Retinopathy of prematurity is a serious disease that can cause blindness in infants and children, mostly in newborns born at less than 37 weeks of gestation or with a birth weight of less than 2,500 grams. Retinopathy of prematurity has a prevalence of 15-30% in preterm infants and is responsible for 1/3 of blind children. It is closely related to the week of gestation and birth weight of the infant. 40% of infants born before 31 weeks of gestation are at risk of developing retinopathy of prematurity, and the more immature they are, the higher the incidence and the more severe the condition. In general, the prematurity of preterm infants weighing less than 1500 g is between 30% and 50%, and the lighter the weight the higher the prevalence, with a prevalence of up to 90% for those weighing less than 750 g and about 45% for those weighing 1000 g to 1200 g. Although there have been some advances in the diagnosis and treatment of retinopathy of prematurity in recent years, it is still the leading cause of visual impairment and blindness in infants and children worldwide. With the increasing demand for treatment and survival of low birth weight infants born prematurely in China, the incidence and severity of retinopathy of prematurity, a disease previously rarely seen, is gradually increasing. Prevention and treatment of retinopathy of prematurity has become an important issue in improving the quality of life of preterm and low birth weight infants. The development of the retinal vessels in the human eye matures with increasing gestational age. Under normal circumstances, the vascular system of the retina begins to develop from the center to the periphery at 15-16 weeks of gestation (3-4 months) in order to adapt to the needs of retinal metabolism; the vascular development is rapid at 24-28 weeks (6-7 months), and by 36 weeks (9 months) the nasal vessels are in place, and all vascular development is complete at 40 weeks (10 months) of birth. Because many organs are not fully developed at birth, especially the lung tissues are not fully functional, leading to respiratory distress and cerebral hypoxia, which are life-threatening and therefore often require oxygen inhalation after birth to ensure the oxygen needs of living tissues. In preterm infants, due to early birth, the retinal vessels are not yet fully developed and have not yet reached the periphery of the retina, which continues to develop after birth. If a preterm infant needs oxygen inhalation at this stage due to unstable systemic condition, the high concentration of oxygen can cause the developing vascular front tissue to occlude and stop development, and the area where the peripheral retinal blood vessels are not yet developed is still avascular. The retina is in a relatively hypoxic state under the influence of other existing systemic factors, such as fluctuations in oxygen saturation, vitamin E deficiency, cyanosis, physical respiration, ventricular hemorrhage, convulsions, ischemic-hypoxic encephalopathy, sepsis, intrauterine ischemia, anemia, aortic insufficiency, pulmonary hyaline membrane disease, etc. The relatively hypoxic retina produces vascular endothelial growth factor to stimulate neovascularization and thus compensate for hypoxia. The new blood vessels are unsound vessels, which are prone to rupture and bleeding, inducing hyperplasia and pulling the retina to cause retinal detachment, which can lead to blindness and eye atrophy in severe cases. Children with retinopathy of prematurity generally have a history of oxygenation in the incubator after birth. Retinopathy often occurs during a period of relative tissue hypoxia when high levels of oxygen administration are rapidly discontinued. Even with normal oxygen use, the risk of retinopathy of prematurity cannot be ruled out because preterm infants are often accompanied by pulmonary respiratory dysfunction, acid-base toxicity, pneumonia, and ischemic-hypoxic encephalopathy, which can leave the child’s organism in a state of metabolic disturbance and relative hypoxia. Retinopathy of prematurity does not always occur in oxygenated preterm infants, but in those without a history of oxygenation, it can also be caused by a rapid increase in fetal hemoglobin (fetal PO2) oxygen saturation and a rapid change in fetal partial pressure of oxygen (fetal PO2) to neonatal PO2. In addition, maternal anemia and multiple fetuses also contribute to the development of this disease. Therefore, the causes of retinopathy of prematurity are multifaceted, and the underlying causes are prematurity, low weight, and immaturity of retinal vascular development. Therefore, premature infants must receive fundus examination at the ophthalmology department in time to detect and treat retinopathy of prematurity to avoid serious loss of vision.