Diabetic retinopathy, also known as diabetic eye disease, is a medical condition in which damage occurs to the retina due to diabetes mellitus. It is a leading cause of blindness.
Diabetic retinopathy affects up to 80 percent of those who have had diabetes for 20 years or more. At least 90% of new cases could be reduced with proper treatment and monitoring of the eyes. The longer a person has diabetes, the higher his or her chances of developing diabetic retinopathy. Each year in the United States, diabetic retinopathy accounts for 12% of all new cases of blindness. It is also the leading cause of blindness in people aged 20 to 64.
Diabetic retinopathy often has no early warning signs. Even macular edema, which can cause rapid vision loss, 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 or drive. In some cases, the vision will get better or worse during the day.
The first stage, called non-proliferative diabetic retinopathy (NPDR), has no symptoms. Patients may not notice the signs and have 20/20 vision. The only way to detect NPDR is by fundus photography, in which microaneurysms (microscopic blood-filled bulges in the artery walls) can be seen. If there is reduced vision, fluorescein angiography can show narrowing or blocked retinal blood vessels clearly (lack of blood flow or retinal ischemia).
Macular edema, in which blood vessels leak their contents into the macular region, can occur at any stage of NPDR. Its symptoms are blurred vision and darkened or distorted images that are not the same in both eyes. Ten percent (10%) of diabetic patients will have vision loss related to macular edema. Optical Coherence Tomography can show areas of retinal thickening due to fluid accumulation from macular edema.[6]
In the second stage, abnormal new blood vessels (neovascularisation) form at the back of the eye as part of proliferative diabetic retinopathy (PDR); these can burst and bleed (vitreous hemorrhage) and blur the vision, because these new blood vessels are fragile. The first time this bleeding occurs, 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 the vision. In extreme cases, a person may 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 funduscopic exam, a doctor will see cotton wool spots, flame hemorrhages (similar lesions are also caused by the alpha-toxin of Clostridium novyi), and dot-blot hemorrhages.
All people with diabetes are at risk – those with Type I diabetes and those with Type II diabetes. The longer a person has had diabetes, the higher their risk of developing some ocular problem. Between 40 and 45 percent of Americans diagnosed with diabetes have some stage of diabetic retinopathy. After 20 years of diabetes, nearly all patients with Type I diabetes and >60% of patients with Type II diabetes have some degree of retinopathy; however, these statistics were published in 2002 using data from four years earlier, limiting the usefulness of the research. The subjects would have been diagnosed with diabetes in the late 1970s, before modern fast-acting insulin and home glucose testing.
Prior studies had also assumed a clear glycemic threshold between people at high and low risk of diabetic retinopathy.
Published rates vary between trials, the proposed explanation being differences in study methods and reporting of prevalence rather than incidence values.
During pregnancy, diabetic retinopathy may also be a problem for women with diabetes. NIH recommends that all pregnant women with diabetes have dilated eye examinations each trimester.
People with Down syndrome, who have extra chromosome 21 material, almost never acquire diabetic retinopathy. This protection appears to be due to the elevated levels of endostatin, an anti-angiogenic protein, derived from collagen XVIII. The collagen XVIII gene is located on chromosome 21.
Diabetic retinopathy is the result of damage to the small blood vessels and neurons of the retina. The earliest changes leading to diabetic retinopathy include narrowing of the retinal arteries associated with reduced retinal blood flow; dysfunction of the neurons of the inner retina, followed in later stages by changes in the function of the outer retina, associated with subtle changes in visual function; dysfunction of the blood-retinal barrier, which protects the retina from many substances in the blood (including toxins and immune cells), leading to the leaking of blood constituents into the retinal neuropile. Later, the basement membrane of the retinal blood vessels thickens, capillaries degenerate and lose cells, particularly pericytes and vascular smooth muscle cells. This leads to loss of blood flow and progressive ischemia, and microscopic aneurysms which appear as balloon-like structures jutting out from the capillary walls, which recruit inflammatory cells; and advanced dysfunction and degeneration of the neurons and glial cells of the retina.
An experimental study suggests that pericyte death is caused by blood glucose persistently activating protein kinase C and mitogen-activated protein kinase (MAPK), which, through a series of intermediates, inhibits signaling through platelet-derived growth factor receptors — signaling that supports cellular survival, proliferation, and growth. The resulting withdrawal of this signaling leads to the programmed cell death (apoptosis) of the cells in this experimental model.
Small blood vessels – such as those in the eye – are especially vulnerable to poor blood sugar (blood glucose) control. An overaccumulation of glucose damages the tiny blood vessels in the retina. During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any change in their vision. Early changes that are reversible and do not threaten central vision are sometimes termed simplex retinopathy or background retinopathy.
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 (PDR) stage, where blood vessels proliferate/grow. 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.
Diabetic retinopathy is detected during an eye examination that includes:
The eye care professional will look at the retina for early signs of the disease, such as:
If macular edema is suspected, FFA and sometimes OCT may be performed.
Diabetic retinopathy also affects microcirculation thorough the body. A recent study showed assessment of conjunctival microvascular hemodynamics such as vessel diameter, red blood cell velocity and wall shear stress can be useful for diagnosis and screening of diabetic retinopathy. Furthermore, the pattern of conjunctival microvessels was shown to be useful for rapid monitoring and diagnosis of different stages of diabetic retinopathy.
In April 2018 the FDA approved a similar device called IDx-DR.[19] IDx-DR is an AI diagnostic system that autonomously analyzes images of the retina for signs of diabetic retinopathy. As an autonomous, AI-based system, IDx-DR is unique in that it makes an assessment without the need for a clinician to also interpret the image or results, making it usable by health care providers who may not normally be involved in eye care.
Google is testing a cloud algorithm that scans photos of the eye for signs of retinopathy. The algorithm still requires FDA approval.
According to a DRSS user manual, poor quality images (which may apply to other methods) may be caused by cataract, poor dilation, ptosis, external ocular condition, or learning difficulties. There may be artefacts caused by dust, dirt, condensation, or smudge.
In the UK, screening for diabetic retinopathy is part of the standard of care for people with diabetes. After one normal screening in people with diabetes, further screening is recommended every two years. In the UK, this is recommended every year. Teleophthalmology has been employed in these programs. In The U.S, a current guideline for diabetic retinopathy is recommendation of annual dilated exams for all patients with diabetes. There are barriers to recommended screening that is contributing to the disparity. Such as the patient factor which includes education about diabetic retinopathy and the availability of the treatment. The health care system also contributes to the disparities in diabetic screening, which includes insurance coverage, long waiting time for the appointment and difficulty scheduling appointments which makes the person less likely to screen. Provider factors also influence the barrier to screening which is a lack of awareness of the screening guidelines, skills or having the right tools to perform eye exams which can affect the diagnosis and treatment. A cross-sectional study showed that when physicians treating black patients had more difficulty providing proper subspecialty care and diagnostic imaging for the patients.
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 95 percent chance of keeping their vision when they get treatment before the retina is severely damaged. These three treatments are laser surgery, injection of corticosteroids or anti-VEGF agents into the eye, and vitrectomy.
Although these treatments are very successful (in slowing or stopping further vision loss), 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 or anti-VEGF drugs. 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.
Obstructive sleep apnea (OSA) has been associated with a higher incidence of diabetic eye disease due to blood desaturation caused by intermittent upper airway obstructions. Treatment for OSA can help reduce the risk of diabetic complications.
The best way of preventing the onset and delaying the progression of diabetic retinopathy is to monitor it vigilantly and achieve optimal glycemic control.
Since 2008 there have been other therapies (e.g. kinase inhibitors and anti-VEGF) drugs available.
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