Diabetes and the Eye

Diabetes mellitus affects almost every ocular structure. It is the leading cause of blindness in working age adults in many countries. About one third of people with diabetes have retinopathy and about 7 to 10 percent have sight threatening disease.

• Ocular manifestations:
  • Retina: nonproliferative and proliferative retinopathy, macular oedema, macular ischaemia, vitreous haemorrhage, tractional retinal detachment.
  • Lens: early cataract (cortical, posterior subcapsular), fluctuating refraction with glucose swings (hyperglycaemia causes myopic shift by lens swelling, rapid correction causes hypermetropic shift).
  • Glaucoma: neovascular glaucoma from retinal ischaemia, and an increased risk of primary open angle glaucoma.
  • Cornea and surface: dry eye, reduced corneal sensation, neurotrophic keratopathy, recurrent erosions, delayed healing, and infection risk.
  • Neuro ophthalmic: ischaemic third, fourth and sixth cranial nerve palsies (pupil sparing third nerve palsy), diabetic papillopathy, anterior ischaemic optic neuropathy, and optic atrophy.
  • Other: orbital infection (mucormycosis in ketoacidosis), recurrent styes, and iris rubeosis.
• Risk of retinopathy rises with disease duration (almost all type 1 and about 60 percent of type 2 after 20 years), HbA1c, hypertension, dyslipidaemia, pregnancy, nephropathy, and smoking.

• Early retinopathy is asymptomatic. Visual symptoms appear with macular oedema (blurred central vision, distortion), vitreous haemorrhage (floaters, sudden loss), or tractional detachment.
• Retinal signs by stage: microaneurysms and dot blot haemorrhages, hard exudates, cotton wool spots, venous beading, loops and intraretinal microvascular abnormalities (severe nonproliferative disease), new vessels on the disc or elsewhere (proliferative disease), preretinal and vitreous haemorrhage, fibrovascular proliferation, and rubeosis iridis with neovascular glaucoma.
• Macular oedema: retinal thickening and exudates within one disc diameter of the fovea.
• Cranial nerve palsy: sudden diplopia with periorbital pain, normal pupil in third nerve palsy, recovery in 3 to 6 months.

• Screening: type 2 diabetes at diagnosis, then every 1 to 2 years if no retinopathy (annually if risk factors); type 1 diabetes from 5 years after diagnosis (or from age 12 years), then annually; pregnancy planning, in the first trimester, and each trimester or more often if retinopathy is present; more frequent for progressive disease.
• Visual acuity, intraocular pressure, slit lamp (including iris for rubeosis and gonioscopy if suspected), dilated fundus examination, and retinal photography (two field or seven field), with grading by severity.
• Optical coherence tomography for macular thickness and fluid; widefield fluorescein angiography for ischaemia and leakage; optical coherence tomography angiography for macular perfusion; B-scan if vitreous haemorrhage obscures the view.
• Systemic assessment: HbA1c, blood pressure, lipids, renal function and urine albumin creatinine ratio, and evaluation for neuropathy.

• Systemic control reduces onset and progression: HbA1c target around 7 percent (53 mmol/mol) for most adults, individualised; blood pressure below 130/80 mmHg (ACE inhibitor or angiotensin receptor blocker as first line, e.g. ramipril 2.5 to 10 mg daily or losartan 50 to 100 mg daily); statin therapy; smoking cessation; fenofibrate 145 mg daily slows progression of retinopathy in type 2 diabetes. Avoid very rapid lowering of HbA1c in advanced retinopathy (rapid improvement can transiently worsen retinopathy) and review retinopathy before starting intensive therapy or semaglutide type agents.
• Nonproliferative retinopathy: observation, optimising systemic factors, and follow up every 3 to 12 months by severity.
• Centre involving diabetic macular oedema with reduced vision: intravitreal anti-VEGF (aflibercept 2 mg or ranibizumab 0.5 mg monthly for 5 doses then every 8 weeks, or bevacizumab 1.25 mg, or faricimab 6 mg), with deferral of laser; intravitreal steroid (dexamethasone implant 0.7 mg every 4 to 6 months, fluocinolone implant 0.19 mg) for pseudophakic or non-responding eyes (monitor pressure and cataract); focal or grid laser for non-central oedema.
• Proliferative retinopathy: panretinal photocoagulation (1200 to 2000 burns in 2 to 3 sessions, 500 micrometre spot, 0.1 seconds) or intravitreal anti-VEGF (aflibercept 2 mg monthly for 3 to 5 doses then as needed), with regular monitoring; vitrectomy for non-clearing vitreous haemorrhage, tractional detachment, or fibrovascular proliferation.
• Neovascular glaucoma: anti-VEGF, panretinal photocoagulation, pressure lowering medication, and drainage device or cyclophotocoagulation.
• Cataract surgery: control macular oedema first, give perioperative anti-VEGF or steroid in eyes with oedema or active proliferative disease, and monitor for progression.
• Dry eye and neurotrophic keratopathy: preservative free lubricants, autologous serum 20 percent, bandage lens; cranial nerve palsies: patching, prisms, and observation.
• Rehabilitation, certification, and education about adherence to screening and systemic control.