Hepatic encephalopathy, as a serious complication of end-stage liver disease, is characterized by high morbidity and recurrent disease, and is associated with poor patient prognosis. Hepatic encephalopathy is a syndrome based on metabolic disorders and central nervous system dysfunction caused by hepatic insufficiency and/or portal shunt on the basis of cirrhosis. About 50% of cirrhotic patients have cerebral edema, and those with a long course of the disease have thinning of the cerebral cortex and reduction of neurons and nerve fibers. The main clinical manifestations can range from personality changes, behavioral abnormalities, and fluttering tremor to the development of impaired consciousness and coma. The main treatment program includes taking out the triggers of hepatic encephalopathy attacks; actively treating the primary disease, improving liver function and reducing the production and absorption of nitrogen-derived toxic substances in the intestines, promoting ammonia metabolism in the body, and lowering blood ammonia. Patients should pay attention to bed rest, prohibit smoking and alcohol, should not take unnecessary drugs and health care products with unclear efficacy to avoid hepatotoxicity damage, food should be easy to digest, less gas-producing staple food, and eat vegetables and fruits often. If hepatic encephalopathy is diagnosed, early standardized treatment is recommended to reduce the adverse effects of the disease.