Fulminant liver failure
Introduction
Introduction to fulminant hepatic failure Fulminant hepatic failure is a syndrome of hepatic encephalopathy caused by a large number of hepatocyte necrosis and severe liver damage caused by various causes, no previous history of liver disease and 8 weeks after the disease. The onset is urgent, the progress is fast, and the mortality rate is high. Early diagnosis and early treatment can reduce the mortality rate. basic knowledge The proportion of illness: 0.0065% Susceptible people: no specific people Mode of infection: non-infectious Complications: hypersplenism, hypoglycemia
Cause
Cause of fulminant hepatic failure
The pathogenesis of this disease has not been fully elucidated, that is, it is believed that the pathogenesis of FHF is mainly primary immune injury, and secondary hepatic microcirculation disorder, with the study of the effects of cytokines (Cytokine) on vascular endothelial cells and the microcirculation of the liver The study of the role of disorders in the pathogenesis suggests that the Schwartz reaction is associated with the pathogenesis of FHF, a group of biologically active protein mediators that are secreted following lymphokine research, such as tumor necrosis factor (TNF), interleukins. -1 (IL-1) and lymphotoxin (LT), among which TNF is a product of endotoxin-stimulated mononuclear macrophages and acts on vascular endothelial cells and hepatocytes, leading to the Schwartz reaction, and thus TNF is considered to be One of the main pathogenesis of FHF, in addition, endotoxemia can increase hepatocyte necrosis and lead to visceral injury (such as renal failure) is also an important pathogenic factor.
Prevention
Fulminant liver failure prevention
The prevention of fulminant hepatic failure should firstly start from the cause, actively prevent hepatitis B, and carry out universal hepatitis B vaccination, especially for vaccination of high-risk groups to effectively prevent the onset of hepatitis B and hepatitis D.
Complication
Fulminant liver failure complications Complications, hypersplenism, spleen hyperfunction
In the extreme stage of the course of the disease, hepatic encephalopathy is mainly manifested, followed by the following symptoms, during which the transition phase is not easily separated.
1. Cerebral edema: When there is a hernia, the cerebral edema is present when the pyramidal tract is positive, or there is conjunctival edema, the pupil is loose, the breathing is slow, the rhythm is irregular, and the papilledema shows cerebral edema.
2. Coagulation dysfunction and hemorrhage: The bleeding site is common to the skin, gums, nasal mucosa, bulbar conjunctiva and gastric mucosa.
(1) Abnormal platelet mass and quantity: platelets are smaller than normal at FHF, vacuoles can be seen by electron microscopy, pseudopods, serosal opacity, normal platelets without hepatic encephalopathy, bone marrow suppression, hypersplenism, and consumption by intravascular coagulation Can cause thrombocytopenia.
(2) Coagulation factor synthesis disorder: all clotting factors in plasma are reduced, especially in the extrahepatic synthesis of factor VII, but increased, prothrombin time is significantly prolonged.
(3) DIC with local secondary fibrinolysis: plasma plasma and its activating substances are decreased, while fibrin/fibrinogen degradation products are increased.
3. Infection: The most common respiratory infections, other urinary infections, mostly G-bacteria, G + cocci, may also have anaerobic and mold infections.
4. Renal failure: 70% of renal function abnormalities in FHF, half of acute tubular necrosis, high urinary sodium, isotonic urine and tubular necrosis, hepatocyte necrosis, endotoxemia, improper use of diuretics, Gastrointestinal hemorrhage caused by low blood volume and low blood pressure and other factors, it is reported that renal failure in the FHF cause of death, it is worth noting.
5. Electrolyte acid-base balance disorder: hyponatremia, hypocalcemia, hypomagnesemia, hypokalemia, respiratory alkalosis, hypokaline alkalosis and metabolic acidosis.
6. Others: hypoglycemia, hypoxemia, pulmonary edema, arrhythmia, portal hypertension and acute pancreatitis.
Symptom
Symptoms of fulminant hepatic failure Common symptoms Hiccups, intestinal palsy, nausea and vomiting, bowel sounds, disappeared, nose, fan, fatigue, persistent fever, liver damage
I. Early symptoms
1. Huangqi has three characteristics:
(1) After the appearance of jaundice, it will rapidly deepen in the short term, such as total bilirubin >171mol/L, and other manifestations of severe liver damage, such as bleeding tendency, prolonged prothrombin time, elevated ALT, etc., if only deeper Astragalus, no other serious liver function abnormalities, shown as intrahepatic cholestatic.
(2) The duration of jaundice is long. Generally, the law of jaundice is deepening, continuing, and subsiding in three stages. If jaundice is still not retreated after 2 to 3 weeks, it indicates that the condition is serious.
(3) After the appearance of jaundice, the condition did not improve. The general rule was acute jaundice hepatitis. When jaundice appeared, the appetite gradually improved, and nausea and vomiting were alleviated. If the symptoms did not improve 1 week after the appearance of jaundice, it was necessary to be alert to severe hepatitis.
2. Continued low fever: There may be low fever at the beginning of the disease. The body temperature drops to normal after the appearance of jaundice. If accompanied by persistent hypothermia with jaundice, it suggests hepatocyte necrosis or endotoxemia.
3. The general situation is extremely poor: such as fatigue, burnout, loss of appetite, and even life can not take care of themselves.
4. Obvious gastrointestinal symptoms: frequent nausea, vomiting, hiccups, obvious abdominal distension, disappearance of bowel sounds, intestinal paralysis.
5. Bleeding tendency: such as skin ecchymosis, purpura, nasal discharge, bleeding gums, a few upper gastrointestinal bleeding, etc., suggesting coagulopathy, liver failure.
6. Ascites appears rapidly: due to the long half-life of albumin (about 2 weeks), hypoalbuminemia usually occurs 2 to 3 weeks after the disease, and ascites often occurs in patients with a course of more than 2 to 8 weeks.
7. Personality changes: if the original character is cheerful, the mutation is melancholy, or conversely, the sleep rhythm is reversed, the language is repeated, the inability to conceive, the disorientation disorder, the behavioral quirks, the behavioral quirks, the casual notes, etc., are signs of hepatic encephalopathy, and then the consciousness appears. Obstacle, enter the liver coma.
8. Progressive liver reduction, liver odor, flapping tremor, increased muscle tone, positive pyramidal tract sign, sputum sputum, etc., suggesting severe liver damage.
9. Increased heart rate, low blood pressure, associated with endotoxemia or internal bleeding.
Second, the symptoms
In the extreme stage of the course of the disease, hepatic encephalopathy is mainly manifested, followed by the following symptoms, during which the transition phase is not easily separated.
1. Cerebral edema: When there is a hernia, the cerebral edema is present when the pyramidal tract is positive, or there is conjunctival edema, the pupil is loose, the breathing is slow, the rhythm is irregular, and the papilledema shows cerebral edema.
2. Coagulation dysfunction and hemorrhagic bleeding sites are common to the skin, gums, nasal mucosa, bulbar conjunctiva and gastric mucosa.
(1) Abnormal platelet mass and quantity: platelets are smaller than normal at FHF, vacuoles can be seen by electron microscopy, pseudopods, serosal opacity, normal platelets without hepatic encephalopathy, bone marrow suppression, hypersplenism, and consumption by intravascular coagulation Can cause thrombocytopenia.
(2) Coagulation factor synthesis disorder: all clotting factors in plasma are reduced, especially in the extrahepatic synthesis of factor VII, but increased, prothrombin time is significantly prolonged.
(3) DIC with local secondary fibrinolysis: plasma plasma and its activating substances are decreased, while fibrin/fibrinogen degradation products are increased.
3. Infection: The most common respiratory infections, other urinary infections, mostly G-bacteria, G + cocci, may also have anaerobic and mold infections.
4. Renal failure: 70% of renal function abnormalities in FHF, half of acute tubular necrosis, high urinary sodium, isotonic urine and tubular necrosis, hepatocyte necrosis, endotoxemia, improper use of diuretics, Gastrointestinal hemorrhage caused by low blood volume and low blood pressure and other factors, it is reported that renal failure in the FHF cause of death, it is worth noting.
5. Electrolyte acid-base balance disorder: hyponatremia, hypocalcemia, hypomagnesemia, hypokalemia, respiratory alkalosis, hypokaline alkalosis and metabolic acidosis.
6. Others: hypoglycemia, hypoxemia, pulmonary edema, arrhythmia, portal hypertension and acute pancreatitis.
Examine
Examination of fulminant liver failure
1. Prothrombin time measurement
This test is one of the most valuable indicators to correctly reflect the severity of the damage, which is helpful for early diagnosis. The test is strict, and it is necessary for experienced people to be responsible for accurate and prolonged prothrombin time.
2. Cholesterol lipase assay
This enzyme is synthesized by hepatocytes, so serum cholesteryl lipase is significantly reduced when severe liver damage occurs.
3. Biliary enzyme separation
The bilirubin is gradually increased and the ALT is decreased. 80% of the ALT is present in the liver cytoplasm. When the liver cells are damaged, the cell membrane permeability changes, and the ALT escapes into the blood. The early ALT can be increased, and the disease is aggravated. At a certain period of time, the enzyme has been depleted, and its half-life is short, and serum ALT is decreased, indicating a poor prognosis.
4. AST/ALT proportional dynamic observation
Determination within 10 days after the disease has a certain significance for predicting the condition and prognosis. ALT is mainly in the liver cytoplasm, AST is mostly present in the mitochondria, and the normal AST/ALT ratio is 0.6. When the liver cells are seriously damaged, AST is discharged from the mitochondria. Its ratio is >1.
5. Amino acid (AA) determination
Including the total amount of urinary amino acids and serum amino acid analysis, since almost all amino acids are metabolized in the liver, hepatocytes synthesize essential proteins. When severe liver damage occurs, AA cannot be used to cause AA metabolic disorders and balance disorders. The total amount of urinary AA increased significantly, and the concentration of aromatic amino acids in serum increased. The ratio of branch/aromatic ratio decreased from normal 3 to 3.5 to <1, indicating a poor prognosis.
Diagnosis
Diagnosis and diagnosis of fulminant hepatic failure
Diagnostic criteria:
1 Hepatic encephalopathy and neuropsychiatric symptoms occurred within 8 weeks of onset.
2 no signs of chronic liver disease.
3 There are clinical manifestations of severe liver damage at the same time.
4 routine biochemical and hematological examinations have hepatocyte dysfunction, early ALT elevation, prolonged prothrombin time.
5 history of hepatitis exposure or drugs, history of liver damage caused by poison.
6 liver pathological examination has large hepatocyte necrosis.
In the course of the disease, due to the involvement of multiple organs, the clinical symptoms are complex and diverse, the onset is acute, and the disease progresses rapidly.
For children and youth should be identified with chronic hepatitis, fulminant hepatitis or cirrhosis.
