1. DIABETIC RETINOPATHY
Dr Samuel Ponraj

2. RISK FACTORS
• Duration of Diabetes
• Poor control of Diabetes
• Pregnancy
• Systemic diseases –
Hypertension,Nephropathy,Hyperlipidemia,
Anemia, Obesity
• Family History

3. Pathogenesis
• Capillaropathy
• Aldose Reductase
• Vasoproliferative factors

4. • Capillaropathy:
Loss of Pericytes
Thickening of Capillary basement
membrane
Endothelial cell damage
Haematological changes –
abnormalities of [erythrocytes and
leucocytes] , increased platelet stickiness,
and increased plasma viscosity
Capillary leakage,occlusion,microaneurysm

5. • Aldose reductase:
GLUCOSE SORBITOL
-Can not diffuse out easily
-Intracellular Concentration rises
Osmotic diffusion of water - Electrolyte imbalance

6. • Vasoproliferative factors:
Capillary Non - Perfusion
Retinal Hypoxia
VEGF induced
Neovascularisation

7. Classification
Proposed disease severity level Findings on Ophthalmoscopy
No apparent retinopathy No abnormalities
Very Mild NPDR Few Microaneurysms only
Mild NPDR Few microaneurysms ,Retinal
haemorrhage, hard exudates in 1 or 2
quadrants
Moderate NPDR Above findings seen in 2 or 3 quadrants
Severe NPDR Above findings in all quadrants & atleast
of the following plus signs
• Cotton wool spots
• > 20 intraretinal hemorrhages in each
of 4 quadrants
•Venous beeding in 2 or more quadrants
•IRMA in 1 or more quadrants
PDR One or more of following:
Extraretinal neovascularisation
Vitreous /preretinal hemorrhages

8. Clinically significant macular oedema
• Retinal thickening within 500 µm of the centre
of the macula
• Exudates within 500 µm of the centre of the
macula, if associated with retinal thickening
(which may be outside the 500 µm .
• Retinal thickening one disc area (1500 µm) or
larger, any part of which is within one disc
diameter of the centre of the macula.

10. Diabetic macular edema
Due to increased retinal capillary
permeability/leakage & localised edema
- Most common cause of visual impairment in
DM
1.Focal DME:
- Well circumscribed retinal thickening
- Hard exudates [circinate pattern]
F/A : HF - leakage , good macular perfusion

11. • Diffuse DME:
- Diffuse thickening ,edema Cystoid spaces
F/A : HF Diffuse leakage – Flower petal look
• Ischaemic DME:
- Due to microvascular blockage
F/A: HF Capillary non perfusion @ FAZ.

12. HIGH RISK CHARACTERISTICS
• NVD - 1/4 TO 1/3 DISC area with or without
VH or PRH
• NVD – ¼ DISC area with VH or PRH
• NVE - > ½ DISC area with VH or PRH

13. Signs:
• Microaneurysms - localized out-pouchings
- focal dilatation of the capillary wall
- fusion of two arms of capillary loop
inner capillary plexus (inner nuclear layer)
F/A : Tiny HF dots due to leakage
• Retinal Haemorrhages :
- Superficial NFL Haemorrhages – flame shaped
[Precapillary arteriole]
-Intraretinal [nuclear]Haemorrhages - Dot & blot
Haemorrhages
[Venous end of capillaries]

14. • Hard Exudates:
-composed of lipoprotein and lipid-filled
macrophages located mainly within the outer
plexiform layer [chronic localized retinal
oedema]
-Waxy yellow lesions – ring/clumps.
F/A: HF - blockage of background
choroidal and retinal capillary fluorescence.

15. • Cotton wool Spots /Soft exudates/ NFL infarcts
- Local ischaemia ,axoplasmic flow block
swollen ends -cytoid bodies ,neuronal debris.
- Small, whitish, fluffy superficial lesions
- focal HF due to blockage of background
choroidal fluorescence

16. • Venous anomalies :
-seen in ischaemia ,Sluggish retinal circulation
- generalized dilatation and tortuosity,
- ‘looping’ ‘beading’ ‘sausage-like’
segmentation
• IRMA:
- Arteriolar-venular shunts - bypassing the
capillary bed [Collaterals]
- Fine, irregular, red intraretinal lines
F/A : HF ,no leakage.

21. Investigations
• Complete blood picture
• Routine & microscopic urine analysis
• Blood sugar fasting & post prandial
• Glycosylated hemoglobin [HbA1C]
• Lipid ,thyroid & renal profile
• Fundus Fluorescein Angiography
• OCT

22. OCT
• Dense material within neurosensory retina
[Hard exudates]

23. NORMAL DME

24. Medical Therapy :
Antiplatelet therapy :
Ticlopidine ,Aspirin reduces stroke ,CVS
morbidity by inhibiting Platelet aggregation.
Anti hypertensive agents :
ACE inhibitors/B- blockers – tight blood
pressure control ,

25. • Antiangiogenesis:
Intravitreal Anti – VEGF to suppress retinal
neovascularization.
• Blood sugar control.

26. Pan retinal Photocoagulation
• Aim: To destroy ischaemic areas ,decrease
production of vasoproliferative factors ,
stimulates release of antiangiogenic factors
from RPE.
• Regression of Neovascularization.
• Use of Argon laser.
• 1200 -2000 burns , 500 um spot size, 0.1 sec
• Scatter pattern over periphery retina.

28. Peripheral retinal Cryotherapy
• Done for anterior retina – inadequate
visualization of fundus due to opaque media.

29. • Focal laser therapy:
- 500–3000 µm from the centre of the macula.
- Spot size -50-100 um, 0.1 sec
• Grid therapy:
- more than 500 µm from the centre of the
macula and 500 µm from the temporal margin of
the optic disc.
-Spot size -100 um ,0.1 sec

30. Pars plana vitrectomy
• Indications:
- Non clearing Vitreous haemorrhage
- Macular threatening traction retinal detachment
- Macular edema with thickened taut posterior
hyaloid
- Severe preretinal macular haemorrhage

31. THANK U