Neonatal hypoxic-ischemic encephalopathy (HIE) is perinatal asphyxia in newborns under the influence of various factors, resulting in hypoxic-ischemic damage to the brain, which not only seriously threatens the life of newborns, but also is one of the most common causes of post-neonatal disability. The main clinical manifestations are low Apgar score, impaired consciousness, and cerebral edema, which seriously threaten the life of newborns as the condition progresses. HIE is a brain-damaging lesion caused by perinatal hypoxia and ischemia, which mostly occurs in utero and during delivery. Hypoxia is the main cause of morbidity, which can lead to intrauterine distress, followed by abnormal heart rate, reduced fetal movement, and fetal feces contamination of amniotic fluid, which can lead to fetal suppression in severe cases; while hypoxia at birth can lead to prolonged intrauterine distress and aspiration of fetal feces during delivery; postpartum hypoxia can produce neonatal The organism oxygenation state is extremely not, such as pulmonary hyaline membrane disease, frequent respiratory respite, shock, etc. Therefore, whenever there is hypoxia, it will adversely affect the newborn, and hypoxia and ischemia are causally related, and certain bleeding ischemia and hypoxia will trigger a series of diseases in the newborn, which will eventually evolve into metabolic disorders in brain tissue and cerebral edema, etc. Especially when the cerebral blood vessels are damaged, intracranial hemorrhage will occur, and HIE will occur as a result. Newborns are in the stage of gradual development and growth of all functions, and their physiology and anatomy have unique characteristics. After the occurrence of post-asphyxia hypoxia and ischemia, the oxidation process of glucose is unable to oxygenate due to lack of oxygen, which increases sugar consumption and lactic acid accumulation, leading to hypoglycemia and metabolic acidosis, which cannot meet the normal needs of the brain. On this basis, ATP production is reduced and the cell membrane sodium and calcium pumps are not functional enough to allow calcium ions to enter the cells, and sodium ions cause cell-derived brain edema. At the same time, hypoxia and ischemia can also lead to cerebrovascular autoregulation dysfunction, forming pressure passive cerebral blood flow. Once the blood pressure is too high, intracranial hemorrhage can easily occur, and the decrease of cerebral blood flow in hypotension can cause ischemic injury, which is mostly seen in the subarachnoid space.