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DIABETIC
RETINOPATHY
DEMYSTIFIED
Dinesh mittal SONALEE MITTAL
DRISHTI THE VISION EYE HOSPITAL , VIJAYNAGAR INDORE
DINESH
MITTAL
SONALEE
MITTAL
Diabetic Retinopathy
remains the leading cause of
blindness among 25 and 75
years of age .
Diabetic Macular Odema
the leading cause of
decrease in vision in
Diabetic Retinopathy
•DR is a microangiopathy of retinal
vasculature .
•Earliest change thickening of
basement membrane & loss of
pericyte .
MICOANEURYSMS
•hypercellular saccular
outpoucings of cappilary wall
•deep red dots
•first visible clinical sign of DR
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
Progressive capillary closure and
resulting retinal ischaemia leads to
 intraretinal microvascular
abnormalities ( IRMA )
 intraretinal haemorrhages
 and venous abnormalities
( eg venous beading )
Cotton wool
spot
small white
patches with
wispy border
ischaemic area
affecting nerve
fiber layer.
retinal thickening of
the posterior pole
and detected by slit
lamp biomicroscopy or
optical coherence
tomography (OCT )
Diabetic macular odema
( DME )
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
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 .
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 .
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
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
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
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 ) .
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.
classification
• Mild non proliferative
diabetic retinipathy
( NPDR )
Few microaneurysms
or haemorrhages may be
present .
classification
• Moderate NPDR
Haemorrhages ,
microaneurysms ,
cotton wool spots ,
venous beading or
IRMA may be
present .
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 .
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
Management
• Modification of systemic
risk factors
• Intensive control of blood
sugar
• Control of blood pressure
• Lowering of lipid levels
• Exercise and food habbits
Management of DR
PDR with HRCs
DRS study
do PRP
pan retinal Photocoagulation
Severe NPDR & early PDR
ETDRS STUDY
consider for
PRP
Early and mod NPDR
no PRP , regular follow up
PRP protocol
•ETDRS ( early treatment
diabetic retinopathy
study ) protocol for full
scatter laser provides
useful guidelines
•Size of burn 500 µm
•Time .1 second
argon laser burn of moderate intensity
placed one half to one burn apart
divided between 2 or more sittings.
Management of macular odema
• If thickening
involves centre
of fovea then
treat other wise
wait .
• ETDRS
recommends
treatment if
CSME is there.
CSME
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.
• 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
DRCR .net protocol I
intravitreal anti vegf
agents
with early or
deferred laser
Superior
Over
laser alone
laser with steroids
steroids alone
or
or
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
Role of steroids in DME
• Retisert , illuven,
ozurdex
dexamethasone
implant &
triamcinolone
• ( 1mg and 4 mg )
are inferior to laser
or intravitreal anti
vegf agents
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
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 .
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
Pt. of PDR with HRCs with DME
involving centre or having CSME
focal or grid laser
followed by PRP .
Give intravitreal anti
VEGF agents
Pt. of PDR with HRCs with DME
involving centre or having CSME
GRID
PRP
injection
DIABETIC RETINOPATHY DEMYSTIFIED

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DIABETIC RETINOPATHY DEMYSTIFIED

  • 2. DRISHTI THE VISION EYE HOSPITAL , VIJAYNAGAR INDORE DINESH MITTAL SONALEE MITTAL
  • 3. Diabetic Retinopathy remains the leading cause of blindness among 25 and 75 years of age .
  • 4. Diabetic Macular Odema the leading cause of decrease in vision in Diabetic Retinopathy
  • 5. •DR is a microangiopathy of retinal vasculature . •Earliest change thickening of basement membrane & loss of pericyte .
  • 6. MICOANEURYSMS •hypercellular saccular outpoucings of cappilary wall •deep red dots •first visible clinical sign of DR
  • 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 )
  • 9. Cotton wool spot small white patches with wispy border ischaemic area affecting nerve fiber layer.
  • 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 .
  • 20. classification • Moderate NPDR Haemorrhages , microaneurysms , cotton wool spots , venous beading or IRMA 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
  • 24. Management of DR PDR with HRCs DRS study do PRP pan retinal Photocoagulation
  • 25. Severe NPDR & early PDR ETDRS STUDY consider for PRP
  • 26. Early and mod NPDR no PRP , regular follow up
  • 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