Diabetic retinopathy Introduction, classification, clinical features, Diabetic macular edema, diagnosis, examination, investigations, management, hallmark studies.

1. DIABETIC
RETINOPATHY
DR. UMAIRA LIAQAT
PG-2

2. INTRODUCTION
 Diabetic retinopathy is a chronic, progressive and
potentially sight-threatening disease of the retinal
vasculature, associated with prolonged hyperglycemia and
other conditions associated with DM, such as
Hypercholesterolemia and Hypertension.

3. EPIDEMIOLOGY
 5th commonest cause of acquired visual loss worldwide
 Leading one among the working population
 Globally, no. of people with Diabetes will increase to 552
million by 2030
 Diabetic retinopathy 191 million
 Vision threatening diabetic retinopathy 56.3 million

4. CLASSIFICATION
 Early Treatment Diabetic Retinopathy Study (ETDRS)
Classification / Modified Airlie House Classification
 AAO classification
 NSC-UK classification
 Scottish Diabetic Retinopathy Grading System

7. Descriptive Classification
1. RETINOPATHY
On the basis of presence or absence of new abnormal vessels:
• NPDR
• PDR
2. MACULOPATHY
• Focal
• Diffuse
• Ischemic
• Clinically significant Macular edema

8. NPDR

9. PDR
Described according to:
 LOCATION:
• NVD (On or within 1 disc diameter of disc margin)
• NVE (Elsewhere in retina more than 1DD from disc margin

10. Maculopathy
 Focal Edema
 Diffuse Edema
 Ischaemic Maculopathy
 Clinically Significant Macular Edema
 Center involving Macular Edema (thickening in the macula
involving central subfield zone that is 1mm in diameter)
 Non-Center involving Macular Edema

11. RISK FACTORS
 NON-MODIFIABLE RISK FACTORS:
1. DURATION & AGE AT ONSET:
• Before the age of 30, after 10yrs incidence of DR: 50%
• After the age of 30, 90%
• Rarely develops within 5 years of onset of diabetes.

12. 2. PUBERTY:
• Physiological increased resistance to insulin at this age
• Surge of Growth Hormone
• Adolescent diabetics are more prone to VTDR, as compared
to adult patients.
3. GENDER:
• Males > Females
• Inherent resistance to some neurodegenerative changes that
precede background DR in type 2 DM

13.  MODIFIABLE RISK FACTORS:
1. GLYCEMIC CONTROL:
• Early control can prevent or delay development and
progression of DR
• More beneficial in Type 1 DM
• Risk of complications can be decreased by 21% per 1%
HbA1c decrement.
2. HYPERTENSION:
• 10mm Hg reduction in mean systolic blood pressure reduces
microaneurysm count, hard exudates and cotton wool spots
over 4-7 years time by 11%

14. 3. PREGNANCY:
• Sometimes associated with rapid progression of DR
• Risk is related to severity of DR in first trimester
• DME developed late during pregnancy may resolve on its
own
4. MISCELLANEOUS:
• Raised Serum Cholesterol
• Nephropathy
• Obesity
• Smoking

15. SYMPTOMS
• Asymptomatic in initial stages
• Blurred vision
• Floaters and flashes
• Distorted vision
• Dark areas in vision
• Poor night vision
• Impaired color vision
• Partial or total loss of vision

16. CLINICAL FEATURES OF NPDR
1. MICROANEURYSMS:
• Localized outpouching of capillary wall.
• Inner nuclear layer
• Tiny red dots, often initially temporal to fovea.
• May leak, producing dot haemorrhage, edema or exudate, or
may thrombose.
• EARLIEST SIGN OF DR.
• FA: tiny hyperfluorescent dots in early frames and diffuse
hyperfluorescence in late frames ,due to leakage.

17. MICROANEURYSMS

18. 2. RETINAL HAEMORRHAGES:
 RETINAL NERVE FIBER LAYER HAEMORRHAGES:
• Larger superficial pre-capillary arterioles
• Flame shaped or splinter haemorrhages because of RNFL
architechture
 INTRARETINAL HAEMRORRHAGES:
• Venous end of capillaries
• Dot/Blot Haemorrhages in the compact middle layers of retina.
 DARK ROUND HAEMORRHAGES:
• Haemorrhagic retinal infarcts in middle retinal layers
• Increased likelihood of progression to PDR

19. RNFL HAEMORHAGES

20. DOT/BLOT HAEMORHAGES

21. DEEP DARK ROUND HAEMORHAGES

22. 3. EXUDATES:
• Caused by chronic localized retinal edema
• Develop at the junction of normal and edematous retina
• Composed of lipoprotein and lipid filled macrophages
• Mainly in Outer plexiform layer
• SIGNS: Waxy yellow lesions with distinct margins
• Arranged in clumps or rings at posterior pole
• Chronic leakage of microaneurysms leads to enlargement and
deposition of cholesterol
• FA: Hypofluorescence only with large dense exudates
• Retinal capillary fluorescence is preserved over the lesions

23. HARD EXUDATES

24. 3. COTTON WOOL SPOTS:
• Accumulation of neuronal debris in RNFL
• Ischaemic disruption of axoplasmic flow at the edge of infarct
• Not Specific to DR
• Removed by autolysis and phagocytosis
• SIGNS: small fluffy white lesions, obscuring underlying
vessels.
• FA: focal hypofluorescence due to local ischaemia and blockage
of background choroidal fluorescence

25. COTTON WOOL SPOTS

26. 4. VENOUS CHANGES:
The extent of retinal area exhibiting venous changes correlates with
progression to PDR
 VENOUS BEADING:
• Foci of venous endothelial cell proliferation that have failed to
develop into new vessels.
• FA: vessel wall staining
 VENOUS SEGMENTATION:
• Usually occurs along venous beading
 VENOUS LOOPS:
• Due to small vessel occlusion and opening of alternative
circulation

27. VENOUS CHANGES

28. 5. INTRARETINAL MICROVASCULAR
ABNORMALITIES:
• Arteriolar-venular shunts bypassing the capillary bed
• Often seen adjacent to areas of marked capillary hypo perfusion
• SIGNS: Fine, irregular, red intraretinal lines running from
arterioles to venules, without crossing major vessels
• FA: focal hypofluorescence with adjacent areas of capillary
dropout without leakage
• They resemble telangiectatic vessels in youngs
• But telangiectatic vessels are leaky and cause retinal edema and
exudation.

29. IRMA

30. 6. ARTERIAL CHANGES:
• Retinal arteriolar dilatation
• Early sign of ischaemic dysfunction.
• Peripheral narrowing
• Obliteration of vessel lumen
• Silver wiring: portion of the narrowed blood vessel develops
such an opaque wall that no blood is visible within it

31. ARTERIAL CHANGES

32. CLINICAL FEATURES OF PDR
1. NEW VESSELS AT DISC (NVD):
• Neovascularization on or within 1 disc diameter from disc
margin
• Normal vessels taper off from disc and do not return
• NVDs always loop back, may form a network and are wider
at top of loop
• Form as a result of generalized retinal ischaemia or even
wide spread macular ischaemia
• Leaky on FA

33. NVD

34. 2. NEW VESSELS ELSEWHERE (NVE):
• Occur along the border between the healthy retina and areas
of capillary occlusion,
• Resemble IRMAs, but IRMAs never form loops
• Any unusual blood vessel forming loops is supposed to be a
new vessel, until proven otherwise.
3. NEW VESSELS ON IRIS (NVI):
• Indicates more wide spread ischemia
• May lead to NVG by formation of new vessels in angle
(NVA)

35. NVE

36. NVI

37.  FLUORESCEIN ANGIOGRAPHY:
• It highlights neovascularization during early phase of angiogram
• Irregular expanding hyperflorescence during late stages, due to
intense leakage
• Can be used to confirm the presence of new vessels
• And to delineate areas of ischemic retina that might be
selectively targeted for laser treatment
4. NEW VESSELS ON ANTERIOR HYALOID FACE:
• Usually occur after vitrectomy if insufficient ablation of
peripheral retina is done

38. 5. NEW VESSELS AT VITREO RETINAL INTERFACE:
• Dynamic interaction between blood vessels and posterior
hyaloid face.
• It leads to an inflammatory response and scar formation
• Scar pulls the new vessels from retinal surface leading to:
o Sub-hyaloid haemorrhage
o When vitreous detaches, subhyaloid blood enters the
vitreous cavity converting into vitreous haemorrhage
o Tractional RD
o Combined traction/rhegmatogenous RD

39. SUBHYALOID HAEMORRHAGE

40. DIABETIC MACULAR EDEMA
• The most common cause of visual impairment in diabetics
• Fluid is located between outer plexiform and inner nuclear layer
initially
• Later it may also involve the inner plexiform and nerve fiber layer,
till full thickness of retina becomes edematous
• With central fluid accumulation, fovea assumes a cystoid appearance
(cystoid macular edema), detected on OCT
• On FA, it assumes a central flower petal pattern

41. DME

42. FA OF CMO

43.  FOCAL MACULOPATHY:
• Well circumscribed retinal thickening associated with complete
or incomplete rings of exudate
• Caused by focal leakage from microaneurysm and dilated
capillary segments
• FA: late focal hyperfluorescence due to leakage
 DIFFUSE MACULOPATHY:
• Diffuse retinal thickening caused by extensive capillary leakage,
may be associated with cystoid changes
• FA: mid and late phase diffuse hyperfluorescence and
demonstrates CMO, if present

44. FOCAL AND DIFFUSE MACULAR EDEMA

45.  ISCHAEMIC MACULOPATHY:
• Signs are variable
• Macula may look relatively normal, despite decreased visual
acuity
• FA: capillary non perfusion at the fovea, enlarged Foveal
avascular zone
• Other areas of capillary non perfusion at the posterior pole and
periphery

46. ISCHAEMIC MACULOPATHY

47.  CLINICALLY SIGNIFICANT MACULAR EDEMA :
• Defined in the ETDRS as:
1. Retinal thickening within 500 micrometers of the centre of
macula
2. Hard exudates within 500 micrometers of center of macula,
associated with retinal thickening of adjacent retina
3. Retinal thickening of one disc diameter or larger, any part of
which is within one disc diameter of the centre of macula

48. CSME

49. CSME

50. DIAGNOSIS
HISTORY:
• Duration, type and treatment of diabetes
• Medical hx ( obesity, hypertension, IHD, CVA, renal disease,
pregnancy, neuropathy, smoking)
• Ocular hx ( trauma, other ocular diseases, injections, surgery,
laser treatment, refractive procedures)
• Medication hx (Pioglitazone)

51. EXAMINATION
• Visual Acuity
• Slit lamp biomicroscopy
• IOP
• Gonioscopy before dilation, when indicated
• Pupillary assessment for optic nerve dysfunction
• Dilated fundoscopy with 78 or 90D lens
• Indirect ophthalmoscopy for examination of peripheral retina

52. INVESTIGATIONS:
• Blood pressure
• FBS
• RBS
• HbA1c
• Lipid profile
• CBC
• RFT
• Electrolytes

53. ANCILLARY TESTS:
• Color and Red free fundus photography
• Optical Coherence tomography (OCT)
• Fluorescein Angiography (FA)
• OCT angiography (OCT-A)
• B-Scan ultrasonography
• Fundus Autofluorescence (FAF)

54. FUNDUS PHOTOGRAPHY:
To detect diabetic retinopathy and to document:
• The severity of disease
• Presence of NVE and NVD
• The response to treatment
• Need for additional treatment on future visits
• Color Fundus photographs are used best for white lesions like
exudates and cotton wool spots
• Other lesions like microaneurysms and retinal haemorrhages are
best visualized by red free fundus photographs.

55. OPTICAL COHERENCE TOMOGRAPHY:
Provides high resolution images of vitreoretinal interface,
neurosensory retina and subretinal space
• Used to quantify and monitor retinal thickening
• To identify vitreomacular traction
• To evaluate the patients with difficult /questionable
examination for DME
• To investigate other causes of macular edema
• To screen a patient with no or mild diabetic retinopathy
• SD-OCT cannot identify foveal ischaemia and widening
of FAZ

56.  FLUORESCEIN ANGIOGRAPHY:
• To guide laser treatment for CSME
• To identify suspected but clinically obscure retinal
neovascularization
• To rule out other causes of macular edema
• To identify areas of capillary non-perfusion and enlarged FAZ
• UWF-FA can reveal more pathology than conventional field
imaging, for example:
o Peripheral microaneurysms and neovascularization
o Vascular non perfusion and leakage
o Peripheral retinal ischaemia

57. OCT-ANGIOGRAPHY:
• Ability to visualize depth-resolved, capillary-level
abnormalities in the three retinal plexuses
• Offering a much more quantitative assessment of macular
ischemia
• Can also detect preclinical microvascular changes
• Quantitative FAZ metrics to demonstrate FAZ area,
acircularity index and axis ratio
• Cannot visualize vascular leakage
• Areas of DME act as flow voids and they appear larger than
the cystoid spaces themselves, giving an inaccurate
impression.

58. B-SCAN ULTRASONOGRAPHY:
• Assessment of the status of the retina in the presence of a
vitreous hemorrhage or other media opacity
• To assess the amount of vitreous hemorrhage
• To define the extent and severity of vitreoretinal traction
• To diagnose diabetic retinal detachments in the setting of
media opacity.

59. FUNDUS AUTOFLUORESCENCE:
• Non-invasive modality
• Short wavelength FAF derives signal mainly from Lipofuscin
in RPE
• Near Infrared FAF derives its signal from melanin in RPE and
Choroid
• It represents the metabolic activity of RPE
• The visual potential may be predicted indirectly by assessing
the status of RPE and photoreceptors.
• Previous laser marks not clinically evident, can easily be
detected with FAF

60. MANAGEMENT:
 General Measures
 Laser Photocoagulation
 Intravitreal Anti-VEGF agents
 Intravitreal Corticosteroids
 Pars plana Vitrectomy

61. GENERAL MEASURES:
• Patient education
• Diabetic control
• Control of hypertension and Hyperlipidemia
• Fenofibrate 200mg daily (reduces progression)
• Smoking cessation
• Treatment of other risk factors like anemia and renal disease

62. LASER PHOTOCOAGULATION:
• Focal/grid laser
• Scatter laser/PRP
INDICATIONS FOR PRIMARY PRP:
• High risk PDR
• Early PDR (when new vessels are flat and NV complexes are
less than 1/3rd DD)
• Severe or Ischaemic NPDR
• Young type 1 Diabetic
• Fellow eye blind from DR
• Family history of blindness from DR
• Poor patient compliance to follow-up
• Prior to cataract operation or pregnancy

63. MACULAR FOCAL LASER:
o Laser applied directly to leaking microaneurysms 500-3000ìm
from center of fovea.
o Spot size: 50-200 micrometer
o Duration: 80-100ms (0.08-0.1sec).
o Power: Adjust power to produce a greyish burn.
o Lesions as close as 300ìm from center may be lased provided
these are not inside FAZ

64. FOCAL LASER

65. MACULAR GRID LASER:
o Applied to areas of diffuse retinal thickening
o Laser performed from 500 to 3000ìm superiorly and inferiorly
and to 3500 µm temporally from fovea.
o No treatment is applied to area within 500ìm of the disc
margin.
o Spot size: 50-200ìm,
o Duration: 80-100ms (0.08-0.1 sec)
o Spacing: 1-1.5burn apart.
o Power: Adjust power to produce a gentle blanching burn.

66. GRID LASER

67.  PROCEDURE OF PRP:
• Anaesthesia: topical/sub-tenon/peribulbar
• Laser: Argon Blue-Green laser
• Contact Lens used: Panfunduscopic lens/ Mainster lens
• Laser parameters:
o Spot size: 400 micrometer
o Duration: 10-50ms
o Spacing: 1-1.5 burn width
o Target: Grey white burns
o Extent of area treated: 1500 in initial setting
o Mild PDR: 2500-3500, Moderate PDR: 4000, Severe
PDR: 7000

68. PRP

69. MECHANISM OF PRP:
• Decreased retinal demand for oxygen
• Decreased release of angiogenic factors
• Mechanical inhibition of NV formation
INDICATORS OF REGRESSION POST-PRP:
• Blunting of vessel tips
• Shrinking and disappearance of NV
• Regression of IRMA
• Increased fibrosis
• Absorption of retinal haemorrhages
• Disc pallor

70. COMPLICATIONS:
1. EARLY:
• Iris burns
• Macular burns
• Retinal tears
• VH
• CME
• Choroidal detachment
• Malignant glaucoma
2. LATE:
• Decreased VA
• Deterioration of night
vision and color vision
• Tractional RD
• ERM
• CNV

71. INTRAVITREAL ANTI-VEGF AGENTS:
• Ranibizumab (Lucentis)(Patizra)
• Bevacizumab (Avastin)
• Aflibercept (Eylea)
INDICATIONS:
• CSMO involving macular center with reduced VA and
significant foveolar thickening on OCT
• PDR with persistent VH with aim to avoid vitrectomy
• As initial treatment of rubeosis iridis whilst a response to PRP
is realized
• For rapid control of very severe PDR to minimize risk of
haemorrhage

72. DOSAGE:
• Ranibizumab: 0.3-0.5 mg/ 0.05ml
• Bevacizumab: 1.25mg/ 0.05ml
• Aflibercept: 2.0mg/0.05ml
TREATMENT REGIMES:
• Fixed monthly injections:
Feasible in the start of therapy for initial 3-6 months
• PRN (pro renata) Regime:
Follow up visits and monitoring adjusted according to
disease response
• Treat and Extend Regime:
Treatment with extended intervals bimonthly or so

73. CONTRAINDICATIONS
• Recent stroke
• Recent MI
• Pregnancy
• Non-healing wounds
• Scheduled major surgery
COMPLICATIONS:
• SCH
• Cataract
• Glaucoma
• Endophthalmitis
• Vitreous Haemorrhage
• Retinal Detachment

74. INTRAVITREAL CORTICOSTEROIDS:
• Ozurdex (Dexamethasone) : 0.7mg
• Iluvien (Flucinolone acetonide) : 0.19mg
• Retisert (Flucinolone acetonide) : 0.59mg
• Triamcinolone Acetonide : 1-4mg/0.05ml
INDICATIONS:
• Anti-VEGF failure: significant edema and poor vision
after 6 injections and laser
• Pseudophakic patient with low glaucoma risk
• Recent cataract surgery (CME component)
• Anti-VEGF Contraindicated: Pregnancy, stroke, non-
healing wounds, myocardial infarction

75. ADVANTAGES:
• Less frequent injections
• Also treats inflammatory component
• Safe in pregnancy
• Ozurdex helpful in vitrectomized patients
DISADVANTAGES:
• Cataract
o Virtually 100%, causing significant problems within a
year
• Glaucoma
o 40% require therapy
o May even need filtration surgery or removal of steroid
implant

76.  SURGICAL TREATMENT:
INDICATIONS OF PPV:
1. COMMON:
• Tractional RD involving macula
• Combined tractional and rhegmatogenous RD
• Persistent VH (>6 months for NIDDM, 3 months for IDDM)
2. LESS COMMON:
• Progressive fibrovascular proliferation (Anterior hyaloid)
• Rubeosis with VH (preventing adequate PRP)
• Dense pre-macular VH
• Ghost cell glaucoma
• Macular edema with macular traction
• Significant recurrent VH despite maximal PRP

77. BENEFITS:
Prevents or delays:
• Persistent intra-gel haemorrhage
• Retinal detachment
• Opaque membranes
• Rubeosis Iridis
 POOR PROGNOSTIC FACTORS:
• Age >40yrs
• Pre-op iris neovascularization
• No previous laser
• Retinal detachment
• Cataract
• VA< 5/60

78. SPECIAL CONSIDERATIONS:
 CATARACT SURGERY & DR:
 PRE-OPERATIVE:
• Plan to operate early, before CSMO or high-risk PDR develops
• If possible, treat CSMO and wait until resolved before operating
• Treat high-risk PDR/NVI preoperatively if possible.
• If no fundus view, perform B-scan. If TRD or VH is present,
refer for possible combined phaco-vitrectomy.
• If high-risk PDR/NVI and unable to complete preoperative PRP,
perform intraoperative indirect PRP

79.  INTRA-OPERATIVE:
• Phacoemulsification technique is preferred.
• Use a large-diameter optic, acrylic IOL
• If intraoperative PRP is required, perform after crystalline lens
removal and before intraocular lens insertion.
 POST-OPERATIVE:
• If ME is present within 1 week, it should be considered due to
diabetes and treated as above.
• ME that develops after 1 week-6 months is probably PPK and
may resolve spontaneously. Manage expectantly for upto 1 year
• Frequent reviews in eyes with severe NPDR or worse, as there is
an increased risk of progression.
• Promptly treat high-risk PDR that occurs in the postoperative
period.

80.  PREGNANCY & DR:
• Ideally, patients should be reviewed preconception to assess
baseline retinopathy.
• Minimum review is at the end of the first trimester, weeks 20–
24, then weeks 30–34.
• Arrange more frequent review if there is severe retinopathy/
maculopathy or poor diabetic control.
• Avoid fluorescein angiography if possible.
• Treat by laser as required.

81. EVIDENCE BASED MANAGEMENT

82. TREATMENT OF DME

83. MAJOR STUDY TRIALS
 ETDRS (Early Treatment of Diabetic Retinopathy Study)
 DRS (Diabetic Retinopathy Study)
 DRVS (Diabetic Retinopathy Vitrectomy Study)
 DCCT (Diabetic Control and Complications Trial)
 UKPDS (UK Prospective Diabetic Study)

89. INTRA-VITREAL INJ TRIALS
 RANIBIZUMAB VS SHAM
• BCVA significantly improved in ranibizumab compared to sham.
• TRIALS: RISE and RIDE
 RANIMIZUMAB VS FOCAL LASER
• Ranibizumab monotherapy or combined with laser showed
superior BCVA improvements over laser treatment alone
• TRIALS: READ – 2, RESTORE and REVEAL

90.  AFLIBERCEPT VS FOCAL LASER
• Mean change in BCVA and CST Values significantly better in
aflibercept vs. laser
• Similar efficacy in monthly vs 2 monthly aflibercept
• TRIALS: VIVID and VISTA
 STEROIDS
• Compared to the sham group, patients receiving the steroid
implants had a significantly greater BCVA gain and CFT
reduction
• There was also significantly higher rate of cataract formation and
glaucoma in steroid groups compared to sham groups
• TRIALS: FAME A & B and MEAD trials

91. COMPARISON TRIALS
 DRCR.NET PROTOCOL I:
• Comparison of laser, ranibizumab + laser and triamcinolone+
laser
• Triamcinolone was not superior to focal/grid laser and had more
adverse outcomes
• Ranibizumab with prompt or deferred focal/grid laser had
superior VA and OCT outcomes compared to laser alone
• Pseudophakic patients gained equivalent in the ranibizumab/laser
as the triamcinolone/laser group but had much higher incidence
of glaucoma

92.  DRCR.NET PROTOCOL T
• Comparison of Ranibizumab, Bevacizumab and Aflibercept in
diabetic macula edema
• Visual acuity improved in all three groups over 2 years
• Overall, in terms of VA improvement, none of the medications
showed any significant advantage over the others
• For subgroups with worse vision at baseline or thicker maculas at
baseline, aflibercept performed better at year one, but at 2 years,
it had no advantage over ranibizumab but still remained superior
to bevacizumab
• Regardless of agent used, number of anti-VEGF injections
required in the 2nd year was reduced

93.  DRCR.NET PROTOCOL S:
• Prompt PRP vs. Ranibizumab + Deferred PRP for PDR
• PRP effective for PDR over last 4 decades; remains effective in
21st century
• Ranibizumab for PDR is at least as good as (non-inferior to) PRP
for visual acuity at 2 years
• It was noted that visual functions and visual fields were better
preserved in Anti-VEGF group.
• No substantial safety concerns for at least 2 years
• 5 years results were published by AAO in 2018
• Unfortunately, the visual benefits which anti-VEGF showed at 2
year could not be maintained. And at 5 years both groups showed
similar outcome in terms of visual functions.

94. LATEST ADVANCES & FUTURE
PROSPECTS IN DR
 SCREENING:
• EYEART: A new FDA autonomous AI system for detecting DR
 IMAGING:
• OCT-Angiography: Uses variation in phase and intensity of a light
signal to infer vascular structures
• DOPPLER OCT
 LASER:
• Frequency doubled Nd-YAG Laser: PASCAL
• Micro-pulse Subthreshold diode Laser

95. PRP THROUGH PASCAL

96. GRID LASER APPLICATION THROUGH PASCAL

97.  PHARMACOLOGICAL AGENTS:
• Long Acting Anti-VEGF: Abicipar Pegol
• Refillable, trans-scleral ranibizumab reservoir
• Anti-VEGF producing encapsulated cell chamber filled with
immortalized RPE cells
• PKC Inhibitors: Ruboxistarin
• Ocriplasmin: Proteolytic enzyme, non-surgically inducing PVD
 VITREORETINAL SURGERY:
• Bimanual dissection techniques with Chandelier lighting or an
illuminated pick
• Mixed gauge Vitrectomy: 27-gauge instruments inserted through 24-
gauge cannulas

99. MCQS
1. An uncontrolled diabetic patient had decreased vision in both eyes.
On examination he had NVD < 1/4th DD, a large pre retinal
hemorrhage inferior to disc & CSME. What could be the best
possible treatment option for this patient?
a. PRP
b. Avastin + Prompt PRP
c. PRP + Focal laser
d. Avastin + Deferred PRP
e. Avastin + Focal laser

100. 2. A pseudophakic, type 2 diabetic patient presents with worsening
vision due to center involving macular edema, CMT less than 370
micron. He has no previous ocular treatment. Which of the
following treatment option would be the most appropriate choice
for this patient?
a. Aflibercept
b. Dexamethasone Implant
c. Focal argon laser
d. Ranibizumab

101. 3. A 58 yrs old college principal had Hx of sudden loss of vision in
her R eye since last 02 months which is static and not improving
without treatment. O/E her BCVA is HM OD & 6/36 OS. Fundus
examination shows dense vitreous hemorrhage in R eye precluding
retina view while L eye has PDR with dry macula. What could be
your next step of management?
a) FFA OS
b) B Scan OD
c) Intra vitreal Avastin OU
d) Vitrectomy OD
e) PRP OU

102. 4. B Scan OD shows no TRD. What could be the best treatment option
for her Right eye?
a. Observation for 03 months
b. Avastin injections monthly
c. Pan Retinal Photocoagulation
d. Avastin F/B 25G PPV+EL
e. Avastin F/B 25G PPV+EL+S.oil

103. 5. A 63 yrs old retired army officer with uncontrolled diabetes presented
to you for diabetic retinopathy screening. His fundus photograph &
OCT macula are given below. What could be the best possible
treatment option for him?
a) Observation
b) Avastin injections
c) Scatter PRP
d) Avastin + PRP
e) Dexamethasone implant