Cirrhosis is a common chronic liver disease, which is caused by one or more reasons for a long time or repeatedly, causing diffuse damage to the liver. Histologically, there are extensive degeneration, necrosis, regeneration and regeneration nodules of hepatocytes, connective tissue proliferation and fibrous septa formation, which lead to the destruction of hepatic lobule structure and the formation of pseudolobule, and the liver gradually deforms and hardens, and develops into cirrhosis. In the early clinical stage, due to the strong compensatory function of liver, there may be no obvious symptoms; In the later stage, multiple systems are involved, with liver function damage and portal hypertension as the main manifestations, and serious complications such as gastrointestinal bleeding, hepatic encephalopathy, secondary infection and canceration often occur.
Etiology:
(1) Viral hepatitis is mainly hepatitis B and C (formerly known as non-A and non-B), and viral hepatitis A generally does not develop into cirrhosis. Its pathogenesis is related to the immune abnormality caused by hepatitis virus, and its pathogenic mode is mainly chronic hepatitis, especially chronic active hepatitis, which gradually evolves into cirrhosis. Most patients with posthepatitic cirrhosis show small nodular cirrhosis. A few cases, such as slow course, mild but uniform inflammatory necrosis, can also show small nodular cirrhosis. The course from viral hepatitis to cirrhosis ranges from a few months to decades.
(2) Schistosoma japonicum is parasitic in the mesenteric vein branch, and the eggs enter the liver with the blood flow, mainly deposited in the portal area. The stimulation of eggs and their toxic products causes a large number of connective tissue hyperplasia, leading to liver fibrosis and portal hypertension. The left lobe of schistosomiasis cirrhosis is seriously involved, and there are large nodules on the liver surface. Because there is no obvious degeneration and regeneration of other liver cells except near egg deposition, the clinical liver function changes slightly, while portal hypertension appears earlier, which used to be called schistosomiasis cirrhosis and should be called schistosomiasis liver fibrosis.
(3) Chronic alcoholism, long-term heavy drinking, direct damage to the liver by acetaldehyde, an intermediate metabolite of alcohol, and the development of cirrhosis through fatty liver are the main pathogenesis of alcoholic cirrhosis. Due to the long-term nutritional imbalance caused by alcoholism, reducing the resistance of the liver to certain toxic substances also plays a role in the pathogenesis.
(IV) Drugs and Chemical Poisons Many drugs and chemical poisons can damage the liver, such as long-term use of isoniazid, tetracycline diacetate, methyldopa, cincofen, etc. Or long-term repeated exposure to certain chemical poisons such as carbon tetrachloride, phosphorus, arsenic, chloroform, etc. It can cause drug-induced or toxic hepatitis and chronic active hepatitis, and then develop into toxic (drug-induced) large nodule or small nodule cirrhosis.
(V) Malnutrition Long-term malnutrition, especially the lack of anti-lipid factors such as protein, B vitamins, vitamin E and choline, can cause hepatocyte necrosis and fatty liver until it develops into malnutrition cirrhosis. However, some people deny that malnutrition is directly related to human cirrhosis. At present, it is believed that long-term malnutrition will reduce the resistance of the liver to other pathogenic factors.
(VI) Chronic congestive heart failure, constrictive pericarditis and hepatic vein occlusion syndrome (Budd-Chiari syndrome) caused by various reasons of circulatory disorders can cause long-term blood stasis and hypoxia in the liver, necrosis of hepatocytes in the lobule center, and proliferation of connective tissue, leading to blood stasis cirrhosis with small nodules. Heart disease, also known as cardiogenic cirrhosis, has hepatomegaly, and the liver function damage is not very serious, but it can also be manifested as mild jaundice, decreased plasma albumin and ascites.
(VII) Cholestasis When intrahepatic cholestasis or extrahepatic bile duct obstruction persists, it can lead to liver cell ischemia, necrosis and fibrous tissue proliferation, leading to cirrhosis. Generally, it can be divided into intrahepatic cholestasis and extrahepatic biliary obstructive biliary cirrhosis. Primary biliary cirrhosis is caused by inflammation and obstruction of intrahepatic small bile duct related to autoimmune factors.
(VIII) Intestinal infection and inflammation Chronic specific or non-specific intestinal inflammation often causes digestive, absorption and nutritional disorders. Toxins produced by intestinal pathogens reach the liver through the portal vein, causing degeneration and necrosis of liver cells and developing into cirrhosis.
(9) Metabolic disease is hereditary and metabolic disease. Because of metabolic disorder, some substances are deposited in the liver, which leads to degeneration and necrosis of liver cells and proliferation of connective tissue, thus forming cirrhosis.
1, hepatolenticular degeneration or Wilson's disease. Due to congenital abnormal copper metabolism, copper deposits in liver and brain tissues and causes diseases. It is characterized by liver cirrhosis and bilateral basal ganglia degeneration. In addition to the symptoms of liver cirrhosis, there are also mental disorders and extrapyramidal symptoms, such as facial expression loss, salivation, difficulty swallowing and speaking, tremors of hands, feet, head and neck, and muscle rigidity.
2. Hemochromatosis is liver cirrhosis caused by iron metabolism disorder and excessive iron deposition in liver tissue. Most of them are small nodules, and in the late stage, they can also show large small micronodular cirrhosis. The main clinical manifestations are cirrhosis, diabetes and skin pigmentation.
Pathology:
The liver shows chronic diffuse damage, and the volume of the liver may be slightly larger in the early stage, but it will shrink due to fibrosis in the later stage, and the texture will become hard and the weight will be reduced. The surface of the liver is covered with brown or grayish brown nodules with grayish white connective tissue around the nodules. Microscopically, it has the following characteristics. ① Hepatocytes were extensively degenerated and necrotic, and regenerated hepatocytes formed irregular regenerative nodules. Regenerated hepatocytes vary in size and are arranged in disorder. Because of the abnormal relationship with biliary tract and portal vein system, their functions are far lower than those of normal liver cells. ② Connective tissue hyperplasia, starting from portal area and under capsule, extending into hepatic lobule, combining with connective tissue in hepatic lobule to form membranous structure, separating hepatic lobule into pseudolobule. ③ In the pseudolobule, the central vein is often located on one side of the lobule, and some pseudolobules are composed of several incomplete hepatic lobules, including two or three central veins, or even no central vein. Direct communication can occur between portal vein, hepatic vein and hepatic artery branches, resulting in short circuit. ④ Inflammatory cells infiltrated in the hyperplastic connective tissue to varying degrees, and bile duct-like structure (pseudobile duct) was seen.
physiopathology
First, abnormal liver function is caused by a large number of necrosis of liver cells, and the function of newborn liver cells is far from normal, which leads to abnormal liver function, such as the synthesis of plasma albumin, the metabolism of bile pigment, the detoxification of harmful substances, the inactivation of estrogen, the increase of antidiuretic hormone, the increase of secondary aldosterone, the manufacture of coagulation factors, etc., which all affect various clinical manifestations.
Secondly, portal hypertension is caused by the destruction of hepatic lobule structure and the proliferation of fibrous tissue, which reduces the blood passage of portal vein. In the regenerative liver cell mass, the capillaries are abnormally bent, which hinders the blood circulation. In addition, the portal vein branch is directly connected with the hepatic artery, and the portal vein pressure is greatly increased. Normal portal vein pressure is lower than 1.96 kPa (200mm water column). When the portal vein pressure exceeds 2.94kpa(300mmH2O), gastrointestinal congestion, splenomegaly, ascites formation and collateral circulation between portal vein and vena cava will occur. The collateral circulation of portal vein and vena cava is mainly found in the following parts: (1) the lower esophagus and the fundus of stomach, and the gastric coronary vein is anastomosed with the esophageal vein. ⑵ In the lower rectum and mesentery, the superior hemorrhoid vein and the inferior hemorrhoid vein anastomosed in the inferior vena cava. (3) Around the navel, the umbilical vein and paraumbilical vein that were locked at birth were reopened and anastomosed with the subcutaneous vein of abdominal wall. ⑷ Contact between abdominal organs and retroperitoneal tissues, such as hepatic phrenic vein and internal vein of spleen and kidney ligament. Among the above side branches, the lower end of esophagus appears earlier, which is easy to rupture and cause massive bleeding, which is life-threatening. The reasons are as follows: ① Esophageal vein is close to portal vein and is easily affected by portal hypertension. ② Esophageal vein is very shallow, and it is in the loose connective tissue of submucosa. When varicose veins occur, this connective tissue will also contract under pressure. ③ Esophageal vein is located in the chest cavity, and it is influenced by negative pressure in the chest cavity when inhaling, which makes portal vein blood flow in more easily.
Three, the formation of ascites in addition to portal hypertension, there are the following factors:
(a) hypoalbuminemia liver albumin synthesis function decreased, protein intake is insufficient, intestinal congestion caused by digestive and absorption disorders. When the plasma albumin is lower than 25-30g/L, ascites and limb edema often occur.
(II) Hepatic lymph imbalance When the outflow tract of hepatic vein is blocked, the plasma infiltrates into the space beside the hepatic sinus (space of disse), resulting in an increase in hepatic lymph production, which can reach 7- 1 1L (normally 1-3L). A large number of lymph exceeds the reflux transport capacity of thoracic duct, and lymph overflows from the surface of hepatic capsule and hilar lymphatic vessels.
(3) Endocrine factors: The increase of antidiuretic hormone increases the reabsorption of water. The activity of the third factor excretory hormone decreased, urinary sodium excretion decreased, and ascites aggravated. Secondary aldosteronism increases the reabsorption of water and sodium. The activity of prostaglandin (PGE, PGE2) atrial natriuretic peptide decreased, but the renal blood flow, sodium excretion and urine volume decreased.
(4) When liver cirrhosis is caused by renal factors, the renal hemodynamics changes obviously, and the effective blood volume decreases. With the increase of abdominal pressure, renal vascular contraction reduces renal blood flow and glomerular filtration rate, and water and sodium remain, resulting in oliguria or anuria. Severe cases can form so-called functional renal failure.
Symptoms:
The onset and course of liver cirrhosis are generally slow, and it can lurk for 3-5 years or more than ten years. Its clinical manifestations can be divided into compensatory stage and decompensated stage of liver function, but the boundary between them is not obvious or overlapping, so it is not suitable to apply mechanically.
First, the symptoms of liver function compensation period are mild, often lacking specificity, mainly manifested as fatigue, anorexia and indigestion. There may be nausea, aversion to oil, flatulence, epigastric 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 accompanying diseases, and can be relieved after rest or proper treatment. Spleen is slightly or moderately swollen, and liver function test results can be normal or slightly abnormal.
Some cases were concealed, only after physical examination, surgery for other diseases, and even at autopsy.
Second, the symptoms of decompensation of liver function are obvious, mainly two clinical manifestations caused by abnormal liver function and portal hypertension, and there may be systemic multi-system symptoms.
1. The general symptoms and nutritional status are poor, emaciation and fatigue, listlessness, and even weakness in bed. Dry and rough skin, dark face. Anemia, glossitis, angular stomatitis, night blindness, polyneuritis and edema are common. There may be irregular low fever, which may be caused by hepatocyte necrosis; Detoxification function of liver decreases, and toxins absorbed by intestine enter systemic circulation; Portal vein thrombosis or endometritis; Secondary infection, etc.
2. Symptoms of digestive tract: obvious loss of appetite. Feel discomfort and fullness in the upper abdomen, nausea and even vomiting after meals. I have a poor tolerance for fat and protein, and eating greasy food is easy to cause diarrhea. Patients feel unbearable abdominal distension due to ascites and gastrointestinal pneumatosis, and toxic flatulence may occur in the late stage. The above symptoms are related to gastrointestinal congestion, edema, inflammation, digestive absorption disorder and intestinal flora imbalance. More than half of the patients have mild jaundice, and a few have moderate or severe jaundice, suggesting progressive or extensive necrosis of hepatocytes.
3. Bleeding tendency and anemia often include nosebleed, gingival bleeding, skin ecchymosis and gastrointestinal mucosal erosion and bleeding. The bleeding tendency is mainly due to the decrease of the function of synthesizing coagulation factors in the liver, thrombocytopenia caused by hypersplenism and the increase of capillary fragility. Patients still have different degrees of anemia, mostly due to nutritional deficiency, low intestinal absorption function, hypersplenism and gastrointestinal blood loss.
4. Endocrine disorders Endocrine disorders include the increase of estrogen, aldosterone and antidiuretic hormone, mainly due to the weakening of inactivation of liver function, but the accumulation in the body and urine excretion increase; When estrogen increases, the feedback mechanism inhibits the function of anterior pituitary gland, affects the function of pituitary-gonad axis and pituitary-adrenal cortex axis, and leads to the decrease of androgen and adrenocortical hormone.
Due to the imbalance between estrogen and androgen, male patients often suffer from decreased sexual desire, testicular atrophy, alopecia and breast development. Female patients with irregular menstruation, amenorrhea and infertility. In addition, some patients may have spider nevus and/or telangiectasia in areas with vena cava drainage such as face, neck, upper chest, back, shoulders and upper limbs. In the palm, thenar muscles and fingers are red, which is called liver palm. It is generally believed that the appearance of spider nevus and liver palm is related to the increase of estrogen, and some vasodilatory active substances that have not been inactivated by the liver also have a certain effect. When the liver function is seriously damaged, the number of spider nevus can increase, and when it improves, the liver function can decrease, shrink or disappear.
When aldosterone increases, it acts on the distal renal tubule, which increases sodium reabsorption; When the antidiuretic hormone increases, it acts on the collecting tube to increase the absorption of water. Sodium-water retention reduces urine volume and edema, and also plays an important role in promoting the formation and aggravation of ascites. If the adrenal cortex function is impaired, skin pigmentation may appear on the face and other exposed parts.
Logo:
The clinical manifestations of portal hypertension constitute three clinical manifestations of portal hypertension: splenomegaly, establishment and opening of collateral circulation and ascites, which has important clinical significance. In particular, the establishment and opening of collateral circulation has diagnostic value.
1. splenomegaly is usually moderate splenomegaly, and some of it can reach below the umbilicus. The main reasons are spleen congestion, toxins and inflammatory factors, which are also related to the proliferation of reticuloendothelial cells. Spleen is mostly medium hardness, smooth surface and blunt edge. Perisplenic inflammation can cause left upper abdominal pain or abdominal pain. If there is more ascites, palpation should be done by impact method. When the upper digestive tract bleeds, the spleen can temporarily atrophy or even cannot be touched, which is of great value in differentiating and determining esophageal variceal bleeding. Spleen enlargement is often accompanied by leukopenia, thrombocytopenia and/or erythropenia, which is called hypersplenism.
2. The establishment of collateral circulation and the increase of portal vein pressure. When it exceeds 1, 96 kpa(200 mmh2o), the blood flow from digestive organs and spleen is blocked, forcing collateral circulation between blood vessels in many parts of portal vein system and systemic circulation. Clinically, the more important ones are: ① varicose veins in the lower esophagus and gastric fundus, gastric coronary veins in portal vein system, etc. It is formed by anastomosis with esophageal vein, intercostal vein and azygos vein in vena cava system. Often due to obvious increase in portal vein pressure, esophagitis, rough and sharp food damage, or sudden increase in intra-abdominal pressure, varicose veins rupture and massive bleeding. ② Abdominal wall and periumbilical varicose veins, when portal hypertension occurs, umbilical vein re-opens and expands, connecting with accessory umbilical vein and abdominal vein. A tortuous vein can be seen in the abdominal wall around the umbilicus, and the blood flow direction is upward from the umbilicus and downward from the umbilicus, which can be distinguished from inferior vena cava obstruction. If the umbilical vein is obviously varicose, the lumen expands and the blood flow increases, sometimes persistent venous murmurs can be heard. (3) The formation of hemorrhoids, which can cause hematochezia.
3. Ascites is the most prominent manifestation of decompensation of liver cirrhosis. The direct cause of ascites is excessive retention of water and sodium. The mechanism is that the decrease of plasma albumin content leads to the decrease of plasma colloid osmotic pressure, lymphatic reflux disorder, endocrine dysfunction and kidney and many other factors (see pathology for details). Ascites often has flatulence before it appears. When there is a lot of ascites, the abdomen bulges and the abdominal wall is tight and shiny, which makes the patient inconvenient to move. Elevated abdominal pressure can compress internal organs and cause umbilical hernia. It can also raise the diaphragm, causing dyspnea and palpitation. Some patients may have pleural effusion, especially on the right side, which is mostly caused by ascites entering the thoracic cavity through lymphatic vessels of diaphragm, which is called hepatic pleural effusion. Mobile dullness appears in ascites above the medium level, and a small amount of ascites is not obvious, which can be detected by ultrasound.
The size, hardness and smoothness of liver palpation are related to liver fat infiltration, hepatocyte regeneration, fibrous tissue proliferation and contraction. In the late stage of liver cirrhosis, the liver is small and hard with nodules on the surface.
Diagnosis:
Decompensated cirrhosis can often be diagnosed according to clinical manifestations and related examinations. The main diagnostic criteria of liver cirrhosis are: ① viral hepatitis, schistosomiasis and long-term drinking history; ② The liver may be slightly larger, often atrophied in the later stage, with hard texture and uneven surface. ③ Liver function damage. ④ Clinical manifestations of portal hypertension. ⑤ False lobules can be seen in liver biopsy.
Treatment:
(a) rest liver function compensation, reduce activities appropriately, you can take part in some work, pay attention to the combination of work and rest. Patients in decompensated stage should mainly rest in bed.
(2) The diet should be nutritious and easy to digest and absorb. Generally, foods with high calorie, high protein and rich vitamins are appropriate. The fat content should not be too much, but there is no need to limit it too strictly. When there is ascites, the diet should be less salt. At present, some people advocate that there is no need for a salt-free diet, because it affects appetite and is not worth the loss. If liver function is obviously damaged or blood ammonia is high, and hepatic encephalopathy tends to occur, the intake of protein should be temporarily restricted. Alcohol should be banned and coarse and hard food should be avoided.
(3) Patients with decompensated support therapy often have nausea, vomiting, eating less or not eating, so they can be infused with glucose intravenously with vitamin C, potassium chloride, inosine and insulin. And pay special attention to maintaining the balance of water, electrolyte and acid-base, especially supplementing potassium salt. In addition, compound amino acids, blood, plasma and albumin can also be used as appropriate.
Second, there is no specific drug for drug treatment at present, so it is not appropriate to abuse drugs, otherwise it will increase the burden on the liver and backfire.
1. Hepatic fibrosis is an inevitable process of the occurrence and development of liver cirrhosis, and anti-fibrosis therapy is of great significance.
2. Chinese medicine has a long history of treating liver cirrhosis, which can really improve symptoms and liver function. Generally speaking, drugs such as softening the liver and dispersing stagnation, promoting blood circulation and removing blood stasis are the main drugs, and the treatment is based on syndrome differentiation.
Third, the treatment of ascites The difficulty of ascites treatment depends on the duration of ascites and the degree of liver function damage. Therefore, the basic measures to treat ascites should focus on improving liver function, including clinical rest, strengthening nutrition and supporting treatment.
(a) 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 sodium chloride).
(2) Increase the discharge of water and sodium.
1. The principle of using diuretics is combined, intermittent and alternate use. The dosage should not be too large, and the diuretic speed should not be too fast, so as not to induce serious side effects such as hepatic coma and hepatorenal syndrome.
2. When the therapeutic effect of cathartic diuretics is not good, traditional Chinese medicine or oral mannitol can be used to excrete water through the gastrointestinal tract, and there is generally no serious reaction. It is suitable for patients with upper gastrointestinal bleeding, diluted hyponatremia and functional renal failure.
3, put ascites and albumin infusion.
(3) Increase the plasma colloid osmotic pressure. Intravenous infusion of fresh blood, plasma or albumin regularly, in small quantities and many times every week is of great help to improve the general condition of the body, restore liver function, increase the colloid osmotic pressure of plasma and promote the regression of ascites.
(4) Concentrated reinfusion of ascites will lose electrolyte and protein, which will easily induce electrolyte disorder and hepatic coma. Ascites can recur quickly, so the method of releasing ascites is generally not used for treatment. Abdominal puncture and drainage can be considered in the following situations; ① Ascites mostly affects cardiopulmonary function; ② The compression of high ascites in renal vein affects blood return; (3) When spontaneous peritonitis is complicated and peritoneal lavage is needed. It is appropriate to drain about 3000ml each time.
Concentrated reinfusion of ascites is a better method to treat refractory ascites. Ascites can be concentrated several times to dozens of times by a concentration device. After blood transfusion, protein can be supplemented, the plasma colloid osmotic pressure can be increased, the effective blood volume can be increased, the renal blood circulation can be improved, and the retained water and sodium can be discharged, so as to achieve the purpose of relieving and eliminating ascites. Side effects include fever, infection and electrolyte disorder, which can be prevented by targeted treatment.
(5) Surgical treatment of abdominal cavity-jugular vein drainage (Leveen drainage). It is one of the effective methods for surgical treatment of liver fibrosis caused by schistosomiasis. Drainage can increase effective blood volume, improve renal blood flow and supplement protein. Ascites infection or suspected cancerous ascites can not be used, because it can be complicated with ascites leakage, pulmonary edema, hypokalemia, superior vena cava thrombosis, infection and DIC, so use it with caution.
Another operation is thoracic catheter-internal jugular vein anastomosis. Hepatic lymph can smoothly flow into internal jugular vein through thoracic catheter, thus reducing lymph flow into abdominal cavity, but the effect is not good.
Fourth, the surgical treatment of portal hypertension and hypersplenism aims to reduce the pressure of portal vein system and eliminate hypersplenism. Commonly used are various shunts and splenectomy. The effect of surgical treatment is closely related to the careful selection of indications and the timing of operation. Portal hypertension in schistosomiasis liver fibrosis is significant, but the damage of liver function is slight. Medical treatment of upper gastrointestinal bleeding is ineffective and there are no surgical contraindications, so surgical treatment can be considered. Patients with advanced liver cirrhosis whose plasma albumin is lower than 30g/L, prothrombin time is obviously prolonged, and liver function damage such as jaundice and ascites is obvious should be listed as contraindications for operation.
Verb (abbreviation of verb) liver transplantation 1963 Complete the first normal liver transplantation. Since then, more than 600 cases have been reported around the world, and the number is increasing, more than half of which were completed after 1980. Due to the adoption of newer immunosuppressive therapy, the improvement of supportive therapy and surgical operation, the survival rate of liver transplantation has been continuously improved. According to foreign statistics, the 3-year survival rate of liver transplantation since 1980 is ranked according to the number of diseases; Late nonalcoholic cirrhosis is about 41%; Alcoholic cirrhosis 20%; Biliary atresia 60%; Hepatocellular carcinoma 20%; Cholangiocarcinoma <10%; Metabolic diseases, mainly α -antitrypsin deficiency, accounted for 60%; Sclerosing cholangitis 25%; Brdd-Chiari syndrome 47%. Since there is no satisfactory treatment for patients with advanced liver disease at present, the survival rate 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 factor affecting liver transplantation is the donor liver problem.
Six, the treatment of complications
First aid measures should be taken to treat upper gastrointestinal bleeding, including fasting, lying still, strengthening monitoring, quickly supplementing effective blood volume to correct hemorrhagic shock, taking effective hemostasis measures and preventing hepatic coma. In order to prevent esophageal varices bleeding or bleeding again after hemostasis, sclerosing agent or vein ligation can be injected into varicose veins through conventional fiberscope, and long-term administration of propranolol and other drugs can reduce portal vein pressure.
(2) Spontaneous peritonitis combined with spontaneous peritonitis and septicemia often aggravate liver damage rapidly, so supportive treatment and application of antibiotics should be actively strengthened. It is emphasized that once the diagnosis is made, antibiotics should be used early, in sufficient amount and in combination, and treatment should not be started after the bacterial culture report of ascites. Choose mainly Gram-negative bacilli and Gram-positive cocci, and then consider adjusting antibiotics according to the treatment response and bacterial culture results.
(III) Treatment of hepatic encephalopathy Patients with liver cirrhosis have mental symptoms such as personality changes, especially when there are incentives for hepatic encephalopathy, they should be examined in time and take treatment measures.
(IV) Treatment of functional renal failure Under the premise of actively improving liver function, the following treatment measures can be taken:
(1) Stop using or avoid using drugs that damage renal function, such as neomycin, gentamicin, kanamycin and nitrogen-containing drugs.
(2) Avoid and control various factors that reduce blood volume, such as strong diuresis, massive ascites, and massive hemorrhage in upper digestive tract.
(3) Strictly control the infusion volume, live within our means, and correct the imbalance of water, electrolyte and acid-base.
(4) Transfusion of dextran, plasma, albumin and ascites is concentrated and reinfusion, so as to increase the circulating blood volume and improve the renal blood flow. On the basis of volume expansion, diuretics were applied.
Reference:
Project unit reference range
Alanine transaminase ALT IU/L 0-40
Uric acid UA umol/L 140-430
Glucose concentration 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 common clinical phenomenon. The liver is the largest detoxification organ in human body, and whether this organ is normal or not is very important to human body. Elevated ALT is an important indicator of liver function problems. Among the common factors, all kinds of hepatitis can cause the elevation of ALT, which is caused by the destruction of the liver. Some drugs, such as anti-tumor drugs and anti-tuberculosis drugs, can cause liver function damage. Excessive drinking and eating certain foods can also cause short-term liver damage.
ALT mainly exists in the cytoplasm of hepatocytes, and its intracellular concentration is 1000-3000 times higher than that in serum. As long as there is 1% hepatocyte necrosis, serum enzymes can be doubled. Therefore, ALT is recommended by the World Health Organization as the most sensitive indicator of liver function damage. But it is not organ-specific, and many diseases can cause its increase. Acute viral hepatitis increased significantly, while chronic hepatitis, active cirrhosis, liver cancer, liver abscess, myocardial infarction, myocarditis and heart failure increased moderately. It can also be slightly improved. Therefore, the evaluation of ALT elevation should be closely combined with clinical practice. Some elevated ALT is related to fatty liver and drinking. There are many liver-protecting drugs commonly used in clinic. However, the therapeutic effects of some drugs are easy to repeat, leading to 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 protect liver function.
Alanine aminotransferase mainly exists in liver, heart and skeletal muscle. Damage or necrosis of liver cells or some tissues will increase alanine aminotransferase in blood. There are many diseases that can cause abnormal transaminase in clinic, so we must identify them.
1, viral hepatitis This is the most common disease that leads to the increase of transaminase. All kinds of acute and chronic viral hepatitis can cause the increase of transaminase. 2, toxic hepatitis A variety of drugs and chemicals can cause the increase of transaminase, but after stopping the drug, transaminase can return to normal.
3. Heavy or long-term drinkers will also increase alanine aminotransferase.
4. Liver cirrhosis, liver cancer cirrhosis active stage, transaminase is higher than the normal level, should be actively treated. 5, biliary tract diseases, cholecystitis, gallstones acute attack, often fever, abdominal pain, nausea, vomiting, jaundice, serum bilirubin and transaminase increased.
6, heart disease acute myocardial infarction, myocarditis, heart failure, alanine aminotransferase and aspartate aminotransferase are elevated, patients often have chest pain, palpitations, shortness of breath, edema. Cardiac examination showed positive signs and abnormal electrocardiogram.
7. Other infectious diseases, such as pneumonia, typhoid fever, tuberculosis and infectious mononucleosis. All of them have elevated transaminase, but these diseases have typical clinical manifestations and can be diagnosed by laboratory examination. In addition, acute soft tissue injury and strenuous exercise can also lead to a transient increase in transaminase. Therefore, it is necessary to go to the hospital for a comprehensive examination, find out the reasons and deal with them in time.