This document discusses diabetic retinopathy and its management. It begins by stating that diabetic retinopathy is the leading cause of vision impairment worldwide. It then describes the clinical presentation and stages of diabetic retinopathy from mild non-proliferative to proliferative, as well as diabetic macular edema. The management section discusses preventing and treating diabetic retinopathy through controlling blood sugar and blood pressure systematically, as well as local treatments like pan-retinal photocoagulation laser, anti-VEGF injections, and vitrectomy surgery. It emphasizes that timely screening and treatment according to guidelines can reduce the risk of severe vision loss to less than 5%.

1. DIABETIC
RETINOPATHY
ANTI VEGF ,STEROIDS,LASER
DRISHTI THE VISION VIJAYNAGAR INDORE 2019

2. INTRODUCTION
• Diabetic retinopathy remains the leading cause of
visual impairment among the working-age
population throughout the world.
• Macular Odema is leading cause of decrease in
vision in Diabetic Retinopathy . Other causes of
decrease in vision in diabetic retinopathy are
• Macular Ischaemia ,
• Retinal And Viterous Haemorrhages And
• Tarctional Retinal Detachment

3. INTRODUCTION
• Diabtic retinopathy is
Progressive dysfunction
of the retinal
vasculature caused by
chronic hyperglycemia
resulting in structural
damage to the neural
retina.
HYPERGLYCAEMIA
RETINAL
VASCULATURE
DYSFUNCTION
STRUCTURAL
DAMAGE TO
NEURAL RETINA

4. INTRODUCTION
2010
• 285 MILLION OF WORLD POPULATION HAS DM
• 6.4%
2015
• 415 MILLION
2030
• PREDICTED DIABETIC POPULATION 552 MILLION
• 7.7%

5. INTRODUCTION
• Diabetic Retinopathy remains the number one
cause of new blindness in most countries because
of delays in seeking treatment.
• The vast majority of diabetic individuals who lose
vision do so not because of an inability to treat
their disease but due to a delay in seeking medical
attention.

6. Risk factors
• Duration of retinopathy is most closely associated
with the incidence of diabetic retinopathy and
remains the best predictor of diabetic retinopathy.
• Other risk factors in development of diabetic
retinopathy are
• poor glycemic control,
• and hypertension.

7. Clinical Picture Diabetic
Retinopathy
• DR is a
microangiopathy of
retinal vasculature .
Earliest change is
Thickening of
basement membrane
and loss of pericyte .

8. Micoaneurysms
• Microaneurysms are the
first ophthalmoscopically
detectable change and are
considered the hallmark of
diabetic retinopathy
• They appear visibly as
deep red dots .

9. Clinical Picture Diabetic
Retinopathy
• Classically, nonproliferative diabetic retinopathy
(NPDR is characterized by microvascular and
intraretinal changes seen on dilated fundus
examination .
• It include microaneurysms, hemorrhages, hard
exudates, cotton wool spots, intraretinal
microvascular abnormalities (IRMAs), and venous
beadings.
• Macular edema could occur in both non
proliferative & proliferative diabetic retinopathies.

10. Intra Retinal
Haemorrhages
• When the wall of a capillary or microaneurysm is
weakened enough, it may rupture, giving rise to an
intraretinal hemorrhage.
• If the hemorrhage is deep ,it usually is round or
oval (“dot or blot”) .If the hemorrhage is superficial,
in the nerve fiber layer, it takes a flame or splinter
shape .

11. Hard exudates
• The intercellular fluid comes
from leaking
microaneurysms or from
diffuse capillary
incompetence.
• it may accumulate in a ring
around a group of leaking
microaneurysms. This
pattern is called circinate
retinopathy .

12. Advanced Nonproliferative
Diabetic Retinopathy
• In advanced NPDR, signs of increasing inner retinal
hypoxia appear, such as
• multiple retinal hemorrhages,
• cotton–wool spots,
• venous beading and vascular loops,
• intraretinal microvascular abnormalities (IRMAs),
and large areas of capillary nonperfusion seen on
fluorescein angiography.

14. Mild non proliferative diabetic
retinopathy ( NPDR )
Few microaneurysms or haemorrhages may be
present .

15. Moderate NPDR
Haemorrhages , microaneurysms ,
cotton wool spots , venous beading
or IRMA may be present.

16. Severe NPDR
• 4-2-1 rule
• Any one of following three features is considered
diagnostic of severe NPDR
• 1. all 4 quadrants contain severe intra retinal
haemorrhages or microaneurysms
• 2. venous beading in 2 or more quadrants .
• 3 IRMA in at least 1 quadrant

17. Proliferative diabetic retinopathy
• PDR is
characterised by
formation of new
vessels and
fibrotic tissue on
retina and optic
disc .

18. PDR with HRCs high risk characteristics
• NVD equal to or greater than ¼ disc area
• NVD any amount with vitreous or pre retinal haemorrhage .
• NVE equal to or greater than ½ disc area with fresh
vitreous or pre retinal haemorrhage

19. Diabetic macular odema ( DME )
• Diabetic macular odema
( DME ) is defined as
retinal thickening of the
posterior pole and
detected by slit lamp
biomicroscopy or
optical coherence
tomography ( OCT ).

20. Diabetic macular odema ( DME
• ETDRS ( early treatment diabetic retinopathy
study ) defines Clinical Significant Macular Odema (
CSME ) on biomicroscopy as
• 1. thickening of retina at or with in 500 µm of
center of macula
• 2. hard exudates at or with in 500 µm of center of
macula associated with thickening of adjacent
retina
• 3. zone of retinal thickening one disc area or
larger any part of which is with in one disc
diameter of center of macula

21. Thickening of retina within 500 µm of
centre of macula
hard exudates at or with in 500 µm of
center of macula associated with
thickening of adjacent retina
zone of retinal thickening one disc
area or larger any part of which is
with in one disc diameter of center of
macula

22. Optical Coherence Tomography
• The application of optical coherence tomography
(OCT) to management of DME has been very useful.
The degree of DME and response to therapy can be
quantified on OCT.
• Specifically, the central subfield thickness (CST)
can be used to follow a patient’s response to
treatment of DME.

23. MANAGEMENT

24. Prevention
PRIMARY to prevent
development of DM
• Daily exercises
• Reduce weight
• Healthy eating habbits
• Regular blood sugar
checkup
SECONDARY to
prevent
complications of DM
• Intensive control of blood
sugar
• Control of blood pressure
• Decrease of blood lipids
TERTIARY to prevent
loss of vision
• Screening through a
dilated pupil by skilled
eye care provider for
early detection and
treatment of diabetic
retinopathy

25. TREATMENT
• Successful management of diabetic retinopathy
requires not only local treatment
1. laser therapy,
2. intravitreal pharmacotherapy,
3. and vitrectomy
but also systemic control of
1. hyperglycemia,
2. blood pressure,
3. and lipids.

26. Management of DR
TYPE OF DR
MANAGEMENT
PDR with HRCs Do PRP ( Pan Retinal
Photocoagulation DRS Study )
Severe NPDR and early PDR consider for PRP ( ETDRS STUDY )
Early and mod NPDR no PRP , regular follow up

27. PRP

28. DRCR .net protocol I
intravitreal anti VEGF
agents with early or
deferred laser
Superior
Over
laser alone
laser with steroids
steroids alone
or
or

29. INTRAVITREAL INJECTION

30. Management of macular odema
• If thickening involves centre of fovea then treat
other wise wait .
Treatment of choice is Intravitreal Anti VEGF
1. Ranibizumab ( Lucentis , Accentrix , Razumab ) .3
mg in .03 ml or
2. IV Bevacimizumab ( Avastin) 1.25mg in .05 ml. or
3. Aflibercept ( Eylea ) 2mg in .05 ml

31. Management of macular odema
• DRCR .net protocol I recommends treating centre
involving DME with 4 to 6 Intravitreal injections of
anti VEGF agents till the macula is relatively dry
followed by focal laser .
• In cases of non centre involving DME , focal or
macular grid is recommended .
• One can add IV injection of steroid triamcinolone
2mg / .05 ml in patients who are not responding to
anti VEGF agents

32. INJECTION dose of drug for dme
Intravitreal drug AVASTIN LUCENTIS,
ACCENTRIX,
RAZUMAB
TRIAMCINOLONE
Intravitreal dose 1.25 mg .3 mg 2 mg
strength in vial 25 mg / ml 10 mg / ml 40 mg / ml
Amt in cc injected .05 ml .03 ml .05 ml
Needle gauge used 30 g 30 g 27 gauge
To be repeated after 1 month 1 month 3 to 4 months
Cost per inj 5 thousand rs 25 thousand rs 500 rs

33. •The major problems with anti-VEGF therapy
are cost and frequency of administration. At
present, ranibizumab at a dose of 0.3 mg has
undergone the most rigorous testing, but due
to cost issues, worldwide, BEVACIZUMAB
1.25 mg is the drug of choice for DME .
• Triamcinolone 2 mg is used to enhance the
effect or to decrease number of required
injections of anti VEGF drugs keeping in
mind its complications of cataract and
glaucoma .
• Focal and grid laser should be used where
indicated .

34. Disease Study treatment
PDR + HRC DRS PRP
SEVERE NPDR
PDR WITHOUT HRC
ETDRS CONSIDER PRP
MILD &
MODERATE NPDR
ETDRS NO PRP
CENTRE INVOLVING
MACULAR ODEMA
DRCR .NET
PROTOCOL I
INTRAVITREAL
ANTI VEGF
CENTRE SPARING ME
ETDRS FOCAL OR GRID
LASER

35. Some clinical
presentations

36. CASE 1
• Vision 6 /6 both eyes
• Moderate NPDR
•Do observation
•& No
intervention

37. CASE 2
• Vision 6/18 involved eye
• FA shows focal leak
OCT macular odema
• Severe NPDR with
centre involving
Macular Odema
• Intravitreal Avastin
injections two or three
depending upon
response supplemented
by focal green laser

38. CASE 3

39. CASE 3
•Do PRP•PDR with no
macular
odema

40. CASE 4
• PDR with DME involving
centre
Intravitreal anti
VEGF AGENTS
add Intravitreal
STEROIDS
FOCAL OR
GRID LASER
PRP

41. CONCLUSION
• If fundus examinations are initiated
before the development of significant
retinopathy and repeated periodically—
and if the recommendations of DRS ,
ETDRS and DRCR.net clinical trials are
applied in the management —the risk
of severe visual loss is less than 5%.

42. CONCLUSION
•The prognosis for diabetic
retinopathy used to be dismal. But
now this has changed for better.
Timely laser photocoagulation as
advocated by the DRS AND ETDRS
and intravitreal anti VEGF therapy
has made this disease treatable.

43. THANK
YOU
DR DINESH
DR SONALEE