Diabetic macular oedema

Overview

Diabetic macular oedema (DMO) is the most important cause of visual loss in the working-age diabetic population in the UK. Fluid accumulates within the retinal layers at the macula and can occur at any stage of diabetic retinopathy.

Pathophysiology

•Chronic hyperglycaemia → pericyte loss + endothelial damage → VEGF upregulation → breakdown of inner blood-retinal barrier tight junctions → fluid leakage into retinal layers → macular oedema

•VEGF is the pivotal mediator - this is why anti-VEGF therapy is so effective

•DMO can coexist with any severity of diabetic retinopathy - not confined to proliferative disease

Presentation

•Blurred central vision - reduced visual acuity for fine detail and reading

•Metamorphopsia - distortion of straight lines; test with Amsler grid

•Asymptomatic - detected on routine diabetic eye screening before symptoms develop

•Fundoscopy: retinal thickening at macula, hard exudates (yellow lipid deposits) in circinate/plaque pattern, microaneurysms at fovea

⚠️

DMO can be present with good visual acuity (even 6/6) - do not be falsely reassured; OCT may still reveal clinically significant oedema warranting treatment.

Investigations

🏆 Gold standard

•optical coherence tomography (OCT) - quantifies central subfield thickness, identifies intraretinal/subretinal fluid, ellipsoid zone disruption, and epiretinal membrane; essential for diagnosis, treatment planning, and monitoring

🥇 First-line

•best corrected visual acuity (BCVA) - establishes baseline and determines treatment eligibility

•slit-lamp biomicroscopy with 78D/90D lens - stereoscopic assessment of retinal thickening and hard exudates

🥈 Second-line

•fluorescein angiography (FFA) - maps vascular leakage, identifies ischaemic maculopathy; important when ischaemia is suspected

•Systemic: HbA1c, blood pressure, lipid profile, eGFR/urine ACR - to identify and optimise modifiable risk factors

Management

•Systemic optimisation (all patients): optimise glycaemic control (HbA1c <53 mmol/mol in most adults with T2DM); BP target <130/80 mmHg (ACE inhibitors/ARBs preferred); statin for dyslipidaemia

•First-line (centre-involving DMO with visual impairment): ranibizumab 0.5 mg intravitreal injection (monthly loading then treat-and-extend/PRN) - NICE-approved anti-VEGF

•First-line alternative: aflibercept 2 mg intravitreal injection - NICE-approved; also binds PlGF; may be preferred where ranibizumab response is suboptimal

🥈 Second-line

•focal/grid macular laser photocoagulation - now used for non-centre-involving DMO or as adjunct to anti-VEGF; not suitable for fovea-threatening oedema

🥉 Third-line

•dexamethasone 0.7 mg intravitreal implant (Ozurdex) - NICE-approved; useful for inadequate anti-VEGF response or pseudophakic patients; avoid in phakic patients (cataract risk)

•fluocinolone acetonide 0.2 micrograms/day intravitreal implant (Iluvien) - long-acting up to 36 months; NICE-approved for chronic DMO insufficiently responsive to other therapies; risk of raised IOP and cataract

⚠️

Intravitreal steroid implants in phakic patients carry significant risk of cataract formation and raised intraocular pressure - must be discussed in informed consent and IOP monitored after implantation.

Complications

•Permanent central visual loss - photoreceptor death from chronic oedema, especially if ellipsoid zone disrupted on OCT

•Subfoveal hard exudate plaque - lipid deposition causes irreversible photoreceptor damage even after oedema resolves

•Macular ischaemia - capillary dropout in foveal avascular zone; not treatable with anti-VEGF; limits visual recovery

•Endophthalmitis - rare but serious complication of intravitreal injection (~0.03% per injection)

Prognosis

•Anti-VEGF therapy achieves average visual acuity gains of ~8-10 ETDRS letters; significant proportion gain ≥15 letters (three lines)

•Poor prognostic markers: ellipsoid zone disruption on OCT, extensive foveal avascular zone enlargement, subfoveal hard exudates, longstanding oedema before treatment