2. INTRODUCTION
Diabetic retinopathy is a chronic progressive sight-threatening disease of
retinal microvasculature associated with prolonged hyperglycaemia &
other conditions linked to diabetes such as hypertension.

3. PREVALENCE
• The total number of people with diabetes is
projected to rise from 285 million in 2010 to
439 million in 2030.
• Diabetes remains a leading cause of legal blindness
between the ages of 25-65 years in the western
world.
• It is responsible for 1.8 million of the 37 million
cases of blindness throughout the world (4.9%).
• 33% of patients with diabetes have signs of
diabetic retinopathy.

4. RISK FACTORS

5. 1) DURATION OF DIABETES
• It’s the best predictor of diabetic retinopathy.
• In patients diagnosed with DM before the age of 30 years, the incidence of DR
after 10 years is 50%, and after 30 years 90%
• After 20 years of diabetes, nearly 99% of patients with type I DM and 60% with
type II have some degree of diabetic retinopathy. This is because PDR is a result
of very high average blood glucose levels that are more likely to be in DM type I
than type II.
• But for some understood reasons, the incidence of maculopathy is more in DM
type II than type I.
• DR rarely develops within 5 years of onset of diabetes or before puberty, but
about 5% of type II diabetics have DR at presentation.

6. Diabetic Eye Disease
Key Points
• Treatments exist but work best
before vision is lost
RECOMMENDED EYE EXAMINATION SCHEDULE
Diabetes type Recommended time
of first examination
Recommended
follow-up*
Type 1 3-5 years after diagnosis Yearly
Type 2 At time of diagnosis Yearly
Prior to pregnancy
(type 1 or type 2)
Prior to conception and
early in the first trimester
No retinopathy to mild-
moderate NPDR -
every 3-12 months
Severe NPDR or worse -
every 1-3 months
*Abnormal findings may dictate more frequent follow-up examinations

7. 2) POOR GLYCAEMIC CONTROL
•The severity of hyperglycemia is the key alterable risk factor associated with the
development of diabetic retinopathy.
•Tight blood sugar control, particularly when instituted early, can prevent or delay
the development or progression of DR.
• As per ‘The Diabetes Control and Complications Trial’,
intensive control reduced the risk of developing retinopathy by
76% and slowed progression of retinopathy by 54%.
• ‘The UK Prospective Diabetes Study’ concluded similar
results in DM type II patients (25% reduction in risk).
• However a sudden improvement in control may be associated
with progression of retinopathy in near term due to increase
in serum IGF level (Chantelau & Kohner).
• Type I diabetic patients appear to obtain greater benefit
from good control than those with type II.
• Raised HbA1c is associated with an increased risk of
proliferative disease. This is because of increased
oxygen-binding capacity of HbA1c leading to hypoxia.
•Target HbA1c level = 6.5-7 %.

8. 3) PREGNANCY
• Sometimes associated with rapid progression of DR.
• Key factors are-
– Greater pre-pregnancy severity of retinopathy
– Poor pre-pregnancy control of diabetes
– Control exerted too rapidly during the early stages of pregnancy
– Development of pre-eclampsia and fluid imbalance

9. 4) HYPERTENSION
• According to “Appropriate Blood-pressure Control in Diabetes
(ABCD) Trial”, target BP should be <140/80.
• Tight control appears to be particularly beneficial in type II diabetics with
maculopathy.
• The “EURODIAB Controlled Trial of Lisinopril in Insulin
Dependent Diabetes (EUCLID)” showed lowered rates of development
of retinopathy in diabetics taking lisinopril for anti-hypertensive medication as
compared to placebo.

10. 5) NEPHROPATHY
• Nephropathy, if severe, is associated with worsening of DR.
• Conversely, treatment of renal disease (ACE inhibitors and Angiotensin II
receptor antagonists) may be associated with improvement of retinopathy.

11. 6) OTHER RISK FACTORS
• Smoking
• Sex : M > F
• Hyperlipidemia (TG, LDL)
• Cataract surgery
• Obesity
• Anemia (leading to hypoxia)
• Carotid artery occlusive disease
• Alcohol (?)

12. High myopia, choroidal degeneration and extensive
old chorio-retinopathy protect against DR
Believed to act in the same manner as pan-retinal photocoagulation by reducing
the metabolic needs of the retina.

13. It is a microangiopathy caused by effect of hyperglycemia on small blood
vessels leading to -
• Retinal capillary occlusion
• Retinal capillary leakage
PATHOGENESIS

14. CELLULAR DAMAGE
Caused by-
• Sorbitol accumulation (Glucose Sorbitol)
• Free radical mediated oxidative stress
• Accumulation of advanced glycation end products (AGEs)
• Excessive activation of protein kinase C and diacyl glycerol
Aldose reductase

15. CAPILLAROPATHY
Characterized by-
• Death of pericytes
• Thickening of capillary basement membrane (sorbitol pathway)
• Loss of vascular smooth muscle cells (capillary acellularity)
• Endothelial proliferation
• Abnormalities of RBCs (leading to defective oxygen transport) and WBCs
• Increased platelet stickiness and adhesion
• Increased plasma viscosity
• Defective fibrinolysis and prolonged
clot lysis time

16. BREAKDOWN OF BLOOD RETINAL BARRIER
• Blood retinal barrier is composed of 2 parts-
– Inner BRB – tight junctions of retinal capillaries, endothelial cells
– Outer BRB – tight junctional complexes (zonula occludens and zonula
adherens) located between adjacent RPE cells
• Breakdown of this BRB leads to leakage of lipoproteins responsible for
formation of exudates.

17. NEOVASCULARISATION
• Caused by capillary non-perfusion leading to retinal hypoxia.
• New vessel growth is thought to be caused by an imbalance between
angiogenic and anti-angiogenic factors in an attempt to re-vascularise the
hypoxic retina.
• IRMA (Intraretinal microvascular abnormalities) are shunts that run between
the retina from arterioles to venules.
ANGIOGENIC FACTORS ANTI-ANGIOGENIC FACTORS
VEGF Endostatin
PDGF Angiostatin
HGF PEDF
FGF
Growth hormone

18. Cotton – wool spot
Neovascularization
Ischemia
Neovascular
glaucoma
Microvascular
Occlusion
Fibrovascular bands
Vitreous
hemorrhage
Increased VEGF
Tractional retinal
detachment
Infarction

19. NON-PROLIFERATIVE DIABETIC RETINOPATHY (NPDR)
NO DR Review in 12 months
VERY MILD
Microaneurysms only
Review most patients in 12 months
MILD
Any or all of:
microaneurysms, retinal hemorrhages, exudates, cotton
wool spots
Review range 6-12 months, depending on
severity of signs, stability, systemic factors,
and patient’s personal circumstances
MODERATE
Severe retinal haemorrhages in 1-3 quadrants or mild IRMA
Significant venous beading in no more than 1 quadrant
Cotton wool spots
Review in approximately 6 months
(PDR in up to 26%, high-risk PDR in up to 8%
within a year)
SEVERE
The 4-2-1 rule-
Severe retinal haemorrhages in all 4 quadrants
Significant venous beading in ≥2 quadrants
Moderate IRMA in ≥1 quadrants
Review in 4 months
(PDR in up to 50%, high-risk PDR in up to 15%
within a year)
VERY SEVERE
≥2 of the criteria for severe
Review in 2-3 months
(High-risk PDR in up to 45% within a year)
ABBREVIATED EARLY TREATMENT DIABETIC RETINOPATHY STUDY (ETDRS) CLASSIFICATION
CATEGORY MANAGEMENT

20. PROLIFERATIVE DIABETIC RETINOPATHY (PDR)
MILD-MODERATE
New vessels on the disc (NVD) < 1/3 disc area
New vessels elsewhere (NVE) < 1/2 disc area
Treatment considered according to severity of signs,
stability, systemic factors, and patient’s personal
circumstances
If not treated, review in up to 2 months
HIGH-RISK
NVD > 1/3 disc area
Any NVD with vitreous or preretinal
hemorrhage
NVE >1/2 disc area with vitreous or preretinal
hemorrhage
Laser photocoagulation
Intravitreal anti-VEGF agents
Intravitreal triamcinolone
Pars plana vitrectomy
Lipid lowering drugs
ADVANCED DIABETIC EYE DISEASE
Preretinal (retrohyaloid) and/or intragel
hemorrhage
Tractional retinal detachment
Tractional retinoschisis
Rubeosis iridis (iris neovascularisation)
Pars plana vitrectomy
CATEGORY MANAGEMENT
PDR requires the presence of newly formed blood vessels or fibrous tissue, or
both, arising from retina or optic disc and extending along the inner surface of
retina or optic disc or into the vitreous cavity.

21. OTHER DECRIPTIVE CATEGORIES
• BACKGROUND DIABETIC RETINOPATHY (BDR)
It’s the earliest phase of DR.
Characterised by microaneurysms, dot and blot hemorrhages and exudates.
• DIABETIC MACULOPATHY
Refers to presence of any retinopathy at the macula.
• PRE-PROLIFERATIVE DIABETIC RETINOPATHY (PPDR)
Cotton wool spots, venous changes, IRMA and deep retinal hemorrhages.
• DIABETIC PAPILLOPATHY
It is a form of optic neuropathy seen in young type I diabetics. It is unrelated to
glycemic control or any other known feature of diabetes.

22. VARIOUS CLASSIFICATION SYSTEMS
Grading of NPDR according to-
International / American Academy of Ophthalmologists (AAO) classification
• Mild
• Moderate
• Severe
National Screening Committee – United Kingdom (NSC-UK) classification
• Background (Level R1)
• Pre-proliferative (Level R2)
Scottish Diabetic Retinopathy Grading Scheme (SDRGS)
• Mild background (Level R1)
• Moderate background (Level R2)
• Severe background (Level R3)

23. PDR according to-
National Screening Committee – United Kingdom (NSC-UK) classification
is Level R3
Scottish Diabetic Retinopathy Grading Scheme (SDRGS)
is Level R4

24. APPROXIMATE EQUIVALENCE OF THE
CLASSIFICATION SYSTEMS
ETDRS NSC SDRGS AAO RCOphth
10 - None R0 - None R0 - None No apparent retinopathy None
20 - Microaneurysms only R1 - Background R1 - BDR Mild NPDR Low risk
35 - Mild NPDR Moderate NPDR
43 - Moderate NPDR R2 - Pre-
proliferative
R2 Moderate BDR High risk
47 - Moderately severe
NPDR
53 A-D - Severe NPDR R3 - Severe BDR Severe NPDR
53 E - Very severe NPDR
61 - Mild PDR
65 - Moderate PDR
R3 - Proliferative R4 - PDR PDR PDR
71, 75 - High risk PDR
81, 85 - Advanced PDR

25. SYMPTOMS
Diabetic retinopathy is asymptomatic in early stages of the disease.
As the disease progresses symptoms may include-
• Blurred vision
• Floaters and flashes
• Fluctuating vision
• Distorted vision
• Dark areas in the vision
• Poor night vision
• Impaired color vision
• Partial or total loss of vision

27. SIGNS OF DIABETIC
RETINOPATHY

29. MICROANEURYSMS
•Focal saccular dilatations of the capillary wall.
•Size = 20-100 µm
•Ophthalmoscopically visible (better on red free illumination) if larger than 30 µm.
Smaller ones can be visualized on angiography.
•Maximally seen in supero-temporal quadrant.
•Caused by-
-focal dilatation of the capillary wall where
pericytes are absent, or
-by fusion of two arms of a capillary loop
•Hyperfluorescent on fluorescein angiography

30. RETINAL HAEMORRHAGES
They may be small and round (dot and blot) or flame shaped depending on
their depth within the retinal layers.
Retinal hemorrhage spreads along the line of least resistance, constrained by
the local anatomy of the particular layer from which it arises. Therefore a
superficial bleed will track parallel to the nerve fiber layer resulting in a
longitudinal spread becoming flame shaped.
However deeper in the retina,
since the layers are vertically oriented
it results in circumscribed, round
hemorrhages (dot and blot).

31. EXUDATES
• Termed ‘hard’ exudates, are caused by chronic localised retinal oedema and
develop at the junction of normal and oedematous retina.
• Composed of lipoprotein and lipid-filled macrophages and are exuded from
microaneurysms.
• Located mainly within the outer plexiform layer.
• Hypofluorescent on FA.

33. DIABETIC MACULAR OEDEMA
• Diabetic maculopathy is the most common cause of visual impairment in
diabetic patients, particularly type II.
• According to the Wisconsin Epidemiologic Study of Diabetic
Retinopathy (WESDR), the prevalence rate of macular oedema is 10 %
in the diabetic population as a whole.
• Oedema is due to capillary leakage and the fluid is initially located
between the outer plexiform and inner nuclear layers. Later it may also
involve the inner plexiform and nerve fibre layers.
• With further accumulation of fluid the fovea assumes a cystoid
appearance: Cystoid Macular Oedema (CMO).
• Hyperfluorescent on FA.
• Best detected by slit-lamp biomicroscopy and stereoscopic fundus
photography.

35. Well-circumscribed retinal thickening Focal hyperfluorescence on FA
Circinate hard exudates Focal photocoagulation, good
prognosis
FOCAL DIABETIC MACULOPATHY
Maculopathy is of 4 types- focal, diffuse, ischemic and mixed.

36. DIFFUSE DIABETIC MACULOPATHY
Diffuse retinal thickening Generalized hyperfluorescence on FA
Frequent cystoid macular oedema Grid photocoagulation, guarded
prognosis

37. ISCHEMIC DIABETIC MACULOPATHY
Macula appears relatively normal Capillary non-perfusion on FA
Poor visual acuity
Occurs as a result of non perfusion of parafoveal capillaries with or without
intraretinal fluid accumulation.

38. MIXED DIABETIC MACULOPATHY
Diabetic maculopathies rarely exist isolated and most commonly have two or
more of the component.
Focal
IschemicDiffuse

39. Retinal thickening
within 500 µm of
centre of macula
Exudates within
500 µm of centre
of macula, if
associated with
retinal thickening
Retinal thickening one disc area (1500 µm)
or larger, any part for which is within
one disc diameter of centre of macula
CLINICALLY SIGNIFICANT MACULAR EDEMA (CSME)
As defined by ETDRS-

40. COTTON WOOL SPOTS
• Described by Mcleod D in 1975
• The term ‘soft exudates’ is a misnomer because cotton wool spots are not
exudates at all, but an accumulation of intracellular fluid and organelles as a
result of local ischemia
• Result from interruption of axoplasmic flow in the nerve fiber layer thereby
causing a gross, localized axonal distention known as ‘cytoid bodies’.
• Hypofluorescent on FA
• Once the cotton wool spot resolves, the nerve fiber and ganglion cells at that
spot atrophy, giving rise to ‘depression sign’.
• Other causes of cotton wool spots- hypertension, retinal vein occlusion,
retinal vasculitis, anemia, leukemia
VENOUS CHANGES
• Generalised dilatation and tortuosity
• ‘Looping’
• ‘Beading’
• ‘Sausage-like’ segmentation

42. IRMA
• Intraretinal microvascular abnormalities are arteriolar-venular shunts that
run from retinal arterioles to venules, thus bypassing the capillary bed
• Hyperfluorescent on FA

43. ARTERIAL CHANGES
• Retinal arteriolar dilatation (early marker of ischemia)
• Peripheral narrowing
• Silver wiring
• Obliteration

44. NEW VESSELS AT THE DISC (NVD) NEW VESSELS ELSEWHERE (NVE)
On or within one disc diameter of the
optic nerve head
Neovascularisation further away from
the disc
PROLIFERATIVE RETINOPATHY

45. NEW VESSELS ON THE IRIS (NVI)
Also known as ‘Rubeosis iridis’.
High likelihood of progression to neovascular glaucoma.

46. RETINAL DETACHMENT
Scar tissue from neovascularization shrinks leading to tractional RD.

47. VITREOUS HAEMORRHAGE
• Caused by bleeding from new vessels.
• When small, it’s perceived as floaters.
• A very large hemorrhage might block out all vision.
• Vitreous hemorrhage alone does
not cause permanent vision loss.
• When the blood clears, vision
may return to its former level
unless the macula has been
damaged.

48. EPIRETINAL MEMBRANE
• Also known as macular pucker, pre-macular fibrosis, surface wrinkling retinopathy
or cellophane maculopathy.
• Develops as a result of proliferation of cells between the vitreous and the macula.

49. BURNED OUT PDR
• When vitreous contraction has reached completion (i.e. when the vitreous has
detached from all areas of the retina except those where vitreo-retinal
adhesions associated with new vessels prevent such detachment), proliferative
retinopathy tends to enter the burned-out or ‘involutional’ stage.
• Vitreous haemorrhages decrease in frequency and severity.
• Some degree of RD is present.
• A marked reduction in the calibre of retinal vessels is characteristic of this
stage. Previously dilated or beaded veins return to normal calibre. Arterioles
decrease in calibre and also the number of visible branches are reduced.
• Only occasional retinal haemorrhages and microaneurysms are present.
• Fibrous tissue may become thinner and more transparent, allowing the retina
to be seen more clearly.
• Marked loss of vision at this stage is
explained by severe retinal ischemia.

50. DIAGNOSTIC TESTING

51. FLUORESCEIN ANGIOGRAPHY
- Identifies macular capillary non-perfusion.
- Identifies subtle areas of NV causing recurrent vitreous hemorrhage.

52. COLOUR FUNDUS PHOTOGRAPHY
For documentation purpose.
MODIFIED AIRLIE CLASSIFICATION uses 7 standard photographic fields to
detect neovascularisation.
RIGHT EYE
Field 1 - Disc
Field 2 - Macula
Field 3 - Temporal to macula
Field 4 - Superior-temporal
Field 5 - Inferior-temporal
Field 6 - Superior-nasal
Field 7 - Inferior-nasal

53. ULTRASONOGRAPHY
- When opaque media preclude retinal examination.
- Useful in ruling out :
1. Retinal detachment
2. Traction threatening macular detachment
3. Vitreous hemorrhage

54. OCULAR COHERENCE TOMOGRAPHY
MACULAR OEDEMA

55. COLOUR VISION ASSESSMENT
- Acquired blue-yellow defect.

56. CLINICAL TRIALS
Three major randomized clinical trials have largely determined the strategies
for appropriate clinical management of patients with DR -
1. Diabetic Retinopathy Study (DRS )
2. Early Treatment Diabetic Retinopathy Study (ETDRS)
3. Diabetic Retinopathy Vitrectomy Study (DRVS)

57. DIABETIC RETINOPATHY STUDY (DRS)
MAJOR ELIGIBILITY CRITERIA
1. Visual acuity ≥ 20/100 (6/36) in each eye
2. PDR in at least one eye or severe NPDR in both
3. Both eyes suitable for photocoagulation
MAJOR DESIGN FEATURES
One eye of each patient was assigned randomly to photocoagulation- scatter
(panretinal), local (for surface vessels) and focal (for macular oedema). The
other eye was assigned to follow-up without photocoagulation
MAJOR CONCLUSIONS
1. Photocoagulation reduced the risk of severe visual loss by 50 % or more
2. Modest risks of decrease in visual acuity and visual field
3. Treatment benefit outweighs risks for eye with high-risk PDR

58. EARLY TREATMENT DIABETIC
RETINOPATHY STUDY (ETDRS)
MAJOR ELIGIBILITY CRITERIA
1. Visual acuity ≥ 20/40 (6/12) {20/400 (60/120) if reduction caused by macular
oedema}
2. Mild NPDR to non-high risk PDR, with or without macular oedema
3. Both eyes suitable for photocoagulation
MAJOR DESIGN FEATURES
1. One eye of each patient was assigned randomly to early photocoagulation and
the to deferral (careful follow-up and photocoagulation if high risk PDR
develops).
2. Patients assigned randomly to aspirin or placebo.

59. MAJOR CONCLUSIONS
1. Focal photocoagulation (direct laser for focal leaks and grid laser for
diffuse leaks) reduced the risk of moderate visual loss by 50 % or more
and increased the chance of a small improvement in visual acuity
2. Both early scatter with or without focal photocoagulation and deferral
were followed by low rates of severe visual loss
3. Focal photocoagulation should be considered for eyes with CSMO
4. Scatter photocoagulation is not indicated for mild to moderate NPDR but
should be considered as retinopathy approaches the high-risk stage and
usually should not be delayed when the high-risk stage is present

60. DIABETIC RETINOPATHY VITRECTOMY
STUDY (DRVS)
GROUP H – Recent Severe Vitreous Haemorrhage
MAJOR ELIGIBILITY CRITERIA
1. Visual acuity ≤ 5/200 (5/60)
2. Vitreous hemorrhage consistent with visual acuity, duration 1-6 months
3. Macula attached
MAJOR DESIGN FEATURES
1. In most patients, only one eye was eligible
2. Eligible eye or eyes assigned randomly to early vitrectomy or conventional
management (vitrectomy if center of macula detaches or if vitreous
hemorrhage persists for 1 year, photocoagulation as needed and as possible)
MAJOR CONCLUSIONS
Chances of recovery of VA ≥ 10/20 (3/6) increased by early vitrectomy, at
least in patients with type I diabetes, who were younger and had more severe
PDR

61. GROUP NR – Very Severe PDR with Useful Vision
MAJOR ELIGIBILITY CRITERIA
1. Visual acuity ≥ 10/200 (3/60)
2. Center of macula attached
3. Extensive, active, neovascular, or fibrovascular proliferations
MAJOR DESIGN FEATURES
Same as Group H (except conventional management included vitrectomy
after a 6 months waiting period in eyes that developed severe VH)
MAJOR CONCLUSIONS
Chances of of VA ≥ 10/20 (3/6) increased by early vitrectomy, at least for eyes
with severe new vessels.
Early vitrectomy for eyes with recent severe VH and VA < 5/200 (5/60) was
beneficial, especially for patients with type I DM. Furthermore, the chances of
achieving VA of 10/20 (3/6) or better increased when early vitrectomy was
performed in eyes with severe new vessels, again especially for patients with
type I DM.

62. TREATMENT

63. INDICATIONS OF TREATMENT
NVD > 1/3 disc in area Less extensive NVD
+ hemorrhage
NVE > 1/2 disc in area
+ hemorrhage

64. TREATMENT OF UNDERLYING DISORDERS
• Glycemic control – Insulin, OHG
• Blood pressure control – Anti-hypertensive medications
• Cholesterol control – Statins, Fibrates
• Support renal function – ACEI, ARB
• Lifestyle modification – Smoking and alcohol cessation, exercise ,weight
control

65. • The history of retinal photocoagulation dates to 400 BC, when Plato described
the dangers of direct sun gazing during an eclipse.
• Czerny and Deutschmann, in 1867 and 1882, respectively, focused sunlight
through the dilated pupils of rabbits and created thermal burns in the animals’
retinas.
• Meyer-Schwickerath undertook the study of retinal photocoagulation in
humans in 1946 using the xenon arc lamp.
• The first clinical ophthalmic use of a laser in humans was reported by Campbell
et al. in 1963 and Zweng et al. in 1964.
• L’Esperance conducted the first human photocoagulation trial for ophthalmic
disease using the argon laser in 1968. He also introduced the frequency-doubled
Nd:YAG and krypton lasers in 1971 and 1972, respectively.
LASER PHOTOCOAGULATION

66. MECHANISM OF ACTION
Though not clear but it has been proposed that it may improve oxygenation
of ischemic inner retinal layers by destroying some of the metabolically
highly active photoreceptor cells and allowing oxygen (diffusing from
choriocapillaries) to continue into the inner layers of retina, relieving hypoxia
and removing the stimulus for expression of angiogenic factors.

67. 1. ARGON LASER (514.5 nm)
• All eyes with CSMO should be considered for laser photocoagulation
irrespective of the level of visual acuity.
• Reduces the risk of visual loss by 50%.
• Two types- focal and grid
i. Focal treatment - Burns are applied to microaneurysms and microvascular
lesions in the centre of rings of exudates located 500-3000 µm from the
centre of the macula.
Spot size - 50-100 µm
Exposure time - 0.1 sec

68. ii. Grid treatment – Burns are applied
to areas of diffuse retinal thickening
more than 500 µm from the centre
of the macula and 500 µm from the
temporal margin of the optic disc.
Spot size - 50-100 µm
Exposure time – 0.1-0.5 sec
• 70% of eyes achieve stable visual acuity after laser photocoagulation
• 15% show improvement
• 15% subsequently deteriorate.

69. 2. FREQUENCY-DOUBLED Nd:YAG LASER (532 nm)
• Less destructive than argon laser.
• PASCAL – Pattern Scan Laser uses frequency-doubled micropulse YAG in single
shot mode or in a predetermined array of up to 56 shots applied in less than a
second. It improves patient comfort.
3. MICROPULSE DIODE LASER (780-850 nm)
• Short duration (microseconds) burns are applied to RPE without significantly
affecting the outer retina and choriocapillaries.
4. DYE LASER (570-630 nm)
Yellow wavelength (577 nm) is absorbed by Hb and therefore direct closure
of microaneurysms and blood vessels can be achieved.
5. KRYPTON LASER (568-647 nm)
No longer in use.
6. YLF (YTTRIUM LITHIUM FLUORIDE) LASER
Currently under clinical trial

70. LASER SETTINGS
• SPOT SIZE depends on the contact lens used.
With Goldmann lens spot size is set at 200-500 µm, but with a
panfundoscopic-type lens it is set at 100-300 µm because of induced
magnification.
Other lenses used are – Volk, Mainster, Rodenstock
• DURATION OF BURN - 0.05-0.1 sec
• POWER - 250-570 mW, sufficient to produce only a light intensity burn
causing stimulation of the retinal pigment epithelium. The end point is a
whitening or darkening of the microaneurysms.
ANAESTHESIA
Topical anesthesia is adequate in most patients, although peribulbar or sub-
Tenon anesthesia may be necessary.

71. ASSESSMENT AFTER LASER PHOTOCOAGULATION
GOOD INVOLUTION POOR INVOLUTION
• Regression of neovascularization leaving
‘ghost’ vessels or fibrous tissue
• Decrease in venous changes
• Absorption of hemorrhages
• Disc pallor
• Persistent neovascularization
• Hemorrhage

72. BENEFITS OF LASER PHOTOCOAGULATION
RISK WITH TREATMENT
RISK WITHOUT TREATMENT0%
5%
10%
15%
20%
25%
30%
35%
40%
MILD NVD WITH
HEMORRHAGE SEVERE NVD
WITHOUT
HEMORRHAGE
SEVERE NVD WITH
HEMORRHAGE SEVERE NVE WITH
HEMORRHAGE
4% 9%
20%
7%
26% 26%
37%
30%

73. FOLLOW-UP
• After 4-6 weeks, the patients are reviewed.
• If some obvious treatable lesions are missed at the initial session, they are
treated 4 months after the initial treatment confirming this with FA.
• Follow-up should be done at 4 monthly intervals.
ADVERSE EFFECTS
• Paracentral scotoma.
• Transient increased edema and decreased vision.
• Choroidal neovascularization.
• Subretinal fibrosis.
• Scar expansion.
• Foveolar burns.

74. INTRAVITREAL ANTI-VEGF AGENTS
0.5 mg Ranibizumab given monthly for 3 months.
1.25 mg Bevacizumab given 3 monthly.
INTRAVITREAL STEROID
0.1 ml (4 mg) Triamcinolone.
Indicated when macular edema is associated with tangential traction from a
thickened and taut posterior hyaloid.
LIPID LOWERING DRUGS
Statins reduce progression of retinopathy by 25-50%.
PERIPHERAL CRYOABLATION
Since the advent of diode laser the role of peripheral cryoablation has decreased
as the infrared wavelength is unable to bypass media opacities such as cataracts
and minimal vitreous hemorrhages.

75. PARS PLANA VITRECTOMY

76. INDICATIONS OF PARS PLANA VITRECTOMY
Severe persistent vitreous hemorrhage Dense, persistent premacular hemorrhage
Progressive proliferation despite laser therapy Retinal detachment involving macula

77. BENEFITS OF PPV
Vitrectomy prevents or delays:
• Persistent intra-gel hemorrhage
• Retinal detachment
• Opaque membranes
• Rubeosis iridis
VISUAL RESULTS OF PPV
• 70 % of cases achieve visual improvement
• 10 % are made worse
• 20 % remain unchanged
POOR PROGNOSTIC FACTORS
• Age > 40 years
• Preoperative iris neovascularisation
• Cataract
• Visual acuity < 5/200 (5/60)
• Retinal detachment
• No previous photocoagulation

78. OTHER TREATMENT MODALITIES USED IN
PAST
• ASPIRIN AND ANTI-PLATELET TREATMENTS
Dipyridamole Aspirin Microangiopathy of Diabetes (DAMAD) Study and
Ticlopidine Microangiopathy of Diabetes Study (TMDS) did not demonstrate
any clinically beneficial effect.
• ALDOSE REDUCTASE INHIBITORS
The Sorbinil Retinopathy Trial using ‘Sorbinil’ drug showed no effect in slowing
of progression of retinopathy.
• PITUITARY ABLATION
Various types of procedures were used to suppress anterior pituitary function
ranging from external irradiation to transfrontal hypophysectomy and they
produced rapid improvement in intraretinal lesions of DR.

79. FUTURE PROSPECTS
• Inhibitors of advanced glycation end products
• Growth hormone antagonists

80. PRACTICAL CONCLUSIONS
The 4 major modes by which visual loss can occur in DR and their brief
management at a glance-
MACULOPATHY
• Fluorescein angiography
• Control diabetes
• Laser photocoagulation
• Vitrectomy (not totally accepted)
VITREOUS HEMORRHAGE
• PRP after spontaneous clearing of
hemorrhage or after vitrectomy
PDR WITH TRACTIONAL RD INVOLVING
OR THREATENING MACULA • Vitrectomy with PRP
INVOLUTED DR • Leave it alone

81. “That’s
all.