known as non-A, non-B) viral hepatitis. Hepatitis A virus is generally not Development of cirrhosis of the liver. Its pathogenesis is related to immune abnormalities caused by hepatitis virus. Its pathogenesis is mainly through the stage of chronic hepatitis, especially chronic active hepatitis, and gradually evolves into cirrhosis. Post-hepatitis cirrhosis mostly manifests as macronodular cirrhosis; a few cases may also manifest as micronodular cirrhosis, such as a slow and protracted disease course with mild but uniform inflammatory necrotic lesions. The course from viral hepatitis to liver cirrhosis can be as short as a few months or as long as dozens of years.

(2) Schistosomiasis schistosomiasis parasitizes in the mesenteric vein branches. The eggs enter the liver with the blood flow and are mainly deposited in the portal area. The stimulation of the eggs and their toxic products causes a large amount of connective tissue hyperplasia, leading to Liver fibrosis and portal hypertension. In schistosomiasis cirrhosis, the left lobe is more severely affected, and there are larger nodules on the liver surface. Because there is no obvious degeneration and regeneration of liver cells in other parts of the liver except for the atrophy of liver cells near the egg deposits, clinical changes in liver function are mild, and portal hypertension appears earlier. In the past, it was called schistosomiasis cirrhosis. Should be called schistosomiasis liver fibrosis.

(3) Chronic alcoholism: Long-term heavy drinking, acetaldehyde, the intermediate metabolite of alcohol, directly damages the liver, and the development of cirrhosis through fatty liver is the main pathogenesis of alcoholic cirrhosis. Long-term malnutrition caused by alcohol abuse reduces the liver's resistance to certain toxic substances, which also plays a certain role in the disease.

(4) Drugs and chemical poisons Many drugs and chemical poisons can damage the liver, such as long-term use of isoniazid, tetracycline diacetate, methyldopa, cinchofen, etc., or long-term repeated exposure to certain Chemical poisons such as carbon tetrachloride, phosphorus, arsenic, chloroform, etc. can cause drug-induced or toxic hepatitis and chronic active hepatitis, and then develop into toxic (drug-induced) macronodular or micronodular cirrhosis.

(5) Malnutrition Long-term malnutrition, especially the lack of protein, B vitamins, vitamin E and anti-lipid factors such as choline, can cause liver cell necrosis and fatty liver, until it develops into nutritional deficiencies. Adverse cirrhosis of the liver. But some people deny the direct relationship between malnutrition and human liver cirrhosis. At present, it is believed that long-term nutritional imbalance can reduce the liver's resistance to other pathogenic factors.

(6) Circulatory disorders, chronic congestive heart failure, constrictive pericarditis and hepatic vein obstruction syndrome (Budd chiari syndrome) caused by various causes can cause long-term blood stasis and hypoxia in the liver. Hepatocyte necrosis and connective tissue hyperplasia in the central lobule area lead to stasis cirrhosis, which is small nodular in shape. Caused by heart disease, also known as cardiogenic cirrhosis, there is liver enlargement and liver function damage may not be very serious, but may also manifest as mild jaundice, reduced plasma albumin, and ascites.

(7) Cholestasis When intrahepatic cholestasis or extrahepatic bile duct obstruction persists, it can lead to liver cell ischemia, necrosis, fibrous tissue proliferation and the formation of cirrhosis. It can generally be divided into intrahepatic cholestasis and extrahepatic bile duct obstruction biliary cirrhosis. Primary biliary cirrhosis is caused by inflammation and obstruction of small intrahepatic bile ducts related to autoimmune factors.

(8) Intestinal infection and inflammation Chronic specific or non-specific intestinal inflammation often causes digestion, absorption and nutritional disorders, and toxins produced by pathogens in the intestine reach the liver through the portal vein, causing hepatocytes to Degeneration and necrosis develop into cirrhosis.

(9) Metabolic diseases: Hereditary and metabolic diseases cause certain substances to be deposited in the liver due to metabolic disorders, causing degeneration and necrosis of liver cells and proliferation of connective tissue to form cirrhosis.

1. Hepato-lenticular degeneration, also known as Wilson's disease.

Due to congenital abnormalities in copper metabolism, copper deposits in the liver and brain tissue and causes disease. It is characterized by the coexistence of liver cirrhosis and bilateral basal ganglia degeneration. Clinically, in addition to symptoms of liver cirrhosis, there are mental disorders and extrapyramidal symptoms, such as lack of facial expression, drooling, difficulty swallowing and speaking, hands, feet and head. Neck tremor, muscle stiffness and other symptoms.

2. Hemochromatosis is a liver cirrhosis caused by iron metabolism disorder and excessive iron deposition in liver tissue. Most of them are small nodules. In the late stage, they can also manifest as macronodular cirrhosis. The main clinical manifestations are liver cirrhosis, diabetes and skin pigmentation.

Pathology:

The liver shows chronic diffuse damage. In the early stage, the liver volume may be slightly larger. In the late stage, the liver shrinks due to fibrosis, becomes hard, loses weight, and the surface is covered with brown color. Or gray-brown nodules of varying sizes, surrounded by gray-white connective tissue. It has the following characteristics under the microscope. ① Extensive liver cell degeneration and necrosis, and regenerated liver cells form irregularly arranged liver cell regeneration nodules. The regenerated liver cells vary in size and are arranged in disorder. Due to the abnormal relationship with the biliary tract and portal vein system, their functions are much lower than that of normal liver cells. ② Connective tissue hyperplasia begins in the portal area and under the capsule, extends into the liver lobules, and combines with the connective tissue in the liver lobules to form a membrane-like structure, which separates the liver lobules and changes them into pseudo lobules. ③In the pseudolobule, the central vein is often located on one side of the lobule. Some pseudolobules are composed of several incomplete liver lobules, and may have two or three central veins, or even no central vein. Direct communication may occur between the portal vein, hepatic vein and small branches of the hepatic artery, resulting in short circuits. ④ There are varying degrees of inflammatory cell infiltration in the proliferated connective tissue, and bile duct-like structures (pseudo bile ducts) can be seen.

Pathology and Physiology

1. Liver hypofunction due to massive necrosis of liver cells, and the function of new hepatocytes is far from normal, resulting in reduced liver function, such as the synthesis of plasma albumin , the metabolism of bile pigments, the detoxification of harmful substances, the inactivation of estrogen, the increase of antidiuretic hormone, the secondary increase of aldosterone, and the production of coagulation factors, etc. are all affected and cause various clinical manifestations.

2. Portal hypertension: Due to the structural destruction of the liver lobules and the proliferation of fibrous tissue, the portal vein blood channels are reduced. In the regenerated liver cell mass, the capillaries are abnormally tortuous, blocking blood flow. In addition, the direct communication between the branches of the portal vein and the branches of the hepatic artery greatly increases the portal vein pressure. The normal portal pressure is lower than 1.96kpa (200mmH2O). When the portal pressure exceeds 2.94kpa (300mmH2O), gastrointestinal congestion, splenic congestion and enlargement, ascites formation, and the establishment of collateral circulation between the portal vein and vena cava will occur. The collateral circulation of the portal vein and vena cava is mainly found in the following locations: (1) The lower esophagus and the fundus of the stomach, and the gastric coronary vein and esophageal vein anastomose. ⑵ In the lower rectum, the superior hemorrhoidal vein of the lower mesentery and the hemorrhoid of the inferior vena cava, the infrahaemorrhoidal vein anastomoses. ⑶ Around the umbilicus, the umbilical vein and paraumbilical vein that have been blocked since birth reopen and anastomose with the subcutaneous veins of the abdominal wall. ⑷The contact point between abdominal organs and retroperitoneal tissues, such as the veins between the liver and diaphragm, the veins in the splenorenal ligament, etc. Among the above-mentioned side branches, those at the lower end of the esophagus appear earlier and are prone to rupture, causing massive bleeding and endangering lives. The reasons are: ① The esophageal vein is close to the portal vein and is easily affected by portal hypertension. ② The esophageal veins are very shallow and located in the loose connective tissue of the submucosa. When varicose veins occur, this layer of connective tissue is also compressed and atrophied. ③ The esophageal vein is located in the chest cavity and is affected by the negative intrathoracic pressure during inhalation, making it easier for portal vein blood to flow in.

3. In addition to portal hypertension, the formation of ascites also has the following factors:

(1) Hypoalbuminemia, decreased function of the liver in synthesizing albumin, and insufficient protein intake , Intestinal congestion causes digestion and absorption disorders. When plasma albumin is lower than 25-30g/L, ascites and limb edema often occur.

(2) Hepatic lymph imbalance When the hepatic venous outflow is blocked, plasma penetrates from the liver sinusoidal wall into the parasinusoidal space (Disse cavity), resulting in increased hepatic lymph production, which can reach 7-7 per day. 11L (normally 1-3L), a large amount of lymph fluid exceeds the reflux and transportation capacity of the thoracic duct, and the lymph fluid overflows from the liver capsule surface and portal lymphatic vessels into the abdominal cavity. This ascites has a high protein content, is produced quickly, and is not easy to absorb.

(3) Endocrine factors Increase in antidiuretic hormone, which increases water reabsorption.

The activity of the third factor adsorption hormone decreases, urinary sodium excretion decreases, and ascites aggravates. Secondary increase in aldosterone increases water and sodium reabsorption. The activity of prostaglandin (PGE, PGE2) atrial natriuretic peptide decreases, resulting in decreased renal blood flow, sodium excretion and urine output.

(4) Renal factors: In liver cirrhosis, renal hemodynamics change significantly, effective blood volume decreases, and abdominal pressure increases. Renal vasoconstriction reduces renal blood flow and glomerular filtration rate, and decreases water and sodium levels. Retention, oliguria or anuria. Severe cases can form so-called functional renal failure.

Symptoms:

The onset and progression of liver cirrhosis are generally slow and can remain dormant for 3-5 years or more than ten years. Its clinical manifestations can be divided into liver function Compensation and decompensation periods, but the boundary between the two periods is not obvious or overlaps, and should not be applied mechanically.

1. Liver function compensation phase Symptoms are mild and often lack specificity, with fatigue, loss of appetite and indigestion being the main symptoms. There may be nausea, oiliness, abdominal bloating, upper abdominal discomfort, dull pain and diarrhea. These symptoms are mostly caused by gastrointestinal congestion, secretion and absorption dysfunction. Symptoms often appear intermittently, aggravated by fatigue or comorbidities, and can be relieved with rest or appropriate treatment. The spleen is mildly or moderately enlarged, and liver function test results can be normal or slightly abnormal.

Some cases occur insidiously and are only discovered during physical examinations, surgeries for other illnesses, or even autopsies.

2. Liver function decompensation stage has significant symptoms, mainly two categories of clinical manifestations caused by decreased liver function and portal hypertension, and may have systemic and multi-system symptoms.

1. Systemic symptoms: The general condition and nutritional status are poor, weight loss, lack of energy, and severe cases are weak and bedridden. The skin is dry and rough, and the complexion is gray and dark. Anemia, glossitis, angular stomatitis, night blindness, polyneuritis and edema are common. There may be irregular low-grade fever, which may be due to liver cell necrosis; reduced liver detoxification function; toxins absorbed by the intestines enter the systemic circulation; portal thrombosis or endotitis; secondary infection, etc.

2. Digestive tract symptoms include significant loss of appetite, epigastric discomfort and fullness after eating, nausea and even vomiting, poor tolerance to fat and protein, and eating greasy food can easily cause diarrhea. Patients experience unbearable abdominal distension due to ascites and gastrointestinal pneumatosis, and toxic tympanic bowel may occur in the later stages. The above symptoms are related to gastrointestinal congestion, edema, inflammation, digestion and absorption disorders and intestinal flora imbalance. More than half of the patients have mild jaundice, and a few have moderate or severe jaundice, the latter indicating progressive or extensive necrosis of liver cells.

3. Bleeding tendency and anemia often include epistaxis, gum bleeding, skin ecchymosis and gastrointestinal mucosal erosion and bleeding. The bleeding tendency is mainly due to the decreased function of the liver in synthesizing coagulation factors, thrombocytopenia caused by hypersplenism, and increased capillary fragility. Patients still have varying degrees of anemia, mostly caused by nutritional deficiencies, low intestinal absorption function, hypersplenism, gastrointestinal blood loss and other factors.

4. Endocrine disorders: Endocrine disorders include increases in estrogen, aldosterone, and antidiuretic hormone. The main reason is that decreased liver function weakens their inactivating effects, and accumulates in the body and increases excretion in the urine. When estrogen increases, it inhibits the function of the anterior pituitary gland through a feedback mechanism. This affects the functions of the pituitary-gonadal axis and the pituitary-adrenocortical axis, resulting in a decrease in male hormones and sometimes a decrease in adrenocortical hormones.

Due to the imbalance between estrogen and male hormones, male patients often suffer from loss of sexual desire, testicular atrophy, hair loss, breast development, etc.; female patients suffer from irregular menstruation, amenorrhea, infertility, etc. In addition, some patients may develop spider nevi and/or telangiectasia on the face, neck, upper chest, back, shoulders, upper limbs and other areas with vena cava drainage; redness and scales may appear on the large and hypothenar muscles of the palms and fingertips. Liver Palm. It is generally believed that the appearance of spider nevi and liver palms is related to the increase in estrogen, and some vasodilator active substances that have not been inactivated by the liver also play a certain role. When liver function damage is severe, the number of spider nevi can increase and increase, and when liver function improves, it can decrease, shrink or disappear.

When aldosterone increases, it acts on the distal renal tubules, increasing sodium reabsorption; when antidiuretic hormone increases, it acts on the collecting ducts, increasing water absorption. Sodium and water retention can lead to decreased urine output and edema. It also plays an important role in promoting the formation and aggravation of ascites. If the adrenal cortex function is impaired, skin pigmentation may occur on the face and other exposed parts.

Signs:

The clinical manifestations of portal hypertension constitute three clinical manifestations of portal hypertension: splenomegaly, establishment and opening of collateral circulation, ascites, and clinical manifestations of portal hypertension. All of the above are of great significance. In particular, the establishment and opening of collateral circulation have characteristic value for diagnosis.

1. Splenomegaly is often moderate splenomegaly, and some may reach below the umbilical cord. The main reason is splenic congestion, toxins and inflammatory factors. Reticuloendothelial cell hyperplasia is also related. The spleen is mostly medium hard, with a smooth surface and blunt edges. If perisplenitis occurs, it can cause left upper quadrant pain or abdominal pain. If there is a lot of ascites, the palpation method must be used. In cases of massive upper gastrointestinal bleeding, the spleen may temporarily shrink or even become untouchable, which is of great value in identifying and determining esophageal variceal bleeding. Splenomegaly is often accompanied by a decrease in white blood cells, platelets, and/or red blood cells, which is called hypersplenism.

2． Establishment and opening of collateral circulation When the portal vein pressure increases and exceeds 1,96kpa (200mmmH2O), the return blood flow from the digestive organs and spleen is blocked, forcing the establishment of collateral circulation between blood vessels in many parts of the portal system and the systemic circulation. The clinically more important ones include: ① Varicose veins in the lower esophagus and gastric fundus, which are formed by anastomosis between the gastric coronary vein of the portal vein system and the esophageal vein, intercostal vein, azygos vein, etc. of the vena cava system. Severe variceal bleeding is often caused by a significant increase in portal pressure, esophagitis, injury from rough and sharp food, or a sudden increase in intra-abdominal pressure. ② Abdominal wall and periumbilical varicose veins. When portal hypertension occurs, the umbilical vein reopens and expands, and is connected to the accessory umbilical vein, abdominal wall veins, etc. Curved veins can be seen on the periumbilical abdominal wall. The direction of blood flow is upward above the umbilicus and downward below the umbilicus. It can be distinguished from inferior vena cava obstruction. If the umbilical vein has significant varicose veins, the lumen will expand and blood flow will increase, and sometimes a continuous venous murmur can be heard. ③ Hemorrhoids form and may cause blood in the stool when they rupture.

3. Ascites is the most prominent manifestation of decompensation of liver cirrhosis. The direct cause of the formation of ascites is excessive water and sodium retention. The mechanism is a reduction in plasma albumin content, which leads to a reduction in plasma colloid osmotic pressure, lymphatic reflux obstruction, endocrine dysfunction, kidney disease, etc. Factors (see pathology for details): There is often flatulence before the appearance of ascites. When there is a large amount of ascites, the abdomen is distended and the abdominal wall is tight and shiny, causing the patient to have difficulty moving. Increased abdominal pressure can compress intra-abdominal organs, causing umbilical hernia, and can also cause The elevation of the diaphragm causes dyspnea and palpitations. Some patients may develop pleural effusion, which is more common on the right side. This is mostly caused by ascites entering the chest cavity through the diaphragmatic lymphatic vessels, which is called hepatic pleural effusion. Moving dullness occurs in moderate or above ascites. Moving dullness is not obvious in small amounts of ascites and can be detected with the help of ultrasound.

Liver palpation The size, hardness and smoothness of the liver are related to the amount of fat infiltration in the liver, liver cell regeneration, fibrous tissue proliferation and contraction. In the late stage of cirrhosis, the liver is small, hard, and has a nodular surface.

Diagnosis:

Decompensated cirrhosis can often be diagnosed based on clinical manifestations and relevant examinations. The main diagnostic basis for liver cirrhosis is: ① There is a history of viral hepatitis, schistosomiasis, long-term drinking, etc.; ② The liver can be slightly larger, but often shrinks, becomes hard, and has an uneven surface in the late stage. ③ Liver function damage. ④Clinical manifestations of portal hypertension. ⑤ Liver biopsy showed pseudolobule formation.

Treatment:

(1) Rest People with compensated liver function should reduce their activities appropriately and be able to participate in some work, and pay attention to the balance between work and rest. Decompensated patients should mainly stay in bed.

(2) Diet should be rich in nutrients, easy to digest and absorb, and generally high-calorie, high-protein, vitamin-rich and delicious foods are suitable. The fat content should not be too high, but it does not have to be too restrictive. When you have ascites, you should eat less salt. Some people currently advocate that you don’t need to eat a salt-free diet, because it will affect your appetite and cause more harm than good. People with significant liver function damage or high blood ammonia who are prone to hepatic encephalopathy should temporarily limit protein intake. Alcohol and rough and hard food should be avoided.

(3) Supportive therapy: Most decompensated patients have nausea, vomiting, eating little or being unable to eat. Glucose can be infused intravenously, and vitamin C, potassium chloride, inosine, insulin, etc. can be added. Special attention should be paid to maintaining water, electrolyte and acid-base balance, especially the supplement of potassium salts. In addition, compound amino acids, blood, plasma and albumin can also be used as appropriate.

2. Drug treatment There is currently no specific drug, and it is not advisable to abuse drugs, otherwise it will increase the burden on the liver and be counterproductive.

1. Liver fibrosis is a necessary process for the occurrence and development of liver cirrhosis, and anti-fibrosis treatment is of great significance.

2. Traditional Chinese medicine has a long history of treating liver cirrhosis and can indeed improve symptoms and liver function. Commonly used drugs are mainly used to soften the liver, dissipate stagnation, activate blood circulation and remove blood stasis, and treatment is based on syndrome differentiation of the disease.

3. Treatment of ascites The difficulty of treating ascites depends on the duration of ascites and the degree of liver function damage. Therefore, the basic measures for treating ascites should focus on improving liver function, including clinical rest, enhanced nutrition and supportive therapy.

(1) Limit the intake of water and sodium. The daily water intake is about 1000ml. If there is significant hyponatremia, it should be limited to 500ml. Sodium should be limited to 10-20mmol per day (equivalent to 0.6-1.2g of sodium chloride)

(2) Increase the excretion of water and sodium

1. Use of diuretics The principle is combined, intermittent and alternating medication. The dose should not be too large, and the diuretic rate should not be too strong to avoid inducing serious side effects such as hepatic coma and hepatorenal syndrome.

2. Catharsis: When diuretic treatment is ineffective, traditional Chinese medicine or oral mannitol can be used to expel water through the gastrointestinal tract. Generally, there is no serious reaction. It is suitable for patients with upper gastrointestinal bleeding, dilutional hyponatremia and functional renal failure.

3. Remove ascites and infuse albumin.

(3) Increase plasma colloid osmotic pressure. Regular, small, and multiple intravenous infusions of fresh blood, plasma, or albumin every week can improve the general condition of the body, restore liver function, and increase plasma colloid osmosis. Pressure and promoting the resolution of ascites are of great help.

(4) Ascites concentration and reinfusion. Ascites drainage will cause loss of electrolytes and proteins, which can easily induce electrolyte disorders and hepatic coma, and ascites can recur quickly, so ascites drainage is generally not used for treatment. Abdominal puncture and drainage may be considered in the following situations: ① high-grade ascites affects cardiopulmonary function; ② high-grade ascites compresses the renal vein and affects blood return; ③ is complicated by spontaneous peritonitis and requires peritoneal flushing. The appropriate amount of liquid dispensed each time is about 3000ml.

Ascitic fluid concentration and reinfusion is a better method to treat refractory ascites. When ascites passes through a concentration device, the protein can be concentrated several to dozens of times. After reinfusion, protein can be supplemented, plasma colloid osmotic pressure can be increased, effective blood volume can be increased, and renal blood circulation can be improved, thereby removing retained water and sodium to achieve the goal of reducing and eliminating ascites. Side effects include fever, infection, electrolyte imbalance, etc., which can be prevented by targeted treatments.

(5) Surgical treatment Abdominal-jugular venous drainage (Leveen drainage). It is one of the effective methods for surgical treatment of schistosomiasis liver fibrosis. It uses drainage to increase effective blood volume, improve renal blood flow, and supplement protein. This method cannot be used in patients with ascites infection or suspected cancerous ascites, as it may be complicated by ascites leakage, pulmonary edema, hypokalemia, superior vena cava thrombosis, infection and DIC, so it should be used with caution.

Another operation is thoracic duct-internal jugular vein anastomosis. The hepatic lymph fluid flows smoothly into the internal jugular vein through the thoracic duct, thus reducing the flow of lymph fluid into the abdominal cavity, but the effect is not good.

IV. Surgical treatment of portal hypertension and hypersplenism The main purpose of treatment is to reduce the pressure of the portal vein system and eliminate hypersplenism. Commonly used are various shunts and splenectomy. The effect of surgical treatment is closely related to careful selection of indications and timing of surgery. Surgical treatment may be considered in patients with schistosomiasis liver fibrosis, significant portal hypertension, mild liver function damage, or severe upper gastrointestinal bleeding that is ineffective in medical treatment and has no contraindications to surgery. Those with advanced liver cirrhosis whose plasma albumin is lower than 30g/L, prothrombin time is significantly prolonged, and those with significant liver function impairment such as jaundice and ascites should be listed as contraindications for surgery.

5. Liver transplantation The first formal liver transplantation in humans was completed in 1963. Since then, more than 600 cases have been reported around the world, and the number is constantly increasing. More than half of them were completed after 1980. Liver transplant survival rates continue to improve due to the use of newer immunosuppressive therapies, improvements in supportive care, and improved surgical procedures. According to foreign statistics, the 3-year survival rate of liver transplantation since 1980, in order of disease type, is: late-stage non-alcoholic cirrhosis 41%; alcoholic cirrhosis 20%; biliary atresia 60%; hepatocellular carcinoma 20%; cholangiocarcinoma <10%; metabolic diseases, mainly α-antitrypsin deficiency 60%; sclerosing cholangitis 25%; Brdd-Chiari syndrome 47%. Given that most patients with advanced liver disease have no satisfactory treatment options, survival rates after liver transplantation will continue to improve. It is expected that more and more patients with various chronic liver diseases will receive liver transplantation in the future.

The main factors affecting liver transplantation are liver donor problems.

6. Treatment of complications

(1) First aid measures should be taken to treat upper gastrointestinal bleeding, including: fasting, lying still, strengthening monitoring, and quickly replenishing effective blood volume To correct hemorrhagic shock, adopt effective hemostatic measures and prevent hepatic coma, etc. To prevent esophageal variceal bleeding or recurrence after hemostasis, regular fiberoptic endoscopy can be used to inject sclerosing agents or venous ligation into the variceal veins, and long-term use of drugs that reduce portal pressure, such as propranolol, can be used.

(2) Spontaneous peritonitis. When spontaneous peritonitis and sepsis are complicated, liver damage often worsens rapidly. Supportive treatment and antibiotic application should be actively strengthened. Emphasize the early, sufficient and combined use of antibiotics as soon as the diagnosis is made, and do not wait for the bacterial culture report of the ascites before starting treatment; choose antibiotics that mainly target Gram-negative bacilli and also take into account Gram-positive cocci, and then use antibiotics based on the response to treatment and the bacteria Culture results, consider adjusting antibiotics.

(3) Treatment of hepatic encephalopathy: Patients with cirrhosis who develop personality changes and other mental symptoms, especially if there are inducements for hepatic encephalopathy, should be promptly examined and treated.

(4) In the treatment of functional renal failure, on the premise of actively improving liver function, the following treatment measures can be taken:

(1) Stop or avoid the use of drugs that damage kidney function , such as neomycin, gentamicin, kanamycin and nitrogen-containing drugs.

(2) Avoid and control various factors that reduce blood volume, such as strong diuresis, large amounts of ascites, and upper gastrointestinal bleeding.

(3) Strictly control the amount of infusion, live within your means, and correct water, electrolyte and acid-base imbalances.

(4) Infusion of dextran, plasma, albumin and concentrated ascites fluid to increase circulating blood volume and improve renal blood flow. On the basis of volume expansion, diuretics are applied.

Reference:

Project unit reference range

Alanine aminotransferase ALT IU/L 0-40

Uric acid UA umol/L 140 -430

Glucose GLU umol/L 3.9-6.1

Triglyceride TG umol/L 0.4-1.8

Total cholesterol T-CHOL umol/L 2.8 -5.69

Elevated alanine aminotransferase (ALT) is a very common clinical phenomenon. The liver is the largest detoxification organ in the human body. Whether this organ is normal is very important to the human body. Elevated ALT is an important indicator of liver function problems. Among common factors, various types of hepatitis can cause elevated ALT, which is caused by damage to the liver. Some drugs, such as anti-tumor drugs and anti-tuberculosis drugs, can cause damage to liver function. Drinking a lot of alcohol and eating certain foods can also cause short-term damage to liver function.

ALT mainly exists in the plasma of liver cells, and its intracellular concentration is 1000-3000 times higher than that in serum. As long as 1% of liver cells are necrotic, serum enzymes can be doubled. Therefore, ALT is recommended by the World Health Organization as the most sensitive detection indicator of liver function damage. However, it is not organ-specific, and many diseases can cause its increase. A significant increase is seen in acute viral hepatitis, a moderate increase is seen in chronic hepatitis, active cirrhosis, liver cancer, liver abscess, and a mild increase is also seen in myocardial infarction, myocarditis, heart failure, etc. Therefore, the evaluation of ALT elevation should be closely combined with clinical practice. Some elevated ALT levels are related to fatty liver disease and alcohol consumption. There are many hepatoprotective drugs commonly used in clinical practice. However, the therapeutic effect of some drugs is effective but easy to relapse, resulting in some liver diseases that cannot be cured for a long time and a large number of liver cells are destroyed. How to protect liver cells is the key to protecting liver function.

Alanine aminotransferase is mainly found in the liver, heart and skeletal muscle. Damage or necrosis of liver cells or certain tissues will increase alanine aminotransferase in the blood. Clinically, there are many diseases that can cause abnormal transaminase, which must be identified

1. Viral hepatitis, which causes transaminase The most common diseases that increase transaminases, various acute and chronic viral hepatitis can cause elevated transaminases. 2. Toxic hepatitis A variety of drugs and chemical agents can cause an increase in transaminase, but after stopping the drug, the transaminase can return to normal.

3. Alanine aminotransferase will also increase in heavy or long-term drinkers.

4. Liver cirrhosis and liver cancer. When liver cirrhosis is active, transaminases are higher than normal levels and should be actively treated.

5. During acute attacks of biliary tract disease cholecystitis and cholelithiasis, fever, abdominal pain, nausea, vomiting, jaundice, and elevated blood bilirubin and transaminases are common.

6. Heart disease In acute myocardial infarction, myocarditis, and heart failure, alanine aminotransferase and aspartate aminotransferase are elevated, and patients often have chest pain, palpitations, shortness of breath, and edema. The cardiac examination showed positive signs and electrocardiogram abnormalities.

7. Certain other infectious diseases, such as pneumonia, typhoid fever, tuberculosis, infectious mononucleosis, etc., all have elevated transaminases, but these diseases each have typical clinical manifestations. The diagnosis can be confirmed with the help of laboratory tests. In addition, acute soft tissue injury and strenuous exercise may also cause transient elevation of transaminases. Therefore, you need to go to the hospital for a more comprehensive examination to find out the cause and deal with it in time.