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Q2 LONG ANSWER 10M ★ High-yield

Describe diabetic retinopathy with its classification and management.

Ophthalmology · 3rd Professional

Epidemiology and Pathogenesis

  • Diabetic retinopathy is the leading cause of blindness in the working-age population, and is of enormous and growing importance in India.
  • The single strongest risk factor is duration of diabetes — after 20 years, nearly all type 1 and the majority of type 2 patients have some retinopathy
  • Modifiable risk factors — glycaemic control, established by the DCCT in type 1 and the UKPDS in type 2, both of which showed that tight control substantially reduces the development and progression of retinopathy; hypertension, which the UKPDS showed is at least as important; dyslipidaemia, which drives hard exudate formation; smoking; and anaemia

Clinical Lesions

LesionNature and significance
Microaneurysm
  • Outpouching of a capillary wall at a site of pericyte loss; the earliest clinically visible lesion.
  • A small red dot, distinguished from a dot haemorrhage only on angiography, where it fills and leaks
Dot and blot haemorrhagesIn the deeper (inner nuclear and outer plexiform) layers, where the compact tissue keeps them round
Flame-shaped haemorrhagesIn the nerve fibre layer, where they spread along the axon bundles
Hard exudates
  • Yellow, waxy, sharply defined deposits of lipid and lipoprotein in the outer plexiform layer, precipitating at the edge of an area of leakage — hence the circinate ring around a leaking group of microaneurysms.
  • Indicate chronic oedema, and are associated with dyslipidaemia
Cotton-wool spotsFluffy white lesions with indistinct margins; they are infarcts of the nerve fibre layer with stasis of axoplasmic flow. Indicate ischaemia
Venous beading and loopsIrregular sausage-like dilatation of the veins; a reliable and important sign of severe ischaemia
IRMA
  • Intraretinal microvascular abnormalities — dilated, tortuous, shunt-like vessels within the retina bridging areas of non-perfusion.
  • They differ from new vessels in being INTRAretinal, not crossing the internal limiting membrane, and not leaking on angiography.
  • A marker of severe ischaemia and of impending proliferation
NeovascularisationNew vessels on the disc (NVD) or elsewhere (NVE), growing forward onto the posterior hyaloid; fragile, leak profusely on angiography, and bleed. They define proliferative disease

Classification

  • The international clinical classification, derived from the ETDRS:
  • NO apparent retinopathy — no abnormalities
  • Mild non-proliferative (NPDR) — microaneurysms only

Management and Screening

  • Systemic control IS the foundation, and comes before any ocular treatment: glycaemic control, blood pressure control, lipid control (fenofibrate has been shown to reduce progression), smoking cessation and management of nephropathy and anaemia
  • Anti-VEGF injection — ranibizumab, aflibercept, bevacizumab or faricimab — is first-line for centre-involving macular oedema, and has transformed outcomes. It is also increasingly used for proliferative disease, though it requires sustained follow-up and a patient lost to follow-up after anti-VEGF alone may do worse than one given laser
  • Focal and grid laser for non-centre-involving oedema and for leaking microaneurysms; it stabilises rather than improves vision
  • Panretinal photocoagulation (PRP) — the standard treatment for proliferative disease. It destroys ischaemic peripheral retina, removing the source of VEGF. It preserves central vision at the cost of peripheral field and night vision, which must be explained. Considered earlier in severe NPDR where follow-up is uncertain, in the only eye, before cataract surgery, and in pregnancy
  • Intravitreal steroid (dexamethasone or fluocinolone implant) for oedema refractory to anti-VEGF, particularly in pseudophakic eyes — noting the risk of cataract and raised pressure
  • Vitrectomy for non-clearing vitreous haemorrhage, tractional retinal detachment involving the macula, and combined tractional-rhegmatogenous detachment
  • Screening schedule — type 1: from 5 years after diagnosis or from puberty; type 2: AT diagnosis, because the disease has often been present for years unrecognised; then annually, or more often with worse grades; and in pregnancy, at booking and each trimester
  • Screening is where the greatest benefit lies in India, since retinopathy is asymptomatic until the macula or the vitreous is involved, and treatment at that late stage preserves far less
  • Microaneurysms are the earliest visible lesion, and fill and leak on angiography whereas dot haemorrhages block

All questions in The Retina and Vitreous

  1. Q1Describe the anatomy and physiology of the retina and the vitreous. ★
  2. Q2Describe diabetic retinopathy with its classification and management. ★
  3. Q3Describe the retinal vascular occlusions with their management. ★
  4. Q4Describe retinal detachment with its types, features and management. ★
  5. Q5Describe age-related macular degeneration with its management. ★
  6. SN1Describe retinitis pigmentosa with its features and associations. ★
  7. SN2Describe retinopathy of prematurity with its screening and treatment. ★
  8. SN3Describe hypertensive retinopathy and the other systemic retinopathies. ★
  9. SN4Describe posterior vitreous detachment, vitreous haemorrhage and vitreous opacities. ★
  10. SN5Describe retinoblastoma with its genetics, presentation and management. ★
  11. SN6Describe central serous chorioretinopathy and macular hole. ★
  12. SN7Describe the investigations used in retinal disease.

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