What Is Acute Liver Failure?

Acute liver failure refers to a variety of causes of large-area necrosis of liver cells or severe liver function damage. A clinical syndrome mainly manifested by jaundice, ascites, hepatic encephalopathy, and coagulopathy. The main clinical features of this disease are rapid onset and rapid progress. In recent years, with the development of liver transplantation, artificial liver and other technologies, the mortality rate has decreased significantly.

Basic Information

Visiting department

Gastroenterology

Common causes

Caused by a viral infection, drug or poison

Common symptoms

Jaundice, ascites, hepatic encephalopathy, and coagulopathy

Contagious

no

1. Viral infection In China, 85% to 90% of acute liver failure is caused by acute viral hepatitis. Acute viral hepatitis B is the most common, followed by viral hepatitis A, viral hepatitis C, and D virus. Hepatitis, viral hepatitis E, etc.
2. Drugs that cause acute liver failure are the most common antituberculosis drugs, non-steroidal anti-inflammatory drugs, antidepressants and anticancer drugs.
3. Acute poisoning (1) Common chemical poisons are phosphorus, antimony, chloroform, nitrobenzene, halothane, carbon tetrachloride, etc.
(2) Drink heavily in the short term.
(3) Common biotoxins include fish gall and toadstool.
4. Ischemic severe trauma, acute circulatory failure such as shock, acute heart failure, portal vein thrombosis, etc., lead to ischemia and necrosis of liver cells.
5. Other acute hepatolenticular degeneration, hepatic amyloidosis, heat stroke, acute fatty liver in pregnancy, sepsis, malignant tumors and autoimmune hepatitis.

1. Early manifestations are rapid onset, rapid progress, and lack of specificity. May be manifested as general weakness, nausea, vomiting, and lack of appetite.
2. Progressive deepening of jaundice and rapid progress.
3. Hepatic encephalopathy Hepatic encephalopathy can be divided into four stages, with neurological and mental changes in the early stages, irritability, delirium, impaired computing and disorientation, convulsions, lethargy, and coma in the late stages.
4. Extensive bleeding of skin, mucous membranes and internal organs due to coagulopathy, which can be life-threatening in severe cases.
5. Cerebral edema Most patients may develop cerebral edema, which is manifested by rapid deepening of coma, frequent convulsions, abnormal changes in pupils, irregular breathing, continuous increase in blood pressure, and disc edema.
6. Progressive liver shrinkage The liver has a large area of necrosis, and liver odor and flutter-like tremor may appear, which is a precursor to liver coma.
7. Acute renal failure caused by acute liver failure in patients with hepatorenal syndrome, patients with oliguria or anuria, acidosis, azotemia, hyperkalemia and other manifestations, most of them functional.

1. Blood biochemical examination (1) The serum bilirubin increases progressively, which can increase by 17.1 to 34.2 mol / L per day, and can reach more than 171 mol / L within a few days. At the same time, serum transaminase increased progressively. In severe cases, "biliary-enzyme separation" occurred, and the AST / ALT ratio was> 1.
(2) Serum protein or prealbumin decreased significantly.
(3) The blood cholesterol level is significantly reduced.
2. Prothrombin time (PT) prolonged (> 15s) and prothrombin activity (PTA) decreased (<40%). Platelets were <50 × 109 / L, fibrinogen decreased (<1.25g / L), and serum cholinesterase activity was <40%.
3. Imaging examination showed progressive reduction of liver volume.
4. Histopathological examination of liver cells showed one-time necrosis, and the area of necrosis exceeded 2/3 of liver parenchyma; or sub-mass necrosis with severe degeneration of living hepatocytes, the sinus wall grid did not collapse or a few incomplete collapses. Due to severe reduction of coagulation function in patients with liver failure, liver puncture has certain risks and should be selected carefully.

The clinical diagnosis of acute liver failure needs to be determined based on comprehensive analysis of medical history, clinical manifestations, and auxiliary examinations.
Acute onset, hepatoencephalopathy of degree or above (divided by degree classification) within 2 weeks and the following manifestations: Extremely weak, and have severe digestive symptoms such as anorexia, abdominal distension, nausea, vomiting; Progressive deepening of jaundice in a short period of time; bleeding tendency, PTA 40%, and other reasons excluded; progressive liver shrinkage.

1. For the treatment of acute liver failure caused by poisons and drugs, the toxic substances should be removed as soon as possible and active detoxification treatment should be carried out.
2. Support the appropriate amount of fresh blood, plasma and albumin.
3. Oral lactulose is used to defecate soft stools 2 to 3 times, and can also be used for enema. Oral antibiotics (such as metronidazole) to reduce the intestinal flora.
4. Prevention and treatment of multiple organ dysfunction syndrome (MODS)
(1) Correct the acid-base imbalance, alkalosis is more common, and it is harmful to patients. Severe alkalosis can be intravenously infused with dilute hydrochloric acid or large doses of vitamin C, and supplement potassium.
(2) Pay attention to anti-infective treatment.
(3) Dehydration agents such as mannitol are required for conscious disturbance and disc edema.
(4) Diuretics can be used when urine volume is too small.
5. Artificial liver adjuvant therapy and liver transplantation The patient's blood is perfused through the animal liver in vitro, or through the adsorption of activated carbon and semi-dialysis to remove harmful substances in the blood of patients with liver failure. Liver transplantation is also available for acute liver failure caused by liver disease. These therapies are expensive and have not yet acquired more mature experience, and further research is needed.