Diabetic retinopathy

What it is

Diabetic retinopathy is the leading cause of preventable blindness in working-age adults worldwide, affecting approximately 1 in 3 people with diabetes — and nearly all who have lived with diabetes for 20 or more years show some degree of retinal change. Also called diabetic eye disease, it is the most common serious microvascular complication of diabetes mellitus. It develops when chronically elevated blood glucose damages the tiny blood vessels supplying the retina, the thin layer of light-sensitive tissue at the back of the eye that converts visual signals to the brain.

In Canada, where more than 3.7 million people are living with diagnosed diabetes (Diabetes Canada, 2023), retinopathy screening rates remain below recommended targets in several provinces — making awareness of the condition and its silent early course especially important for Canadian patients.

The condition progresses through two broad stages:

Stage	Key features	Vision threat
Non-proliferative DR (NPDR) — mild to severe	Microaneurysms, haemorrhages, hard exudates, vessel leakage	Diabetic macular edema (DME) can develop at any NPDR stage
Proliferative DR (PDR)	Abnormal new vessel growth (neovascularization), vitreous haemorrhage, traction retinal detachment	High risk of severe or permanent vision loss

Diabetic macular edema (DME) — swelling of the central retina caused by fluid leakage — can occur at any stage and is the most common cause of vision loss in people with diabetes.

Causes and mechanism

Diabetic retinopathy develops from sustained hyperglycaemia damaging the retinal microvasculature through several overlapping processes:

1. Pericyte loss — pericytes wrap around retinal capillaries and maintain their structural integrity; high blood glucose causes them to die, weakening vessel walls.
2. Microaneurysm formation — weakened walls balloon into small pouches that leak or rupture.
3. Increased vascular permeability — damaged vessels allow fluid and lipids to seep into retinal tissue.
4. Ischemia — blocked or damaged vessels reduce oxygen delivery to the retina.
5. VEGF upregulation — oxygen-deprived retinal tissue releases excess vascular endothelial growth factor (VEGF), triggering growth of fragile, abnormal new vessels in the proliferative stage.

Key modifiable risk factors include poor glycaemic control (elevated HbA1c), high blood pressure, elevated cholesterol, and smoking. Non-modifiable factors include diabetes duration, diabetic kidney disease (which shares the same microvascular pathway), and pregnancy. Emerging research also suggests that the hormonal transition of menopause in women with type 2 diabetes may influence retinopathy development, though the mechanism is not yet fully characterized.

Symptoms and diagnosis

Diabetic retinopathy is a silent disease in its early stages. Significant retinal damage can accumulate before any vision change is noticed. Symptoms that may appear as the condition advances include:

• Floaters or dark strings drifting across the visual field (often from minor vitreous bleeding)
• Blurred or fluctuating vision
• Impaired colour perception
• Dark or empty patches in the visual field
• Sudden vision loss — a medical emergency indicating vitreous haemorrhage or retinal detachment

Diagnosis relies on:

• Dilated fundus examination — the ophthalmologist examines the retina after pupil dilation for microaneurysms, haemorrhages, exudates, and new vessels.
• Optical coherence tomography (OCT) — provides high-resolution cross-sectional retinal images, essential for detecting DME.
• Fluorescein angiography — maps vessel integrity and identifies leaking or non-perfused areas.
• Wide-field retinal photography — increasingly used for screening; available through many Canadian optometry practices and LifeLabs or Dynacare-affiliated imaging centres in some provinces.

Diabetes Canada recommends that people with type 1 diabetes have their first dilated eye exam within 5 years of diagnosis, and those with type 2 diabetes at the time of diagnosis — both followed by annual examinations thereafter.

Treatment options

Treatment is stage-dependent, and optimizing glycaemic control, blood pressure, and cholesterol remains the most important intervention at every stage.

For NPDR: Close monitoring with regular retinal examinations. The landmark DCCT trial showed that intensive blood glucose control in type 1 diabetes reduced the risk of developing retinopathy by 76% and slowed progression by 54%. The UKPDS demonstrated comparable benefits in type 2 diabetes.

For PDR and advanced disease:

• Pan-retinal photocoagulation (PRP) — laser applied to peripheral retinal tissue to reduce VEGF-driven neovascularization; substantially lowers the risk of severe vision loss.
• Anti-VEGF intravitreal injections (e.g., ranibizumab, bevacizumab, aflibercept) — used alongside or instead of laser for PDR; also first-line for DME. Coverage varies by province under public drug benefit programs; patients should confirm eligibility with their provincial formulary.
• Corticosteroid implants — for DME cases that do not respond to anti-VEGF therapy.
• Vitrectomy surgery — surgical removal of the vitreous gel when persistent haemorrhage or traction retinal detachment threatens central vision.

When to see a clinician in Canada

Anyone with diabetes should follow the Diabetes Canada screening schedule: type 1 — first exam within 5 years of diagnosis, then annually; type 2 — at diagnosis, then annually. Seek same-day or urgent ophthalmological assessment if you experience:

• A sudden increase in floaters or new flashing lights
• Sudden or rapidly worsening vision loss
• A dark curtain or shadow spreading across part of your visual field

These symptoms may signal vitreous haemorrhage or retinal detachment, both of which require urgent intervention to preserve sight. Referrals can be initiated through a family physician, endocrinologist, or optometrist. In provinces with telehealth access, platforms such as Maple or similar services can help triage urgency and facilitate rapid specialist referral.

Limitations and open questions

Research is still emerging on several fronts. The role of hormonal changes — particularly the estrogen decline of menopause — in modifying retinopathy risk in women with type 2 diabetes is an active area of investigation, and no clinical guidelines yet incorporate menopausal status into screening recommendations. The optimal sequencing of anti-VEGF therapy versus laser for PDR is not fully settled, and long-term comparative data on newer anti-VEGF agents remain limited. Health Canada has not issued specific guidance on AI-assisted retinal screening tools, though several are in use internationally and are being evaluated in Canadian pilot programs. Genetic susceptibility to retinopathy at a given level of glycaemic exposure is real but not yet actionable in routine clinical practice — no validated pharmacogenomic test currently guides individualized screening intervals.