DIABETES RETINOPATHY BY DNYANESHWAR BHAGWAN POTFODE

1. Diabetes retinopathy
DNYANESHWAR B. POTFODE
OPHTHALMIC OFFICER

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. Retina

4. Retina

5. Retina

6. Microscopic structure of the retina.

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. 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. Pathogenesis of diabetic retinopathy.

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. 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. 1. Mild NPDR
• At least one microaneurysm or intraretinal
hemorrhage.
• Hard/soft exudates may or may not be
present.

13. Mild NPDR

14. 2. Moderate NPDR
• Moderate microaneurysms/intraretinal
hemorrhage.
• Early mild IRMA.
• Hard/soft exudates may or may not present

15. Moderate NPDR

16. 3. Severe NPDR.
• Four quadrants of severe microaneurysms/
intraretinal hemorrhages.
• Two quadrants of venous beading.
• One quadrant of IRMA changes

17. Severe NPDR

18. 4. Very severe NPDR
• Four quadrants of severe microaneurysms/
intraretinal hemorrhages.
• Two quadrants of venous beading.
• One quadrant of IRMA changes.

19. Very sever NPDR

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. 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. 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. Investigations
• Urine examination,
• Blood sugar estimation.
• Fundus fluorescein angiography should be
carried out to elucidate areas of
neovascularisation, leakage and capillary
nonperfusion

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. Medical treatment
1. Control of systemic risk factors
2. Role of pharmacological
modulation.
3. Role of intravitreal steroids

26. III. Photocoagulation.
• i. Macular photocoagulation.
Focal treatment
Grid treatment.
• ii. Panretinal photocoagulation

27. Focal treatment

28. Grid treatment

29. Panretinal photocoagulation

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.