Liver failure

Introduction When the liver is damaged by certain pathogenic factors, it can cause damage to the liver's morphological structure (denaturation, necrosis, cirrhosis) and abnormal liver function. However, due to the huge reserve capacity and regenerative capacity of the liver, the mild damage is generally not caused by the liver's compensatory function. If the damage is more serious and extensive (one-time or long-term repeated damage), abnormal liver metabolism caused by obvious substance metabolism disorder, detoxification function, bile formation and excretion disorder and bleeding tendency is called hepatic insufficiency. Severe liver damage, can not eliminate the toxic metabolites in the blood, or the imbalance of the metabolism of the substance, causing central nervous system dysfunction (hepatic encephalopathy), called hepatic failure.

Cause

Cause:

Fulminant liver failure:

1. Various types of viral hepatitis: such as hepatitis A, B, C, D, E virus hepatitis. It can also be caused by a mixture of two or more hepatitis viruses or overlapping infections.

2. Drugs: antipyretic analgesics such as paracetamol, angtong, aspirin, anti-tuberculosis drugs such as Remi seal, rifampic; other such as halothane, methyldopa, bismuth, arsenic, sulfa drugs, etc. .

3 poisoning. Such as poisonous poisoning, stinky rice poisoning, carbon tetrachloride poisoning.

4 hypoxic liver injury: such as heart failure for a certain period of time, hepatic sputum caused by shock, hypoxia.

an examination

Related inspection

Liver function test hepatitis A antibody

1. Overworked, over-tired, weak, even extremely weak, with mild mental symptoms such as abnormal behavior, sexual analysis or change of consciousness.

2, severe vomiting can not eat, and there is a hiccup phenomenon, serum bilirubin exceeds 171mol / L, or daily increase at a rate of 34.2mol / L, liver function damage is separated by enzyme bile.

3. Cholinesterase and cholesterol decreased significantly, albumin decreased rapidly, and white and globulin were inverted.

4, prothrombin activity continued to decline, accompanied by bleeding tendency, hemorrhoids, jaundice increased, fever does not retreat, both white blood cells and neutrophils increased.

Differential diagnosis

Identification:

(1) Acute liver failure: Liver cells show one-time necrosis, necrotic area 2/3 of liver parenchyma, or sub-macro necrosis, or bridging necrosis, with severe degeneration of viable hepatocytes, and sinusoidal stents do not collapse or Complete collapse.

(2) Subacute liver failure: sub-macro necrosis or bridging necrosis of the liver tissue is old and new, the reticular fiber collapses in the old necrotic area, or collagen fibers are deposited, and the residual hepatocytes are regenerated to varying degrees. Fine, small bile duct hyperplasia and cholestasis can be seen.

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