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Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which could eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all diabetics who have had diabetes for 15 years or more. Despite these intimidating statistics, research indicates that at least 90% of these new cases could be reduced if there was proper and vigilant treatment and monitoring of the eyes.
Additional recommended knowledge
Signs and symptoms
Diabetic retinopathy often has no early warning signs. Even macular edema, which may cause vision loss more rapidly, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read and drive. In some cases, the vision will get better or worse during the day.
As new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy (PDR), they can bleed (haemorrhage) and blur vision. The first time this happens, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots, floating in a person's visual field, though the spots often go away after a few hours.
These spots are often followed within a few days or weeks by a much greater leakage of blood, which blurs vision. In extreme cases, a person will only be able to tell light from dark in that eye. It may take the blood anywhere from a few days to months or even years to clear from the inside of the eye, and in some cases the blood will not clear. These types of large hemorrhages tend to happen more than once, often during sleep.
On fundoscopic exam, a doctor will see cotton wool spots, flame hemorrhages, and dot-blot hemorrhages.
Diabetic retinopathy is result of microvascular retinal changes. Hyperglycemia-induced pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls. These damages change the formation of the blood-retinal barrier and also make retinal blood vessel become more permiable.
Small blood vessels – such as those in the eye – are especially vulnerable to poor blood sugar control. An overaccumulation of glucose and/or fructose damages the tiny blood vessels in the retina. During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any changes in their vision.
Some people develop a condition called macular edema. It occurs when the damaged blood vessels leak fluid and lipids onto the macula, the part of the retina that lets us see detail. The fluid makes the macula swell, which blurs vision.
As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage. The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina. Fibrovascular proliferation can also cause tractional retinal detachment. The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause neovascular glaucoma. Nonproliferative diabetic retinopathy shows up as cotton wool spots, or microvascular abnormalities or as superficial retinal hemorrhages. Even so, the advanced proliferative diabetic retinopathy (PDR) can remain asymptomatic for a very long time, and so should be monitored closely with regular checkups.
All people with diabetes mellitus are at risk – those with Type I diabetes (juvenile onset) and those with Type II diabetes (adult onset). The longer a person has diabetes, the higher the risk of developing some ocular problem. Between 40 to 45 percent of Americans diagnosed with diabetes have some stage of diabetic retinopathy.  After 20 years of diabetes, nearly all patients with type 1 diabetes and >60% of patients with type 2 diabetes have some degree of retinopathy.
During pregnancy, diabetic retinopathy may also be a problem for women with diabetes. It is recommended that all pregnant women with diabetes have dilated eye examinations each trimester to protect their vision.
Diabetic retinopathy is detected during an eye examination that includes:
Of the 18 million to 20 million diabetics in the United States, only about half receive annual eye examinations for retinopathy risk. In an effort to increase diabetic patient’s compliance for regular eye exams, Digital Healthcare, a Wake Forest, NC company specializing in retinal risk assessment, has announced the introduction of Retasure, a new retinal imaging risk assessment solution that connects primary care physicians with ophthalmic specialists to perform retinal imaging.
Retasure allows primary care physicians to capture digital images of diabetic patients’ retinas in a non-invasive procedure that takes just a few minutes. The images are then transmitted over a secure, HIPPA compliant network to a board certified ophthalmologist at an accredited reading center for examination. Results are returned to the primary care physician within 72 hours.
Retasure has been available throughout Europe, and more than one million people have benefited from the system annually.
The eye care professional will look at the retina for early signs of the disease, such as: (1) leaking blood vessels, (2) retinal swelling, such as macular edema, (3) pale, fatty deposits on the retina (exudates) – signs of leaking blood vessels, (4) damaged nerve tissue (neuropathy), and (5) any changes in the blood vessels.
Should the doctor suspect macular edema, he or she may perform a test called fluorescein angiography. In this test, a special dye is injected into the arm. Pictures are then taken as the dye passes through the blood vessels in the retina. This test allows the doctor to find the leaking blood vessels.
There are three major treatments for diabetic retinopathy, which are very effective in reducing vision loss from this disease. In fact, even people with advanced retinopathy have a 90 percent chance of keeping their vision when they get treatment before the retina is severely damaged. Still, the best way of addressing diabetic retinopathy is to monitor it vigilantly and ensure that it does not happen in the first place by careful blood glucose control and limitation of dietary fructose.
These three treatments are laser surgery, injection of triamcinolone into the eye and vitrectomy. It is important to note that although these treatments are very successful, they do not cure diabetic retinopathy. Caution should be exercised in treatment with laser surgery since it causes a loss of retinal tissue. It is often more prudent to inject triamcinolone. In some patients it results in a marked increase of vision, especially if there is an edema of the macula.
Avoiding tobacco use and correction of associated hypertension are important therapeutic measures in the management of diabetic retinopathy. 
A type of laser surgery called panretinal photocoagulation, or PRP, is used to treat severe macular edema and proliferative retinopathy. The goal is to create 1 000 - 2 000 burns in the retina with the hope of reducing the retina's oxygen demand, and hence the possibility of ischemia. In treating advanced diabetic retinopathy, the burns are used to destroy the abnormal blood vessels that form at the back of the eye.
Before the surgery, the ophthalmologist dilates the pupil and applies anesthetic drops to numb the eye. In some cases, the doctor also may numb the area behind the eye to prevent any discomfort. The lights in the office are also dimmed to aid in dilating the pupil. The patient sits facing the laser machine while the doctor holds a special lens to the eye. The physician can use a single spot laser or a pattern scan laser for two dimensional patterns such as squares, rings and arcs. During the procedure, the patient may see flashes of light. These flashes may eventually create an uncomfortable stinging sensation for the patient. After the laser treatment, patients should be advised not to drive for a few hours while the pupils are still dilated. Vision may remain a little blurry for the rest of the day, though there should not be much pain in the eye.
Scatter laser treatment
Rather than focus the light on a single spot, the eye care professional may make hundreds of small laser burns away from the center of the retina, a procedure called scatter laser treatment or panretinal photocoagulation. The treatment shrinks the abnormal blood vessels. Patients may lose some of their peripheral vision after this surgery, but the procedure saves the rest of the patient's sight. Laser surgery may also slightly reduce colour and night vision.
A person with proliferative retinopathy will always be at risk for new bleeding as well as glaucoma, a complication from the new blood vessels. This means that multiple treatments may be required to protect vision.
Instead of laser surgery, some people need an eye operation called a vitrectomy to restore vision. A vitrectomy is performed when there is a lot of blood in the vitreous. It involves removing the cloudy vitreous and replacing it with a saline solution made up of salt and water. Because the vitreous is mostly water, there should be no change between the saline solution and the normal vitreous.
Studies show that people who have a vitrectomy soon after a large hemorrhage are more likely to protect their vision than someone who waits to have the operation. Early vitrectomy is especially effective in people with insulin-dependent diabetes, who may be at greater risk of blindness from a hemorrhage into the eye.
Vitrectomy is often done under local anesthesia. The doctor makes a tiny incision in the sclera, or white of the eye. Next, a small instrument is placed into the eye to remove the vitreous and insert the saline solution into the eye.
Patients may be able to return home soon after the vitrectomy, or may be asked to stay in the hospital overnight. After the operation, the eye will be red and sensitive, and patients usually need to wear an eyepatch for a few days or weeks to protect the eye. Medicated eye drops are also prescribed to protect against infection.
|Conjunctivitis - Pterygium - Pinguecula - Subconjunctival hemorrhage
|Sclera and cornea
|Scleritis - Keratitis - Corneal ulcer - Snow blindness - Thygeson's superficial punctate keratopathy - Fuchs' dystrophy - Keratoconus - Keratoconjunctivitis sicca - Arc eye - Keratoconjunctivitis - Corneal neovascularization - Kayser-Fleischer ring - Arcus senilis - Band keratopathy
|Iris and ciliary body
|Iritis - Uveitis - Iridocyclitis - Hyphema - Persistent pupillary membrane - Iridodialysis - Synechia
|Cataract - Aphakia - Ectopia lentis
|Choroid and retina
|Retinitis - Chorioretinitis - Choroideremia - Retinal detachment - Retinoschisis - Retinopathy (Hypertensive retinopathy, Diabetic retinopathy, Retinopathy of prematurity) - Macular degeneration - Retinitis pigmentosa - Retinal haemorrhage - Central serous retinopathy - Macular edema - Epiretinal membrane - Macular pucker
|Optic nerve and visual pathways
|Optic neuritis - Papilledema - Optic atrophy - Leber's hereditary optic neuropathy
accommodation and refraction
|Paralytic strabismus: Ophthalmoparesis - Progressive external ophthalmoplegia - Palsy (III, IV, VI) - Kearns-Sayre syndrome
Other strabismus: Esotropia/Exotropia - Hypertropia - Heterophoria (Esophoria, Exophoria) - Brown's syndrome - Duane syndrome
|Visual disturbances and blindness
|Amblyopia - Leber's congenital amaurosis - Subjective (Asthenopia, Hemeralopia, Photophobia, Scintillating scotoma) - Diplopia - Scotoma - Anopsia (Binasal hemianopsia, Bitemporal hemianopsia, Homonymous hemianopsia, Quadrantanopia) - Color blindness (Achromatopsia) - Nyctalopia - Blindness/Low vision
|Anisocoria - Argyll Robertson pupil - Marcus Gunn pupil/Marcus Gunn phenomenon - Adie syndrome
|Trachoma - Onchocerciasis
|Nystagmus - Miosis - Mydriasis - Glaucoma - Ocular hypertension - Floater - Leber's hereditary optic neuropathy - Red eye - Keratomycosis - Xerophthalmia - Aniridia
|See also congenital