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
ļ intraretinal microvascular
abnormalities ( IRMA )
ļ intraretinal haemorrhages
ļ 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 Āµm of center of macula
2 hard exudates at or with
in 500 Āµm 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
ā¢ NVD equal to or greater
than 1/ 4 to 1/3 disc area
ā¢ any amount of NVD with
fresh vitreous / pre
retinal haemorrhage
ā¢ NVE equal to or greater
than Ā½ disc area with
fresh viterous /pre
retinal haemorrhage .
14. Evaluation
ā¢ Previous history of diagnosis
or treatment if any should be
taken thoroughly.
ā¢ Comprehensive eye
examination including VISUAL
ACUITY , IOP measurement ,
ā¢ slit lamp examination of
anterior segment and dilated
funduscopic examination
15. Evaluation
ā¢ ophthalmoscopy in a dilated pupil
remains the standard for clinical
diagnosis and further
classification .
ā¢ posterior pole examination is
best done with slit lamp
biomicroscopy with accessory
lenses .
ā¢ imaging modalities commonly
used in the management are
fundus photography , FA & OCT
16. OCT and FA
are the most useful investigations in DME
ā¢ Confirm presence macular edema
ā¢ Know type of macular edema
ā¢ Assess macular thickness
ā¢ Know response to intravitreal
pharmacotherapy
ā¢ For follow up and documentation
OCT role in DME
17. FA role
ā¢ Type of leak focal
or diffuse
ā¢ 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
ā¢ 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.
ā¢ OCT has become gold standard in
monitoring the progression and treatment
response in DME
ā¢ give micrometer sensitive measurements in
central retinal thickness.
19. classification
ā¢ Mild non proliferative
diabetic retinipathy
( NPDR )
Few microaneurysms
or haemorrhages may be
present .
21. classification
ā¢ 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
ā¢ NVD ā„ than Ā¼ to 1/3 disc area.
ā¢ NVD any amount with vitreous
or pre retinal haemorrhage .
ā¢ NVE ā„ than Ā½ disc area with
fresh vitreous or pre retinal
haemorrhage
23. Management
ā¢ Modification of systemic
risk factors
ā¢ Intensive control of blood
sugar
ā¢ Control of blood pressure
ā¢ Lowering of lipid levels
ā¢ Exercise and food habbits
27. PRP protocol
ā¢ETDRS ( early treatment
diabetic retinopathy
study ) protocol for full
scatter laser provides
useful guidelines
ā¢Size of burn 500 Āµm
ā¢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
ā¢ If thickening
involves centre
of fovea then
treat other wise
wait .
ā¢ 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. ā¢ 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
ā¢ all the three anti vegf
agents RANIBIZUMAB ,
BEVACIMIZUMAB &
AFLIBERCEPT are effective
in management of DME .
ā¢RANIBIZUMAB is slightly
better than BEVACIMIZUMAB
but latter is more economical
34. Role of steroids in DME
ā¢ Retisert , illuven,
ozurdex
dexamethasone
implant &
triamcinolone
ā¢ ( 1mg and 4 mg )
are inferior to laser
or intravitreal anti
vegf agents
35. Role of steroids in DME
ā¢Intravitreal steroids has
main complication of
cataract and glaucoma .
ā¢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
ā¢ Direct treatment
of leaking
microaneurysms in
area of retinal
thickening 500 to3000
Āµm centre of macula .
ā¢ Spot parameter 50
Āµm , barely visible
and .05 to .1 sec burn
duration .
37. Grid treatment
ā¢500 to 3000 Āµm superiorly
, nasally and inferiorly
ā¢500 to 3500 Āµm
temporally from macular
centre .
ā¢No burn in 500 Āµm of
optic disc
ā¢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