What about retinopathy of prematurity?

Early fetal retinal development vitreous artery and choroid supply nutrition. At 100 mm of embryonic age, the vitreous vessels cross the optic disc, while small branches extend from the disc to the peripheral retina. Initially, they are seen only in the nerve fiber layer, but later on they begin to reach the deeper layers. In normal fetuses, vascular proliferation is prominent at 6 to 7 months of age. In preterm infants, the retina is not yet fully developed, and the peripheral part is the least mature. In a hyperoxic environment, retinal vascular constriction and obstruction cause local ischemia, hypoxia, and induce abnormal retinal vascular proliferation, which leads to a series of changes such as exudation, hemorrhage, and mechanization. The abnormally proliferated retinal blood vessels can develop through the inner boundary membrane to the retinal surface and extend into the vitreous, and as a result of vascular mechanization within the exuded vitreous, connective tissue membrane is formed behind the crystal, which can also cause retinal detachment due to traction. Clinical manifestations】 It is common in the first 3-6 weeks of life, and is clinically divided into the active phase and the fibrous membrane formation phase (Reese, 1953). 1. Active phase: divided into five stages (1) Vascular change stage: seen early in the course of the disease. The arteries and veins are tortuous and dilated. The venous diameters are sometimes 3 to 4 times larger than normal. Brush-like capillaries can be 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. The retinal neovascularization increases, mostly located near the equatorial part, but also seen before the equatorial part or in the posterior pole, and 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 proliferating vascular stripe and progresses intravitreally, causing a small retinal detachment in the peripheral part (most) or posterior pole (a few) of the fundus. (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 the disease has a duration of 3 to 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 to 5 degrees from mild to severe depending on the degree: degree I: retinal blood 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 also has small cloudy, 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. Fold 905 is located temporally and 105 is located nasally. It is rare to find them on the superior-inferior temporal side. The retinal vessels are not distributed along this fold, unlike the congenital retinal fold. Grade IV: A fibrous membrane or a detached part of the mechanized retina is visible behind the lens, and the pupil collar is obscured. The red light reflection of the fundus is visible from the unobscured start of the ophthalmoscopic examination. Degree 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. The eye may also be cloudy due to secondary glaucoma or extensive anterior iris adhesions, and the eye is smaller and more sunken than normal. [Differential diagnosis] The majority of this disease occurs in premature infants with a history of excessive guilt absorption in the incubator. Accordingly, the diagnosis can be made, in addition to congenital retinal folds, Coats disease, retinoblastoma, septic endophthalmitis and intravitreal accumulation of blood and formation of mechanized substances, the following diseases should also be noted to differentiate. (1) Bloch-Sülzberger syndrome (pigmentary disorder incontinentia pigmenti) This syndrome is an ectopic systemic histopathy at birth or after birth with a family history. A few cases are combined with posterior crystalline fiber atrophy, which is different from this disease. (2) Retinal dysplsia (retinal dysplasia) This syndrome also has the presence of posterior crystalline fibers. However, it is different from this disease because of the presence of bilateral microphthalmia at birth, post-iris adhesions, family history of mental retardation, somatic dysplasia, cerebral edema, cardiovascular disease, polydactyly and other systemic diseases. (3) Congenital encephalo-ophthalmic dysplasia This disease is also seen in preterm infants and also has posterior fibrous membrane and retinal hypoplasia and detachment. However, there is cerebral edema, ptosis, and abnormal development of the cerebellar cerebellum, which can be differentiated from this disease. (4) Persistent hyperplastic primary vitreous and pseudophacia fibrosa The former is also called persistent posterior fetal fibrovascular sheath of the congenital lens. fibrovascular sheath of the lens). The fetal fibrovascular sheath should be completely gone by the time the fetus is 8.5 months old, and permanent residuals that occur during this process form congenital posterior fetal fibrovascular sheath remnants. Although there are also changes such as microphthalmia and secondary glaucoma, the disease is seen in full-term infants who are not significantly underweight, monocular, with pupils and deviated crystals, etc. There are many differences to distinguish it from this disease. When the posterior vascular membrane of the lens overproduces the posterior scaring of the crystal and causes cataract, while the cortex is absorbed, mesenchymal tissue invades and forms a connective tissue membrane called fibrous pseudophakic lens. (5) Familial exudative vitreoretinopathy is similar to this disease in terms of its fundus. However, it is mostly autosomal dominant and occurs in full-term neonates without a history of oxygen absorption, unlike this disease. The only effective preventive measure is to strictly limit the use of oxygen in early infants, except when there is a risk of life due to cyanosis, oxygen at a concentration of 40% can be given, and the time should not be too long. In addition, high doses of vitamins applied early may also have some preventive effect. Early detection and timely administration of condensation or laser photocoagulation have been reported to prevent further deterioration of the lesion. In order to prevent the development of secondary glaucoma, the pupil must be dilated frequently in active, severe cases to avoid post-iris adhesions. The pupil dilator should be 2% omatropine to avoid atropine poisoning and to prevent long-term dilated pupils from causing anterior adhesions in the peripheral part of the iris. The prognosis of the disease varies according to the severity of the disease and the extent of fibrous membrane remaining during the active phase. Those who can stop on their own in the first two stages of the disease will not have much damage to their vision; those who have fibrous membrane remnants but do not involve the macula will also retain good vision. When fibrous membrane formation is 4 to 5 degrees, the vision is highly poor.