Hepatic encephalopathy is a neuropsychiatric syndrome caused by hepatic insufficiency, which can occur in people with acute hepatic insufficiency or in people with chronic liver disease, especially in patients with portal shunt. Patients usually have a history of severe liver disease, and most have predisposing factors, such as eating too much protein, upper gastrointestinal bleeding, taking amines, massive diuresis, and releasing ascites. The development of hepatic encephalopathy shows progressive changes. Prodromal phase: mild personality and behavioral changes, such as apathy or excitement, often with no or only mild neurological signs; Pre-comatose phase: confusion, impaired calculation, orientation and comprehension, marked neurological signs such as positive pathological reflexes, hepatic odor and fluttering tremor; Stupor: drowsiness and light coma predominate, various neurological signs persist or worsen, and a few have extreme psychomotor excitement; Coma: comatose stage, not responsive to all kinds of stimuli. For the treatment program of hepatic encephalopathy, the current clinical practice is mainly aimed at removing the cause of the disease and stopping the production and absorption of ammonia-containing toxins. In principle, patients should limit oral protein and replace animal protein with plant protein, as well as take lactulose and keep the bowels clear. Pay attention to maintain the water electrolyte and acid-base balance of the amount of intake, the best daily adult not more than 1500 ml or the previous day’s urine volume plus 500 ml. Follow the doctor’s instructions to apply intestinal non-absorbable or seldom-absorbable antimicrobial drugs, such as neomycin, metronidazole and so on. If the disease is serious, plasma exchange therapy and plasma dialysis therapy can be applied. It is recommended that patients go to regular hospitals for treatment in time according to their own symptoms, so as not to delay the condition and cause serious consequences.