A complete source of information intended for ophthalmologists. Includes everything from risk factors to pathophysiology to management.

1. DIABETIC RETINOPATHY
PRESENTATION BY
Dr. Sumeet Agrawal
PG II Year

2. • Chronic retinal disorder characterized by
gradually progressive alterations in the retinal
microvasculature in patients with diabetes
mellitus

3. OVERVIEW
• EPIDEMIOLOGY
• RISK FACTORS
• PATHOGENESIS
• PATHOLOGIC ENTITIES
• DISEASE ENTITIES
• DIFFERENTIAL DIAGNOSIS
• MANAGEMENT
• FOLLOW UP

4. EPIDEMIOLOGY

5. EPIDEMIOLOGY
• 31.7 million diabetic subjects in
• Largest number of diabetics in any single country.
• 12. 5 % of urban population & 4 % of the rural
population
• Expected to increase to 79.4 million by 2030
• Type 2 diabetes in Indians differs from that in
western population :
– onset is at a younger age,
– obesity is less common,
– genetic factors appear to be stronger.
Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes, estimates for the year 2000 and projections for 2030. Diabetes Care.
2004;27:1047–1053.
Mohan V, Ramachandran A, Snehalatha C, Mohan R, Bharani G, Viswanathan M. High prevalence of maturity onset diabetes of the young
(MODY) among Indians. Diabetes Care. 1985;8:371–374.
Joshi SR. Metabolic syndrome: emerging clusters of the Indian phenotype. J Assoc Physicians India. 2003;51:445– 456.

6. +
[1]
[1] Rema M et al. Prevalence of Diabetic Retinopathy in Urban India: The Chennai
Urban Rural Epidemiology Study (CURES) Eye Study, I.Invest. Ophthalmol. Vis. Sci;
July 2005 vol. 46: 328-333

7. [6]R Piyush et al.Prevalence of Diabetic Retinopathy in Western Indian Type 2 Diabetic Population: A Hospital – based Cross – Sectional
StudyJournal of Clinical and Diagnostic Research. 2013 Jul, Vol-7(7): 1387-1390
[7] Agrawal RP, Ranka M, Beniwal R, Gothwal SR, Jain GC, Kochar DK et al. Prevalence of diabetic retinopathy in type 2 diabetes in relation to
risk factors: Hospital based study. Int J Diab Dev Countries. 2003;23:16-19.
[8] Rema M, Premkumar S, Anitha B, Deepa R, Pradeepa R, Mohan V. Prevalence of diabetic retinopathy in urban India: The Chennai Urban
Rural Epidemiology Study (CURES) Eye Study, I. Invest Ophthalmol Vis Sci. 2005; 46 : 2328-33.
[11] Rema M, Ponnaiya M, Mohan V. Prevalence of retinopathy in non insulin dependent diabetes mellitus at a diabetes centre in southern
India. Diabetes Res Clin Pract.1996; 34: 29-36.
[12] Narendran V, John RK, Raghuram A, Ravindran RD, Nirmalan PK, Thulasiraj RD. Diabetic retinopathy among self reported diabetics in
southern India: a population based assessment. Br J Ophthalmol. 2002;86:1014–18.
[13] Mahesh G, Giridhar A, Saikumar SJ, Anna Elisa, Ramkumar, Bhat S. Prevalence of Diabetic Retinopathy in a Rural Population of South ndia.
[6]
INDIANSTUDIES

8. Epidemiology of DME
• 10-year incidence of DME
– 20.1% among patients diagnosed before age 30 years (younger
onset)
– 39.3% among patients diagnosed after age 30 (older onset)
• Diabetes Control and Complications Trial (DCCT)
– 27% of patients develop macular edema within 9 years of diabetes
• 3% in eyes with mild nonproliferative diabetic retinopathy
(NPDR),
• 38% with moderate to severe NPDR, and
• 71% with proliferative diabetic retinopathy (PDR) develop
DME
• Older onset diabetics are at a higher risk
Anderson JM, Itallie CMV. Tight junctions and the molecular basis for regulation of paracellular permeability. Am J Physiol. 1995;269:G467—76
Klein R, Klein BEK, Moss SE. Th e epidemiology of ocular problems in diabetes mellitus. in SS F (ed): Ocular problems in diabetes mellitus. Boston, Blackwell Scientifi c Publications, 1991, p. 1--51
Klein R, Klein BEK, Moss SE, Cruickshanks KJ. Th e Wisconsin epidemiologic study of diabetic retinopathy. XV. Th e long term incidence of macular edema. Ophthalmology. 1995;102:7—16
Vitale S, Maguire MG, Murphy RP, et al. Clinically signifi cant macular edema in Type 1 diabetes. Incidence and risk factors. Ophthalmology. 1995;102. 117--6.
Klein R, Klein BEK, Moss SE. Visual impairment in diabetes. Ophthalmology 1984; 91:1-8

9. RISK FACTORS

10. • DURATION OF DIABETES
• GLYCEMIC CONTROL
• HYPERTENSION
• RENAL DYSFUNCTION
• DYSLIPIDEMIA
• PREGNANCY
• OBESITY
• ANEMIA

11. RISK FACTORS
• DURATION OF DIABETES
– Single most important risk factor
DURATION OF
DM
PREVALANCE
OF DR
DURATION OF
DM
PREVALANCE
OF DR
> 5 yrs. very low 11 – 13 yrs. 23 %
5 – 10 yrs. 27 % 13 – 16 yrs. 44 %
TYPE 1 10 – 20 yrs. 71 – 90 % TYPE 2 16 – 20 yrs. 60 %
> 20 yrs. 95 % [20-30%
PDR]
20 – 30 yrs. 77 %
> 30 yrs 96 %
Klein R., Klein B., Moss S., et al: The Wisconsin epidemiologic study of diabetic retinopathy. XIV. Ten-year incidence and progression of diabetic retinopathy. Arch
Ophthalmol 1994; 112:1217-1228.
Yanko L., Goldbourt U., Michaelson C., et al: Prevalence and 15-year incidence of retinopathy and associated characteristics in middle-aged and elderly diabetic men. Br J
Ophthalmol 1983; 67:759-765.
Kostraba J.N., Dorman J.S., Orchard T.J., et al: Contribution of diabetes duration before puberty to the development of microvascular complications in IDDM
subjects. Diabetes Care 1989; 12:686-693.

12. [1] Rema M et al. Prevalence of Diabetic Retinopathy in Urban India: The Chennai
Urban Rural Epidemiology Study (CURES) Eye Study, I.Invest. Ophthalmol. Vis. Sci;
July 2005 vol. 46: 328-333
[1]

13. [6]R Piyush et al.Prevalence of Diabetic Retinopathy in Western Indian Type 2 Diabetic
Population: A Hospital – based Cross – Sectional Study Journal of Clinical and Diagnostic
Research. 2013 Jul, Vol-7(7): 1387-1390

14. PREVALENCE OF DIABETIC RETINOPATHY IN TYPE 2 DIABETES IN RELATION TO RISK FACTORS:
HOSPITAL BASED STUDY. A Raghav et al. INT. J. DIAB. DEV. COUNTRIES. 2003; 23: 16-9

15. GlobalPrevalenceandMajorRiskFactorsofDiabeticRetinopathyEYE
DISEASE(META-EYE)STUDYGROUPDiabetesCare2011;35:556–564.

16. • Duration of DM before puberty is not
important.

17. Role of Glycemic Control
DCCT (1993)
• 1441 subjects with
IDDM followed for
6.5yrs
• Randomized into strict
and conventional t/t
• Strict control group had
average HbA1c 7.2%
– Conventional: 8.8%
• Strict control resulted in…
– Reduced risk of retinopathy by 76%
– Reduced risk of progression by 54%

19. Role of Blood Pressure
UKPDS (1998)
• 1148 hypertensive type-2 diabetics randomized into
tight and less-tight BP control and followed for 8.4
yrs
• Average BP:
– Tight: 144/82
– Less tight: 154/87
• Tighter BP control
resulted in…
– 34% reduction in
progression of DR
– 47% reduced risk of loss of 3 lines VA

20. Role of Cholesterol
• WESDR (1991): Higher serum cholesterol increased risk of hard
exudates in type-1 DM
• ETDRS (1996): Higher serum lipids increased risk of hard
exudates and loss of VA
• Elevated lipids may increase the morbidity of diabetic macular
edema

21. ‘Earliest’ in DR
• Ophthalmoscopically detectable change
• Histopathological change
• Symptom
• Electrophysiological abnormality

22. • Poor night vision (dark adaptation)
• Poor recovery from bright lights (photo stress)
• Diminution of the amplitude of the oscillatory
potentials (OP's) of the electroretinogram at a
time when both the a- and b-waves are normal
• Ischemia in the inner nuclear layer
• Predictor of progression
• Severity inversely proportional to the amplitude
of the b-wave

23. Color vision assessment:
Acquired blue-Yellow defect
(patients would be unable to accurately match
self – monitored color - dependent urine or
blood-glucose tests)
NOTE :
Macular disorders : Blue-yellow defects (Exceptions : Cone dystrophy, Stargardt’s disease
Optic nerve disorders : Red-green defects (Exceptions : glaucoma, autosomal dominant optic
neuropathy)

24. PATHOGENESIS

25. • ALDOSE REDUCTASE
– Converts sugars, when present in high concentration, into alcohols.
(glucose to sorbitol)
– Sorbitol cannot easily diffuse out of cells,
– Osmotic forces draw water into the cells resulting in electrolyte
imbalance.
– Retinal pericytes and Schwann cells,
• VASOPROLIFERATIVE FACTORS
– Vascular endothelial growth factor (VEGF),
– In the vitreous of patients with diabetic retinopathy
– Decreases after PRP
• GROWTH HORMONE
– Reversal of florid diabetic retinopathy in women who had postpartum
hemorrhagic necrosis of the pituitary gland
– Growth hormone deficiency was found to be somewhat protective
against retinopathy

26. • PLATELETS AND BLOOD VISCOSITY
– Platelets in diabetic patients are “stickier” than
platelets of patients without diabetes
– Diabetic platelets are especially sensitive to
thromboxane and to other aggregating agents
such as epinephrine.
– Focal capillary occlusion and focal areas of
ischemia in the retina

27. • Microvascular leakage
• Microvascular occlusion

28. Microvascular leakage
Degeneration and loss of pericytes
Plasma leakage
Hard exudate
(Circinate pattern)
Capillary wall weakening
microaneurysm
Retinal edema
Intraretinal hemorrhage

29. Microvascular occlusion
Neovascularization
and fibrovascular proliferation
VEGF
Increased plasma viscosity
Deformation of RBC
Increased platelets stickiness
Decreased capillary blood flow
and perfusion
Endothelial cell damage and proliferation
Capillary basement membrane thickening
Retinal hypoxia
A-V shunt
IRMA
Cotton wool spots
Proliferative
retinopathy
Rubeosis
iridis

30. PATHOGENESIS OF DME
• BREAKDOWN OF BLOOD RETINAL BARRIER
– changes in the tight junctions,
– pericyte loss,
– endothelial cell loss,
– retinal vessel leukostasis,
– up-regulation of vesicular transport,
– increased permeability of the surface membranes of
retinal vascular endothelium and RPE cells,
– activation of the AGE receptor,
– downregulation of glial-cell,
– derived neurotropic factor (GDNF),
– retinal vessel dilation

31. • VASOACTIVE FACTORS
– VEGF,
– protein kinase C [PKC],
– heparin,
– angiotensin II,
– PEDF,
– biochemical pathways
• VITREORETINAL INTERFACE

32. PATHOLOGIC ENTITIES

33. • MICROANEURYSM
• CAPILLARY NON PERFUSION
• INTRARETINAL HEMORRHAGES
• HARD EXUDATES
• COTTON WOOL SPOTS
• VENOUS BEADING
• INTRARETINAL MICROVASCULAR
ABNORMALITIES (IRMA)

34. MICRO ANEURYSMS
• Pericytes : Mesothelial cells
• Surround and support the capillary endothelium
• 1:1
• Weakens the capillaries => thin-walled
dilatations
• Endothelial cells proliferate
• Layers of basement membrane material
• Fibrin &/or erythrocytes, may occlude the
lumen
• Small red dots; 20-200 μ; OPL/INL
• Temporal to the fovea
• Venous side => arterial side
• Permeable to lipid and fluid

36. • FFA differentiates
– Patent micro aneurysms and dot hemorrhages
– Cannot if it is filled with clotted blood
– Many more seen in FFA than ophthalmoscopically
• Rupture => intra retinal hemorrhage
– Deep (OPL/INL) :
• Dot (venous end of the capillaries),
• blot (superficial precapillary arterioles; larger)
– Superficial (NFL) : flame shaped, splinter
(hypertensives)

40. HARD EXUDATES
• Outer plexiform layer
• Accumulated lipoproteins
• Circinate pattern
• Centre usually contains a micro aneurysm
• Differentiate from drusens

42. COTTON WOOL SPOTS
• White fluffy lesions in nerve fibre layer
• Occlusion of retinal pre-capillary arterioles
• Swelling of local nerve fibre axons
• “Soft exudates" or "nerve fibre layer infarctions"
• FFA
– no capillary perfusion in the area of the soft exudate
• Very common in DR with concomitant hypertension

45. VENOUS BEADING & LOOPS
• Indicates sluggish retinal circulation
• Nearly always adjacent to extensive areas of
capillary nonperfusion
• Focal vitreous traction

46. INTRA RETINAL MICROVASCULAR
ABNORMALITIES (IRMA) :
• Dilated, tortuous retinal capillaries
• Shunt between arterioles and venules.
• Adjacent to areas of capillary closure.
• May resemble focal areas of flat NVE .
– In IRMA :
• Intraretinal location
• Absence of profuse leakage on FFA
• Failure to cross over major retinal blood vessels.

48. PROLIFERATIVE DIABETIC RETINOPATHY
• Usually arise from veins
• NVD: within 1 disc diameter of the optic disc
• NVE: further than 1 disc diameter away
• Capillary non-perfusion is more extensive in
NVD
• More often in younger patients (<40 yrs.)

50. • Vessels grow along the path of least resistance
– Absent ILM over the optic disc
– Posterior hyaloid face
• Associated with fibrous proliferation
– Vascular (into the vitreous cavity, surface of
retina/disc)
– Avascular (thickening of the posterior hyaloid)

51. PDR and the Vitreous
• PVD in diabetics leads to shrinkage of the
entire vitreous
• New vessels are pulled into the vitreous by
it’s contracting forces
• Vitreous hemorrhage, breaks and RD
• Vitrectomy inhibits neovascularisation

52. Hemorrhage in PDR
• Location:
– Subhyaloid: settles down and absorbed faster
– Into the vitreous: very slow clearing
– Sub-ILM: round/oval/boat shaped
• Increased progression to RD

53. DIABETIC RD
• TRACTION ALONE (Non-rhegmatogenous)
– Confined to the posterior pole (rarely beyond
2/3rd distance to the equator
– Taut and shiny surface
– Concave towards the pupil
– No shifting/subretinal fluid

55. DISEASE ENTITIES

56. • CLASSIFICATION
– NPDR
• Mild
• Moderate
• Severe
– PDR
– Advanced diabetic eye disease
• DIABETIC MACULOPATHY
• DIABETIC PAPILLOPATHY

57. MicroaneurysmsMild NPDR
Mild NPDR plus hemorrhages, hard exudates, cotton wool
spots .
Moderate NPDR
Moderate NPDR plus one of :
1. Intraretinal Hges in four quadrants .
2. Marked venous beading in two or more quadrants
3. IRMA one or more quadrants.
Severe NPDR
(4-2-1 rule)
Two or more of the above features described in severe NPDRVery severe
NPDR

58. New vessels and/or fibrous proliferations; or preretinal
and/or vitreous hemorrhage
Early PDR
1. NVD ≥ 1/3 of DD.
2. less extensive NVD, if vitreous or preretinal
hemorrhage is present .
3. NVE ≥ half disc area, if vitreous or preretinal
hemorrhage is present
PDR with High
Risk
Characteristics
1. Extensive vitreous hemorrhage precluding grading.
2. Retinal detachment involving the macula.
3. Phthisis bulbi .
Advanced
Diabetic Eye
Disease
Early Treatment Diabetic Retinopathy Study Research Group: Early Photocoagulation for diabetic
retinopathy. ETDRS Report Number 9. Ophthalmology 98:766, 1991
Approximately 50% of patients with severe NPDR progress to proliferative retinopathy with high-
risk characteristics within 1 year.

59. Diabetic Maculopathy
• Macular ischemia
– Retinal capillary non-perfusion
– Progressive NPDR
• Macular edema
– Increased retinal vascular permeability
– Seen in both NPDR and PDR
– Most common cause of visual loss in DR

60. Clinically Significant Macular Edema
(CSME)
1. Retinal edema within 500 µm of the center of the
fovea .
2. Hard exudates within 500 µm of the fovea, if
associated with adjacent retinal thickening (which
may be outside the 500 µm limit) .
3. Retinal edema that is one disc area (1500 µm) or
larger, any part of which is within one disc
diameter of the center of the fovea.

64. Focal macular edema
Diffuse macular edema

65. Macular ischemia

66. DIAGNOSING DME
• Slit lamp biomicroscopy
– Contact lens
– 78 D / 90 D
• FFA
– leakage on the FA does not equate to clinical retinal thickening
or edema
– focal leakage: well-defined focal area of leakage from
microaneurysms or dilated capillaries
– diffuse leakage: presence of widespread leakage from IRMA,
retinal capillary bed
– diffuse cystoid leakage: diffuse leakage and pooling of dye in
the cystic spaces of the macula in the late phase of the
angiogram
– Macular ischemia

71. Brian Y. Kim S, Scott D et al. Optical Coherence Tomographic Patterns of Diabetic Macular
Edema .Am J Ophthalmol 2006;142:405–412.

72. • Sponge like Thickening
– most common presentation
– mostly in outer retinal layers while internal layers
maintain their normal reflectivity
– spongy appearance with increased retinal
thickness

73. • Cystoid Spaces
– second most common pattern
– intra-retinal cystoid spaces
– involves variable depth of retina and
has intervening septa in between
– progresses gradually to involve the
whole of retinal thickness

74. • Serous Detachment
– Seen as a hypo-reflective area between neurosensory retina
and RPE
• Taut Posterior Hyaloid Membrane
– Taut, thickened, shiny, glistening hyper-reflective membrane
– Striations on retina over the posterior pole
– Attachment to the disc and the top of the elevated macular
surface
– Retinal thickness is greatly increased
– Intra-retinal hyporeflective cyst like cavities (corresponding
to fluid accumulation)
– Foveal detachment

75. • Atypical form of nonarteritic anterior ischemic optic
neuropathy (NAION)
• No visual symptom
• Non-specific minimal visual disturbance such as
painless mild blurring or distortion
• Visual acuity is usually normal or mildly diminished,
except coexisting diabetic maculopathy occurs
• Usually resolves within 2-10 months with residual mild
optic atrophy
DIABETIC
PAPILLOPATHY

76. DIFFERENTIAL DIAGNOSIS
• Radiation retinopathy
• Hypertensive retinopathy
• Retinal venous obstruction (central retinal vein
occlusion (CRVO), branch retinal vein occlusion (BRVO))
• Ocular ischemic syndrome
• Anemia
• Leukemia
• Coats’ disease
• Idiopathic juxtafoveal retinal telangiectasia
• Sickle cell retinopathy

77. ASYMMETRIC DR
• CAUSES
– Myopia ≥5 D,
– Anisometropia >1 D,
– Amblyopia,
– Unilateral elevated intraocular pressure,
– Complete posterior vitreous detachment,
– Unilateral carotid artery stenosis,
– Ocular ischemic syndrome, and
– Chorioretinal scarring

78. MANAGEMENT

79. METABOLIC CONTROL
• SINGLE MOST IMPORTANT STEP
– HbA1C < 7%
– Lipid profile
– Systoilc BP < 130 mmHg
– KFTs
– Proteinuria

80. MEDICAL THERAPY
• ASPIRIN
• TICLOPIDINE
• PENTOXIFYLLINE
• No significant role

81. LASER TREATMENT
• 1959, first reported by Meyer-Schwickerath,
who used a xenon arc photocoagulator
• Goal
– Cause regression of existing neovascular tissue
– prevent progressive neovascularization.

82. LASER TREATMENT
• Neovascularisation with high risk characteristics
• Severe NPDR in both eyes
• One-eyed patient with severe NPDR- other eye lost
because of complications of PDR
• Pregnant ladies with severe NPDR
• Diabetics with severe NPDR likely to undergo
cataract surgery in near future
• Unlikely to follow-up regularly
• Significant areas of capillary nonperfusion and
leakage.

83. MECHANISM OF ACTION
• Increase in oxygenation from the choroid to the inner retina
through the laser scars due to the thinning of the retina in the
treated area
• Autoregulatory response to breathing pure oxygen improves
• Decreases choroidal circulation in the midperiphery, which in
turn shunts blood flow centrally, (“reverse choroidal steal”)
• Hypoxic retina to anoxic
• Destroys highly metabolically active outer retinal cells, reducing
retinal oxygen consumption
• Increase in vasoinhibitors

85. • DRS
– 50% reduction in severe visual loss in eyes with severe
NPDR or PDR
– Visual acuity of 20/100 or better that had
– Risk of severe visual loss with PDR at the 2-year
follow-up
• 6% in the treated eyes compared
• 16% in the control group
• High-risk characteristics,
– 11% in the treated eyes
– 26% in the control group.

86. • Macular edema should be treated first
• Treat the inferior quadrant first
• Limits:
– Posteriorly : Superiorly & Inferiorly - temporal vascular
arcades
– Nasally - ½ DD from disc
– Temporally - 2 DD from foveal center
• Avoid the horizontal meridians
• Avoid in areas of prominent fibrovascular
membranes, vitreoretinal traction and tractional
retinal detachment
• Green, red or diode laser photocoagulation may be
used when vitreous hemorrhage or cataract
prevents the use of an argon laser.

87. Under topical anesthesia
Argon green (514 nm)
Half to one burn width apart
500 u spot size with the Goldmann lens
200 u with the Rodenstock panfundoscopic or Volksuperquad lens
Burn intensity : mild whitening of retina

91. SIDE EFFECTS
• Pain during the treatment
• Decrease in night vision,
• Impaired colour vision,
• Impaired peripheral vision (5%),
• Loss of 1 or 2 lines of visual acuity (3%),
• Mydriasis,
• Glare,
• Temporary loss of accommodation,
• Photopsias,
• Macular edema may be aggravated,
• Exudative retinal detachment,
• Retinal breks,
• Ciliochoroidal effusion,
• Elevated intraocular pressure,
• Angle-closure glaucoma,
• Subretinal or epiretinal fibrosis
• Damage to cornea/iris/lens
Stoltz RA, Brucker AJ: Lasers in diabetes; in Fankhauser F, Kwasniewska S (eds):
Lasers in Ophthalmology. The Hague, Karger Publications, 2003, pp 229–240.

92. • Topical non-steroidal anti-inflammatory drops
• 2 weeks and 4 weeks (to see for any untoward
complications),
• Follow-up visits at 3-month
• Additional laser is needed in at least 30% of
patients
• Between prior laser scars
• Peripheral retina

93. • Signs of a good successful laser:
– Reduced number of exudates and hemorrhages,
– Stabilization / sometimes improvement of visual
acuity,
– Reduction in the angry look of NVD / NVE,
– Appearance of fibrous component in the areas of
previous new vessels,
– Reduced caliber of retinal vessels

95. • The Early Treatment
Diabetic Retinopathy
Study (ETDRS) set the
guidelines for
treatment of DME :
– Glycemic control
(DCCT),
– O ptimal BP control
(UKPDS) and
– Macular focal/grid
photocoagulation
reducing the risk of
moderate vision loss by
50% (from 24% to 12%
after 3 years).

96. LASER THERAPY FOR DME
• FOCAL TREATMENT (leaking microaneurysm 500 –
3000 u from center)
– Aim : closure of leak
• GRID TREATMENT (diffuse leak 500 u away form
center)
– Aim : stimulate retinochoroidal pump

97. ETDRS protocol

98. VEGF

99. ANTI VEGF THERAPY
• Bevacizumab (Avastin)
– monoclonal antibody to VEGF which binds to and
neutralize all the active forms of the VEGF molecule
– 4 to 6 weekly injections
• Ranibizumab (Lucentis)
– humanized, antigen-binding fragment (Fab) of a second-
generation, recombinant monoclonal antibody directed
against VEGF
• Aflibercept (Eylea)
– recombinant fusion protein consisting of vascular
endothelial growth factor (VEGF)-binding portions from
the extracellular domains of human VEGF receptors 1 and
2, that are fused to the Fc portion of the human IgG1
immunoglobulin
– 8 weekly injections

101. ANTI VEGF THERAPY

105. • DA VINCI (2008)
– VEGF Trap Eye Vs laser in DME
– Change in BCVA at 24 and 52 weeks
– VEGF Trap eye significantly better
• VISTA DME (2011)
– VEGF Trap Eye in center involving DME

106. STEROIDS
• Intravitreal Triamcinolone Acetonide
– 4mg/0.1 mL
• Flucinolone acetonide implant
– low-dose (0.23 micrograms/day) or high-dose (0.45
micrograms/day) insert that lasts for 36 or 24 months
respectively
– FAME trial (2011)
• Ozurdex
• Posurdex
• Frequent side effects

107. • Diabetic Retinopathy Clinical Research Network
(drcr.net),
– 150 clinical centers and
– 500 physicians in United States,
– 840 eyes, intravitreal TA (1 mg or 4 mg) was compared
with focal/grid photocoagulation in patients with
DME.
• After a two-year period,
– photocoagulation produced superior visual acuity and
retinal thickness measurements and had fewer side-
effects than TA

108. SURGICAL MANAGEMENT
• INDICATIONS OF PPV:
– Dense, non-clearing vitreous hemorrhage (6
months)
– TRD involving/threatening the macula
– Combined TRD and RRD
– Diffuse DME with posterior hyaloid traction
– Significant recurrent vitreous hemorrhage despite
maximal PRP

109. • Severe progressive fibrovascular proliferation
• Anterior hyaloid fibrovascular proliferation
• Intractable ghost cell glaucoma
• Anterior segment neovascularisation with
media opacities (PRP not possible)
• Dense premacular hemorrhage

110. Objectives of Vitrectomy in DR
• Removal of axial opacities
• Relief of anteroposterior and tangential traction
• Segmenting or peeling of epiretinal membranes
• Endolaser treatment
• Effecting hemostasis
• Closure of all retinal breaks
• Treatment and prophylaxis of complications

111. • PVD induction is a major issue
• Segmentation,
• Delamination, and
• en bloc delamination

112. DRVS STUDY
• Vitrectomy 1 to 4 months after the onset of
severe vitreous hemorrhage for type 1
diabetics yields final vision greater than or
equal to 20/40 in 36% of this sub-group as
compared to only 12% with conventional
management (p =.001)

113. PHARMACOLOGIC VITREOLYSIS
• Ocriplasmin (JETREA)
• Recombinant protease with activity against
fibronectin and laminin
• FDA approval on 17 October 2012

114. FOLLOW UP

117. • Diabetic retinopathy induces vision loss
– Type 1 diabetes
• proliferative retinopathy,
– Type 2 diabetes,
• macular edema, and proliferative retinopathy is
relatively rare.