retinopathy
- Related Topics:
- retina
- retinopathy of prematurity
- retinal diseases
What are the main types of retinopathy?
How does diabetic retinopathy develop?
How is retinopathy treated?
retinopathy, damage affecting the small blood vessels in the retina, the light-sensitive layer at the back of the eye, that may lead to partial or complete vision loss. Depending on the underlying cause, symptoms of retinopathy may vary, and the condition may develop gradually or abruptly. Though retinopathy sometimes improves on its own, in many instances, treatment is necessary to halt retinal damage and restore vision.
Types and causes
There are four main types of retinopathy: diabetic retinopathy, retinopathy of prematurity (ROP), hypertensive retinopathy, and central serous chorioretinopathy. Each type differs from the others in cause, progression, and treatment.
Diabetic retinopathy
Diabetic retinopathy, which may develop in individuals who have type 1 or type 2 diabetes mellitus, is the most commonly occurring type of retinopathy, affecting about 146 million adults with diabetes worldwide. The condition develops when excess glucose in the blood damages vessels in the retina. In early diabetic retinopathy, known as nonproliferative diabetic retinopathy, this damage causes blood vessels to leak fluid into the retina, impairing vision. In the advanced stage of diabetic retinopathy, called proliferative diabetic retinopathy, new blood vessels grow that are structurally unstable, causing bleeding and, in some instances, the formation of scar tissue, which can cause retinal detachment.
Symptoms of diabetic retinopathy include blurred vision, blank or dark spots in the visual field, difficulty seeing in the dark, sudden loss of vision in one or both eyes, and recently developed color blindness. Symptoms may not become apparent until a late stage of the disease.
Retinopathy of prematurity
Retinopathy of prematurity (ROP) occurs in infants who are born prematurely, especially those with low birth weight. In mild forms, developing blood vessels within the retina, which originate at the optic disk, temporarily stop growing toward the retinal periphery. The vessels usually resume development without deleterious consequences. However, in severe forms of ROP, the stalled vessels break through to the surface of the retina and proliferate extensively. These fragile tangles are susceptible to breaking, bleeding, and scarring, and they may pull on the underlying retina, causing complex retinal detachments and blindness.
Hypertensive retinopathy
Hypertensive retinopathy develops in individuals who are affected by hypertension (high blood pressure). Chronic hypertension damages the small blood vessels in the retina, leading to bleeding, swelling, and vision problems. Swelling of the optic nerve may occur with sudden high blood pressure. When left untreated, hypertensive retinopathy may result in a loss of visual clarity. Symptoms are often not present until later stages of the disease.
Central serous chorioretinopathy
Central serous chorioretinopathy—in which fluid leaks from the choroid (a vascular layer between the outer wall of the eyeball and the retina) and accumulates beneath the retina, in the retinal pigment epithelium—develops for reasons that are unclear. Factors that are thought to contribute to the condition include stress, high blood pressure, the use of steroid drugs (e.g., prednisone or hydrocortisone), autoimmune disorders, and sleep-related disorders. Symptoms include blurred or distorted vision and poor vision in the dark. The condition may lead to retinal detachment. It most often occurs in men between ages 30 and 50.
Diagnosis and treatment
Diagnosis of retinopathy is often made following a routine eye exam and consideration of other vision-related symptoms. In hypertensive retinopathy, for example, diagnosis may be based on a combination of factors, including the presence of headaches and blurred, dim, or double vision. Such symptoms typically warrant examination of the eyes for signs of bleeding, swelling, and other indications of blood vessel damage. To diagnose diabetic retinopathy, the retina and interior of the eye are examined with an ophthalmoscope; a dye may be used to spot leaky blood vessels. To diagnose central serous chorioretinopathy, the eyes are investigated for bubblelike fluid between the retinal layers. In the early stages of ROP, symptoms are not outwardly present, and the eyes must be examined for abnormalities. In severe cases, signs of ROP include nystagmus (rapid side-to-side eye movements) and leukoria (white pupils).
Treatment for retinopathy, especially diabetic retinopathy, depends on the cause and stage. Mild nonproliferative diabetic retinopathy, for example, may not require treatment. As diabetic retinopathy progresses, however, injections of vascular endothelial growth factor (VEGF) inhibitors may be administered to slow the growth of abnormal blood vessels. Laser treatments to seal leaky blood vessels or to create scars that shrink or slow blood vessel growth may also be used. Surgical procedures, such as vitrectomy to remove all or part of the vitreous (the gel-like material filling much of the eyeball) or scleral buckling to reattach the retina, may be necessary.
Treatment for ROP is typically not recommended in the early stages of the disease, as most cases resolve on their own; however, close monitoring is crucial. In advanced stages of ROP, injections of VEGF inhibitors, laser treatments, vitrectomy, or scleral buckling may be recommended. Children with ROP have an increased risk of developing glaucoma, cataracts, amblyopia (lazy eye), myopia (nearsightedness), or strabismus (crossed eyes).
There are no specific treatments for hypertensive retinopathy. Though existing damage to the retina may persist, taking medications to lower blood pressure may lead to improvements in retinal health and prevent further damage to the retina. If sudden high blood pressure causes swelling of the optic nerve, emergency intravenous steroid treatment may be required. In the case of central serous chorioretinopathy, the disease usually resolves in three to four months without treatment; full visual acuity is generally restored within six months. However, if the disease persists, an ophthalmologist may recommend corticosteroid therapy or laser treatment.