Relation of diabetes and retina
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diabetic retinopathy fundus findings microaneurysms neovascularization
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Diabetes and the Retina — Diabetic Retinopathy
Overview
Diabetic retinopathy (DR) is the commonest cause of new blindness in industrialized countries among working-age adults. It is a microvascular complication of diabetes that ultimately affects more than 50% of people with long-standing disease, though with effective screening and modern treatment the risk of severe visual loss can be reduced to less than 5%.
— Kanski's Clinical Ophthalmology, p. 506
Ophthalmic Complications of Diabetes
| Frequency | Complication |
|---|---|
| Common | Maculopathy (DME, macular ischaemia), Retinopathy (ischaemia → neovascularization, vitreous haemorrhage), Unstable refraction |
| Uncommon | Recurrent styes, Xanthelasma, Accelerated cataract |
| Serious | Tractional retinal detachment, Neovascular glaucoma, Ocular motor nerve palsies |
| Rare | Diabetic papillopathy, acute-onset cataract, rhino-orbital mucormycosis |
Pathogenesis
DR is predominantly a microangiopathy. Chronic hyperglycaemia causes direct damage to retinal small vessels through several mechanisms:
- Pericyte loss — the supporting cells of retinal capillaries are selectively destroyed
- Basement membrane thickening
- Altered retinal blood flow
- Capillary leakage — damaged vessels leak protein, red blood cells, and lipids → retinal oedema
- Capillary occlusion → retinal hypoxia → upregulation of VEGF (Vascular Endothelial Growth Factor)
- Neovascularization — VEGF drives growth of new, fragile, abnormal vessels prone to rupture
— Goldman-Cecil Medicine, p. 1556; Kanski's Clinical Ophthalmology, p. 522
Risk Factors
| Factor | Notes |
|---|---|
| Duration of diabetes | Most important predictor; DR rarely appears within 5 years or before puberty |
| Poor glycaemic control (HbA1c ↑) | DCCT and UKPDS confirm tight control prevents/delays DR |
| Hypertension | Must be controlled <140/80 mmHg; particularly important in T2DM maculopathy |
| Nephropathy | Severe nephropathy worsens DR; renal transplantation may improve it |
| Pregnancy | Can accelerate progression, especially if pre-existing DR or pre-eclampsia |
| Hyperlipidaemia | Fenofibrate may slow progression |
| Type 1 > Type 2 | Prevalence in T2DM is 67% at 10 years; 10% develop proliferative disease |
| Drugs | Pioglitazone → worsening DME; GLP-1 agonists with rapid glycaemic improvement may worsen DR |
Note: A sudden improvement in glycaemic control paradoxically can cause transient worsening of DR.
— Kanski's Clinical Ophthalmology, p. 507; Harrison's Principles of Internal Medicine 22E, p. 3267
Classification
ETDRS / International Classification
| Stage | Clinical Features | Follow-up |
|---|---|---|
| No DR | Normal | 12 months |
| Mild NPDR | Microaneurysms only | 12 months |
| Moderate NPDR | Microaneurysms, blot haemorrhages, hard exudates, cotton-wool spots, venous beading | 6 months |
| Severe NPDR ("4-2-1 rule") | >20 intraretinal haemorrhages in all 4 quadrants, or venous beading in ≥2 quadrants, or IRMA in ≥1 quadrant | Refer promptly |
| PDR | NVD, NVE, and/or vitreous/preretinal haemorrhage | Urgent treatment |
| DME | Retinal thickening ± hard exudates at/near fovea | Can occur at any stage |
Descriptive clinical categories (Kanski):
- Background DR (BDR): Microaneurysms, dot/blot haemorrhages, hard exudates — the earliest signs
- Preproliferative DR (PPDR): Cotton-wool spots, venous beading, IRMA — signify progressive retinal ischaemia
- Proliferative DR (PDR): NVD (≤1 disc diameter of disc) ± NVE; High-risk PDR = vitreous haemorrhage + neovascularization ≥1/3 disc area
- Advanced diabetic eye disease: Tractional retinal detachment, persistent vitreous haemorrhage, neovascular glaucoma
— Goldman-Cecil Medicine, Table 210-13; Kanski's Clinical Ophthalmology, p. 522; Wills Eye Manual, p. 811
Retinal Signs (What You See on Fundoscopy)
| Sign | Significance |
|---|---|
| Microaneurysms | Earliest sign — focal outpouchings of weakened capillary walls |
| Dot & blot haemorrhages | Intraretinal bleeding from microaneurysms |
| Hard (waxy) exudates | Lipid/protein deposits from leaking capillaries |
| Cotton-wool spots | Nerve fibre layer infarcts → ischaemia marker |
| Venous beading | Irregular vein calibre — severe ischaemia |
| IRMA | Intraretinal microvascular abnormalities — dilated collateral vessels |
| Neovascularization (NVD/NVE) | New fragile vessels → bleed easily |
| Vitreous/preretinal haemorrhage | Rupture of new vessels |
| Tractional retinal detachment | Fibrovascular membranes contract |
| Neovascular glaucoma | Iris/angle neovascularization → IOP rise |
Fundus Images
NPDR — Moderate stage (microaneurysms, dot-blot haemorrhages, cotton-wool spots):
PDR — Proliferative stage (neovascularization of disc and elsewhere, preretinal haemorrhage):
NPDR vs PDR comparison diagram:
Workup
- Dilated fundus exam — 90D/60D lens at slit lamp; indirect ophthalmoscopy for peripheral retina
- Fluorescein angiography (IVFA) — perfusion abnormalities, foveal ischaemia, subclinical NVE
- OCT — macular thickness, detect DME
- OCT-Angiography (OCTA) — central macular ischaemia
- Systemic labs: HbA1c, fasting glucose, lipid panel, blood pressure
— Wills Eye Manual, p. 813
Treatment
Diabetic Macular Oedema (DME)
- Anti-VEGF agents (first-line for centre-involving DME): ranibizumab, aflibercept, bevacizumab (off-label)
- Intravitreal corticosteroids: dexamethasone implant, fluocinolone acetonide — for anti-VEGF non-responders; risk of cataract and elevated IOP
- Focal macular laser: for extrafoveal microaneurysms; adjunctive role
Proliferative DR (PDR)
- Panretinal photocoagulation (PRP) — indicated for high-risk characteristics (NVD > ¼ disc area, any NVD with haemorrhage, NVE > ½ disc area with haemorrhage, any NVI/NVA)
- Anti-VEGF therapy — alternative to PRP; preferred if DME coexists or if vitreous haemorrhage limits view
- Vitrectomy — for dense non-clearing VH, traction retinal detachment threatening macula, traction-rhegmatogenous detachment
Systemic Prevention
- Tight glycaemic control (HbA1c target); tight BP control (<140/80 mmHg)
- Fenofibrate to lower triglycerides
- Fenofibrate may reduce DR progression independent of lipid-lowering effect
— Harrison's, p. 3267; Wills Eye Manual, p. 813–814; Goldman-Cecil, p. 1556
Screening Guidelines
- Type 1 DM: Screen at 5 years after diagnosis, then annually
- Type 2 DM: Screen at diagnosis (hyperglycaemia often pre-dates clinical recognition), then annually
- Requires dilated eye exam by ophthalmologist/optometrist or retinal photography with remote grading — routine non-dilated exams are inadequate
- Pregnant women with DM: screen before and during pregnancy; DME in late pregnancy often resolves spontaneously
Key Clinical Pearls
- DR is largely asymptomatic even in severe PDR — screening is essential
- Duration of diabetes is the single most important risk factor
- In T1DM, presence of CKD without retinopathy should prompt investigation for alternative kidney disease causes
- Aspirin does NOT influence the natural history of DR and can be continued in patients on anti-VEGF therapy
- The risk of severe visual loss can be reduced to <5% with proper screening and treatment
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