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Diabetes retinopathy

DIABETES RETINOPATHY BY DNYANESHWAR BHAGWAN POTFODE

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Diabetes retinopathy

  1. 1. Diabetes retinopathy DNYANESHWAR B. POTFODE OPHTHALMIC OFFICER
  2. 2. Normal structure • Retina- • The innermost tunic of the eyeball, is a thin, delicate and transparent membrane. It is the most highly-developed tissue of the eye. It appears purplish-red due to the visual purple of the rods and underlying vascular choroid.
  3. 3. Retina
  4. 4. Retina
  5. 5. Retina
  6. 6. Microscopic structure of the retina.
  7. 7. DIABETIC RETINOPATHY • Retinal changes seen in patients with diabetes mellitus. With increase in the life expectancy of diabetics, the incidence of diabetic retinopathy (DR) has increased.
  8. 8. Etiopathogenesis • 1. Duration of diabetes is the most important determining factor. Roughly 50 percent of patients develop DR after 10 years, 70 percent after 20 years and 90 percent after 30 years of onset of the disease. • 2. Sex. Incidence is more in females than males (4:3). • 3. Poor metabolic control is less important than duration, but is nevertheless relevant to the development and progression of DR. • 4. Heredity. It is transmitted as a recessive trait without sex linkage. • 5. Pregnancy may accelerate the changes of diabetic retinopathy. • 6. Hypertension, when associated, may also accentuate the changes of diabetic retinopathy. • 7. Other risk factors include smoking, obesity .
  9. 9. Pathogenesis of diabetic retinopathy.
  10. 10. Classification I. Non-proliferative diabetic retinopathy (NPDR) Mild NPDR Moderate NPDR Severe NPDR Very severe NPDR II. Proliferative diabetic retinopathy (PDR) III. Diabetic maculopathy IV. Advanced diabetic eye disease (ADED)
  11. 11. Clinical feature • Microaneurysms in the macular area • Retinal haemorrhages both deep and superficial haemorrhages . • Hard exudates-yellowish-white waxy-looking patches are arranged in clumps or in circinate pattern. These are commonly seen in the macular area. • Retinal oedema characterized by retinal thickening. • Cotton-wool spots (if > 8, there is high risk of developing PDR). • Venous abnormalities, beading, looping and dilatation. Intraretinal microvascular abnormalities (IRMA). • Dark-blot haemorrhages representing haemorrhagic retinal infarcts.
  12. 12. 1. Mild NPDR • At least one microaneurysm or intraretinal hemorrhage. • Hard/soft exudates may or may not be present.
  13. 13. Mild NPDR
  14. 14. 2. Moderate NPDR • Moderate microaneurysms/intraretinal hemorrhage. • Early mild IRMA. • Hard/soft exudates may or may not present
  15. 15. Moderate NPDR
  16. 16. 3. Severe NPDR. • Four quadrants of severe microaneurysms/ intraretinal hemorrhages. • Two quadrants of venous beading. • One quadrant of IRMA changes
  17. 17. Severe NPDR
  18. 18. 4. Very severe NPDR • Four quadrants of severe microaneurysms/ intraretinal hemorrhages. • Two quadrants of venous beading. • One quadrant of IRMA changes.
  19. 19. Very sever NPDR
  20. 20. II. Proliferative diabetic retinopathy (PDR) • Proliferative diabetic retinopathy develops in more than 50 percent of cases after about 25 years of the onset of disease. • • The hallmark of PDR is the occurrence of neovascularisation over the changes of very severe non-proliferative diabetic retinopathy. • • Vitreous detachment and vitreous haemorrhage may occur in this stage
  21. 21. III. Diabetic maculopathy • Changes in macular region need special mention, due to their effect on vision. • The diabetic macular edema occurs due to increased permeability of the retinal capillaries. • It is termed as clinically significant macular edema. • Thickening of the retina at or within 500 micron of the centre of the fovea.
  22. 22. IV. Advanced diabetic eye disease • It is the end result of uncontrolled proliferative diabetic retinopathy. • • Persistent vitreous haemorrhage, • Tractional retinal detachment and • Neovascular glaucoma.
  23. 23. Investigations • Urine examination, • Blood sugar estimation. • Fundus fluorescein angiography should be carried out to elucidate areas of neovascularisation, leakage and capillary nonperfusion
  24. 24. Management • I. Screening for diabetic retinopathy. • Every year, till there is no diabetic retinopathy or there is mild NPDR. • Every 6 months, in moderate NPDR. • Every 3 months, in severe NPDR. • Every 2 months, in PDR with no high risk characteristic
  25. 25. Medical treatment 1. Control of systemic risk factors 2. Role of pharmacological modulation. 3. Role of intravitreal steroids
  26. 26. III. Photocoagulation. • i. Macular photocoagulation. Focal treatment Grid treatment. • ii. Panretinal photocoagulation
  27. 27. Focal treatment
  28. 28. Grid treatment
  29. 29. Panretinal photocoagulation
  30. 30. IV. Surgical treatment. • It is required in advanced cases of PDR. Pars plana vitrectomy is indicated for dense persistent vitreous haemorrhage, tractional retinal detachment, and epiretinal membranes. Associated retinal detachment also needs surgical repair.

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