Summary: accumulate in the blood, leading to encephalopathy. In patients with cirrhosis, the presence of portacaval anastomoses allows ammonia-rich blood to bypass the liver and reach the brain, resulting in hepatic coma. Additionally, the liver's failure to clear toxic substances, such as drugs and metabolic by-products, contributes to the development of hepatic encephalopathy. The clinical manifestations of hepatic coma include neuropsychic disturbances, motor abnormalities, and characteristic flapping tremor. EEG changes show bilateral, synchronous delta waves. The pathogenesis of hepatic coma involves a complex interplay of liver dysfunction, circulation alterations, and cerebral intoxication, highlighting the critical role of the liver in maintaining brain function and metabolic balance.