7. sharply demarcated extravascular
deposits of lipid material resultIng
from spillage and incomplete
resorption of lipoproteins .
often present at border between
edematous & non edematous
retina .
they may exist as circinate ring
pattern around the
Hard exudates
8. Progressive capillary closure and
resulting retinal ischaemia leads to
intraretinal microvascular
abnormalities ( IRMA )
intraretinal haemorrhages
and venous abnormalities
( eg venous beading )
10. retinal thickening of
the posterior pole
and detected by slit
lamp biomicroscopy or
optical coherence
tomography (OCT )
Diabetic macular odema
( DME )
11. 3 zone of thick retina one
disc area or larger any
part of which is with in
one disc diameter of
center of macula
ETDRS defines
CSME
1 thickening of retina at or with
in 500 µm of center of macula
2 hard exudates at or with
in 500 µm center macula
with thick adjacent retina
12. Proliferative diabetic retinopathy
( PDR )
PDR formation of new
vessels and fibrotic
tissue on retina and
optic disc
contraction of fibrous
tissue lead to
tractional retinal
detachment and
viterous haemorrhage .
13. PDR with HRC s
• NVD equal to or greater
than 1/ 4 to 1/3 disc area
• any amount of NVD with
fresh vitreous / pre
retinal haemorrhage
• NVE equal to or greater
than ½ disc area with
fresh viterous /pre
retinal haemorrhage .
14. Evaluation
• Previous history of diagnosis
or treatment if any should be
taken thoroughly.
• Comprehensive eye
examination including VISUAL
ACUITY , IOP measurement ,
• slit lamp examination of
anterior segment and dilated
funduscopic examination
15. Evaluation
• ophthalmoscopy in a dilated pupil
remains the standard for clinical
diagnosis and further
classification .
• posterior pole examination is
best done with slit lamp
biomicroscopy with accessory
lenses .
• imaging modalities commonly
used in the management are
fundus photography , FA & OCT
16. OCT and FA
are the most useful investigations in DME
• Confirm presence macular edema
• Know type of macular edema
• Assess macular thickness
• Know response to intravitreal
pharmacotherapy
• For follow up and documentation
OCT role in DME
17. FA role
• Type of leak focal
or diffuse
• Rule out macular
ischaemia
Increasingly OCT is being used for evaluation of macular edema .
Spectral domain ( SD OCT ) has replaced time domain OCT ( TD OCT ) .
18. Diabetic macular odema
• Slit lamp biomicroscopy , color fundus
photography or ophthalmoscopy may not be
able to detect mild DME . Here OCT is very
helpful in measuring central foveal thikness.
• OCT has become gold standard in
monitoring the progression and treatment
response in DME
• give micrometer sensitive measurements in
central retinal thickness.
19. classification
• Mild non proliferative
diabetic retinipathy
( NPDR )
Few microaneurysms
or haemorrhages may be
present .
21. classification
• Severe NPDR 4-2-1 rule
Any one of following three
features is considered
diagnostic of severe NPDR
all 4 quadrants contain severe
intra retinal haemorrhages/
microaneurysms
venous beading in 2 or more
quadrants .
IRMA in at least 1 quadrant .
22. PROLIFERATIVE DIABETIC
RETINOPATHY
Early PDR
New vessels and criterion not
met for high risk PDR
PDR with HRCs
• NVD ≥ than ¼ to 1/3 disc area.
• NVD any amount with vitreous
or pre retinal haemorrhage .
• NVE ≥ than ½ disc area with
fresh vitreous or pre retinal
haemorrhage
23. Management
• Modification of systemic
risk factors
• Intensive control of blood
sugar
• Control of blood pressure
• Lowering of lipid levels
• Exercise and food habbits
27. PRP protocol
•ETDRS ( early treatment
diabetic retinopathy
study ) protocol for full
scatter laser provides
useful guidelines
•Size of burn 500 µm
•Time .1 second
28. argon laser burn of moderate intensity
placed one half to one burn apart
divided between 2 or more sittings.
29. Management of macular odema
• If thickening
involves centre
of fovea then
treat other wise
wait .
• ETDRS
recommends
treatment if
CSME is there.
CSME
30. DRCR .net protocol I
treat centre involving DME with
intravitreal inj of anti vegf agents till the
macula is relatively dry followed by focal
laser .
RANIBIZUMAB ( LUCENTIS )
.3 mg in .05 ml
Or
BEVACIMIZUMAB ( AVASTIN)
1.25mg in .05 ml.
31. • to reduce the burden
and cost of injections
usually three
intravitreal anti vegf
injections are given and
then switched to as
required PRN dosing
.one can add intravitreal
injection Triamcinolone
1mg / .025 ml
32. DRCR .net protocol I
intravitreal anti vegf
agents
with early or
deferred laser
Superior
Over
laser alone
laser with steroids
steroids alone
or
or
33. DRCR .net protocol T
• all the three anti vegf
agents RANIBIZUMAB ,
BEVACIMIZUMAB &
AFLIBERCEPT are effective
in management of DME .
•RANIBIZUMAB is slightly
better than BEVACIMIZUMAB
but latter is more economical
34. Role of steroids in DME
• Retisert , illuven,
ozurdex
dexamethasone
implant &
triamcinolone
• ( 1mg and 4 mg )
are inferior to laser
or intravitreal anti
vegf agents
35. Role of steroids in DME
•Intravitreal steroids has
main complication of
cataract and glaucoma .
•In pseudophakic patients
IV TA plus laser benefit is
comparable to IV ANTI
VEGF agents and
superior to that seen in
laser group
36. Modified ETDRS focal / grid laser
protocol as used by DRCR .net
• Direct treatment
of leaking
microaneurysms in
area of retinal
thickening 500 to3000
µm centre of macula .
• Spot parameter 50
µm , barely visible
and .05 to .1 sec burn
duration .
37. Grid treatment
•500 to 3000 µm superiorly
, nasally and inferiorly
•500 to 3500 µm
temporally from macular
centre .
•No burn in 500 µm of
optic disc
•Burn parameter two
visible burns width apart
38. Pt. of PDR with HRCs with DME
involving centre or having CSME
focal or grid laser
followed by PRP .
Give intravitreal anti
VEGF agents
39. Pt. of PDR with HRCs with DME
involving centre or having CSME
GRID
PRP
injection