The pathophysiological basis of hepatic encephalopathy is liver cell failure and collateral shunt caused by operation or naturally formed between portal veins. Many toxic metabolites, mainly from the intestine, have not been detoxified and cleared by the liver, entered the systemic circulation through collateral branches and reached the brain through the blood-brain barrier, causing brain dysfunction.

There are many metabolic disorders in hepatic encephalopathy. The occurrence of encephalopathy may be the result of the combined action of many factors, but the metabolic disorders of nitrogen-containing substances including protein, amino acids, ammonia, mercaptan and the accumulation of inhibitory neurotransmitters may play a major role. Sugar water and electrolyte metabolism are disordered, and hypoxia can interfere with the energy metabolism of the brain and aggravate encephalopathy. The increase of short-chain fatty acids also played an important role.

Extended data

There are many factors that induce hepatic encephalopathy, such as massive potassium excretion, diuresis, ascites, sleep, sedation, anesthetics, constipation, uremia, infection or surgical trauma. These factors are mainly through: increasing the production of neurotoxic substances or improving the toxic effects of neurotoxic substances; Improve the sensitivity of brain tissue to various toxic substances; Increase the permeability of blood cerebrospinal fluid barrier and induce encephalopathy.

The primary diseases of hepatic encephalopathy include severe viral hepatitis, severe toxic hepatitis, drug-induced liver disease, acute fatty liver during pregnancy, various types of liver cirrhosis, portosystemic shunt, primary liver cancer and other end-stage diffuse liver diseases. Hepatic encephalopathy is the most common among patients with liver cirrhosis, accounting for about 70%.

Baidu encyclopedia-hepatic coma