Overview of hepatic failure
Hepatic failure (hepatic failure) refers to the clinical syndrome that occurs when liver cells are extensively and severely damaged and the metabolic functions of the body are severely disturbed, referred to as liver failure. Hepatic failure occurs in the course of many serious liver diseases, the condition is dangerous and the prognosis is poor. Clinical manifestations are loss of appetite, nausea and vomiting, jaundice, liver odor, bleeding, ascites, pulmonary hydrops, coma, purpura. Treatment of patients should be absolutely bedridden, avoid and remove triggers that induce hepatic coma, prevent and control infections, promptly rescue bleeding, and strengthen symptomatic supportive therapy.
Questions you may be concerned about
What are the consequences of liver failure
Cirrhosis, hepatocellular carcinoma and other diseases leading to liver failure may result in upper gastrointestinal hemorrhage, hepatic encephalopathy, hepatorenal syndrome or even life-threatening conditions.
Liver cirrhosis advanced stage, liver cancer and other diseases will lead to liver failure in serious state, because liver portal vein is an important blood return channel of gastrointestinal and digestive tract, when cirrhosis and liver cancer occurs, this pathway is blocked, which leads to portal hypertension, varicose veins of the lower esophagus, and upper gastrointestinal hemorrhage occurs after swallowing harder food, and shock or even death occurs in serious cases.
In addition, liver as an important detoxification and metabolism organ of the whole body, the function of processing of blood ammonia and other substances is seriously insufficient after liver failure, which in turn leads to hepatic encephalopathy coma or even death; due to the influence of the blood reflux and blood supply of the whole body, kidneys are more sensitive to ischemia, and renal dysfunction will occur in a very short period of time.
It is recommended that patients with hepatitis, cirrhosis, hepatocellular carcinoma and other diseases should consult a doctor in time, improve the abdominal ultrasound liver function and other auxiliary examinations, and carry out the corresponding medication or surgical treatment under the guidance of the doctor’s advice.
Causes
1. Hepatitis
Various types of viral hepatitis, such as A, B, C, D, E, F, G viral hepatitis. It can also be caused by mixed or overlapping infections of two or more hepatitis viruses.
2. Drugs
Antipyretic and analgesic drugs, such as paracetamol, analgin, aspirin, etc.; anti-tuberculosis drugs, such as remifent, rifampicin, etc.; other drugs, such as halothane, methyldopa, antimony, arsenic, sulfonamides, etc.
3 Poisoning
Such as muscarinic poisoning, carbon tetrachloride poisoning, etc.
4. Hypoxic liver injury
Such as hepatic stasis and hypoxia caused by heart failure and shock lasting for a certain period of time.
5.Other
Such as acute hepatomegaly (Wilson’s disease). Chronic liver failure: mostly occurs in the course of chronic severe hepatitis, various types of liver cirrhosis and other diseases.
Differential diagnosis
Mainly differentiated from the following diseases:
1. Sepsis
Sepsis has many similarities with acute hepatic failure (AHF), e.g., encephalopathy, jaundice, abnormal coagulation function can also occur, and it is easy to be misdiagnosed as AHF. Factor VIII test is important for differential diagnosis, and it is normal in AHF, but lowered in sepsis.
2. Acute fatty liver of pregnancy
It is difficult to distinguish AHF from acute fatty liver of pregnancy, and even more so when the two overlap. However, the treatment of both is the same: termination of pregnancy.
3. Biliary hepatitis
Biliary hepatitis also has many similarities with AHF, especially when severe gastrointestinal symptoms are caused by other reasons. However, the treatment of the two is very different, so attention should be paid to the differentiation of the two. The characteristics of hepatitis silt type are: (1) there are often clinical and biochemical features of obstructive jaundice, but there is no dilatation of intra- and extra-hepatic bile ducts in ultrasound; (2) the examination of plasminogen time (PT) and plasminogen activity (PTA) is usually normal or mildly abnormal; (3) the liver does not shrink or even enlarged; (4) hepatic encephalopathy does not usually occur.
Examination
1. Measurement of prothrombin time
This test is one of the most valuable indicators to correctly reflect the severity of the damage, which is helpful for early diagnosis. This test requires strict requirements and should be performed by experienced persons to ensure accuracy. It is characterized by a significant prolongation of the prothrombin time.
2. Measurement of cholinesterase
This enzyme is synthesized by hepatocytes, therefore, serum cholinesterase is obviously reduced in severe liver damage.
3. Separation of bile enzymes
Bilirubin gradually rises while glutamate aminotransferase (ALT) decreases. 80% of ALT exists in the plasma of hepatocytes, when hepatocyte damage, the permeability of cell membrane is changed, ALT escapes into the blood, ALT can be elevated in the early stage, and with the aggravation of the disease, the enzyme has been depleted by a certain period of time, coupled with the short half-life of the enzyme, the decline in serum ALT, suggesting that the prognosis is not good.
4. Dynamic observation of AST/ALT ratio
Measured within 10 days after the disease, it has certain significance in predicting the condition and prognosis.ALT is mainly found in hepatocyte plasma, and most of AST is found in mitochondria, the normal ratio of AST/ALT is 0.6.When the hepatocyte is seriously damaged, AST is discharged from the mitochondria, and the ratio is >1.
5. Amino acid (AA) measurement
Including total urinary amino acid and serum amino acid analysis. Almost all amino acids are metabolized in the liver and synthesized by hepatocytes as essential proteins. When severe liver damage, AA can not be utilized and cause AA metabolism disorder and imbalance. Firstly, the total amount of urinary AA increases significantly, the aromatic amino acids in serum increase, and the branch/aromatic ratio decreases from the normal 3~3.5 to below 1.0.
Treatment principle
Early detection and early treatment of the cause are very important, but most patients have a poor prognosis. Patients should be absolutely bedridden, avoiding and removing triggers of hepatic coma, preventing and controlling infections, timely treatment of bleeding, and strengthening symptomatic supportive therapy. Liver transplantation should be considered if available.