Diabetic Retinopathy: How Diabetes Damages the Retina, and What Can Be Done
World Diabetes Day falls on 14 November. It is a reasonable moment to ask a question most people with diabetes have never been asked: when was your retina last examined?
For a great many Indians, the honest answer is never. India's National Blindness and Visual Impairment Survey examined more than 56,000 people aged 50 and above across 21 states and union territories. Among those who already knew they had diabetes, 89.9% had never had a retinal examination. Only 6.3% had had one in the preceding year. Of those found to have sight-threatening diabetic retinopathy, only 13.6% had received laser treatment.
That gap matters because the damage is silent until it is not. By the time vision changes, the disease is usually well established. Almost everything that can be saved is saved by looking early.
Understanding the diabetic retinopathy stages and seeking timely screening can help detect retinal changes before significant vision loss occurs.
India's diabetes burden, in numbers
The ICMR-INDIAB study, the largest national survey of its kind, surveyed 113,043 people across 31 states and union territories. It estimated 101 million Indians living with diabetes (11.4%) and a further 136 million with prediabetes (15.3%) — meaning more Indians are on the runway to diabetes than have already arrived. It also found hypertension in 35.5%, abdominal obesity in 39.5% and raised cholesterol in 24%. Those three travel with diabetes, and as this article explains, all three affect the retina.
The International Diabetes Federation puts India second in the world for absolute numbers, with roughly 89.8 million adults aged 20 to 79 affected in 2024 and a projection of 156.7 million by 2050. Around 43% — some 38.6 million people — do not know they have it.
Why diabetes is rising: what the evidence says
A 2025 review in Diabetologia examined why type 2 diabetes prevalence varies so widely between populations. Its conclusions are worth stating plainly, because they are often replaced in public conversation by folklore:
Urbanisation and industrialisation: Across 207 countries, urbanisation, population density and income per head track prevalence in middle-income countries. Sedentary work and energy-dense processed food are the mechanism, and sugar intake has been identified as a key mediator.
Obesity is among the strongest modifiable risk factors. Global adult obesity more than doubled between 1990 and 2021. In one US cohort, a BMI of 30 or above carried more than a tenfold increase in ten-year diabetes risk compared with a BMI under 25. The Global Burden of Disease 2021 analysis ranks high body mass index as the single largest contributor to type 2 diabetes burden, ahead of dietary risks, environmental and occupational risks, tobacco, low physical activity and alcohol.
The nutritional transition: Refined grains, added sugar and processed foods displacing traditional diets, with Asia and India named specifically.
Genetic predisposition and ethnicity: Real, but not the whole story — polygenic risk scores do not account for the differences observed between populations.
Undernutrition before birth: The thrifty phenotype hypothesis: poor nutrition in utero followed by an energy-rich childhood raises later risk. This is directly relevant to the generation of Indians now in middle age.
Earlier onset: South Asian people develop type 2 diabetes roughly 10 to 15 years earlier than white populations. Earlier onset means more years of exposure, and more years of exposure is what drives retinopathy.
Globally, the Global Burden of Disease study counted 529 million people with diabetes in 2021 and projects 1.3 billion by 2050.
Recognising diabetic retinopathy symptoms and undergoing regular retinal examinations are important for detecting diabetic eye disease.
How high blood sugar damages the eye
Sustained high glucose is toxic to blood vessels throughout the body. The vessels that show it first are the smallest and most metabolically demanding: those of the kidney, the peripheral nerves and the retina. This is why diabetic kidney disease, diabetic neuropathy and diabetic retinopathy tend to appear together, and why a finding in one should prompt a look at the others.
The retina has one particular advantage for medicine: it is the only part of the body where these small vessels can be examined directly, through the pupil, without a single incision. What a retina examination shows is a readout of what high sugar is doing to small vessels everywhere.
Stage 1: Pericyte loss and Microaneurysms — mild NPDR
Wrapped around the outside of every retinal capillary is a layer of supporting cells called pericytes. They provide structural support and help regulate blood flow. Chronic hyperglycaemia kills them.
Once that external support is lost, the capillary wall bulges at its weakest points. These outpouchings are called microaneurysms, and on examination they appear as small red dots scattered across the retina. Their appearance marks mild non-proliferative diabetic retinopathy (NPDR).
At this stage vision is usually completely normal. There is nothing to feel. This is precisely the stage at which a patient benefits most from being found, and precisely the stage at which nobody comes.
Stage 2: Leakage and Hard Exudates — moderate NPDR
Damaged vessel walls do not only bulge, they leak. Fluid and lipid-rich plasma seep into the retinal tissue. The water is reabsorbed; the fatty, protein-rich residue is not, and settles as yellowish deposits called hard exudates. Alongside more numerous dot and blot haemorrhages, this picture defines moderate NPDR.
Here symptoms begin. Where the leakage occurs in the macula — the small central area responsible for reading, faces and fine detail — the retina swells. This is diabetic macular oedema (DME), and it is the commonest reason a person with diabetes loses reading vision. Straight lines may look bent, print may look smudged, and vision may fluctuate from day to day.
An important point about sequence: macular oedema can occur at any stage of retinopathy. A patient with otherwise mild changes can have significant central swelling, and a patient with advanced retinopathy can have a dry macula and good vision. The stage of retinopathy and the state of the macula are two separate questions, and both are answered at every visit.
Stage 3: Vessel Closure and Ischaemia — severe NPDR
Running in parallel with pericyte loss, the basement membrane of the capillary wall thickens. Combined with changes in the blood itself, this progressively occludes the capillaries. Areas of retina lose their blood supply.
On examination this appears as more extensive haemorrhages in all four quadrants, beading of the veins and abnormal shunt vessels. On OCT angiography it appears directly, as dark zones where no flow can be detected. This is severe NPDR, and it is the point at which the eye stops being merely damaged and starts being dangerous.
Stage 4: New Vessels — Proliferative Diabetic Retinopathy
An oxygen-starved retina does what starved tissue does anywhere: it signals for new blood supply. The principal signal is vascular endothelial growth factor (VEGF).
The vessels that grow in response are not normal. They are fragile, poorly formed, leak readily and bleed easily, and they grow along the surface of the retina and into the vitreous gel rather than where they are needed. Their appearance defines proliferative diabetic retinopathy (PDR), the advanced stage.
Not all proliferative disease carries the same risk. The Diabetic Retinopathy Study defined high-risk characteristics (HRC), and the definition still guides treatment today:
New vessels on the optic disc (NVD) measuring at least one-third of a disc area; or
Any NVD accompanied by vitreous or preretinal haemorrhage; or
New vessels elsewhere in the retina (NVE) of at least half a disc area accompanied by vitreous or preretinal haemorrhage.
Disc neovascularisation is the one to respect most, because new vessels at the disc imply widespread retinal ischaemia rather than a local problem. An eye with high-risk PDR needs treatment, not observation.
The warning sign people ignore: floaters and black spots
When a new vessel bleeds, blood enters the vitreous gel. The patient sees floaters, cobwebs, a shower of black spots, or a sudden smoky haze across the vision. It may clear partly over days, which is exactly what makes it dangerous, because it invites waiting.
In a person with diabetes, new floaters or black spots are a reason to have the retina examined within days. It is not a nuisance. It is the retina reporting that new vessels have formed and have already started bleeding.
If that report is ignored, which in practice happens often, two things follow. The bleed may become dense and persistent — a vitreous hemorrhage that does not clear. Or the fibrous scaffold accompanying the new vessels contracts and pulls the retina off its bed, producing a tractional retinal detachment. Both need surgery, and the visual results of operating on a detached, ischaemic diabetic retina are far poorer than the results of treating the same eye six months earlier.
What the stages look like together
Stage | What is happening in the retina | What the patient notices | What we usually do |
Mild NPDR | Pericyte loss, microaneurysms (red dots) | Nothing | Control sugars, BP, lipids; review in 12 months |
Moderate NPDR | Leakage, hard exudates, more hemorrhage; macular oedema may appear | Often nothing; blurring or distortion if the macula is involved | OCT at every visit; anti-VEGF injection if the macula is swollen; review in 6 to 12 months |
Severe NPDR | Capillary closure, widespread hemorrhage, venous beading, ischemia | Usually nothing, which is the problem | Review every 3 to 4 months; consider laser or injections to reduce progression risk |
PDR | New vessels on the disc or retina, driven by VEGF | Floaters, black spots, sudden haze if they bleed | Pan-retinal laser and/or anti-VEGF; review every 2 to 4 months |
Advanced PDR | Non-clearing vitreous hemorrhage; tractional retinal detachment | Marked or sudden vision loss | Vitrectomy surgery |
Follow-up intervals above follow the American Academy of Ophthalmology's 2024 Preferred Practice Pattern, and shorten when macular oedema is present.
What the long-term studies tell us about the odds
The Wisconsin Epidemiologic Study of Diabetic Retinopathy followed a population cohort for decades and remains the reference for natural history. Over ten years, retinopathy developed in 89% of those with younger-onset diabetes, 79% of insulin-treated older-onset patients and 67% of those not on insulin. Progression to proliferative disease occurred in 30%, 24% and 10% respectively. At 25 years in the younger-onset cohort, 97% had some retinopathy, 83% had progressed, and 42% had developed proliferative disease.
Those are sobering figures, and they are also the point. Retinopathy in long-standing diabetes is close to universal. Blindness from it is not. What separates the two is control and timing, and both are modifiable.
The same study identified the factors that predicted progression: higher HbA1c, higher body mass index, proteinuria and systolic blood pressure. Each 1% rise in HbA1c over four years carried an 18% higher risk of proliferative disease.
Investigations: what we actually look at
Dilated retinal examination remains the foundation, and validated retinal photography is an accepted alternative for screening.
Optical coherence tomography (OCT) is the workhorse. It gives a cross-sectional image of the retina to a few microns, showing whether the macula is swollen, how much, where the fluid sits, and whether the photoreceptor layers are intact. Every treatment decision about macular oedema, and every decision about whether a further injection is needed, is made on OCT. It takes seconds, needs no dye and no injection.
OCT angiography (OCTA) is the more recent and, in diabetic eyes, the more revealing. It maps blood flow through the retinal capillary networks without injecting any dye, so areas of capillary closure, enlarged foveal avascular zones and early new vessels can be seen directly rather than inferred. At Claritas Eye & Retina Institute, under Dr Mayank Bansal, OCT angiography is available on site and used routinely. Being able to see the ischaemia that drives the disease, rather than only the fluid it produces, changes how precisely treatment can be timed.
Fluorescein angiography, which requires an intravenous dye, has a much reduced role as a result. It retains a place where very wide-field imaging of peripheral ischaemia is needed, or where a specific diagnostic question remains unanswered, but it is no longer a routine step for most diabetic eyes.
Treatment, Part One: The ABC
Before any injection, laser or operation, there is the part the patient controls, and the part with the best evidence behind it. We call it the ABC.
What it means | What the evidence shows | |
A — HbA1c | Glycated haemoglobin, an average of blood sugar over about three months. A single fasting reading tells you about one morning; HbA1c tells you about the quarter. | In the DCCT, intensive control reduced the risk of developing retinopathy by 76% and its progression by 54%, with reductions of 47% for proliferative disease and 56% for the need for laser. In type 2 diabetes, UKPDS 33 showed a 25% reduction in microvascular endpoints and a 29% reduction in retinal photocoagulation. ACCORD-Eye reduced four-year progression from 10.4% to 7.3%. |
B — Blood pressure | Treated to target, not merely measured. | In UKPDS 38, tight blood pressure control over 7.5 years reduced retinopathy progression by 34%, the need for retinal photocoagulation by 35%, and loss of three or more lines of vision by 47%. Pushing systolic below 120 adds nothing further, as ACCORD showed. |
C — Cholesterol | Lipids, and fenofibrate specifically. | In the FIELD study, fenofibrate reduced the need for first laser treatment by about 31%. In ACCORD-Eye, fenofibrate added to simvastatin cut four-year progression from 10.2% to 6.5%. The 2024 LENS trial, run inside Scotland's national screening programme in 1,151 patients, found a 27% lower risk of referral or treatment for retinopathy over four years. |
One caveat worth hearing from a retina surgeon rather than discovering by surprise: when very high sugars are brought down very fast, retinopathy can transiently worsen before it settles. In the DCCT this early worsening occurred within 12 months in 13.1% of the intensively treated group against 7.6% of controls, and most had recovered by 18 months. The lesson is not to avoid control. It is to bring sugars down steadily, and to have the retina examined before starting an intensive regimen, including the newer weight-loss and GLP-1 based injections now widely used in India.
The DCCT also demonstrated something remarkable called metabolic memory. Years after both groups' HbA1c had converged, the previously intensively treated group still had 53% less progression at ten years. Good control today keeps paying for a decade. The reverse is also true.
Treatment, Part Two: Injections Into The Eye
Patients often ask why we cannot simply prescribe drops. The answer is anatomical. A drop placed on the surface of the eye reaches the cornea and the front chamber reasonably well, but very little of it crosses the full depth of the eye to reach the retina at the back. To act on the retina, the drug has to be delivered into the vitreous cavity. That is what an intravitreal injection is.
The drugs used are anti-VEGF agents. They block the VEGF signal that is driving both the leakage causing macular oedema and the growth of new vessels in proliferative disease. The swelling settles, the retina dries, leaking stops, and new vessels regress. The injection is given in the clinic under anaesthetic drops after the surface is cleaned, and takes a few minutes.
The agents available in India:
Drug | Brand names in India | Typical treatment interval |
Ranibizumab | Accentrix, Razumab, Lucentis | About 1 month |
Bevacizumab | Avastin (used off-label) | About 1 month |
Aflibercept 2 mg | Eylea, Anyra | About 2 months |
Brolucizumab | Pagenax | About 3 months |
Aflibercept 8 mg | Eylea 8 mg (being introduced) | Up to 4 to 5 months in responders |
Faricimab | Vabysmo | Up to 4 months in responders |
The DRCR Retina Network's Protocol T compared the three original agents head to head in 660 eyes with macular oedema. At one year, mean gains were 13.3 letters with aflibercept, 11.2 with ranibizumab and 9.7 with bevacizumab, with aflibercept's advantage concentrated in eyes that started with worse vision. Protocol AC later showed that starting with bevacizumab and switching to aflibercept when needed gave two-year results statistically equivalent to aflibercept from the outset. For Indian practice, where cost decides whether a course is completed at all, that is a useful and under-quoted result.
Protocol I established that anti-VEGF with laser, as needed, beat laser alone for centre-involving oedema. Protocol V showed that for eyes with macular oedema but still-excellent vision of 20/25 or better, careful observation with prompt treatment if vision drops performs as well as treating immediately. Not every swollen macula needs an injection this week, and knowing which ones do is the whole skill.
How many injections are needed is the question every patient asks. The honest answer is that it depends on the eye, and that the number falls over time. At Claritas, the aim is deliberately to use as few injections as the disease requires, with that judgement made on OCT and OCT angiography at every follow-up visit rather than on a fixed calendar.
Treatment, Part Three: Laser, and Where it Still Belongs
Laser is older than the injections and is still irreplaceable. Pan-retinal photocoagulation (PRP) treats the ischaemic peripheral retina, reducing the drive for VEGF production and causing new vessels to regress.
The Diabetic Retinopathy Study, in 1,742 patients, established that photocoagulation reduced the risk of severe visual loss by at least half, and that the benefit was concentrated in eyes with high-risk characteristics. Eyes with severe NPDR or proliferative disease without high-risk features showed no clear benefit — which is why the HRC definition above still matters at the slit lamp.
For macular oedema, the Early Treatment Diabetic Retinopathy Study showed that focal laser roughly halved the risk of moderate visual loss in clinically significant macular oedema. Anti-VEGF injections have since largely displaced focal laser as first-line treatment for centre-involving oedema, but laser retains a role for persistent, well-defined extrafoveal leakage.
The choice between laser and injections for proliferative disease is now an informed one rather than an obvious one. DRCR Protocol S randomised eyes with proliferative disease to ranibizumab or PRP. At five years, vision was equally good in both arms, around 20/25, and severe visual loss was uncommon either way. The injection arm had less visual field loss, less macular oedema (22% against 38%) and fewer vitrectomies (15% against 22%), but required a mean of 19.2 injections over five years against 5.4 in the laser arm.
That trade-off is the crux of real practice. Injections preserve more peripheral field but demand that the patient keeps coming back, for years. Laser is largely done once. For a patient who travels from another city, or who cannot reliably attend every two months, laser is often the safer choice precisely because it does not depend on attendance. Protocol S itself had substantial loss to follow-up, and its authors concluded that patient circumstances should guide the decision. Any surgeon who tells you one is simply better than the other has not read the five-year data.
Treatment, Part Four: Vitrectomy Surgery
Surgery is for two situations. A vitreous haemorrhage that does not clear, and a tractional retinal detachment. In both, the operation is a vitrectomy: the blood-filled gel is removed, the fibrous membranes pulling on the retina are dissected away, laser is applied, and the retina is flattened.
Timing matters. DRCR Protocol AB randomised 205 patients with vitreous haemorrhage from proliferative disease to initial aflibercept or to immediate vitrectomy with PRP. At two years, average vision was essentially the same in both arms, and both approaches were judged viable first-line options. But a third of the injection-first group needed vitrectomy anyway during follow-up, and tractional detachment was found in 13% of those eyes before the haemorrhage cleared. Starting with injections is reasonable; drifting with injections while traction develops is not.
There is more on this on our vitrectomy surgery page, and more on the injection procedure itself on our intravitreal injections page.
What is changing: Four developments worth knowing
Newer anti-VEGF agents, and longer intervals: Faricimab blocks two pathways rather than one — VEGF-A and angiopoietin-2, which destabilises vessels and promotes leakage. In the phase 3 YOSEMITE and RHINE trials, 62% of patients in the treat-and-extend arm were on 16-weekly dosing by week 96, with a median of 11 injections over two years and mean gains of around 10.6 letters. Aflibercept 8 mg received an extended FDA label in April 2026 allowing intervals of up to 20 weeks in macular oedema after the first year, on the strength of the PHOTON trial, in which 44% of patients completing 96 weeks were on intervals of 20 weeks or more. The direction of travel is unambiguous: equal control, fewer visits.
Port delivery systems: In February 2025 the US FDA approved Susvimo for diabetic macular oedema: a refillable reservoir implanted into the eye in a single outpatient procedure, which releases ranibizumab continuously and is refilled in the clinic. In the phase 3 Pagoda trial of 634 patients, a refill every six months gave 9.6 letters of improvement against 9.4 letters with monthly injections. For a working adult in Delhi making a 90-minute journey for every injection, two clinic visits a year instead of eight is not a marginal improvement. It is a different disease to live with. It is not yet available in India, and it carries its own surgical and endophthalmitis considerations, but it is the clearest signal of where treatment burden is heading.
Minimally invasive vitreoretinal surgery (MIVS): Diabetic vitrectomy is now routinely performed through 25-gauge and 27-gauge instruments — incisions well under a millimetre, which mostly seal themselves without sutures. In a randomised comparison in proliferative diabetic retinopathy, 27-gauge beveled-tip instrumentation produced less intraoperative bleeding, needed less electrocautery, removed membranes more efficiently and required suturing less often than 25-gauge, with equivalent visual recovery. The gain is not better final vision; it is a quieter eye, a faster return to normal life and less post-operative discomfort, in a group of patients who often need surgery in both eyes.
Continuous glucose monitoring (CGM): This is the development most likely to matter at population scale, and it is not an eye treatment at all. HbA1c is an average, and averages conceal swings. CGM measures glucose continuously and reports time in range. In 3,262 patients with type 2 diabetes, the prevalence of vision-threatening retinopathy fell from 9.7% in the lowest quartile of time in range to 3.5% in the highest, independent of HbA1c. More striking, a 2025 study of matched cohorts in non-proliferative retinopathy found that patients who started CGM had substantially lower two-year risks: proliferative disease 30% lower, macular oedema 20% lower, vitreous haemorrhage 48% lower, tractional detachment 61% lower, and need for vitrectomy 62% lower. These are observational data with the usual caveats, but the direction and the size of the effect are hard to ignore. A sensor on the arm appears to protect the retina more than most things we can offer once damage has started.
See a retina specialist urgently if you have diabetes and notice
New floaters, cobwebs or a shower of black spots
A sudden smoky haze or curtain across the vision
Straight lines appearing bent or wavy
A blurred or missing patch in the centre of your vision
A drop in reading vision in one eye
Any sudden change in an eye already known to have diabetic retinopathy
Need a Retinal Examination in Delhi?
If you have diabetes, regular retinal examinations are important even when your vision seems normal. For an assessment of diabetic retinopathy, retinal imaging or treatment options, you can contact Claritas Eye & Retina Institute and Book an Appointment with Dr. Mayank Bansal, a retina specialist in Delhi.
Frequently Asked Questions
I have diabetes but my vision is fine. Do I still need a retina check?
Yes, and this is the single most important sentence on this page. Mild and moderate retinopathy are usually symptomless, and severe non-proliferative retinopathy — the stage immediately before new vessels form — very often is too. Nearly 90% of Indians with known diabetes have never had a retinal examination, and that is the reason diabetic retinopathy still causes avoidable blindness here. Normal vision tells you nothing about the state of your retina.
How often should my retina be examined?
If you have type 2 diabetes, from the time of diagnosis. If you have type 1, five years after onset. After that, following the American Academy of Ophthalmology's recommendations: every 12 months with no retinopathy or mild changes, every 6 to 12 months with moderate changes, every 3 to 4 months with severe non-proliferative or early proliferative disease, and every 2 to 4 months with high-risk proliferative disease. Intervals shorten if the macula is swollen. If you are pregnant, you need examination soon after conception and then every 1 to 3 months depending on severity, because pregnancy can accelerate retinopathy.
Can diabetic retinopathy be cured or reversed?
Partly, and the distinction matters. Macular swelling can be dried out and vision regained, often substantially. New vessels can be made to regress. What cannot be restored is retinal tissue that has already died from lack of blood supply, or vision lost to long-standing scarring. So treatment reliably protects what you still have and often recovers some of what you have recently lost. It cannot undo years of damage, which is the entire argument for coming early.
Will I go blind?
For the large majority of patients who are examined in time and treated, no. Retinopathy in long-standing diabetes is close to universal; blindness from it is not. In DRCR Protocol S, after five years of treatment with either laser or injections, average vision was around 20/25 and severe visual loss was uncommon in both arms. The patients who lose vision are overwhelmingly those who present late or who stop attending.
Why can't I just use eye drops instead of an injection?
Because a drop cannot reach the retina. Eye drops penetrate the front of the eye well, but very little of the drug travels the full depth to the retina at the back. The retina has to be reached either through the bloodstream, which requires doses with systemic effects, or directly, by placing a small volume of drug into the vitreous cavity. That is what the injection does, and it is why it works where drops do not.
Does the injection hurt? Is it safe?
The eye is numbed with anaesthetic drops and the surface is cleaned with antiseptic. Most patients describe pressure rather than pain, and the injection itself takes seconds. Mild grittiness or a red spot at the injection site for a day or two is common. The serious risk is infection inside the eye, which is rare but is the reason the procedure is done under sterile conditions and the reason you are told to report pain, redness or falling vision in the days afterwards rather than waiting for your next appointment.
How many injections will I need?
It depends on the eye, and the number generally falls over time. Some eyes need a short course and stay dry. Others need ongoing treatment, and in those the newer longer-acting agents can often stretch intervals to three or four months. At Claritas the explicit aim is the fewest injections the disease requires, decided on OCT and OCT angiography at each visit rather than by a fixed schedule.
Is laser still used, or have injections replaced it?
Both are in active use and the choice is a real clinical decision. For proliferative disease, five-year data from DRCR Protocol S found equally good vision with laser or with injections. Injections preserved more peripheral visual field and caused less macular oedema, but required a mean of 19 injections over five years against 5 laser-related treatments. Laser is largely done once and does not depend on the patient returning every two months. For someone who travels a long distance or cannot attend reliably, that makes laser the safer option, not the inferior one.
Does controlling my sugar still help once retinopathy has started?
Very much. In the Wisconsin study, each 1% rise in HbA1c over four years carried an 18% higher risk of progressing to proliferative disease. And the DCCT showed that the benefit of a period of good control persists for at least a decade after it ends. One caution: if your sugars are very high, bring them down steadily rather than crashing them, and have your retina examined before starting an intensive regimen, including the newer weight-loss and GLP-1 based injections. Rapid correction can transiently worsen retinopathy before it improves.
Should I use a continuous glucose monitor?
It is worth discussing with your physician, and there is now eye-specific evidence behind the question. Time in range is associated with retinopathy severity independently of HbA1c, and patients with non-proliferative retinopathy who began CGM had markedly lower two-year rates of proliferative disease, vitreous haemorrhage, tractional detachment and vitrectomy. It is not a treatment for retinopathy, but it appears to be one of the more effective ways to slow it.
I see floaters and black spots. Is that serious?
In a person with diabetes, treat it as urgent. It often means a new vessel has bled. The bleeding may clear partially on its own, which is what tempts people to wait, and waiting is how eyes are lost to tractional detachment. Have the retina examined within days.
What does diabetic retinopathy treatment cost in Delhi?
It depends on what the eye needs: the number of injections, which drug is used, whether laser or surgery is involved. Drug costs have fallen substantially — an indigenously developed aflibercept biosimilar launched in February 2026 and the originator reduced its price by about 44% in April 2026 — and bevacizumab remains a legitimate and far cheaper first-line option with two-year outcomes equivalent to aflibercept in DRCR Protocol AC. We give a written estimate before starting treatment, and we will tell you plainly where a cheaper option performs as well.
Do I need a diabetic retinopathy specialist, or will any eye doctor do?
Screening can be done by any ophthalmologist or through validated retinal photography, and should be. Once there is macular oedema, proliferative disease, a vitreous haemorrhage or any question of traction, the eye should be seen by a vitreoretinal specialist with OCT and OCT angiography on site, because the decisions from that point involve injections, laser, surgery and timing between them.
About the author
Dr Mayank Bansal is a vitreoretinal surgeon and Director of Claritas Eye & Retina Institute, New Delhi, and Senior Consultant in Vitreo-Retinal Surgery at Fortis Memorial Research Institute. He trained at AIIMS, holds FRCS (Glasgow) and FACS (USA), and completed a fellowship at UCLA's Stein Eye Institute. He has performed over 20,000 retina and cataract surgeries, and is a PhD scholar at CSIR-Institute of Genomics and Integrative Biology.
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