OP9.2 | Diabetic Retinopathy — Summary & Reflection

KEY TAKEAWAYS

Diabetic retinopathy is a microvascular disease caused by hyperglycaemia-induced pericyte loss, basement membrane thickening, microaneurysm formation, and progressive vascular leakage and occlusion. It is classified into NPDR (non-proliferative: microaneurysms, dot-blot haemorrhages, hard exudates, cotton-wool spots, IRMA, venous beading — NO new vessels) and PDR (proliferative: neovascularisation on disc [NVD] or elsewhere [NVE], vitreous haemorrhage, tractional retinal detachment). CSME (clinically significant macular oedema) can occur at any stage and is the leading cause of visual loss. Severe NPDR meets the 4-2-1 rule and carries 50% PDR progression risk in 12 months. Management is staged: systemic control (HbA1c <7%, BP <130/80, statins/fenofibrate) for all stages; anti-VEGF injections and/or focal laser for CSME; pan-retinal photocoagulation (PRP) for PDR; vitrectomy for vitreous haemorrhage or tractional retinal detachment. Screening starts at T2DM diagnosis and 5 years after T1DM onset (or at diagnosis in adults), annually when no retinopathy, more frequently as disease progresses. The NPCBVI supports community screening via digital fundus photography in India.

REFLECT

Reflect on the following:
- Why do you think a disease that causes no symptoms in its most treatable stages is also a leading cause of blindness? What does this tell you about the role of proactive clinical screening versus symptom-driven medicine?
- A diabetic patient you see today is reluctant to have his eyes examined, saying 'I feel fine and my blood sugar has been okay lately.' How would you explain to him, in plain language without medical jargon, why you need to look at his eyes even when he sees normally?
- If you were designing a diabetic retinopathy screening clinic at a district hospital in rural India with limited specialist resources, what three key elements would you prioritise, and why?
- Consider the NPDR vs PDR distinction: why does it matter clinically whether haemorrhages come from microaneurysms vs new vessels? What is fundamentally different about the two types of lesions that justifies completely different management?