Retinopathy of prematurity (ROP) is a condition in which the unvascularized retina of preterm infants born at less than 36 weeks of gestation, with low birth weight and prolonged oxygenation, undergoes fibrovascular proliferation and constriction, and further causes retinal detachment and blindness by traction. It was previously referred to as Terry syndrome or posterior lens fibrodysplasia, but the latter reflects only the late manifestations of the disease. The incidence can be 60% to 80% in those with shorter gestation periods or lower birth weights. Etiology Caused by vasoconstriction and vasoproliferation of the incompletely vascularized retina in response to oxygen. Normal retinal vessels reach the nasal margin at about 36 weeks of embryonic development and the temporal margin at 40 weeks. Exposure to high concentrations of oxygen during this period causes capillary endothelial cell damage, vascular occlusion, and stimulation of fibrovascular tissue proliferation. Clinical manifestations Commonly occurring 3 to 6 weeks after birth, it is clinically divided into active phase and fibrovascular formation phase. 1. Active phase (1) Vascular change stage: seen early in the course of retinopathy of prematurity. The arterioles are tortuous and dilated. The venous diameter is sometimes 3 to 4 times larger than normal. Brush-like capillaries are seen at the end of the vessels in the peripheral part of the retina. (2) Retinopathy stage: The lesion develops further, the vitreous appears cloudy, and the fundus is hazier than before. Retinal neovascularization increases, mostly located near the equatorial part, but also seen before the equatorial part or in the posterior pole. The retina in this area is obviously elevated, with blood vessels crawling on its surface, often accompanied by retinal hemorrhages of different sizes. (3) Early proliferative stage: The above-mentioned limited retinal bulge appears as a proliferative vascular stripe and progresses intravitreally, causing a small retinal detachment in the peripheral part of the fundus (most) or the posterior pole (a few). (4) Moderate proliferation stage: The detachment extends to more than half of the retina. (5) Extreme hyperplasia stage: total retinal detachment. Sometimes a large accumulation of blood in the vitreous cavity may also be seen. The active stage of retinopathy of prematurity has a course of 3-5 months. Not all cases go through the above 5 stages, about 1/3 cases stop in the first stage, 1/4 stop in the second stage, and the rest stop in the third, fourth and fifth stages respectively and enter the fibrous membrane formation stage. 2.Fiber film formation period In cases that cannot subside on their own during the active period, they finally scarred and formed fiber film, which is divided into 1~5 degrees from mild to severe depending on the degree: Degree I: retinal vessels are thin and narrow, the peripheral part of the retina is gray and cloudy, mixed with small irregularly shaped pigment spots, and the nearby vitreous body is also cloudy with small pieces, often accompanied by myopia. Grade II: organic masses in the peripheral part of the retina, the optic disc and retinal vessels are pulled to one side, there are pigment arcs on the edge of the contralateral optic disc, and the optic disc is discolored. Degree III: The fibrous mechanized membrane pulls on the retina to form one or several folds. Each fold is connected to a membrane-like mechanized mass in the peripheral part of the retina. The retinal vessels are not distributed along this fold, unlike the congenital retinal folds. Grade IV: The fibrous membrane or detached part of the mechanized retina is visible behind the lens, and the pupil is obscured. Grade V: The entire posterior lens is covered by the fibrous membrane or detached mechanized retina. On dilated pupil examination, a jagged elongated ciliary process is visible in the peripheral part of the pupil. The anterior chamber is very shallow, often with anterior and posterior iris adhesions. It can also be secondary to glaucoma or extensive anterior iris adhesions resulting in corneal clouding and a smaller, more sunken eye than normal. Examination 1. History taking Most of them occur in premature babies with a history of excessive oxygenation in the incubator. 2. Fundus examination (1) Time of the 1st examination: It is advocated that fundus examination should be started 4 weeks after birth for preterm infants with gestational age <32 weeks and birth weight <1500g. < span=""> (2) Follow-up examination: No lesions or only stage I lesions in both eyes: 1 review every other week until ROP regresses and retinal vessels grow to the serrated edge. Stage II lesions or pre-threshold lesions or Rush lesions: review once a week. decreasing degree of ROP, may be examined every 2 weeks until the lesion is completely regressed. Stage III lesions: review 2 to 3 times per week. (3) Examination method: Before examination: Half an hour before using Medorrhinum ophthalmic solution to fully dilate the pupil. During the examination: perform surface anesthesia with Benoxyl ophthalmic solution, separate the eyelids with a lid opener, and perform fundus examination with an indirect fundoscope and a lens with a refraction of 20~30D or RETCAM (wide field fundus photography for children). Vital signs were monitored at the same time as the examination to prevent bradycardia due to the oculocardiac reflex. After the examination: 30 minutes to 2 hours before eating, the smaller the weight the longer the fasting period, but to prevent the occurrence of hypoglycemia. (4) Symptoms: Endothelial proliferation nodules of capillaries appear in the nerve fiber layer of the retina, the vessels are in the shape of small spheres, and there may be proliferation of spindle-shaped mesenchymal cells around them, resulting in thickening of the nerve fiber layer, and there may be small hemorrhages and edema. The nerve fiber layer is further thickened, and the new capillary buds penetrate the inner boundary membrane to reach the retinal surface. In severe cases, they may further enter the vitreous, where they may continue to grow into vascular fiber membrane, producing hemorrhage or tractional retinal detachment. Vascular fibrous membrane formation is seen to varying degrees behind the lens and is connected to the fibrous strips between the retina. Peripheral anterior adhesions, posterior adhesions, pupillary membrane formation, and changes of secondary glaucoma are seen in the iris. 3.Doppler ultrasonography Adjust the gain to the maximum and apply the 8-point inspection method for a comprehensive examination of the vitreous. Then attenuate the gain to the normal range and observe the morphological changes of the lesion. Diagnosis Retinopathy of prematurity occurs in the majority of premature infants. The diagnosis can be made accordingly. Treatment The disease, once it occurs, progresses rapidly and has a narrow window of time in which it can be effectively treated. Therefore, premature infants under 37 weeks of age should be examined promptly after birth, and those at high risk should be examined weekly. In stages 2 to 3, laser or cryotherapy is feasible to coagulate the avascular area. In stage 4~5, vitreous surgery is performed to remove proliferating fibrovascular tissue and photocoagulation is done at the same time to save vision. Prognosis The prognosis of retinopathy of prematurity vision varies depending on the severity of the active phase and the extent of the residual fibrous membrane. Those who are able to stop on their own in the first two stages of the active phase do not have much damage to their vision; those who have fibrous membrane residue but do not involve the macula may also retain good vision. When the fibrous membrane formation is 4~5 degrees, the visual acuity is highly poor.