Fulminant liver failure

Introduction to fulminant hepatic failure Fulminant hepatic failure (FHF) refers to a type of hepatic encephalopathy (HE) that occurs in patients with pre-existing disease without hepatic disease and sudden onset of massive hepatocyte necrosis or significant liver function abnormalities within 8 weeks after the onset of the first symptom. Syndrome. The causes of fulminant hepatic failure are various. According to the pathogen, it can be divided into infectious, toxin, metabolic, invasive, autoimmune, ischemic, radiological, and unexplained. basic knowledge Proportion of disease: 0.5% of patients with hepatitis Susceptible people: no specific people Mode of infection: non-infectious Complications: upper gastrointestinal bleeding, coma

Cause of fulminant hepatic failure

(1) Causes of the disease

The causes of fulminant hepatic failure are various. According to the pathogen, it can be divided into infectious, toxin, metabolic, invasive, autoimmune, ischemic, radiological, and unexplained.

1. Infectious viral infections, especially viral hepatitis, are the most common cause of fulminant hepatic failure in China, and other viruses are occasionally found.

(1) Hepatitis virus: There are 7 kinds of hepatitis viruses currently found, which are hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (hepatitis C virus). , HCV), hepatitis D virus (HDV), hepatitis E virus (HEV), hepatitis G virus (HGV also known as GBV-C) and TTV (TT is In its body, the initial name of the patient whose virus was first found in the body), HAV infection rarely causes fulminant hepatic failure, and its risk is about 0.01% to 0.1%. In 1988, Shanghai's hepatitis A epidemic was common, with a total incidence of more than 300,000. People, only 25 patients died of HAV alone, but the risk of fulminant hepatic failure was significantly increased in patients with hepatitis A and other chronic hepatitis, especially with chronic active hepatitis B, chronic hepatitis C or cirrhosis. However, HBsAg carriers with hepatitis A have a good prognosis. HBV infection or HDV infection alone is the main cause of fulminant hepatic failure. When the GA point mutation occurs at the 1896th position in the pre-HB region of HBV, the original color ammonia is used. The acid password TGG becomes Stopping the TAG, leading to the interruption of the synthesis of pre-C protein, HBeAg turned negative, this mutant can cause HBeAg-negative fulminant hepatitis B, HBeAg-positive fulminant hepatitis B is caused by wild strain, HDV is a kind Defective virus, HBV's surface antigen HBsAg is required as the outer shell of its virus, so HDV infection can be infected with HBV at the same time, or it can be overlapped with HDV in chronic HBV infection. The risk of fulminant hepatic failure in HDV infection is much greater than that. In patients with HBV infection alone, HBV chronic carriers may also experience fulminant hepatic failure after infection with HDV. The role of HCV in causing fulminant hepatic failure is unclear. HCV infection in Japan and other Asian countries may be the main cause of fulminant hepatic failure. One.

(2) Other viral infections: low immunity, immunosuppression, infection of other viruses in neonates and AIDS patients can also lead to fulminant hepatic failure, such as herpes simplex virus infection, especially for disseminated infections and immune dysfunction in newborns. Fatal liver failure leading to lethality, AIDS patients and immunosuppressed patients infected with varicella-zoster virus, can cause varicella hepatitis, fulminant hepatic failure, fulminant hepatic failure caused by EB (Epstein-Barr) virus infection 16 cases have been reported, and immune function can also occur in normal cases, the mortality rate is as high as 87%, other such as cytomegalovirus, paramyxovirus infection can also lead to fulminant hepatic failure.

Toxin

(1) Drug-specific reaction: Many drugs can cause fulminant hepatic failure. Common drugs include anesthetic halothane, isoflurane, methoxyflurane, chloroform, etc., anti-tuberculosis drugs such as isoniazid, Fuping, antidepressants such as phenelzine and phenytoin sodium, cocaine, chlorpromazine, etc., anticoagulants such as dicoumarin, sulfonamides such as salicylic acid azosulfonamide, non-sterol androgen antagonism Medicine Bicalutamide, alcohol poisoning drug disulfiram disulfiram, recreational drug "dance medicine" ecstasy, antihypertensive drug acetophenone, anti-epileptic drug valproic acid, and anti-thyroid drugs, non- Sterol anti-inflammatory drugs, amphotericin B, methyldopa, cyclophosphamide, 5-fluorouracil, 6-mercaptopurine, sedatives, and the like.

(2) Toxic reaction: Acetaminophen (acetaminophen) is one of the most common drugs and the most common cause of fulminant hepatic failure in Europe and the United States. In the case of malnutrition or starvation, liver glutathione is reduced. Increased sensitivity to drugs, even therapeutic doses of acetaminophen can cause fulminant hepatic failure, as well as phenacetin and salicylate, and certain chemical toxicants and prodrugs can cause outbreaks. Liver failure, the former such as carbon tetrachloride, galactosamine, alcohol, tetracycline, phosphorus, etc., the latter including certain herbs and poisonous mites (such as calves, white poison umbrella, corn scorpion, etc.), aflatoxin , bacterial toxins, etc.

3. Metabolic fulminant hepatic failure The most common metabolic disease is Wilson's disease, also known as Wilson's disease, which may be accompanied by hemolytic anemia or hemolytic crisis. The cornea may have a Kayser-Fleischer ring, serum transaminase and Alkaline phosphatase levels are relatively low, sometimes with blurred vision and acalculous cholecystitis.

4. Invasiveness, including fat infiltration and tumor infiltration, can lead to the occurrence of fulminant hepatic failure. Liver infiltration of fat includes acute fatty liver in pregnancy, Reye syndrome, etc. A large number of fat droplets occupy most of the volume of liver cells, making Hepatocytes can not function normally. The use of valproic acid or intravenous high-dose tetracycline can also cause similar lesions. Liver tumor infiltration leads to fulminant hepatic failure, an uncommon manifestation of primary or metastatic tumors of the liver. Caused by, including melanoma, malignant lymphoma, small cell lung cancer, urothelial carcinoma, etc., sometimes the tumor can be widely transferred to the hepatic sinus, but no metastatic nodules can be detected in the liver, and the clinical manifestation is fulminant hepatic failure.

5. Autoimmune autoimmune liver disease refers to a series of immune diseases involving the liver, including autoimmune hepatitis, autoimmune sclerosing cholangitis and autoimmune hepatitis after liver transplantation. Clinical examination may have smooth muscle antibodies, anti- Nuclear antibodies and liver and kidney microsomal antibodies are positive. The former two are mainly due to genetic abnormalities that are prone to autoimmunity. The liver autoantigen polypeptides are recognized by T lymphocytes and produce autoimmune damage against the liver. Autoimmune after liver transplantation. The pathogenesis of sexual hepatitis remains unclear. A type of rheumatic disease, the adult case of Still disease, sometimes involves the liver leading to fulminant hepatic failure.

6. Ischemic vascular factors lead to fulminant hepatic failure, liver ischemia can be caused by systemic hemodynamic changes (such as cardiogenic shock, heat stroke and recurrent arrhythmia, etc.) Sexual hemodynamic disorders (such as acute pre-hepatic venous obstruction).

7. Radiation-induced radiation damage caused by fulminant hepatic failure is rare. Acute radiation sickness or local high-dose radiotherapy sometimes causes fulminant hepatic failure.

8. Other hepatitis B virus carriers may have worse liver function when they are treated with interferon and immunosuppressive drugs, sometimes leading to fulminant hepatic failure. In addition, in addition to the above causes, there are about 1/3 of the causes of fulminant hepatic failure. Unknown, it is generally believed that the cause of this part of patients is related to hepatitis virus, which can be collectively referred to as non-A-G hepatitis.

(two) pathogenesis

The pathogenesis of fulminant hepatic failure varies with the etiology. Viral hepatitis in China is the most common cause of fulminant hepatic failure. The pathogenesis of hepatitis B is the most widely studied. It is currently considered to be cytotoxic T lymphocytes (cytotoxic). T lymphocyte (CTL) is the main effector cell leading to extensive necrosis of hepatocytes. CTL cells attack HBV-infected hepatocytes through a dual recognition mechanism, which is restricted by major histocompatibility complex (MHC)-I. The membrane antigens HBcAg and MHC-I of HBV should be simultaneously expressed on the attacked hepatocyte membrane. CTL must also recognize both antigens in order to bind to target cells, release perforin and other lymphokines to attack the target cells; CTL cells also surface Lymphocyte function associated antigen-1 (LFA-1), LFA-1 ligand-intercellular adhesion molecule-l (ICAM-l) So that hepatocytes can attract CTL cells expressing LFA-1 and adhere them to hepatocytes.

Fulminant liver failure prevention

It should be prevented from further deterioration of fulminant hepatic failure. When hepatic encephalopathy occurs, all of the above measures should be carried out as soon as possible in the middle of the night and promptly transferred to the liver disease treatment center.

Fulminant liver failure complications Complications upper gastrointestinal bleeding coma

1. The pathogenesis of hepatic encephalopathy with hepatic encephalopathy has not yet been fully elucidated. Related to the theory of ammonia poisoning, the imbalance of the ratio of branched-chain amino acids to aromatic amino acids, the pseudo-neurotransmitter theory, the gamma-aminobutyric acid theory, etc. The increase of toxic substances, such as thiols, short-chain fatty acids, glutamine and -ketoglutaric acid, is related to the occurrence of hepatic encephalopathy. Hepatic encephalopathy can occur in the late stage of liver failure. In patients with extensive portal-cavity collateral circulation or portal-cavity shunt, hepatic encephalopathy can also be induced by eating too much protein or upper gastrointestinal bleeding.

Early symptoms of hepatic encephalopathy include personality changes, euphoria or depression, mental retardation, changes in sleep habits, and inappropriate behavior. The most characteristic neurological signs are flapping tremor, and late stage may appear drowsiness or coma, according to clinical Performance can be divided into four stages of hepatic encephalopathy:

(1) Prodromal period (Phase I): Mild personality and behavioral changes, such as silence, apathy or excitement, euphoria often have no or only slight neurological signs.

(2) Pre-coma (phase II): minor insanity, abnormal behavior, calculation, orientation and comprehension, neurological signs, such as hyperreflexia, increased muscle tone, pathological reflex, liver odor and/or flapping Tremor.

(3) Sleeping period (stage III): mainly with lethargy or shallow coma, various neurological signs continue or aggravate, and a few have extreme mental or sports excitement.

(4) Coma period (stage IV): in a coma state, no response to various stimuli.

2. The mechanism of cerebral edema in cerebral edema fulminant hepatic failure is not fully understood. It may be the result of a combination of vascular and brain cytotoxicity, disintegration with the blood-brain barrier, impaired mitochondrial function of brain cells, and brain cell membrane Na- K-ATPase is inhibited, and the synergistic action of bile acid-endotoxin-ammonia causes the osmolar amino acid-taurine/glutamine to be accumulated in astrocytes, and the osmotic pressure regulation function is impaired. Enlargement, cerebral microvascular thrombosis and cerebral vascular responsiveness to carbon dioxide lead to brain resistance vasodilation, loss of autoregulatory function of cerebral blood flow, deep coma after cerebral edema, vomiting, elevated blood pressure, optic disc edema Such as the increase in intracranial pressure, may have pupil dilation, fixation and slow breathing, bradycardia, positive pyramidal tract sign, sputum sputum, severe cases can form cerebral palsy, such as the formation of the midbrain, can appear Chen -Cheyne-Stokes breathing, pupil diminution, eye gaze upwards and personality changes, such as the formation of the middle lobe of the brain, the loss of consciousness, pupil dilation, hemiplegia, etc. For example, the formation of cerebellar tonsil occipital foramen magnum can lead to loss of consciousness, irregular breathing or even suspension, and can die quickly if not treated promptly.

3. Secondary infections Due to the decline of immune function and invasive diagnosis and treatment and the application of broad-spectrum antibiotics, patients with fulminant hepatic failure are prone to secondary infections. Common secondary infections include pulmonary infection, sepsis, and urine. Road infection, biliary and intestinal infections, fungal infections, etc., the pathogens are mainly G bacteria, the most common is Staphylococcus aureus, followed by Staphylococcus epidermidis, other intestinal bacteria and anaerobic bacteria, fungal infections It is one of the main causes of death of patients. Patients may have fever, peripheral white blood cell counts increase, neutrophil classification increases, the nuclear shifts to the left, the condition deteriorates sharply, and the corresponding symptoms of various systemic infections may occur.

4. The cause of primary peritonitis in fulminant peritonitis with fulminant hepatic failure may be related to intestinal translocation through the gastrointestinal barrier into the bloodstream and the body's resistance to abdominal cavity decline, there are data indicating ascites protein < The probability of primary peritonitis in 10g/L is 10 times that of ascites protein >10g/L. The clinical features of primary peritonitis include:

(1) Acute onset without perforation of hollow organs.

(2) fever, mostly for continuous low fever, but also for relaxation and high fever and chill.

(3) There may be abdominal pain, weakened bowel sounds, and there may be signs of peritoneal irritation such as muscle tension and rebound tenderness, but most of them are lighter.

(4) The ascites increased rapidly and the diuretic effect was poor.

(5) Ascites examination was yellow turbidity, Rivalta test was positive, ascites white blood cell count>0.5×109/L, classified neutrophils>50%, or polymorphonuclear granulocyte count>0.25×109/L had diagnostic significance. Ascites culture should be inoculated with 10 ml in a blood culture bottle at the bedside to increase the positive rate.

(6) The positive rate of blood culture is 40% to 60%, and there is a certain positive rate in urine culture.

(7) Peripheral blood white blood cell count increased, neutrophil classification increased, but the original spleen hyperactivity white blood cell count may not increase.

5. Hepatorenal syndrome Hepatorenal syndrome is caused by portal hypertension after severe hepatocyte necrosis, increased vasodilators in the body, decreased peripheral vascular resistance, and relatively reduced circulating blood volume, resulting in renin-angiotensin- Aldosterone system, increased sympathetic nervous system activity and increased secretion of antidiuretic hormone, produces ascites and edema and renal vasoconstriction, surpasses the compensatory function of renal function, produces functional renal insufficiency, and produces hepatorenal syndrome in patients with fulminant hepatic failure Mostly acute, patients with severe hepatic insufficiency with ascites, or patients with hepatic encephalopathy, bacterial infection or bleeding, oliguria or anuria, plasma urea nitrogen and creatinine levels increase rapidly, urine routine examination Normal or mild abnormalities, urinary/plasma osmotic pressure ratio >1.0, urinary sodium concentration <10mmol/L, urinary/plasma creatinine ratio>30, often accompanied by ascites, dilute hyponatremia, hypotension and jaundice, expanded treatment No lasting improvement can be achieved.

6. Upper gastrointestinal hemorrhagic fulminant hepatic failure patients have obvious coagulation mechanism disorder, coupled with the formation of portal hypertension, the liver inactivation of gastrin and histamine and other substances lead to high gastric acid secretion, endotoxemia, etc. Factors, prone to upper gastrointestinal bleeding, the most common cause of upper gastrointestinal bleeding in patients with fulminant hepatic failure is acute diffuse gastric mucosal erosion, esophageal varices bleeding is less common, bleeding is often sudden, generally no obvious aura Signs, a small number of patients may have frequent hiccups, manifested as a sudden large amount of vomiting blood, rapid decline in blood pressure into the state of shock, after the occurrence of bleeding, the patient's original liver damage is further aggravated, jaundice progressively deepens, prothrombin time is further extended, and in number Serious complications such as hepatic encephalopathy, hepatorenal syndrome or primary peritonitis occur during the day. Upper gastrointestinal bleeding is the most common fatal complication of fulminant hepatic failure and the cause of other serious complications.

7. Coagulation dysfunction The cause of coagulopathy caused by fulminant hepatic failure is related to the following factors:

(1) Reduced or excessive consumption of clotting factors.

(2) thrombocytopenia and dysfunction.

(3) Diffuse intravascular coagulation (DIC).

(4) Abnormal anticoagulation system in the blood.

(5) Invalid abnormal fibrinogen formation.

(6) Vitamin K-dependent clotting factor abnormalities.

The incidence of fulminant hepatic failure is 73%, of which 30% is severe. The most common bleeding site is the gastrointestinal tract. Others include the nasopharynx, lung, retroperitoneum, kidney, injection site, etc. Intracranial hemorrhage is rare. However, the consequences are serious. After the occurrence of DIC, extensive microthrombus formation occurs in capillaries and small blood vessels, which consumes a large amount of blood coagulation factors and platelets, and then causes secondary fibrinolysis, resulting in more severe bleeding. The clinical manifestations are skin and extensive mucosal bleeding. Causes circulatory failure and dysfunction of vital organs such as kidney and brain, and accelerates death.

8. Respiratory failure and liver and lung syndrome, about 30% of patients with fulminant hepatic failure develop adult respiratory distress syndrome (ARDS), patients with difficulty breathing frequency, heart rate, cyanosis, irritability, and progressive exacerbation, respiratory rate > 35 Times / min, bloody sputum can occur, it is difficult to relieve by conventional oxygen supply, early cardiopulmonary examination can be no abnormality, as the disease progresses, wet snoring and wheezing sounds and inspiratory blasting sounds can be heard. Signs of consolidation, no abnormalities in the early stage of X-ray examination or slight increase in lung texture, patchy or large shadows or even "white lungs" in the middle and late stage, blood gas analysis arterial oxygen partial pressure <8kPa and progressive decline, alveolar gas - Arterial oxygen partial pressure difference increases, diagnosis based on clinical manifestations and blood gas analysis results is not difficult to make, but should be noted with cardiogenic pulmonary edema identification.

Hepatopulmonary syndrome is a concept put forward in the past 10 years. It refers to severe hypoxemia caused by pulmonary vasodilatation and pulmonary arteriovenous shunt and arterial oxygenation dysfunction due to basal lesions of the liver. Due to the reduced inactivation of pulmonary vasodilators in the liver, the content of cAMP and cGMP in the cells is increased, resulting in loss and expansion of pulmonary vascular hypoxic contraction. Clinically, there are cyanosis, clubbing, portal hypertension and high power circulation. The performance may include orthodeoxidation (referring to a decrease in PaO2 of more than 10% when the patient changes from a supine position to a standing position) and platypnea (referring to a shortness of breath when the patient changes from a supine position to a standing position. The next step is to relieve the blood gas analysis with PaO2 as the main feature. The light PaO2 can also be normal, but the alveolar-arterial blood oxygen pressure difference is obviously increased by >2.0 kPa. The chest radiograph can be normal or the nodule density is increased. In contrast, contrast-enhanced echocardiography revealed intra-arterial and dilatation in the lungs, and a 99-netne-macroaggregated albumin system scan revealed an indication of extrapulmonary organs.

9. Low albuminemia in fulminant hepatic failure due to massive hepatocyte necrosis, leading to albumin synthesis failure, due to the half-life of albumin in vivo is 13 days, so if the patient recovers or dies within 2 weeks, serum albumin The level can be maintained at normal or original level. If the course of disease exceeds 2 weeks, albumin is gradually decomposed in the body, and the albumin is rarely synthesized in the liver, and hypoalbuminemia may occur.

10. Cardiovascular and hemodynamic abnormalities Cardiovascular complications during fulminant hepatic failure mainly include damage to the heart itself, high power circulation and acute portal hypertension. The damage of the heart itself may be mainly due to the invasion of the heart by the virus and the coagulation mechanism. Obstruction leads to hemorrhagic heart damage, clinical manifestations of arrhythmia and ECG changes, common bradycardia, ventricular escape, atrioventricular block and ST-T changes, the mechanism of high power circulation is still unclear May be associated with increased vasodilators in the circulation, extensive blood flow short-circuit and increased nitric oxide production. The clinical manifestations are warm skin, fingertip capillary pulsation, pulse pulsation, hypotension and reduced cycle time. High power circulation combined with insufficient blood oxygenation caused by short circuit of blood flow in the lungs can easily cause hypoxia in tissues and aggravate the damage of various organs. Acute portal hypertension is caused by hepatic sinus collapse due to extensive necrosis of hepatocytes, hepatocyte edema Caused by sinusoidal stenosis, reducing intravascular lumen, intrahepatic blood circulation disorder, coupled with high power circulation, increased portal blood flow When the portal pressure exceeds 1.33 kPa (10 mmHg), acute portal hypertension tends to be lower than that of chronic ones.

11. Hypoglycemia, water and electrolyte balance disorder and acid-base imbalance, about 40% of patients with fulminant hepatic failure have severe hypoglycemia, the mechanism of which includes gluconeogenesis, decreased insulin inactivation, and reduced glycogen storage in hepatocytes. Obstacles, etc., are common in children, hypoglycemia can occur quickly, easily mistaken for hepatic encephalopathy, and can aggravate hepatic encephalopathy and cerebral edema. Generally, patients with liver failure should be supplemented with at least 300g of glucose per day, when blood sugar is lower than 3.5mmol. /L, should immediately inject 50% glucose 50 ~ 100ml, try to apply hypertonic (30% ~ 50%) glucose solution to reduce water intake.

In liver failure, due to the action of renin-angiotensin-aldosterone system and antidiuretic hormone, the kidney reabsorbs sodium, but due to the serious water retention, patients often have dilute hyponatremia, and the clinical manifestations are not obvious. In the early stage of liver failure, patients often have hypokalemia, and in the later stage, refractory hyperkalemia occurs due to renal dysfunction; in addition, due to vomiting and the application of potent diuretics, low chlorine may occur. Hyperemia aggravates metabolic alkalosis, induces hepatic encephalopathy, hypocalcemia, and hypomagnesemia can also be seen. Various acid-base imbalances can occur in liver failure, the most common of which is respiratory alkalosis, followed by metabolic alkali Poisoning or respiratory alkalosis with metabolic alkalosis, respiratory alkalosis with metabolic alkalosis and metabolic acidosis in the late stage, generally in the early stages of liver failure, due to hypoxemia, high blood ammonia, Causes of hypokalemia and anemia, stimulating the respiratory center to cause excessive ventilation, causing respiratory alkalosis, with the development of the disease, the increase of hypokalemia, excessive alkali supplementation and the use of sodium glutamate and other alkaline Deaminating drugs, combined with metabolic alkalosis on the basis of respiratory alkalosis, to the late stage of the disease, due to co-infection, liver and kidney syndrome, hemorrhage, shock and hypoxia, etc. caused by acid accumulation, in the base of the base Metabolic acidosis occurs on the basis of alkali.

12. Acute pancreatitis found that about one-third of patients with hemorrhagic liver failure died of hemorrhagic necrotizing pancreatitis, the mechanism of which is unknown, some people have statistics on the incidence of acute pancreatitis in patients with fulminant hepatic failure of 23% ~33%, because the patient is in a coma, it is extremely difficult to diagnose before birth, and once it is enough to cause death, regular detection of blood amylase in patients with fulminant hepatic failure may be helpful in diagnosis, but only 1/3 of patients have elevated amylase .

Symptoms of fulminant hepatic failure Common symptoms Intestinal palsy, persistent fever, progressive liver reduction, nasal wing fanatic nausea, low fever, bowel sounds disappear

1. The performance of the primary disease may have relevant clinical manifestations according to the cause of the disease. For example, fulminant hepatic failure based on chronic liver disease or cirrhosis may have liver disease face, liver palm and skin vascular spider mites, etc. The cause may have corresponding poisoning performance. The person with Wilson's disease may have corneal KF ring, and the tumor infiltration may have the performance of primary tumor.

2. The manifestation of liver failure The jaundice is rapidly deepened in a short period of time, accompanied by a marked increase in serum transaminases and a prolonged prothrombin time and a significant decrease in activity; in the early stages of the disease, there may be low fever, such as low fever persisting. Endotoxemia or persistent hepatocyte necrosis; poor general condition, such as poor appetite, extreme fatigue, irritability, etc.; intractable hiccups, nausea, vomiting and obvious bloating; obvious bleeding tendency, can appear Subcutaneous deposition, ecchymosis, often more obvious at the injection site, may have gingival bleeding, nose bleeding, severe upper gastrointestinal bleeding; ascites quickly appeared, generally more than 2 weeks, more ascites and low albumin blood The liver is progressively reduced; the liver odor can occur; the manifestations of hepatic encephalopathy, such as personality changes, circadian rhythm upside down, verbal repetition, excessive excitement, behavioral quirks, casual urine, etc., severe conscious disturbance; other neuropsychiatric Abnormalities such as increased muscle tone, positive pyramidal tract signs, sputum and/or sputum, directional and computational dysfunction; tachycardia and hypotension.

3. The manifestations of complications The clinical manifestations of fulminant hepatic failure are characterized by the diversity of their complications.

Examination of fulminant hepatic failure

Biochemical examination

(1) Liver function test: serum bilirubin levels are often significantly elevated, and some patients may rise rapidly, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are significantly elevated. ALT/AST<1, suggesting severe damage to liver cells. In addition, enzyme-cholestasis may occur in the terminal phase, that is, ALT gradually decreases with the increase of jaundice. If the course of disease exceeds 2 weeks, serum albumin levels also decrease. A decrease indicates a persistent severe damage to the liver cells.

(2) Blood ammonia test: It is still one of the important indicators reflecting hepatic encephalopathy and should be checked regularly.

(3) renal function test: can reflect the degree of kidney damage, because urea is synthesized in the liver, in the severe liver damage, urea nitrogen can not rise, serum creatinine level can better reflect kidney function.

(4) Electrolyte determination: It helps to find electrolyte imbalance in time.

(5) blood gas analysis: early detection of acid-base imbalance and hypoxemia, easy to timely treatment.

(6) Alpha-fetoprotein measurement: in the late detection of the disease, if elevated, suggesting regeneration of liver cells.

(7) Determination of serum cholesterol and cholesterol esters: Cholesterol in patients with fulminant hepatic failure is significantly reduced, even in severe cases, the cholesterol ester is often lower than 40% of total cholesterol.

(8) Blood glucose measurement: hypoglycemia can be found in time.

(9) Determination of blood Gc protein: Gc protein is an alpha globulin synthesized by the liver. One of its main functions is to remove actin released by necrotic hepatocytes. Gc protein is significantly reduced in fulminant hepatic failure. At 100 mg/L, the prognosis was poor.

(10) Others: Regular detection of amylase helps to detect pancreatitis in time. Blood amino acid analysis can detect the decrease of the ratio of branched chain amino acid/aromatic amino acid in time, and should be corrected in time to prevent and treat hepatic encephalopathy.

2. Hematology examination

(1) Blood routine: The degree of hemorrhage and the effect of hemostasis can be judged according to the rate of hemoglobin decline. White blood cell count and classification are often significantly increased in fulminant hepatic failure, and platelet examination also helps to judge the condition.

(2) Prothrombin time and activity: It is the most valuable indicator reflecting the degree of liver damage. In severe liver cell damage, the blood coagulation factor decreases rapidly, causing prolonged prothrombin time and decreased activity.

(3) Detection of coagulation factors: If the coagulation factor V<20% indicates a poor prognosis, and the increase in coagulation factors and fibrinogen degradation products may reflect liver regeneration.

(4) Others: Check the DIC if necessary.

3. Microbiological and immunological examination

(1) Examination of viral hepatitis: including anti-HAV-IgM, HBsAg, anti-HBs, HBeAs, anti-HBe, anti-HBc, anti-HBc-IgM, HBV-DNA, DNA polymerase, anti-HCV, HCV -RNA, HDV-RNA, anti-HEV, GBV-C/HGV-RNA, TTV-RNA, etc. and detection of anti-cytomegalovirus and Epstein-Barr virus antibodies.

(2) Bacteriology examination: blood culture, urine culture, culture, sputum culture and ascites culture should be carried out according to need. The ascites culture should be inoculated with the blood culture bottle bed, and if necessary, fungal smear microscopy and culture.

(3) Endotoxin test: feasible sputum test.

(4) Immunological examination: The detection of autoimmune antibodies includes antinuclear antibodies, anti-smooth muscle antibodies, anti-mitochondrial antibodies, serum total complement and complement C3, and detection of circulating immune complexes.

4. B-mode ultrasound examination of liver size and exclusion of bile duct obstruction and gallbladder disease.

5. The EEG waveform is consistent with the clinical, with the increase of the amplitude of the disease, the frequency is slowed down, and is divided into six grades A to F, the grade A is the normal EEG, the patient is conscious, and the B to D grade EEG The amplitude of the increase is slowed down, the mind is confused (Grade B), the stupor (Grade C), the coma (Class D), and the D-class is a three-phase wave of hepatic encephalopathy, which is a high-voltage, slow-frequency diffuse three-phase. Wave, the E-level amplitude is reduced at the same frequency, the patient is deeply comatose, and the F-level EEG activity is completely stopped.

6. Intensive care can detect arrhythmia and blood potassium changes and breathing, abnormal blood pressure.

7. CT can observe changes in liver size and can be compared before and after, and can observe the condition of brain edema.

8. Magnetic resonance examination Magnetic resonance spectroscopy is used to determine the lactate content in the brain. If the lactate in the brain is elevated, the prognosis is poor.

9. Liver radionuclide scanning computerized gamma photography with 99T-diethylenetriaminepentaacetic acid galactosyl human serum albumin (99mTc-GSA) after injection Of gamma-camera), observe the receptor binding of 99mTc-GSA to the liver, help to determine the reserve of liver function and determine the prognosis.

10. Epidural intracranial pressure monitoring is generally recommended to be installed in grade III-IV hepatic encephalopathy for monitoring intracranial pressure. After treatment, intracranial pressure should be lower than 2.7 kPa (20 mmHg).

Diagnosis and diagnosis of fulminant hepatic failure

Diagnosis of hepatic failure The diagnosis of fulminant hepatic failure should be based on clinical jaundice, liver shrinkage and encephalopathy. Biochemical examination has hyperbilirubinemia, elevated transaminase activity, and extremes of coagulation factors such as prothrombin and coagulation factor V. Reduced to make, abdominal ultrasound examination can observe liver size and structural changes, with or without chronic liver disease signs or space-occupying lesions, as well as vascular and bile duct conditions, pathogen diagnosis should be based on detailed clinical analysis and serological and toxicological experiments Finally, histological examination can also be performed. Because of the severe coagulopathy disorder in these patients, liver biopsy should be performed through the jugular vein rather than percutaneous liver biopsy.

Differential diagnosis

1. Mental illness The only manifestation of hepatic encephalopathy with psychiatric symptoms is easily misdiagnosed as a mental illness. Therefore, patients with unclear causes of mental disorder should be alert to the possibility of hepatic encephalopathy.

2. Metabolic encephalopathy such as diabetic ketoacidosis, hypoglycemia, uremia, hypernatremia, hyponatremia, etc. According to the corresponding basic disease history, combined with relevant laboratory tests, blood gas analysis is helpful for identification.

3. Cranial lesions of various cerebrovascular accidents (cerebral hemorrhage, cerebral infarction, subdural hemorrhage), intracranial tumors, brain abscess, encephalitis, meningitis, etc. may appear coma and lethargy, according to the symptoms and signs of the nervous system, Combined with cranial CT or MR examination, as well as cerebrospinal fluid examination, most can be clearly diagnosed.

4. Toxic encephalopathy caused by alcoholism, drug poisoning, and heavy metal poisoning, according to the history of alcohol abuse, medication history and special occupational exposure history, combined with laboratory tests, help differential diagnosis, especially attention to alcohol-related diseases Identification, such as acute alcoholism and abstinence syndrome after withdrawal, is similar to HE. The key to identification is drinking history, elevated blood alcohol concentration, bradycardia during abstinence, fever, and tremor.

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