definition, types, clinical features, management, investigations

1. DIABETIC
RETINOPATHY
Dr Fahmida Hoque

2. DIABETIC RETINOPATHY
•It is the “disease of the retina” caused by
microangiopathy due to long term effect of
diabetes leading to progressive damage of the
retina & blindness.
•Most common cause of severe bilateral visual
loss in working age group.

3. Risk factors
 Age at diagnosis of diabetes
 Duration of diabetes
 Poor metabolic control
 Pregnancy
 Hypertension
 Nephropathy
 Others - smoking, obesity, hyperlipidemia, anemia

4. Pathophysiology
• DR is a microangiopathy primarily affecting the
precapillary arterioles, capillaries, venules and post
capillary venules.
• The basic component of damaging process are
microvascular occlusion & microvascular leakage.

6. • Capillary changes:
 Degeneration & loss of pericytes
 Thickening of Basement membrane
 Damage & proliferation of endothelial cells
• Hematological changes:
 Deformation of RBC & rouleaux formation
 Increased plasma viscosity
 Increased platelet stickiness & aggregation

7. Pathophysiology
Capillary changes hematological changes
micro vascular occlusion
Retinal capillary non- perfusion
Tissue hypoxia
Retinal ischemia
Release of VEGF
Neo- vascularization
NVD NVE NVA NVI (rubeosis iridis)

8. NVD, NVE
Pre – retinal hge fibro- vascular proliferation
Sub – hyaloid hge fibrous glial tissue proliferation
Vitreous hge contraction of F. P.
traction on Retina
TRD
rhegma forms
combined R. D.

9. NVA, NVI
NVG
Secondary open angle glaucoma
Secondary angle closure glaucoma
Optic atrophy
Absolute eye

11. Clinical Features:

12. Clinical features:
Microaneurysm:
 Earliest sign of D. R.
 Appear as tiny red dots.
 It is focal saccular dilatation of capillary walls where pericytes
are absent.
 Located in the outer plexiform layer & inner nuclear layer.
 Usually at posterior pole, especially temporal to the fovea.
 In FFA – present at the edge of area of capillary non- perfusion
(hyper fluorescence dots)

13. Retinal Hemorrhages:
Dot & blot hge:
•Due to rupture of wall of capillary or Microaneurysm, giving
rise to intra retinal hge.
•If the hge is deep (i.e. in the inner layer of OPL) it is usually
is round or oval (dot/ blot hge)

14. Retinal Hemorrhages:
Flame shaped Hge:
•Arise from superficial precapillary arterioles.
•the hge is more superficial & in the nerve fiber layer, it takes
a flame/ splinter shape as they follow the architecture of the
nerve fiber layer.

15. Exudates
Hard exudates:
•These are yellow deposits of
lipid, lipoprotein & lipid filled
macrophages within the outer
plexiform & inner nuclear layer.
•They are arranged in clumps or
form circinate pattern around the
Microaneurysm frequently at
posterior pole.
•These are sign of current/
previous Macular edema.
Cotton wool Spot (soft
exudates):
•They are white fluffy lesion in
nerve fiber layer.
•Caused by capillary occlusion at
NFL due to infarction.

16. Intraretinal microvascular abnormality (IRMA):
•Abnormal dilated, tortuous retinal capillaries that act as a
shunt between arterioles & venules.
•It’s within the internal limiting membrane.
Venous changes:
In the form of “beading”, “looping” & “severe segmentation”
due to venous stagnation.

17. Classification
ETDRS CLASSIFICATION:
NON PROLIFERATIVE DIABETIC RETINOPATHY
MILD NPDR MA, retinal hemorrhage, hard exudates
MODERATE NPDR Mild NPDR plus cotton wool spots, venous changes &
IRMA
SEVERE NPDR
4:2:1 rule
Moderate NPDR plus one of –
•MA, retinal hge in all four quadrants
•Venous changes in 2/ more quadrants
•IRMA atleast in 1 quadrant
VERY SEVERE NPDR Two or more of the above features on severe NPDR

18. Proliferative diabetic retinopathy:
•early/ mild/ non – high risk PDR
•High risk:
New vessel on Disc:
o More than 1/3rd
of Optic disc diameter with/ without hge
o Less than 1/3rd
of optic disc diameter with hge (preretinal
& vitreous hge)
New vessel elsewhere in fundus:
o More than ½ of Optic disc diameter with/ without hge
o Less than ½ of Optic disc diameter with hge. (preretinal &
vitreous hge)

19. CLINICALLY SIGNIFICANT
MACULAR EDEMA:
Modified Airlie- House
criteria:
•Retinal edema within 500
micron of central fovea
•HE within 500 micron of
fovea centralis associated
with adjacent retinal
thickening
•Retinal edema that is 1 disc
diameter or larger, any part
of which is with in 1 disc
diameter of the fovea
centralis.

20. Management
1) History from patient
2) Clinical features
3) Ocular examination
 BCVA
 Slit lamp examination
 Cornea
 Iris
 lens
 Funduscopy

21. Investigation:
 Laboratory test :
 Blood sugar- FBS, RBS, 2HPPBS
 Serum lipid profile
 Medical evaluation of HbA1c
 Ancillary test
 Color fundus photograph
 Fundus Fluorescein Angiography
 OCT

22. Treatment:
• LASER TREATMENT:
Focal laser
Grid laser
Pan retinal photocoagulation
• INTRA VITREAL INJECTION:
Anti- VEGF injection

23. Laser
Indication:
•Grid + focal laser – CSME
•PRP:
• PDR --
High risk
Early PDR –
 In pts with poor compliance
 During pregnancy
 Pt with systemic disease
 Pending cataract surgery/ YAG laser capsulotomy
 Rubeosis iridis
 Severe/ very severe NPDR (irregular F/U)

24. Laser (M/A)
Focal laser:
•Burns only Microaneurysm
Grid laser:
•Around the edema except the Foveolar avascular zone.
PRP:
•It burns the viable retina which is suffering from ischemia,
thus reduces the oxygen demand of retina & prevents
hypoxia.
•As it burns the ischemic retina, so reduces VEGF secretion
by the ischemic retina.

25. Anti- VEGF
It’s a humanized monoclonal antibody fragment.
M/A:
Anti- VEGF
binds with VEGF
Neutralization of VEGF
So, VEGF cant bind to receptor
No neovascularization reduces vascular permeability
inhibits leakage
reduces macular edema

26. Anti- VEGF
Commonly used:
Bevacizumab (Avastin):
dose – 1.25 mg &
Ranibizumab (Lucentis) :
dose – 0.5 mg
Indication:
• NPDR with CSME
• PDR with CSME
• ARMD with CNVM
• CME
• CSCR
• NVG
• CRVO, BRVO
Complication:
•SCH
•Cataract
•Glaucoma
•Vitreous hemorrhage
•Endophthalmitis
•RD