This document discusses diabetic retinopathy, including: - The two main types of diabetes and how they relate to retinopathy risk and onset age. - Diabetic retinopathy as a leading cause of blindness and its impact. - Key risk factors like diabetes duration, glycemic control, and other systemic factors. - The characteristic lesions and stages of non-proliferative and proliferative retinopathy. - Treatment approaches including laser photocoagulation, anti-VEGF injections, steroids, and surgery. - Screening guidelines based on diabetes type and risk level.

1. Dr. Atul Kumar Anand
Senior Resident
AIIMS Patna

2. Retina is frequently affected by systemic
diseases & its manifestations are termed
as retinopathy, e.g. – diabetic retinopathy,
hypertensive retinopathy

3. Two main types of diabetes :
 Insulin-dependent diabetes (IDD):
- known as type 1 .
- develops most frequently between 10
and 20 years of age .
 Non-insulin-dependent diabetes (NIDD):
- also known as type 2.
- develops most frequently between the
ages of 50 and 70 years.

4. Diabetic retinopathy is a leading cause of
new cases of blindness in people aged 20
to 74 years
It has a considerable impact on both the
patient and the society because it typically
affects individuals in their most productive
years

5. Blindness is 25 % more common in
diabetics than non diabetics.
Prevalence of PDR is much more in type I
than type II.
Diabetic retinopathy more severe in type I
than type II.

6. 1. The duration of diabetes :
 the most important factor.
 5-10 yrs of diabetes – 27%
 >10yrs – 71-90%
 20-30 yrs – 95% ( 30-50 % PDR)

7. It is extremely rare for DR to develop
within 5 years of the onset of diabetes.
about 5% of Type II have NPDR at
presentation perhaps due to the lag
between onset and diagnosis.

8. 2 . Glycemic control : 2nd important risk factor
the only important modifiable factor
 Although good metabolic control of diabetes will not
prevent DR, but it may delay its development &
progression by a few years.
 increased severity of diabetic retinopathy is
associated with poorer glucose control.
 insulin treatment is associated with a decreased
risk of either the development or progression of
diabetic retinopathy in patients with type 1 diabetes.

9. With strict control of DM:
- risk of developing retinopathy was
reduced by 75% .
- 50% reduction in the rate of progression
of retinopathy in existing retinopathy
Diabetes Control and Complications Trial (DCCT) Research Group N Engl J Med
1993; 329:977-986.

10. 3 . Miscellaneous factors :
- pregnancy (Hormonal changes) – 10% new
onset and 4% NPDR to PDR
- systemic hypertension – independent risk
factor
- renal diseases
- anaemia.( ↓oxygen )
- elevated serum lipid.
- smoking
- Alcohol. ( ? )
- Obesity.

11. PVD :
• complete PVD may prevent the
development of PDR because the hyaloid
is needed as a scaffold for retinal
neovascularization.
• attached posterior hyaloid has also been
associated with an increased risk for DME

12. High myopia :
• choroidal degeneration and extensive old
chorioretinopathy protect against DR.
• believed to act in the same manner as pan
retinal photocoagulation by reducing the
metabolic needs of the retina

13. Removal of cataract :
• DR may progress after cataract surgery.
• If the cataract preclude retina evaluation
and treatment, prompt postoperative
retinal evaluation and treatment should
considered.

14. Diabetic retinopathy is a microangiopathy
affecting the retinal precapillary arterioles,
capillaries and venules .
Retinopathy has features of both:
- microvascular leakage. (mild- mod NPDR)
- microvascular occlusion .(severe NPDR-
PDR)

15. Microvascular leakage is caused by:
Loss of pericytes
 The pericytes are wrapped around the capillaries and are
thought to be responsible for the structural integrity of the
vessel wall.
Impairment of endothelial tight junctions
Weakening of capillary walls
Elevated levels of vascular endothelial
growth factor (VEGF)

16. Loss pericytes
Microvascular leakage
haemorrhage retinal oedema
Diffuse
Localized
Microanurysm”
”

17.  Microvascular occlusion : caused by
1. thickening of the capillary basement
membrane.
2. capillary endothelial cell damage and
proliferation.
3. changes in red blood cells leading to
defective oxygen transport, and
increased stickiness and aggregation
of platelets

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

20. New vessel proliferation
Fibrous glial
tissue
proliferaion
Tractional RD
RD
IRMA

21. Diabetic retinopathy is asymptomatic in early
stages of the disease
As the disease progresses symptoms may
include
• Blurred vision
• Floaters
• Fluctuating vision(Flactuating refractive error
& cataract)
• Distorted vision
• Dark areas in the vision
• Poor night vision
• Impaired color vision
• Partial or total loss of vision

22.  Microaneurysms :
- located in the inner nuclear layer .
- the first clinically detectable lesions .
- small round dots .(20-200 μ)
- mostly located near and temporal to the
macula.
- When coated with blood they may be
indistinguishable from dot
haemorrhages.

23. MICROANEURYSM

24.  Haemorrhages :
The clinical appearance depending on location
- 'dot' and 'blot' :
originating from the venous end of the
capillaries. located in the compact middle
layers of the retina .
- Flame-shaped :
originate from the more superficial precapillary
arterioles, follow the course of the retinal nerve
fibre layer. (linear disrtibution)

26. Hard exudates :
- located between the outer plexiform and
inner nuclear layers of the retina.
- They are often distributed in a (circinate
pattern) .
- The centres of rings of hard exudates
usually contain microaneurysms .
- Made up of accumulated lipoproteins .

28. Retinal oedema :
- located between the outer plexiform and
inner nuclear layers.
- Later it may involve the inner plexiform and
nerve fibre layers, until eventually the
entire thickness of the retina may become
oedematous.
- with further accumulation of fluid, the
fovea assumes a cystoid appearance .

29. Macular edema types: (FFA + Clinical)
1. Focal ME :which has identifiable leakage
source.
2. Diffuse ME: which has multiple
unidentifiable source of leakage.
3. Cystoid ME: in which fluid accumulate in
OPL and INL to form cystoid spaces.

30.  Vascular changes :
- venous changes :in the form of 'beading',
'looping' and 'sausage-like'
segmentation.
- It represent endothelial cell proliferation.
- arterioles may also be narrowed and
even obliterated, resembling a BRAO .
- The most powerful predictors for
development of PDR.

31.  Cotton-wool spots : (Soft exudates )
- Nerve fiber layer infarction.
- caused by capillary occlusion in the
retinal nerve fibre layer.
- The interruption of axoplasmic flow
caused by the ischaemia, and
subsequent build-up of transported
material within the nerve axons, is
responsible for the white and opaque
appearance of these lesions.
- Disappear within weeks to months.

32. HARD AND SOFT EXUDATES

33.  Intraretinal microvascular abnormalities (lRMA)
:
- Dilated, tortous retinal capillaries that act as a
shunt between arterioles and venules.
- frequently seen adjacent to areas of capillary
closure.
- IRMA may resemble focal areas of flat NVE . But
in IRMA :
1. intraretinal location.
2. absence of profuse leakage on fluorescein
angiography.
3. failure to cross over major retinal blood vessels.

34. IRMA- Intraretinal microvascular anomalies

35.  New Vessels:
- Unlike IRMA, they arise on the retinal
surface and may extend or be pulled into
the vitreous cavity.
- NVD : NV appears on or within one DD of
disc margin .
- NVE : any other location .

38. I. Non-proliferative DR (NPDR)
 Mild
 Moderate
 Severe
 Very severe
II. Proliferative DR (PDR)
 Early PDR
 PDR with HRC
 Advanced diabetic eye disease
III. Clinically significant macular edema (CSME)
- May exist by itself or along with NPDR and PDR

39. At least one microaneurysm - earliest
clinically detectable lesion
 Retinal hemorrhages
 Hard exudates

40. Microaneurysms and/or dot and blot
hemorrhages in at least 1 quadrant
Soft exudates (Cotton wool spots)

42. Any one of the following 3 features is
present
Severe hemorrhages in all 4 quadrants
Significant venous beading in 2 or more
quadrants
Moderate IRMA in at least 1 quadrant
Known as the 4-2-1 rule

43. Any two of the features of the 4-2-1 rule is
present

45. Characterized by
Proliferation of new
vessels from retinal
veins
 New vessels on the
optic disc or within 1
disc diameter(NVD)
 New vessels
elsewhere on the
retina (NVE)

47.  defined as the presence of one or more of the
following features:

1. Retinal oedema within 500 µm of the centre 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 oedema that is one disc area (1500
µm) or larger, any part of which is within one
disc diameter of the centre of the fovea.

49. Background DR(BDR): have microaneurysm,
haemorrhage, & exudates
Diabetic Maculopathy: presence of any retinopathy
at macula
Pre proliferative DR(PPDR): featutes of BDR +
IRMA, venous changes.
 Indicates progressive retinal ischemia with a
heightened risk of progression to retinal
neovascularization

50. PDR: have neovascularization( NVD/NVE)
Advanced diabetic eye disease(ADED):
have tractional RD, persistant VH, NVG

51. ADVANCED
DIABETIC
EYE
DISEASE
A. TRD
B. Rubeosis
C. Preretinal and
vitreous
haemorrhage

52.  Nonproliferative DRP :
Microaneurysms, retinal hemorrhage and hard
exudate
Mild NPDR
Mild NPDR plus 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
Two or more of the above features described in severe
NPDR
Very severe
NPDR
4 : 2 :
1
Rule

53.  Proliferative DRP :
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 HRC
1. Extensive vitreous hemorrhage precluding
grading.
2. retinal detachment involving the macula.
3. phthisis bulbi .
Advanced PDR

54.  Type 1 diabetes - screen within 3-5 years of diagnosis
after age 10
 Type 2 diabetes - screen at time of diagnosis
 Pregnancy - women with preexisting diabetes should be
screened prior to conception and during first trimester

55. Fluorescein Angiography :
- Not needed to identify CSME or PDR.
- But :
1. As a guide during CSME treatment.
2. Identify macular capillary nonperfusion

56. Color Fundus photography :
- For Documentation purpose .
Ultrasonography :
- When opaque media preclude retinal
examination.
- Useful in ruling out :
1. RD.
2. Traction threatening macular detachment.

57. Medical Therapy :
• Glycemic control :
Tight control decrease risk of progression
of retinopathy , nephropathy and
neuropathy as well.
• Blood pressure control.
• Blood lipids control.

58. Laser :
The treatment of depends on the severity
of retinopathy and the presence or
absence of CSME, which may be present
at any stage .

59. All eyes with CSME should be considered
for treatment with laser photocoagulation
irrespective of the level of visual acuity
because treatment reduces the risk of
visual loss by 50%.

60. Treatment of clinically significant
macular oedema
• For microaneurysms in centre of hard
exudate rings located 500-3000 m
from centre of fovea
Focal treatment
• Gentle whitening or darkening of
microaneurysm (100-200 m, 0.10
sec)
• For diffuse retinal thickening located
more
than 500 m from centre of fovea and
500 m from temporal margin of disc
Grid treatment
• Gentle burns (100-200 m, 0.10 sec),
one burn width apart

61.  Focal or Grid
• CSME in both NPDR and
PDR
 Panretinal (PRP)
• PDR

62.  The aim of treatment is to:
1. induce involution of new vessels .
2. prevent vitreous haemorrhage.
 Initial treatment involves the placement
of about 2000-3000 burns in a scatter
pattern, extending from the posterior
fundus to cover the peripheral retina in
one or more sessions.

63.  The technique of PRP is as follows:
1. Topical corneal anaesthesia is adequate
in most patients.
2. - The spot size :depends on which
contact lens is being used. (500 - 200
µm).
- The duration : between 0.10 and 0.05
second
- The power level : produces a gentle
burn

64. Indications for treatment of proliferative
diabetic retinopathy
NVD > 1/3 disc in area Less extensive NVD
+ haemorrhage
NVE > 1/2 disc in area
+ haemorrhage

65. • Spot size (200-500 m) depends
on contact lens magnification
• Gentle intensity burn (0.10-0.05 sec)
• Follow-up 4 to 8 weeks
• Area covered by complete PRP
• Initial treatment is 2000-3000 burns
Laser panretinal photocoagulation

67. Intra vitreal injection of bevacizumab (avastin)
or ranibizumamb(lucentis)
Intra vitreal injection of steroid: triamcinolone
acetonide (IVTA)

68. OZURDEX
 sustain-released dexamethasone intravitreal implant
 22 G needle
 last 6 mths
 FDA approved for
 BRVO/CRVO associated ME
 non-infectious uveitis
NEW COMERS

69. OZURDEX
NEW COMERS

70. Indications for vitreoretinal surgery: PPV
Retinal detachment involving
macula
Severe persistent vitreous
haemorrhage
Dense, persistent premacular
haemorrhage
Progressive proliferation
despite laser therapy

71. Strict glycemic control along with control of
blood pressure & blood lipid
CSME/PDR: laser(focal or grid or PRP){argon,
krypton, diode, frequency doubled YAG}
DME: anti VEGF, IVTA, ozurdex
ADED: surgery(PPV)
Follow up

72. Suggested follow-up
Retinal Finding
Annually
Normal
Every 9 months
Mild NPDR
Every 6 months
Moderate NPDR
Every 4 months
Sever NPDR
Every 2- 4 months
CSME
Every 6 months
CNSME
Every 2-3 months
PDR

73. Simulation of defective vision as experienced by a
Diabetic whose vision has been affected by Diabetic
retinopathy
Normal Defective