Why diabetic eye disease is different
Most eye conditions announce themselves. Diabetic retinopathy does not. The small blood vessels supplying the retina weaken, leak and close off over years, and for most of that time the patient sees perfectly well. Vision changes only once the damage reaches the macula or the disease triggers bleeding — and by then a good deal of what was lost is not recoverable.
Kerala has a high prevalence of diabetes, and a substantial number of people carry retinopathy without knowing it. Screening exists precisely because the disease is silent.
How it develops
In the early stage, called non-proliferative diabetic retinopathy, vessels balloon into microaneurysms and leak fluid, blood and fats into the retina. Often there is nothing to notice.
If leakage collects at the macula — the small central area responsible for reading and recognising faces — it causes diabetic macular oedema. This is the commonest way diabetic patients lose central vision, and it can occur even in otherwise early disease.
In proliferative diabetic retinopathy, so many vessels have closed that the retina, starved of oxygen, grows fragile new ones. These bleed into the vitreous and pull on the retina as they contract, which can cause a tractional retinal detachment. This is the advanced, sight-threatening stage.
Symptoms, when they finally appear
- Blurred or fluctuating vision
- Dark floaters or sudden patches blocking vision, from bleeding
- Difficulty reading or recognising faces
- Dark or empty areas in the field of vision
- Poor night vision
Fluctuating vision with changing blood sugar is common and not in itself a sign of retinopathy — but it is a reason to get the retina examined rather than to wait and see.
How we assess it
Screening is a dilated retinal examination. Drops widen the pupil, and the retina is examined and photographed. Because the drops blur near vision for a few hours, bring someone with you.
Where more detail is needed, OCT scanning measures retinal thickness precisely and shows macular swelling that is not visible on examination alone. Fundus photography documents the retina so that changes can be compared year on year — which is how progression is actually detected, rather than relying on memory.
How it is treated
Control first. Blood sugar, blood pressure and lipids are the foundation. No eye treatment substitutes for them, and this part is managed with your physician.
Laser photocoagulation seals leaking vessels and, in proliferative disease, treats the oxygen-starved peripheral retina to stop new vessels growing. Pan-retinal photocoagulation is an established, effective treatment for advanced disease.
Intravitreal injections deliver anti-VEGF medication or steroid directly into the eye to reduce macular swelling and suppress abnormal vessel growth. They are the mainstay for diabetic macular oedema. A course is usually required, with the interval adjusted to response — see intravitreal injections.
Vitrectomy surgery is needed where there is persistent bleeding into the vitreous or tractional detachment. See vitrectomy.
Treatment is chosen on examination and scan findings, and most patients need a combination over time rather than one intervention.
What to do if you have diabetes
Book a dilated eye examination now if you have not had one in the past year, regardless of how well you see. Keep the annual interval even when the result is normal. Tell us if you are pregnant or planning to be, since retinopathy can progress faster in pregnancy. And bring your recent HbA1c and blood pressure readings — they change how your retina is interpreted.
Sampada VR runs screening for diabetic retinopathy and retinopathy of prematurity as a deliberate focus of the centre, because both are conditions where the difference between early and late detection is measured in vision that is kept or lost.