Stage	Key Features	Investigations	Management
1️⃣ Background DR 👓	Microaneurysms (earliest sign) Dot/blot haemorrhages Hard exudates (lipid leakage)	Digital fundus photography; slit-lamp biomicroscopy	Optimise HbA1c, BP, lipids Annual NHS screening
2️⃣ Non-Proliferative DR 🔬	Cotton wool spots (nerve fibre infarcts) Venous beading IRMA (intraretinal microvascular abnormalities)	Fundoscopy ± fluorescein angiography; OCT for macular oedema	Intensify systemic control Anti-VEGF or focal/grid laser for DME Review every 3–6 months
3️⃣ Proliferative DR 🚨	Neovascularisation (disc or elsewhere) Pre-retinal or vitreous haemorrhage Fibrovascular tissue → tractional detachment	Fundoscopy, OCT, fluorescein angiography	Pan-retinal photocoagulation (PRP) Intravitreal anti-VEGF Vitrectomy if non-clearing haemorrhage
4️⃣ Macular Oedema 🎯	Macular thickening Blurred or distorted central vision	OCT (gold standard); fluorescein angiography	Anti-VEGF (first-line) Steroid injections if refractory Focal/grid laser in selected cases
5️⃣ Advanced Disease ⚡	Tractional retinal detachment Recurrent vitreous haemorrhage Neovascular glaucoma	OCT, fundus photography, fluorescein angiography	Vitrectomy ± anti-VEGF Glaucoma management Lifelong ophthalmology follow-up

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👁️ Diabetic retinopathy (DR) is the leading cause of blindness in working-age adults in the UK. It reflects chronic hyperglycaemia-driven damage to the retinal microvasculature and is often asymptomatic until advanced stages. The NHS Diabetic Eye Screening Programme (DESP) offers annual retinal photography to all people with diabetes aged ≥12 years to enable early detection and prevention of sight loss.

🔬 Pathophysiology (Think: Leak → Ischaemia → New Vessels)

Chronic hyperglycaemia → polyol (sorbitol) pathway activation, oxidative stress.
Pericyte loss + basement membrane thickening → microaneurysms.
Capillary leakage → haemorrhages, hard exudates, macular oedema.
Capillary closure → retinal ischaemia → ↑ VEGF.
VEGF-driven neovascularisation → fragile vessels, haemorrhage, fibrosis, detachment.

🧠 Stage-by-Stage Clinical Reasoning

1️⃣ Background (Mild Non-Proliferative)

Key idea: Early microvascular damage, usually asymptomatic.
Action: Optimise metabolic control; reinforce screening adherence.

2️⃣ Moderate–Severe Non-Proliferative

Key idea: Increasing ischaemia predicts progression.
Action: Shorter follow-up intervals; treat macular oedema if present.

3️⃣ Proliferative DR

Key idea: Sight-threatening stage due to neovascularisation.
Action: PRP to reduce VEGF drive ± anti-VEGF; surgery if complications.

4️⃣ Diabetic Macular Oedema (DME)

Key idea: Main cause of visual loss at any stage.
Action: Anti-VEGF first-line; OCT guides response.

5️⃣ Advanced Diabetic Eye Disease

Key idea: Structural damage and secondary glaucoma.
Action: Surgical and palliative strategies; vision preservation focus.

🚨 Red Flags (Urgent Ophthalmology)

Sudden painless vision loss (vitreous haemorrhage).
Painful red eye with raised IOP (neovascular glaucoma).
Rapid progression (pregnancy, type 1 diabetes, very poor control).

📝 Exam & Teaching Pearls

Earliest lesion: Microaneurysms.
Most common cause of vision loss: Diabetic macular oedema.
Most urgent stage: Proliferative DR.
Prevention works: Tight glycaemic, BP, and lipid control reduces progression by >30%.
UK context: DESP detects disease before symptoms—attendance matters.

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Diabetic Eye Disease

📊 Stages of Diabetic Retinopathy – At a Glance