Retinopathy of premature babies
Currently, the understanding of the pathogenesis mechanism as well as the proper regulation of the incubator oxygen level has significantly reduced the incidence of blindness caused by the disease.
Premature retinopathy (also known as post-vitreous fibrosis) was the most important cause of childhood blindness. The disease occurs in premature babies, low birth weight and is cared for in an environment with high oxygen concentration in incubators. In recent years, thanks to advances in the care of premature babies, the rate of surviving premature babies with low birth weight has increased, so premature retinopathy has become an increasing problem. Currently, the understanding of the pathogenesis mechanism as well as the proper regulation of the incubator oxygen level has significantly reduced the incidence of blindness caused by the disease. Premature retinopathy, if detected and treated early, can prevent blindness.
The pathogenesis of retinopathy at present is still unclear. One of the most popular current theories is related to oxygen concentration. Increased oxygen concentration leads to contraction of incomplete blood vessels in the peripheral retina, thereby causing ischemia and proliferation and fibrosis in the retinal ischemic, and eventually retinal detachment. Many factors are associated with the onset of the disease, such as birth weight, number of months of age at birth, respiratory distress syndrome, or birth control infection. Of these, low birth weight is the most important risk factor for the disease. The lower the birth weight born premature, the higher the risk of developing retinopathy. About 50% of babies born with a weight less than 1250 g show signs of retinopathy of a premature baby.
Figure - Stage 1 and 2 premature retinopathies
Retinopathy of premature babies usually appears on the peripheral retina, especially on the temples. The disease progresses in 3 stages: Stage 1, there is a clear boundary (ie the short bridge between the artery and veins) between the retinal area with blood vessels and the retinal area without blood vessels. Stage 2, emerges a raised ridge (the bridge turns off larger). Stage 1 and stage 2 have a good prognosis, the disease can be self-reversing. Stage 3, from the ridge, generates new vessels that develop into the vitreous. New vessels may also appear in the posterior polar retina (complementary phase). Stage 3 and the complementary phase have a severe prognosis, as neovascularization can affect vision and cause fibrous proliferation and contractility leading to retinal detachment.
Figure - Stage 3 and 4 premature retinopathies
It is necessary to distinguish retinopathy of premature babies from diseases with white pupil signs such as cataracts, Coats disease, cancer of the retina, uveitis, primary vitreous hyperplasia, or some other congenital damage to the retina.
Treatment of retinopathy of premature babies is mainly by surgery, at an early stage can be treated with cryotherapy, laser photocoagulation to destroy the anemia retinal areas. In the late stage, treatment with vitreous-retinal dissection.