Diabetic Retinopathy
Diabetic retinopathy is the leading cause of blindness in working-age adults in the UK, classified as non-proliferative or proliferative, with the NHS Diabetic Eye Screening Programme enabling early detection and treatment.
Key Facts
Diabetic retinopathy is the leading cause of blindness in working-age adults in the UK Affects approximately 40% of people with type 1 diabetes and 20-30% with type 2 after 20 years NHS Diabetic Eye Screening Programme (DESP): annual digital retinal photography for all people with diabetes aged ≥12 Classification: background (R1), pre-proliferative (R2), proliferative (R3) ± maculopathy (M1) Background (R1): microaneurysms, dot/blot haemorrhages, hard exudates Pre-proliferative (R2): cotton wool spots, venous beading, IRMA (intraretinal microvascular abnormalities) Proliferative (R3): new vessel formation (disc NVD, elsewhere NVE); risk of vitreous haemorrhage and tractional retinal detachment Treatment: tight glycaemic control (HbA1c <53mmol/mol), BP control (<140/80), pan-retinal photocoagulation (PRP) for proliferative; anti-VEGF/laser for maculopathy
Overview
Key Facts
Diabetic retinopathy is a microvascular complication of diabetes. Prevention through glycaemic and blood pressure control, early detection through screening, and timely treatment are the pillars of management.
Epidemiology
- ~4.9 million people with diabetes in the UK; ~1.4 million have some retinopathy
- Leading cause of blindness in 16-64 year olds
- Risk factors: duration of diabetes (most important), poor glycaemic control, hypertension, dyslipidaemia, pregnancy, nephropathy
Aetiology
- Chronic hyperglycaemia → microvascular damage to retinal capillaries
- Duration of diabetes is the strongest risk factor
- HbA1c is the most important modifiable factor (DCCT/UKPDS trials)
Pathophysiology
- Hyperglycaemia → polyol pathway activation, AGE formation, PKC activation → pericyte loss → endothelial dysfunction → capillary closure → retinal ischaemia
- Ischaemia → VEGF production → neovascularisation (proliferative)
- Increased capillary permeability → macular oedema (fluid and lipid leakage)
- New vessels are fragile → vitreous haemorrhage; fibrosis → tractional retinal detachment
Clinical Presentation
Background Retinopathy (R1)
- Usually asymptomatic
- Microaneurysms (earliest sign; red dots)
- Dot and blot haemorrhages
- Hard exudates (lipid deposits — yellow waxy deposits)
Pre-proliferative (R2)
- Cotton wool spots (retinal nerve fibre layer infarcts)
- Venous beading and looping
- IRMA (intraretinal microvascular abnormalities)
- Deep dark blot haemorrhages
- Indicates worsening ischaemia
Proliferative (R3)
- New vessels on disc (NVD) or elsewhere (NVE)
- Pre-retinal or vitreous haemorrhage (sudden visual loss)
- Tractional retinal detachment (if fibrovascular proliferation)
- Rubeosis iridis (new vessels on iris) → neovascular glaucoma
Diabetic Maculopathy (M1)
- Reduced central visual acuity
- Hard exudates within 1 disc diameter of fovea
- Clinically significant macular oedema (CSMO)
Red Flags
- Sudden visual loss (vitreous haemorrhage, retinal detachment)
- New vessels on examination
- Rubeosis (new iris vessels — neovascular glaucoma imminent)
- Macular involvement (central visual threat)
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Hypertensive retinopathy | Silver wiring, AV nipping, flame haemorrhages | BP measurement, fundoscopy |
| Retinal vein occlusion | Sector haemorrhages, cotton wool spots | Fundoscopy, OCT, FFA |
| Radiation retinopathy | Post-radiation, similar to DR | History, fundoscopy |
| Sickle cell retinopathy | Sickle cell disease, "sea fan" neovascularisation | Hb electrophoresis |
Diagnosis / Investigation
Bedside
- Visual acuity (Snellen)
- Dilated fundoscopy (slit lamp biomicroscopy)
- NHS DESP screening photograph
Bloods
- HbA1c (glycaemic control)
- BP measurement (target <140/80)
- Lipid profile
- U&Es (nephropathy associated with worse retinopathy)
Imaging
- OCT: gold standard for macular oedema assessment (fluid, thickness)
- Fundus fluorescein angiography (FFA): identifies ischaemia, leakage, neovascularisation
- Wide-field retinal imaging: captures peripheral retina
Special Tests
- Grading of retinopathy (NSC classification: R0-R3, M0-M1)
- 7-field stereo photography (research gold standard)
Management
Non-pharmacological
- Glycaemic control: HbA1c <53 mmol/mol (7%); DCCT: 76% reduction in retinopathy progression with intensive control
- Blood pressure control: target <140/80 (UKPDS: 34% reduction with tight BP control)
- Lipid management: statins as per cardiovascular risk
- Annual screening: NHS DESP; more frequent if higher-grade retinopathy
- Smoking cessation
Pharmacological
- Diabetic macular oedema (centre-involving):
- Anti-VEGF intravitreal injections: aflibercept 2mg or ranibizumab 0.5mg (NICE TA274/TA346)
- Loading: 3-6 monthly injections then PRN/treat and extend
- Non-centre-involving macular oedema: macular laser photocoagulation
- Intravitreal steroid implant (dexamethasone — Ozurdex; fluocinolone — Iluvien): for persistent DMO, especially pseudophakic patients
Surgical/Interventional
- Pan-retinal photocoagulation (PRP): for proliferative retinopathy
- Burns peripheral retina → reduces ischaemic drive → regression of new vessels
- Side effects: reduced peripheral vision, reduced night vision
- Macular laser: focal/grid laser for non-centre-involving DMO
- Vitrectomy: for non-clearing vitreous haemorrhage, tractional retinal detachment involving macula, epiretinal membrane
Referral Criteria
- R1 (background): annual screening
- R2 (pre-proliferative): ophthalmology referral within 13 weeks
- R3 (proliferative): urgent ophthalmology referral within 2 weeks
- M1 (maculopathy): ophthalmology referral within 13 weeks
- Sudden visual loss: emergency ophthalmology referral
Prognosis
- Background retinopathy: not sight-threatening; requires monitoring and risk factor optimisation
- Proliferative retinopathy: sight-threatening without treatment; PRP prevents severe visual loss in >95% (DRS trial)
- Diabetic macular oedema: anti-VEGF improves visual acuity (DRCR.net Protocol T: aflibercept superior for worse baseline VA)
- Tight glycaemic control: DCCT showed 76% reduction in retinopathy development; UKPDS confirmed in type 2
- Screening: NHS DESP has significantly reduced diabetes-related blindness in the UK
Other Relevant Information
NHS Diabetic Eye Screening Classification
| Grade | Features | Action |
|---|---|---|
| R0 | No retinopathy | Annual screening |
| R1 | Background: microaneurysms, haemorrhages, exudates | Annual screening |
| R2 | Pre-proliferative: cotton wool spots, venous beading, IRMA | Ophthalmology <13 weeks |
| R3 | Proliferative: new vessels, vitreous haemorrhage | Ophthalmology <2 weeks |
| M1 | Maculopathy: exudates/haemorrhage near fovea | Ophthalmology <13 weeks |
Key Trials
| Trial | Finding |
|---|---|
| DCCT | Intensive glycaemic control reduces retinopathy by 76% (T1DM) |
| UKPDS | Tight glycaemic and BP control reduce retinopathy in T2DM |
| DRS | PRP reduces severe visual loss by >50% |
| DRCR.net Protocol T | Aflibercept best for DMO with baseline VA 20/50 or worse |