Cirrhosis of the liver is a common chronic liver disease, which is caused by one or more causes of long-term or repeated action, causing diffuse liver damage. In histopathology, there are extensive liver cell degeneration, necrosis, regeneration and regeneration of nodules, connective tissue hyperplasia and fibrous septum formation, leading to the destruction of liver lobule structure and the formation of pseudo-lobules. The liver gradually deforms, hardens and develops cirrhosis . In the early clinical stage, due to the strong liver function compensation, there may be no obvious symptoms; in the later stage, multiple systems are affected, with liver function damage and portal hypertension as the main manifestations, and gastrointestinal bleeding, hepatic encephalopathy, secondary infections, and Severe complications such as cancer.
There are many causes of liver cirrhosis, and their pathological changes and clinical manifestations are also different. The same etiology can develop into different pathological types of cirrhosis; and the same pathological type of cirrhosis can also evolve from multiple etiologies, so there is no unified classification based on the etiology and its pathological form in theory and clinical practice. At present, they are still classified according to etiology and pathology.
1. Etiology classification "There are many causes of liver cirrhosis. In China, viral hepatitis is the most common type of cirrhosis. In foreign countries, especially in North America and Western Europe, alcoholic cirrhosis is more common.
(1) Viral hepatitis is mainly type B and C (in the past called non-A non-B) viral hepatitis. Viral hepatitis A generally does not develop into cirrhosis. Its pathogenesis is related to immune abnormalities caused by hepatitis virus, and its pathogenesis is mainly through chronic hepatitis, especially chronic active hepatitis, and gradually evolves into cirrhosis. Most liver cirrhosis after hepatitis is manifested as macronodular cirrhosis; a few diseases such as a slow course of disease, inflammatory necrosis are mild but more uniform, and can also be manifested as small nodular cirrhosis. The course from viral hepatitis to cirrhosis can be as short as several months and as long as several decades.
(2) Schistosomiasis schistosomiasis parasitizes on the branches of the mesenteric vein, and the eggs are mainly deposited in the portal area after entering the liver with the bloodstream. The stimulation of the 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 more involved, and there are larger nodules on the liver surface. Except for the hepatocytes in the vicinity of the egg deposition, there is no obvious degeneration and regeneration of other liver cells, so the clinical changes in liver function are mild, and portal hypertension appears earlier, which was called schistosomiasis cirrhosis in the past. Should be called schistosomiasis liver fibrosis.
(3) Chronic alcoholism long-term heavy drinking, the intermediate metabolite of alcohol, acetaldehyde, directly damages the liver. The development of liver cirrhosis through fatty liver is the main pathogenesis of alcoholic cirrhosis. The long-term malnutrition caused by alcohol abuse reduces the liver's resistance to certain toxic substances and 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 diacetin, methyldopa, cinchofene, 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) nodules or small nodular 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, fatty liver, and develop into malnourished liver cirrhosis. But some people deny the direct relationship between malnutrition and human liver cirrhosis. At present, it is believed that long-term malnutrition 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, and hepatocyte necrosis in the center of the lobule. Hyperplasia of connective tissue leads to congestive cirrhosis, which is small nodular in shape. Caused by heart disease, it is also called cardiogenic cirrhosis. There is liver enlargement and liver function damage is not very serious, but it can also be manifested as mild jaundice, decreased plasma albumin, and ascites.
(7) Cholestasis: When intrahepatic cholestasis or extrahepatic bile duct obstruction persists, it can cause liver cell ischemia, necrosis, and fibrous tissue proliferation to form liver cirrhosis. Generally can be divided into intrahepatic cholestasis and extrahepatic bile duct obstructive biliary cirrhosis. The inflammation and obstruction of the small bile ducts in the liver related to autoimmune factors is called primary biliary cirrhosis.
(8) Intestinal infection and inflammation Chronic specific or non-specific intestinal inflammation often causes digestion, absorption, and nutritional disorders, and the toxins produced by pathogens in the intestine reach the liver through the portal vein, causing degeneration and necrosis of liver cells and developing cirrhosis .
(9) Metabolic Diseases "Inherited and metabolic diseases, certain substances are deposited in the liver due to metabolic disorders, causing liver cell degeneration and necrosis, connective tissue hyperplasia and cirrhosis.
1. Hepato-lenticular degeneration or Wilson disease. Due to the abnormality of congenital copper metabolism, copper deposits in liver and brain tissues and causes disease. It is characterized by the simultaneous presence of liver cirrhosis and degeneration of the bilateral basal ganglia. In addition to the symptoms of liver cirrhosis, there are clinically mental disorders and extrapyramidal symptoms, such as lack of facial expression, salivation, difficulty swallowing and speaking, hands, feet and head Neck tremor, muscle rigidity and other manifestations.
2. Hemochromatosis (hemochromatosis) is caused by iron metabolism disorder and excessive iron deposition in liver tissue. Most of them are small nodules, and later can also be manifested as large nodular cirrhosis. Clinically, it mainly manifests as liver cirrhosis, diabetes and skin pigmentation.
(10) The cause is unknown. It is difficult to determine the cause of the disease for a while, which is called cryptogenic cirrhosis. It is probably not a special type, and some of the cases may be related to the insidious hepatitis without jaundice.
2. Pathological classification: In the past, it was divided into portal veins and post-necrotic cirrhosis. The currently confirmed pathological classification was formulated by the International Conference in 1974 and is divided into 4 types:
(1) Small nodular liver cirrhosis. The nodules are relatively uniform in size, with a diameter of 3-5mm, generally no more than 1cm. The fibrous septum is thinner and the pseudolobules are relatively uniform. This type is the most common and is equivalent to the previous portal cirrhosis.
(2) Macronodular cirrhosis: The nodules are thicker and vary in size. The diameter is generally 3-5mm, and the maximum can reach 5cm. The nodules are composed of multiple lobules, and the fibrous septa are of different widths and generally wider. This type is mostly caused by large-scale liver necrosis, which is equivalent to past post-necrotic cirrhosis.
(3) Mixed liver cirrhosis with large and small nodules is a mixture of the above two types. This type of liver cirrhosis is also very common.
(4) Incompletely separated liver cirrhosis, also known as regenerative nodule cirrhosis. It is characterized in that most liver lobules are surrounded by fibrous septa to form nodules. The fibrous septa can extend into the liver lobules, but the liver lobules are not completely separated, and the regeneration nodules are not significant. The cause of this type of disease is schistosomiasis in China.
The liver is chronically diffusely damaged. In the early stage, the liver may be slightly larger, and in the late stage, it may shrink, harden, and lose weight due to fibrosis. The surface is covered with brownish-yellow or gray-brown nodules of various sizes, and there are grayish white around the nodules Surrounded by connective tissue. The microscope has the following characteristics. ① Extensive degeneration and necrosis of liver cells, the regenerated liver cells form irregularly arranged liver cell regeneration nodules. The regenerated liver cells vary in size and are arranged disorderly. Because of their abnormal relationship with the biliary tract and portal vein system, their function is much lower than that of normal liver cells. ②The connective tissue hyperplasia begins in the portal area and under the capsule, extends into the liver lobules, and forms a membrane-like structure with the connective tissue in the liver lobules, separating the liver lobules and changing them into pseudo-lobules. ③In the pseudolobules, the central veins often lie on one side of the lobules. Some pseudolobules are composed of several incomplete liver lobules, which may have two or three central veins, or even no central vein. There may be direct communication between the portal vein, hepatic vein and the small branches of the hepatic artery and short circuit. ④ There are varying degrees of inflammatory cell infiltration in the hyperplastic connective tissue, and bile duct-like structures (pseudo bile ducts) can be seen.
1. Hypofunction of the liver is caused by a large number of necrosis of liver cells, and the function of new hepatocytes is far from normal, which leads to hypofunction of liver, such as the synthesis of plasma albumin, the metabolism of bile pigment, the detoxification of harmful substances, and the elimination of estrogen. Many functions such as the increase of antidiuretic hormone, secondary aldosterone increase, and the production of coagulation factors are affected and cause various clinical manifestations.
2. Portal hypertension: Due to the destruction of the liver lobule structure and the proliferation of fibrous tissue, the portal vein blood passage is reduced. In the regenerated liver cell mass, the capillaries are abnormally tortuous, obstructing blood flow. Coupled with the direct traffic between the branches of the portal vein and the branches of the hepatic artery, the portal vein pressure is greatly increased. The portal pressure is normally 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 the vena cava, etc. occur. The collateral circulation of the portal vein and the vena cava is mainly found in the following parts: (1) The lower part of the esophagus and the bottom of the stomach, and the gastric coronary vein is anastomosed with the esophageal vein. ⑵In the lower rectum, the superior hemorrhoidal vein of the lower mesenteric and the hemorrhoids of the inferior vena cava, the inferior hemorrhoidal vein anastomoses. ⑶ Around the umbilical area, the umbilical veins and paraumbilical veins that have been blocked since birth reopened and anastomosed with the subcutaneous veins of the abdominal wall. ⑷The contact between abdominal organs and retroperitoneal tissues, such as the veins between the liver and the diaphragm, and the veins in the spleen and kidney ligaments. Among the above-mentioned collateral branches, the lower end of the esophagus appears earlier, and it is easy to rupture, causing hemorrhage and endangering life. The reasons are as follows: ①The esophageal vein is close to the portal vein and is easily affected by portal hypertension. ②The esophageal veins are very shallow and are located in the loose connective tissue of the submucosa. When the varicose veins expand, this connective tissue is also compressed and shrunk. ③The esophageal vein is located in the thoracic cavity and is affected by the negative pressure in the chest during inhalation, which makes it easier for blood to flow into the portal vein.
Third, the formation of ascites, in addition to portal hypertension, there are several other factors:
(1) Hypoalbuminemia the liver's ability to synthesize albumin is reduced, protein intake is insufficient, and intestinal congestion causes digestion and absorption disorders. When the plasma albumin is lower than 25-30g/L, ascites and limb edema are often present.
(2) Hepatic lymphatic fluid imbalance. When the hepatic vein outflow tract is blocked, plasma penetrates from the wall of the liver sinusoid to the parasinusoidal space (Disse cavity), resulting in increased hepatic lymph fluid production, which can reach 7-11L per day (normally 1-3L ), a large amount of lymph fluid exceeds the capacity of the thoracic duct to reflux and transport. Lymph fluid overflows from the surface of the liver capsule and hilar lymphatic vessels to the abdominal cavity. This ascites has high protein content, is produced quickly, and is not easily absorbed.
(3) The endocrine factor, the increase of antidiuretic hormone, increases the reabsorption of water. The third factor excretion hormone activity decreases, urinary sodium excretion decreases, and ascites increases. Secondary aldosterone increases, increasing the reabsorption of water and sodium. Prostaglandin (PGE, PGE2) atrial natriuretic peptide activity is reduced, and renal blood flow, sodium excretion and urine output decrease.
(4) Kidney factors: In liver cirrhosis, renal hemodynamic changes are obvious, effective blood volume decreases, and abdominal pressure increases, renal vasoconstriction reduces renal blood flow and glomerular filtration rate, water and sodium retention, oliguria or anuria . Severe punishment can cause so-called functional renal failure.
The pathophysiological changes of liver cirrhosis are summarized as follows: (Table 2-11-1)
Table 2-11-1 Pathophysiological changes of liver cirrhosis
Decreased liver function Bile pigment metabolism disorder
Protein synthesis disorder
Elevated blood ammonia, amines, etc., promote liver coma
Plasma albumin decreased, colloidal osmotic pressure decreased, coagulation factor Ⅱ, Ⅴ, Ⅶ, Ⅸ, Ⅹ deficiency, ascites and bleeding tendency
Portal hypertension Hormone inactivation disorder
Splenomegaly, hypersplenism, collateral circulation of portal and systemic veins
Increased aldosterone and antidiuretic hormone
Indigestion, nutritional disorders
Decreased white blood cells, red blood cells and platelets, esophagus, gastric fundus varices, bleeding, abdominal wall varicose veins
Interstitial reaction Fibrosis
Cushion cell dysfunction
Increased monoamine oxidase activity
The onset and course of liver cirrhosis are generally slow, and can be hidden for 3-5 years or more than ten years. Its clinical manifestations can be divided into liver function compensation and decompensation phases, but the distinction between the two phases is not obvious or There is overlap and should not be applied mechanically.
1. Compensation period of liver function "Symptoms are mild and often lack specificity, mainly fatigue, loss of appetite and indigestion. There may be nausea, oiliness, abdominal distension, upper abdominal discomfort, dull pain and diarrhea. These symptoms are mostly caused by gastrointestinal congestion, secretion and absorption dysfunction. Symptoms often appear intermittently, and are aggravated by fatigue or accompanying disease, and can be relieved after rest or appropriate treatment. The spleen was slightly or moderately enlarged, and the liver function test results may be normal or mildly abnormal.
Some cases were concealed and were only discovered during physical examination, surgery for other diseases, or even autopsy.
Second, liver function decompensation period” Significant symptoms, mainly two types of clinical manifestations caused by liver function decline and portal hypertension, and may have systemic symptoms.
(1) Clinical manifestations of decreased liver function
1. Systemic Symptoms The general condition and nutritional status are poor, weight loss, fatigue, lack of energy, and the severely ill are weak and bedridden. The skin is dry and rough, and the complexion is gray and dark. Anemia, glossitis, angular cheilitis, night blindness, polyneuritis and edema are common. Irregular low-grade fever may be caused by necrosis of liver cells; the detoxification function of the liver is reduced and the toxins absorbed by the intestine enter the systemic circulation; portal thrombosis or endometritis; secondary infections, etc.
2. Gastrointestinal symptoms appetite is significantly reduced, after eating, you feel upper abdominal discomfort and fullness, nausea, and even vomiting, poor tolerance to fat and protein, eating greasy food, easy to cause diarrhea. The patient feels unbearable abdominal distension due to ascites and gastrointestinal gas, and toxic tympanum may appear in the late stage. 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 suggesting progressive or extensive necrosis of liver cells.
3. Bleeding tendency and anemia: epistaxis, gum bleeding, skin ecchymosis and gastrointestinal mucosal erosion and bleeding are common. The bleeding tendency is mainly due to the decreased function of the liver to synthesize coagulation factors, thrombocytopenia caused by hypersplenism, and increased capillary fragility. Patients still have varying degrees of anemia, mostly caused by nutritional deficiency, low intestinal absorption, hypersplenism, and gastrointestinal blood loss.
4. Endocrine disorders Endocrine disorders include increased estrogen, aldosterone and antidiuretic hormones, mainly due to decreased liver function, which weakens their inactivation effects, but accumulates in the body and increases excretion in the urine; when estrogen increases, the feedback mechanism inhibits the function of the anterior pituitary gland. Thereby affecting the function of the pituitary-gonadal axis and the pituitary-adrenal cortex axis, resulting in a decrease in male hormones and sometimes adrenal cortex hormones.
Due to the imbalance between estrogen and male hormones, male patients often experience loss of libido, testicular atrophy, hair loss, and breast development; female patients have irregular menstruation, amenorrhea, and infertility. In addition, some patients may develop spider nevi and/or telangiectasias in areas with vena cava drainage on the face, neck, upper chest, back, shoulders, and upper extremities; redness and scales on the palms, small thenar muscles, and finger tips Liver palm. It is generally believed that the appearance of spider veins and liver palms is related to increased estrogen, and some vasodilatory active substances that are not destroyed by the liver also have a certain effect. When the liver function is severely damaged, the number of spider moles can increase, and when the liver function improves, it can decrease, shrink or disappear.
When aldosterone increases, it acts on the distal renal tubules and increases sodium reabsorption; when antidiuretic hormone increases, it acts on the collecting duct and increases water absorption. Sodium and water retention reduce urine output and swelling, and also contribute to the formation and aggravation of ascites. Play an important role in promoting. If the function of the adrenal cortex is impaired, skin pigmentation may appear on the face and other exposed parts.
(2) The clinical manifestations of portal hypertension. The three clinical manifestations that constitute portal hypertension are splenomegaly, the establishment and opening of collateral circulation, ascites, and are of clinical significance. Especially the establishment and opening of collateral circulation has characteristic value for diagnosis.
1. Splenomegaly is usually moderate splenomegaly, some of which can reach below the umbilical cord. The main cause is splenic congestion, toxins and inflammatory factors. The proliferation of reticuloendothelial cells is also related. The spleen is mostly of medium hardness, with a smooth surface and round edges. The large spleen can touch the splenic notch. If the spleenitis occurs, it can cause pain or abdominal pain in the upper left abdomen. If there is more ascites, palpate with impact method. When the upper gastrointestinal bleeding occurs, the spleen can be temporarily reduced or even inaccessible, which is of great value for the identification and determination of bleeding from esophageal varices. Splenomegaly is often accompanied by a decrease in white blood cells, white small plates, and/or red blood cells, which is called hypersplenism.
2. The establishment and opening of collateral circulation. When the portal vein pressure increases, when the pressure exceeds 1,96kpa (200mmmH2O), the return blood flow from the digestive organs and spleen is blocked, forcing the establishment of collateral circulation between the blood vessels in many parts of the portal system and the systemic circulation. Clinically important ones include: ①The lower esophagus and gastric varices, the gastric coronary vein of the portal vein system and the esophageal vein of the vena cava system, intercostal vein, and atypical veins are formed by anastomosis. Often due to a significant increase in portal pressure, esophagitis, rough and sharp food damage, or a sudden increase in intra-abdominal pressure, causing bleeding from varicose veins. ② Abdominal wall and periumbilical varicose veins, when portal hypertension, the umbilical vein reopens and expands, and connects with accessory umbilical vein, abdominal wall vein, etc., the periumbilical abdominal wall can be seen with curved veins, the blood flow direction is above the umbilicus and below the umbilicus It can be distinguished from inferior vena cava obstruction. If the umbilical vein is significantly varicose, the lumen dilates and blood flow increases, and sometimes continuous venous murmurs can be heard. ③ Hemorrhoids form, which can cause blood in the stool when they rupture.
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, kidneys and many other factors. Factors (see pathology for details). Intestinal flatulence is common before ascites appears. When a large amount of ascites occurs, the abdomen is swollen and the abdominal wall is tight and shiny, which makes the patient inconvenient to move. Increased abdominal pressure can compress abdominal internal organs, which can cause umbilical hernia, and can also cause Diaphragm elevation causes difficulty breathing and palpitations. Some patients may have pleural effusion. It is more common on the right side. It is mostly caused by ascites entering the thoracic cavity through the lymphatic vessels of the diaphragm, called hepatic pleural effusion. Mobile dullness occurs in ascites above medium level, and it is not obvious when there is a small amount of ascites, which can be detected by ultrasound.
(3) Liver palpation: The size, hardness, and smoothness of the liver is related to the amount of fat infiltration in the liver, liver cell regeneration, and fibrous tissue proliferation and contraction. In the late stage, the liver is reduced, hard, and nodular in surface.
Liver cirrhosis often leads to death due to complications.
1. Upper gastrointestinal bleeding is the most common complication of this disease, which often occurs suddenly, with heavy bleeding, often accompanied by blood in the stool, in addition to vomiting blood. Prone to shock and induce hepatic encephalopathy, with a high mortality rate. Many patients have a history of gastrointestinal bleeding in the past. In upper gastrointestinal bleeding in patients with liver cirrhosis, in addition to the rupture of esophageal and gastric varices, the cause of bleeding in some patients is complicated by acute gastric mucosal disease or peptic ulcer. Endoscopy is required for identification.
2. Hepatic encephalopathy, found in patients with severe liver disease, is a syndrome of the central nervous system based on metabolic disorders, and clinically manifested mainly by disturbances of consciousness and coma. It is the most common cause of death in liver cirrhosis, and can also be seen in patients after severe hepatitis, liver cancer, severe obstructive jaundice, and portal vena cava shunt.
(1) The etiology and pathogenesis is not yet fully understood. However, it is generally believed that the pathophysiological basis is liver failure and surgical shunt or naturally formed collateral circulation between the portal vein. Due to the decreased liver function, the detoxification effect is reduced, and the necessary substances for maintaining brain function are reduced. Nitrogen and other toxic substances cannot be effectively detoxified by the liver; the extensive shunt between the portal vena cava allows toxic substances to bypass the liver and directly It enters the brain through collateral branches. In addition, increased sensitivity of the brain may also be an important factor. Metabolic disorders in the body during hepatic encephalopathy are multifaceted, and the occurrence of encephalopathy is the result of multiple factors.
1. Ammonia poisoning theory increases blood ammonia is one of the clinical features of hepatic encephalopathy. The urease and amino acid oxidase of intestinal bacteria can act on nitrogenous substances to produce ammonia. Normal people absorb 4 grams of ammonia from the gastrointestinal tract every day. Skeletal muscle also produces ammonia. When a large amount of ammonia is combined with α-ketoglutarate in the brain tissue to form glutamate, the trihydroxy acid cycle is impaired, which seriously affects cell metabolism and energy sources. There are many factors that affect ammonia poisoning, such as blood pH. The mutual conversion of NH3 and NH4+ is affected by pH. NH3 is easier to pass through the blood-brain barrier and cause ammonia poisoning. Any factor that can cause alkalosis can increase the toxicity of ammonia. Ammonia can stimulate the respiratory center, so hepatic encephalopathy often has hyperventilation and respiratory alkalosis, which aggravates the increase in blood ammonia. ②The blood volume is too low. ③ Hypoxia. ④Infection, etc. can increase the toxicity of ammonia. Increased blood ammonia is very important in the pathogenesis, and clinical treatment often has certain effects. However, the increase of blood ammonia is not parallel to the degree of coma. In some cases, blood ammonia does not increase, indicating that ammonia poisoning is not the only cause of hepatic encephalopathy.
2. Synergistic toxicity of ammonia, mercaptans and short-chain fatty acids. Methyl mercaptan is a product of methionine metabolized by bacteria in the intestine. Methyl mercaptan and its converted dimethyl sulfoxide can cause coma. Liver odor may be the volatile odor of methyl mercaptan and dimethyl disulfide. The concentration of methyl mercaptan in the blood of severe liver disease increases, and the increase is more obvious in patients with hepatic encephalopathy.
Short-chain fatty acids (mainly valeric acid, caproic acid and caprylic acid) are significantly increased in the plasma and cerebrospinal fluid of patients with hepatic encephalopathy.
In animal experiments, any one of ammonia, mercaptans and short-chain fatty acids is used alone, if the dose is small, the concentration into the brain is low, which is not enough to cause hepatic encephalopathy; if the combined use is unchanged, it can also induce encephalopathy. symptom. For this reason, it was suggested that the three synergistic effects may play an important role in the pathogenesis.
3. Pseudo-neurotransmitter theory. Aromatic amino acids such as tyrosine and phenylalanine in food are transformed into tyramine and phenethylamine by the action of intestinal bacteria decarboxylase, and then form snakehead in the brain by the action of hydroxylase. Amine (β-hydroxytyrosine) and phenethanolamine. The chemical structure of the latter two is similar to that of the neurotransmitter norepinephrine, but the function of transmitting nerve impulses is weak, so they are called pseudo-neurotransmitters, which cause abnormalities in the cerebral cortex. Inhibition, disturbance of consciousness and coma.
The normal extrapyramidal basal ganglia maintain a balance of inhibition and excitement. When dopamine is replaced by a pseudoneurotransmitter, acetylcholine can be dominant, causing flutter tremor. Levodopa can pass through the blood-brain barrier, so levodopa has been used clinically to treat hepatic encephalopathy, but the effect is uncertain.
So far, the theory of pseudoneurotransmitter has not been fully confirmed.
4. The theory of imbalanced amino acid metabolism; Aromatic amino acids such as phenylalanine, tyrosine and tryptophan increased in the patient’s plasma; while branched chain amino acids such as valine, leucine and isoleucine decreased, the metabolism of the two amino acids It was unbalanced. In liver failure, the inactivation effect of insulin in the liver is reduced, and the blood concentration is increased. Insulin has the effect of promoting branched chain amino acids to enter the muscle tissue, resulting in a decrease in plasma content. The increased tryptophan in the brain can derive more serotonin, which has an inhibitory effect on the central nervous system, and can antagonize norepinephrine and cause coma. Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the mammalian brain, produced by intestinal bacteria. In recent years, it has been found that in animal models of experimental hepatic encephalopathy, the plasma concentration of GABA is increased, the receptors in the brain tissue are increased, and the permeability of the blood-brain barrier is also increased. Some people think that the coma is related to it.
5. Increased brain sensitivity. In severe liver disease, it is extremely sensitive to hypoxia, infection, hypotension, hypoglycemia, electrolyte disturbances, morphine barbiturates, benzodiazepines, and psychiatric symptoms and even coma.
(2) Common causes of hepatic encephalopathy
1. Upper gastrointestinal bleeding” is the most common cause. A large amount of blood is decomposed in the intestine to form ammonia, or other neurotoxic substances are absorbed and induced hepatic encephalopathy.
2. Excessive intake of nitrogenous substances, such as excessive protein in the diet, oral ammonium salt, methionine, etc.
3. Disturbance of water and electrolyte and imbalance of acid-base balance. A large amount of ascites and diuresis cause electrolyte disturbance, hypovolemia and hypoxia, which can lead to prerenal azotemia and increase blood ammonia. Low eating, vomiting, diarrhea, potassium excretion and diuresis, secondary aldosterone increase and ascites, etc., can all lead to hypokalemic alkalosis, thereby promoting NH3 to enter the brain through the blood-brain barrier.
4. Hypoxia and infection increase the catabolism of tissues and increase ammonia production. Hypoxia and high fever increase the toxicity of ammonia.
5. Hypoglycemia, the oxidative phosphoric acid process of glucose helps the combination of NH3 and glutamate, so hypoglycemia can increase the toxicity of ammonia.
6. Constipation, prolongs the contact time of ammonia, amines and other toxic derivatives with colonic mucosa, which is conducive to the absorption of poisons.
7. Sleeping pills, tranquilizers, and surgery. Anesthesia and surgery can increase the burden on liver, kidney, and brain functions. Sedative and sleeping pills can directly inhibit the brain, while inhibiting the respiratory center from causing hypoxia.
(3) Clinical manifestations: The clinical manifestations of hepatic encephalopathy are often inconsistent due to the nature of the original liver disease, the severity of liver cell damage, and the different inducements. In order to observe the dynamic changes of encephalopathy, it is conducive to early diagnosis, treatment and analysis of curative effect. According to the degree of consciousness disturbance, neurological manifestations and changes in EEG, hepatic encephalopathy is divided into four stages from mild mental changes to deep coma.
1. The first stage prodromal stage Mild personality changes and behavioral disorders, such as euphoria or indifferent speech, slow thinking, slow response, accurate response, but unclear and slow speech. There may be flutter-like tremor, also known as liver tremor. When the patient is instructed to spread the arms and fingers apart, the hand will be deviated to the outside, and the metacarpophalangeal joints, wrist joints, and even the elbow and shoulder joints will have rapid and irregular flutters. Jitter. Most of the EEG is normal, and this period lasts from several days to several weeks. Sometimes the symptoms are not obvious and easy to be ignored.
2. The second stage pre-coma is mainly caused by confusion, behavioral disorders and sleep disturbances. The symptoms in the previous stage are aggravated. Orientation and understanding are diminished, and the concepts of time, place, and characters are confused. They cannot perform simple calculations and intellectual actions, such as building blocks and swinging a five-pointed star with a matchstick. Slurred speech, handwriting, abnormal behavior, such as disheveled clothing, and drowning. Most of the sleep time is reversed, and wake up day and night. May have hallucinations, fear, mania, and easily be mistaken for mental illness. There are obvious neurological signs, such as increased muscle tone, tendon hyperreflexia, ankle clonus, and positive pathological reflexes. In addition, involuntary movements and dyskinesias can still occur. This period of flutter-like tremor is easy to detect, and the EEG shows diffuse slow waves, which have certain characteristics.
3. The third stage lethargic phase is dominated by lethargy and severe mental confusion. Various neurological signs continue or worsen. The patient is lethargic most of the time, but can wake up. There is often confusion and confusion when waking up, and often hallucinations. Fluttering tremor can still be detected, muscle tension increases, and limb movement is resistant. Pyramidal tract signs are often positive and EEG is abnormal.
4. The fourth stage coma stage gradually turns from a shallow coma to a deep coma. Complete loss of consciousness, unable to wake up. In light coma, he still responds to painful stimuli, and his tendon reflexes and muscle tone are still hyperactive. In a deep coma, various reflexes disappear, muscle tone decreases, and paroxysmal convulsions, ankle clonus, and hyperventilation may occur. The EEG is obviously abnormal.
The above staging boundaries are not necessarily obvious, and there are often overlapping periods before and after. Some people have recently advocated increasing subclinical hepatic encephalopathy, some people call it stage 0 hepatic encephalopathy. A new technique for measuring visual evoked potentials (VEP) has been developed, which can more accurately reflect the electrical activity of the brain and can detect hepatic encephalopathy before the onset of symptoms.
Hepatic encephalopathy with severe liver damage often has obvious jaundice, bleeding tendency and liver odor. It is easy to be complicated by various infections, cerebral edema and liver and kidney syndrome, which makes the clinical manifestations more complicated.
3. Infected patients with cirrhosis have low resistance, decreased function of Kupffer cells in the liver, combined with intestinal stasis, bacteria can easily enter the abdominal cavity through the intestinal wall, or enter the portal vein and directly enter the systemic circulation through the collaterals, so they often have complicated infections such as pneumonia , Biliary tract infections, gram-negative bacilli sepsis and primary peritonitis. The pathogenic bacteria of spontaneous peritonitis are mostly Escherichia coli and para-E.coli. Recently, it has been discovered that anaerobic bacteria are also one of the pathogenic bacteria. Generally, the onset is more rapid, mainly manifested as abdominal pain and bloating. There is fever, nausea, vomiting and diarrhea, and severe cases have shock. The patient’s ascites grew rapidly, and there was mild abdominal tenderness and peritoneal irritation. Ascites is mostly exudate, but because the exuded ascites is often diluted by the original leaking ascites, its nature can be between leakage and exudate. Ascites should be cultured for ordinary bacteria and anaerobic bacteria and sensitive to drugs test. This complication is serious and requires timely detection and active treatment.
4. Functional renal failure (hepatorenal syndrome): When cirrhosis has a large amount of ascites, due to factors such as insufficient effective circulating blood volume, functional renal failure may occur, also known as hepatorenal syndrome. It is characterized by spontaneous oliguria or anuria, dilutional hyponatremia, hyponatremia and azotemia. The patient's kidney lacks organic changes, and transplanting it to others can exert normal renal function, indicating that renal failure is functional rather than organic damage. Upper gastrointestinal bleeding, shock, large amounts of ascites and strong diuresis, endotoxemia and sodium-water metabolism disorders are closely related to this disease.
5. Disorders of electrolyte and acid-base balance. Patients with liver cirrhosis have electrolyte disturbances before ascites appear. After ascites and other complications appear, electrolyte disturbances become more serious. The common ones are hyponatremia, hypokalemia, hypochloremia and metabolic alkalosis, and induce hepatic encephalopathy. Therefore, it should be corrected in time.
6. Primary liver cancer "A considerable number of primary liver cancers occur on the basis of liver cirrhosis. When patients with liver cirrhosis have progressive enlargement of the liver, persistent liver area pain, liver masses, and ascites turning bloody in a short period of time, especially when alpha-fetoprotein is increased, one should be alert to the possibility of primary liver cancer.
Laboratory and other inspections
1. Blood routine the compensatory period is usually normal, the decompensation period is usually anemia of varying degrees, and the white blood cell and platelet counts decrease during hypersplenism.
2. Urine routine and urinary bilirubin. When there is jaundice and ascites, the urine bilirubin in the urine increases, and bilirubin may also appear. Sometimes there may be protein and casts.
3. Liver function test. Serum albumin decreased and globulin increased, white/globulin ratio decreased or inverted, albumin decreased and γ-globulin increased significantly in serum protein electrophoresis; serum bilirubin increased to varying degrees; serum cholesterol lipid Decrease; serum transaminase SGPT is slightly or moderately increased. When liver cells are severely necrotic, AGOT activity is often higher than AGPT; due to fibrous tissue proliferation, monoamine oxidase (MAO) tends to increase; thrombin is prolonged to varying degrees, and vitamin K injection cannot be corrected ; Liver indigo green (ICG) clearance test, indigo green is a dye that is selectively taken up by the liver after intravenous injection, excreted into bile, not excreted from the kidneys, nor does it participate in the enterohepatic circulation. It is a very practical trial for clinical screening of patients with liver disease. The dose was 0.5mg/kg, and the retention rate was measured 15 minutes later. The normal value was 7.83±4.31%. The retention rate of liver cirrhosis, especially in the decompensated stage, was significantly higher, about 50% or more.
IV. Immunological examination: The markers of hepatitis B and C can be detected in patients with viral hepatitis. About half of the patients with cellular immune examination have reduced T lymphocytes, and reduced E-rosette and lymphocyte transformation rates. Humoral immunity showed increased serum immunoglobulin, with the most obvious increase in IgG, usually parallel to the increase in gamma globulin. The increase mechanism is due to the intestinal nature of multiple antigenic substances, which cannot be degraded after being absorbed in the liver. immune response. In addition, autoantibodies such as anti-nuclear antibodies, smooth muscle antibodies, mitochondrial antibodies, and anti-hepatocyte-specific lipoprotein antibodies are still present.
5. Ascites examination is usually leaking fluid; if it is complicated by spontaneous peritonitis, it can be transformed into exudate, or between the leak and the exudate. Bacterial culture and drug susceptibility test should be sent in time; if it is bloody, in addition to considering concurrent tuberculosis peritonitis, cancer should be highly suspected, and cytology and alpha-fetoprotein should be tested.
6. B-mode ultrasound examination can show the morphological changes of the size of the liver and spleen, whether the portal vein and splenic vein are widened, if there is ascites, there may be a liquid dark area and an estimate of the amount of ascites. In addition, cancer can be found.
7. Endoscopy. Fiber or electronic gastroscopy can clearly show the location and extent of varicose veins. When upper gastrointestinal bleeding is complicated, it is of great value in detecting the location and cause of bleeding. Laparoscopy can directly observe the liver surface, color, edge and spleen, and can be used for selective needle biopsy under direct vision. It is very useful for identifying liver cirrhosis, chronic hepatitis, primary liver cancer, and clarifying the cause of liver cirrhosis. helpful.
8. X-ray examination: Barium swallow examination of the esophagus can show esophageal and gastric varices. Computerized tomography (CT) is not only helpful in the diagnosis of liver cirrhosis, but also can be found for cancer.
9. Radionuclide examination can show that the liver uptake of nuclide is reduced, the distribution of nuclide is uneven, the spleen nuclide is concentrated and enlarged, and the destruction of 51 chromium-labeled red blood cells in the spleen is enhanced when there is hypersplenism.
X. Liver biopsy: Percutaneous liver biopsy can be done when necessary for difficult cases to confirm the diagnosis
Decompensated liver cirrhosis can often be diagnosed based on clinical manifestations and related examinations. Early-stage patients should be carefully asked about the history of viral hepatitis, schistosomiasis, long-term alcoholism, or nutritional disorders, and pay attention to checking the liver and spleen, combining liver function and other necessary examinations to confirm the diagnosis. The main diagnostic criteria for liver cirrhosis are: ① History of viral hepatitis (type B and C), history of schistosomiasis, alcoholism and nutritional disorders. ②The liver can be slightly larger, often shrinks in the late stage, the texture becomes hard, and the surface is uneven. ③The liver function is decreased. ④Clinical manifestations of portal hypertension. ⑤Pseudo lobules formed in liver biopsy.
1. To differentiate from diseases accompanied by hepatomegaly and splenomegaly, such as chronic hepatitis and primary liver cancer. Others include clonorchiasis, hepatic hydatid disease, congenital liver cysts and certain metabolic diseases involving the liver. Blood diseases, such as chronic leukemia, often have splenomegaly, which should be distinguished.
2. Distinguish from diseases that cause ascites and abdominal swelling. Common ones include constrictive pericarditis, tuberculous peritonitis, intra-abdominal tumors, giant ovarian cysts, and chronic nephritis.
3. Diseases differentiated from complications of liver cirrhosis
(1) Upper gastrointestinal bleeding” should be differentiated from peptic ulcer, acute and chronic gastric mucosal lesions, gastric cancer, esophageal cancer and biliary bleeding.
(2) Hepatic coma should be differentiated from coma caused by hypoglycemia, diabetes, uremia, drug poisoning, severe infection and cerebrovascular accident.
(3) Functional renal failure” should be differentiated from chronic nephritis, chronic pyelonephritis, and acute renal failure caused by other causes.
1. General treatment
(1) Those who have rest and liver function compensation should reduce their activities appropriately, participate in part of the work, and pay attention to the combination of work and rest. Patients in the decompensated period should rest in bed.
(2) Diet should be rich in nutrients, easy to digest and absorb, generally high-calorie, high-protein, vitamin-rich and delicious food is appropriate. The fat content should not be too much, but it need not be too restrictive. When there is ascites, the diet should be less salty. At present, some people advocate that it is not necessary to have a salt-free diet, because it affects the appetite and the gain is not worth the loss. Patients with significant liver damage or high blood ammonia who are prone to hepatic encephalopathy should temporarily limit protein intake. Avoid alcohol and avoid eating harsh and sharp foods.
(3) Supportive therapy should be added during the decompensation period. Because most severely ill patients have nausea, vomiting, eating less or unable to eat, intravenous glucose can be infused, and vitamin C, potassium chloride, inosine, insulin, etc. can be added. Particular attention should be paid to maintaining water, electrolyte and acid-base balance, especially the supplement of potassium salt. In addition, compound amino acids, blood, plasma and albumin can also be used as appropriate.
2. Drug treatment: There is no specific medicine at present, and it is not advisable to abuse drugs, otherwise it will increase the burden on the liver and backfire.
(1) Supplement various vitamins. Vitamin C, E and B vitamins can improve liver cell metabolism, prevent fatty degeneration and protect liver cells. Yeast tablets can also be taken. Supplement vitamin K, B12 and folic acid as appropriate.
(2) Drugs that protect liver cells, such as Gantai Le, Vitamin C, Ganning, Yiganling (silymarin tablets), inosine, etc. Vitamin C, B6, potassium chloride, and soluble insulin are added to the 10% glucose solution.
(3) Traditional Chinese Medicine: Traditional Chinese Medicine has unique insights into the diagnosis and treatment of chronic liver disease. The combination of traditional Chinese and Western medicine often yields better results. Traditional Chinese medical scientists believe that liver cirrhosis is caused by damp heat, stagnation of liver qi, which affects the spleen and stomach, resulting in poor blood circulation, clogged arteries and collaterals, causing accumulation or symptom, and water guts appear in the later stage. Syndrome differentiation is mostly of liver stagnation and spleen stagnation or bulging water accumulation. The former can be used with Chaihu Shugan Decoction (San), Fugan Decoction, etc.; the latter can be used with Wulingsan or Wupi drink.
3. Ascites treatment: The difficulty of ascites treatment depends on the duration of ascites and the degree of liver damage. Therefore, the basic measures for the treatment of ascites should focus on improving liver function, including clinical rest, strengthening 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. Diuretics "The principle of use of diuretics is combined, intermittent, and alternating medication. The dosage should not be too large, and the diuretic speed should not be too strong, so as to avoid serious side effects such as hepatic coma and hepatorenal syndrome. Diuretics include potassium retention and potassium excretion diuretics. In principle, the potassium retention diuretic spironolactone 20 mg 3 times a day should be used first, and if the diuresis is not significant after 3 to 5 days, it can be added to 40 mg 3 times a day; or Use triamterene 50mg 3 times a day. When the above treatment effect is not good, potassium excretion diuretic furosemide 20-40mg 3 times a day should be added; or dihydrochloride 25-50mg 3 times a day. Pay attention to potassium supplementation when diuresis. For patients with ascites without limb edema, the weight loss due to diuresis should not exceed 300g per day, or less than 2kg per week. When the diuretic effect of the combined medication gradually weakens, it can be stopped for a few days in order to restore blood volume, and then continue to use or switch to another group of diuretics. During the diuretic treatment, the water, electrolyte, and acid-base balance should be closely observed and supplemented and corrected in time.
2. When the effect of catharsis and diuretics is not good, 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) Increasing plasma colloidal osmotic pressure regularly, small amounts, and multiple intravenous infusions of fresh blood, plasma or protein every week, which can improve the general condition of the body, restore liver function, increase plasma colloidal osmotic pressure, and promote the disappearance of ascites. It helps a lot.
(4) Abdominal puncture and discharge and ascites concentrated reinfusion. The release of ascites will lose electrolytes and proteins, which can easily induce electrolyte disorders and hepatic coma, and ascites can recur quickly, so ascites removal is generally not used for treatment. Abdominal puncture and drainage can be considered in the following situations: ① High ascites affects cardiopulmonary function; ② High ascites compresses renal veins and affects blood return; ③ Complicated with spontaneous peritonitis, when abdominal cavity washing is required. The appropriate amount of liquid for each discharge is about 3000ml.
Concentrated ascites reinfusion is a better way to treat refractory ascites. Ascites passes through the concentrating device, which can concentrate protein several times to several tens of times. After reinfusion, it can replenish protein, increase plasma colloidal osmotic pressure, increase effective blood volume, and improve renal blood circulation, so as to clear the retained water and sodium to reduce and eliminate ascites. Side effects include fever, infection, electrolyte disorders, etc., which can be prevented by targeted treatment.
(5) Surgical treatment: Abdominal cavity-jugular drainage (Leveen drainage). It is one of the effective methods for surgical treatment of schistosomiasis liver fibrosis. Drainage is used to increase effective blood volume, improve renal blood flow, and supplement protein. Patients with ascites infection or suspected cancerous ascites cannot use this method, because ascites leakage, pulmonary edema, hypokalemia, superior vena cava thrombosis, infection, and DIC may be complicated, it should be used with caution.
Another operation is thoracic catheter-jugular vein anastomosis. The hepatic lymph fluid flows smoothly into the internal jugular vein through the thoracic catheter, thereby reducing the lymph fluid flowing into the abdominal cavity, but the effect is not good.
4. Surgical treatment of portal hypertension and hypersplenism. The main purpose of treatment is to reduce the pressure of the portal vein 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 timing of surgery. Patients with schistosomiasis liver fibrosis with significant portal hypertension, mild liver damage, ineffective medical treatment of upper gastrointestinal hemorrhage and no contraindications to surgery may consider surgery. Patients with advanced liver cirrhosis whose plasma albumin is lower than 30g/L, prothrombin time is significantly prolonged, and those with significant liver damage 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, there have been more than 600 reports from all over the world, and it is constantly increasing. More than half of them were completed after 1980. Due to the use of newer immunosuppressive therapies, improvements in supportive therapies and improvements in surgical procedures, the survival rate of liver transplantation continues to increase. According to foreign statistics, the three-year survival rate of liver transplantation since 1980 is based on the number of diseases; about 41% of advanced non-alcoholic cirrhosis; 20% of alcoholic cirrhosis; biliary atresia 60%; hepatocellular carcinoma 20%; cholangiocarcinoma <10%; metabolic disease, mainly α-antitrypsin deficiency 60%; sclerosing cholangitis 25%; and Brdd-Chiari syndrome 47%. In view of the fact that most patients with advanced liver disease have no satisfactory treatment, and the survival rate after liver transplantation will continue to improve. It is expected that more and more patients with chronic liver diseases will receive liver transplantation in the future. The main factor affecting liver transplantation is the problem of the donor liver.
Six, treatment of complications
(1) Treatment of upper gastrointestinal bleeding emergency measures should be taken. Strengthen monitoring, make the patient quiet and eliminate fear.
1. General treatment
(1) Absolutely rest in bed, closely observe changes in the condition, and measure blood pressure and pulse regularly. Timely record the volume and frequency of hematemesis, blood in stool.
(2) Fasting usually 24 to 48 hours after the bleeding stops, the liquid diet can be started.
(3) Blood transfusion and fluid supplementation quickly replenish effective blood volume to correct hemorrhagic shock. Transfusion should try to transfuse fresh blood, because it contains more clotting factors and less ammonia, which is beneficial to hemostasis and prevent hepatic encephalopathy.
2. Hemostatic agent, carboxybenzylamine and 6-aminocaproic acid can be used, and vitamin K is routinely used.
3. For patients with acute gastric mucosal damage or with peptic ulcers, ① cimetidine 400-800mg or furanonitramine 150mg can be infused intravenously, once every 6-8 hours, to inhibit gastric acid secretion to achieve hemostasis. ②For local administration, 8mg of norepinephrine is added to 100ml of normal saline or cold boiled water for oral administration, once every 4-6 hours, and once every 2 hours if necessary.
4. Pituitary vasopressin can constrict visceral blood vessels and reduce portal blood flow, thereby reducing portal pressure and helping to stop bleeding. The method of use can be divided into large-dose intravenous intermittent injection and small-dose continuous infusion. In the former, 20 units of pituitary vasopressin were added to 10% glucose solution, and the drip was completed in about half an hour, once every 4 hours, for 4-6 times. Low-dose continuous infusion method, the dose should be controlled at 0.2 units per minute, continuous intravenous drip. During the medication period, attention should be paid to observe whether there are side effects such as increased blood pressure and increased heart rate. If found, the infusion rate should be slowed down. Pituitary vasopressin can cause coronary vasospasm and uterine contraction, so it is not used for coronary heart disease, hypertension and pregnant women. Long-acting pituitary vasopressin-glycyl vasopressin has good curative effect and few side effects, so it is optional.
5. Airbag compression method uses three-lumen tube airbag compression to stop bleeding. It has a good temporary hemostasis effect on rupture of esophageal and gastric varices. It is generally used as an emergency measure for hematemesis. Sometimes it can win time to create conditions for surgical treatment.The method is to first check the three-chamber tube airbag into the stomach through the nasal cavity, and then inject 300-400ml of air into the stomach airbag with a pressure of 5.33-6.67kpa (40-50mmHg) after the blood in the stomach is exhausted. Then pull the three-lumen tube outwards to make the gastric balloon press tightly against the fundus and cardia of the stomach, and then inject 150-200ml of air into the esophageal sac, maintaining the pressure at 4.0-5.33 (30-40mmHg). Stomach contents should be pumped regularly from the stomach tube to observe the hemostatic effect. Every 4 hours, deflate the esophageal air sac to depressurize, observe whether there is continued bleeding, and prevent continuous compression and esophageal mucosal erosion. The placement time is generally not more than 3-4 days. The esophageal balloon deflation and decompression time can be gradually extended. After the bleeding stops, it is still necessary to observe for 24 hours. When the bleeding stops, the gastric sac is deflated and the three-lumen tube is taken out. When using this method, the pressure of the gastric sac and esophageal sac should be closely observed, and nursing should be strengthened to prevent the three-lumen tube from sliding upward and oppressing the trachea to cause suffocation. Saliva, sputum and other secretions should be sucked out at any time to prevent lung infection caused by inhalation into the lungs .
6. Sclerotherapy (sclerotherapy) injects sclerosing agent into or around the varicose esophageal vein under the direct vision of a fiber endoscope or an electronic endoscope. The hemostasis effect is better than traditional methods, and it can also be used for patients with poor liver function, jaundice and ascites. The commonly used hardener is 5% ethanolamine oleate, 2ml per injection point, the total amount generally does not exceed 20ml. After the injection, the endoscope can be taken out by compressing it for 3-5 minutes.
In recent years, a window-opening plastic sleeve for sclerotherapy has been made. It is inserted into the esophagus with the endoscope during treatment. The cannula is rotated to expose the varicose veins to the window, which makes it very convenient to inject the sclerosant. The new injection point and the cannula play a role of compression and hemostasis on the injection site. Sclerotherapy is to cause thrombosis in the varicose veins and non-infectious fibrosis in the surrounding tissues, so that the varicose veins are occluded and compressed to stop bleeding. Within 24-48 hours after surgery, patients may have low-grade fever and pain behind the breastbone, which may be caused by esophagitis or peri-esophageal inflammation. In addition, there has recently been endoscopic ligation of esophageal varices.
7. Embolization Therapy Percutaneous transhepatic embolization of varices (percutaneous transhepatic embolization of varices) is preoperatively with sedatives, under local anesthesia, hepatic puncture and portal vein contrast via B-mode ultrasound, and then the catheter is selectively inserted into the left or short gastric vein. And inject a small elastic steel ring with fibers as embolism and clotting substance gelatin sponge to cut off the blood flow of the esophageal varicose vein. After the operation, the contrast agent was injected to observe the embolism. This method should only be considered when the aforementioned treatments are ineffective. Complications include blood abdomen, hemothorax and portal vein thrombosis.
8. Propranolol Propranolol can reduce the number of heartbeats and cardiac output, thereby reducing visceral blood flow and portal pressure, which can prevent bleeding from esophageal and gastric varices. Generally 10-15 days after the bleeding stops, the hemodynamics has returned to the state before bleeding. The dosage starts from 10-20mg 3 times a day and gradually increases to 40-60mg 3 times a day. The objective indicator of dose is based on the original heart rate, with a 25% slowdown as an indicator. To achieve the purpose of prevention and treatment, it is necessary to take Propranolol for a long time. Some people believe that Propranolol can reduce liver blood flow, which may damage liver function and induce hepatic encephalopathy. Therefore, further observation is needed for the long-term efficacy of patients with more severe disease.
9. Surgical treatment is ineffective to medical treatment, and if there is heavy or repeated bleeding, emergency surgical operation should be performed as soon as possible, such as esophageal vein suture, gastric fundus cerclage and dissection, splenectomy and shunt, etc.
The success rate of first bleeding in this complication is higher, and the prognosis is worse as the disease progresses and the number of bleeding increases.
(2) Treatment of hepatic encephalopathy. Currently, there is no special treatment. Comprehensive measures should be taken for treatment. Early prevention is very important. Once the signs of the prodromal stage appear, they should be closely observed, looking for incentives, and promptly corrected.
1. Elimination of incentives. The upper gastrointestinal bleeding and infection should be prevented in time, and rapid potassium excretion and diuresis and ascites should be avoided, and attention should be paid to correct the imbalance of water, electrolyte and acid-base balance. In liver cirrhosis, the half-life of the drug in the body is prolonged, the clearance is reduced, and the sensitivity of the brain increases. For this reason, most patients cannot tolerate anesthesia. Analgesic, sleeping, sedation and other drugs, if used carelessly, the patient can quickly fall into lethargy, until irreversible coma. When the patient is agitated or sucking animals, morphine, barbitur, dolanidine, chloral hydrate and paraaldehyde should be prohibited, and a small amount of diazepam, scopolamine, antihistamines such as diphenhydramine, Chlorpheniramine can sometimes be used as a substitute for stabilizers.
2. Reduce the production and absorption of intestinal poisons
(1) Diet limit protein intake, fasting protein when in a coma, daily supply of calories about 5000-6700KJ (1200-1600Kcal), containing sufficient vitamins, carbohydrate-based food. Those who are in a coma and unable to eat can use nasal feeding, or a large vein cannula infusion of 20-40% glucose solution and essential amino acids to maintain nutrition. At the same time, attention should be paid to potassium supplementation to prevent heart failure and cerebral edema. After consciousness is clear, gradually increase protein. 25 grams of protein per day, 10 grams every 3 to 5 days as the condition improves, preferably not more than 50 grams in the short term. Plant protein contains methionine and aromatic amino acids, while ammonia-producing amino acids are less, which is more beneficial than animal protein.
(2) Enema or catharsis can be used to clear intestinal food or blood accumulation with normal saline or weak acid solution (500ml normal saline plus 50g vinegar) enema, or use 50% sorbitol 10-20ml or 25% magnesium sulfate 40-60ml diarrhea.
(3) Inhibit the growth of intestinal bacteria. Orally take 4 grams of neomycin daily, or use ampicillin, kanamycin, etc., to inhibit the growth of E. coli and reduce the production of ammonia. At the same time, 0.2 grams of metronidazole 4 times a day is expected to achieve better results. Neomycin and other treatments should be continued until the patient can tolerate 50 grams of protein per day.
(4) Lactulose is not absorbed after oral administration. The bacteria in the colon decompose into lactic acid and acetic acid, making the intestine acidic and reducing the formation and absorption of ammonia. In the case of renal impairment or hearing impairment, neomycin is avoided, or long-term treatment is required, lactulose is the first choice. The usual dose is 10-20 grams, 3 times a day, or about 65% of lactulose syrup, 50-200ml a day, orally in divided doses. Start with a small dose and adjust to fecal 2-3 times a day, and the pH of feces is 5-6. Side effects include fullness, abdominal pain, nausea, and vomiting. Recently, it has been discovered that certain disaccharides such as lactose and polyol sugars such as sorbitol are fermented by bacteria in the colon, which can also lower the pH of feces and reduce the content of ammonia. The effect is similar to that of lactulose, but the price is cheap. It can be made into powder and taken. Convenience.
3. Promote the metabolism and elimination of toxic substances, correct the disorder of amino acid metabolism
(1) Ammonia-lowering drugs ①Potassium glutamate (6.3g/20ml each, 34mmol/L potassium) and sodium glutamate (5.75g/20ml, 34mmol/L sodium), each dose is different 2 bottles, intravenous infusion with glucose solution, 1-2 times a day, the ratio of potassium glutamate to sodium in the medication depends on the serum potassium, sodium concentration and the condition. Use potassium with caution when oliguria, ascites and edema are obvious Use sodium with caution. Both potassium and sodium glutamate are alkaline. For those with metabolic alkalosis, it is best to use drugs that can acidify blood pH, such as intravenous infusion of large amounts of vitamin C or arginine. ②Add 10-20 grams of arginine to glucose solution by intravenous drip, once a day. This drug is acidic and is suitable for patients with metabolic alkalosis. It may be more effective when applied with potassium and sodium glutamate.
(2) Correct the disorder of amino acid metabolism by intravenous infusion of branched-chain amino acid mixture (containing 16.5 g of leucine, 13.5 g of isoleucine, 12.75 g/100 ml of valine), and the amount of each time is 500-1000ml, do not exceed the amount Long-term application, so as not to produce new amino acid imbalance.
4. Other symptomatic treatment
(1) Correct the imbalance of water, electrolyte and acid-base balance. It is advisable that the total daily intake of fluid should not exceed 2500ml. The fluid volume of patients with liver cirrhosis and ascites is generally controlled within 1000 ml of urine volume to avoid blood dilution, hyponatremia and aggravation of coma. Correct potassium deficiency and alkalosis in time.
(2) Protect brain cell function: Use ice cap to lower the intracranial temperature to reduce energy consumption and protect brain cell function.
(3) To protect the unobstructed respiratory tract and deep coma, consider tracheotomy and give oxygen.
(4) Prevention and treatment of cerebral edema, intravenous drip of hypertonic glucose, mannitol and other dehydrating agents.
(5) Prevention and treatment of bleeding and shock. See the treatment of complications of upper tract bleeding for details.
For drugs that have not yet proven effective, such as levodopa, bromocriptine, etc., it may not be used. Acetohydroxamic acid and adrenal cortex hormones that have been proven ineffective should not be reused.
(3) Treatment of infections: After spontaneous peritonitis and sepsis, the liver damage is often rapidly aggravated, and supportive treatment and the application of antibiotics should be actively strengthened. The principle of antibiotic use is early, adequate and combined medication, and it must be performed immediately after the clinical diagnosis is clear, and treatment cannot be started after ascites or blood culture reports. The selection of antibiotics is mainly for gram-negative bacilli and also for gram-positive cocci. Commonly used antibiotics include ampicillin, cephalosporins, penicillin, chloramphenicol, etc., choose 2~3 kinds of combined application, and then adjust the antibiotic as appropriate according to the culture result and the response to the treatment. The dose should be large for the first few days and the condition is stable The dose can be reduced later, and the medication time is generally at least two weeks. Metronidazole can be used for the treatment of anaerobic bacteria.
(4) Treatment of functional renal failure. Under the premise of actively improving liver function, the following treatment measures can be taken:
(1) Stop or avoid using 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, massive ascites, and upper gastrointestinal bleeding.
(3) Strictly control the amount of infusion, measure the intake and correct the imbalance of water, electrolyte and acid-base.
(4) Infusion of dextran, plasma, albumin and ascites concentrate back infusion to increase circulating blood volume and improve renal blood flow. On the basis of volume expansion, diuretics are used.
(5) Vasoactive drugs, such as vasopressin, dopamine can improve renal blood flow and increase glomerular filtration rate.
The prognosis of liver cirrhosis varies greatly with the cause, type of disease, degree of liver damage, and the presence or absence of complications, such as schistosomiasis cirrhosis, alcoholic cirrhosis, secondary biliary cirrhosis and cirrhosis caused by circulatory disorders. If it has not progressed to the decompensation stage, after active treatment of the primary disease to eliminate the cause, the disease may tend to stop, and the prognosis is better than that of viral hepatitis cirrhosis. A part of liver cirrhosis with small nodular or unobvious regenerating nodules can be in the compensatory period for life; but large nodular and mixed cirrhosis often die due to progressive liver failure in a short period of time. In decompensated patients, jaundice persists, prothrombin time continues to prolong, and complications occur, the prognosis is poor. The causes of death are often hepatic coma, upper digestive bleeding and secondary infections.