Diabetic retinopathy PPT by Dr Ajai (aiims Rishikesh)

1. DIABETIC RETINOPATHY

2. Acknowledgement
◦ Photographs in this presentation are courtesy of Dr.J J
Kanski
( Kanski JJ et al: Retinal vascular disease. In: Kanski JJ et
al,
eds: Synopsis of Clinical Ophthalmology. 3rd ed.
Philadelphia,
PA: Saunders; 2013:241-65.)
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3. Diabetes and eye disease – Learning
Objectives
◦ At the end of the class, students shall be able to
◦ Recognize the importance of diabetic retinopathy as a
public health problem
◦ Identify the risk factors for diabetic retinopathy
◦ Describe and distinguish between the stages of diabetic
retinopathy
◦ Understand the role of risk factor control and annual
dilated eye examinations in the prevention of vision loss
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4. Diabetes Mellitus
Diabetes Mellitus is a group of diseases characterized by high
blood glucose levels. Diabetes results from defects in the
body's ability to produce and/or use insulin.
◦ Type 1 diabetes is usually diagnosed in children and young
adults. In type 1 diabetes, the body does not produce insulin.
About 10% of people with diabetes have this form of the
disease.
◦ In Type 2 diabetes, either the body does not produce enough
insulin or the cells ignore the insulin. This is the most
common form of diabetes.
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5. Diabetic Retinopathy (DR)
Definition
◦Progressive dysfunction of the retinal blood
vessels caused by chronic hyperglycemia.
◦DR can be a complication of type 1 or type
2 diabetes
◦Initially, DR is asymptomatic
◦If not treated, it can cause low vision and
blindness.
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6. Diabetic Retinopathy
Epidemiology
◦The total number of people with diabetes is
projected to rise from 285 million in 2010 to
439 million in 2030.
◦Diabetic retinopathy is responsible for 1.8
million of the 37 million cases of blindness
throughout the world .
◦Diabetic retinopathy (DR) is the leading
cause of blindness in people of working age
in industrialized countries.
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7. Risk factors for Diabetic Retinopathy
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8. Duration of diabetes
◦ The best predictor of diabetic retinopathy is
duration of the disease
◦ After 20 years of diabetes, more than 90% of
patients with type 1 diabetes and 60% with type
2 have some degree on diabetic retinopathy
◦ 33% of patients with diabetes have signs of
diabetic retinopathy
◦ People with diabetes are 25 times more likely to
become blind than the general population.
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9. Other Risk factors
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• Poor Blood Sugar control
• Hypertension
• Hyperlipidemia
• Pregnancy
• Nephropathy
• Others: Smoking, Obesity,
Anemia

10. Pathogenesis of Diabetic Micro angiopathy
Diabetic Retinopathy is a microvasculopathy that causes:
◦ Retinal capillary occlusion
◦ Retinal capillary leakage
Microvascular occlusion is caused by:
◦ Thickening of capillary basement membranes
◦ Abnormal proliferation of capillary endothelium
◦ Increased platelet adhesion
◦ Increased blood viscosity
◦ Defective fibrinolysis
Microvascular leakage is caused by:
◦ Impairment of endothelial tight junctions
◦ Loss of pericytes
◦ Weakening of capillary walls
◦ Elevated levels of vascular endothelial growth factor (VEGF)
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11. Cotton –
wool spots
Neovascularization
Ischemia
Neovascula
r glaucoma
Microvascular
Occlusion
Fibrovascular
bands
Vitreous
hemorrhage
Increased
VEGF
Tractional
retinal
detachment
Infarction
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12. Edema
Retinal
hemorrhag
es
Hard
exudates
Microvascular
Leakage
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13. Pathogenesis
Normal Diabetic retinopathy

14. Healthy Retina Diabetic
Retinopathy
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15. Diabetic retinopathy
symptoms
Asymptomatic in early stages of the disease
As the disease progresses symptoms may include
◦ Blurred vision
◦ Floaters
◦ Fluctuating vision
◦ Distorted vision
◦ Dark areas in the vision
◦ Poor night vision
◦ Impaired color vision
◦ Partial or total loss of vision
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16. Natural History of Diabetic
Retinopathy
◦Mild nonproliferative
diabetic retinopathy
(NPDR)
◦Moderate NPDR
◦Severe NPDR
◦Very Severe NPDR
◦Proliferative diabetic
retinopathy (PDR) 16

17. Findings Obsd
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18. No retinopathy
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19. Histology of retina
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1 RPE
2 Layers of Rods & Cones
3 External Limiting Membrane
4 Outer Nuclear layer
5 Outer Plexiform layer
6 Inner Nuclear layer
7 Inner Plexiform Layer
8 Ganglion Cell layer
9 Nerve Fibre layer
10 Internal limiting membrane

20. Microaneurysms
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• Focal dilatations of retinal capillaries
• Appear as red dots.
• Seen at the posterior pole, especially
temporal to the fovea.
• The first ophthalmoscopically detectable
change in diabetic retinopathy.

21. Retinal Haemorrhages
21
Dot haemorrhages
• In the inner nuclear layer or outer plexiform
layer
• Bright red dots (same size as large
microaneurysms).
Dark Blot/ round haemorrhages
• Larger lesions
• Located within the mid retina
• Extent – marker for neovascularization
Flame Shaped haemorrhages
• Superficial and in the nerve fiber layer

22. Non-proliferative diabetic retinopathy (NPDR)
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23. Non-proliferative diabetic retinopathy (NPDR)
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24. Hard exudates ( Intra-retinal lipid exudates )
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•Yellowish waxy looking patches with
distinct margins
•Outer plexiform layer
•Surrounding capillaries and
microaneurysms, in a circinate pattern.

25. Hard exudates ( Intra-retinal lipid exudates )
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26. Cotton Wool Spots
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•Occlusion of retinal pre-capillary
arterioles supplying the nerve fibre
layer with concomitant swelling of
local nerve fibre axons.
•“Soft exudates" or "nerve fibre layer
infarctions"
•White, fluffy lesions in the nerve fibre
layer.

27. Cotton Wool Spots
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28. Late non proliferative changes
Intra-retinal microvascular abnormalities (IRMA)
• Represent intraretinal arteriolar-venular shunts
which have not breached the internal limiting
membrane of the retina.
• Indicate severe non-proliferative diabetic
retinopathy that may rapidly progress to
proliferative retinopathy.
Venous beading
• Focal narrowing and sausage-shaped dilatation
of the retinal veins.
• Sign of severe non proliferative diabetic
retinopathy.
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29. Late non proliferative changes
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30. 30
Clinical Findings
◦Microaneurysms
◦Management/Treatment
◦Annual follow-up
MILD NONPROLIFERATIVE
DIABETIC RETINOPATHY

31. MILD NONPROLIFERATIVE
DIABETIC RETINOPATHY
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Microaneurysms

32. 32
◦ Clinical Findings
◦ Microaneurysms/ medium to large Intraretinal
haemorrhages in 1- 3 quadrants
◦ Mild Intraretinal Microvascular Abnormalities
(IRMA’s)
◦ Venous beading in not more than 1 quadrant
◦ Cotton wool spots
◦ Management/Treatment
◦ 6-12 month follow-up without CSME
◦ Color fundus photography
Moderate Nonproliferative Diabetic Retinopathy
(NPDR)

33. Moderate Nonproliferative
Diabetic Retinopathy (NPDR)
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Hard exudates
Flamed shaped
hemorrhage
Microaneurysm

34. Severe Nonproliferative Diabetic
Retinopathy (NPDR)
34
Clinical Findings
Any of the following: (4-2-1 Rule)
◦ More than 20 intraretinal hemorrhages in each of four quadrants
◦ Definite venous beading in two or more quadrants
◦ Prominent Intraretinal Microvascular Abnormalities (IRMA) in
one or more quadrants
◦ And no signs of proliferative retinopathy

35. Severe Nonproliferative Diabetic Retinopathy
(NPDR)
Management/Treatment
• 3-4 month follow-up
• Color fundus photography
• Possible panretinal photocoagulation
• CSME present: color fundus photography, fluorescein
angiography, focal photocoagulation, 3-4 month follow-up
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36. Severe Nonproliferative Diabetic
Retinopathy (NPDR)
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Venous beading

37. 37
◦Clinical Findings
◦Ischemia induced neovascularization
◦at the optic disk (NVD)
◦elsewhere in the retina (NVE)
◦New vessels on the iris (NVI)
◦Vitreous hemorrhage/Pre-retinal haemorrhage
◦Retinal traction, tears, and detachment
Proliferative Diabetic Retinopathy
(PDR)

38. Proliferative Diabetic Retinopathy (PDR)
38
•Management/Treatment
–2-4 month follow-up
–Color fundus photography
–Panretinal photocoagulation (3-4
month follow-up)
–Vitrectomy

39. ROLIFERATIVE
DIABETIC
ETINOPATHY
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Neovascularization
Neovascularization
Hard exudate
Cotton-wool
spot
Blot hemorrhage

40. PROLIFERATIVE DIABETIC
RETINOPATHY
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41. High-Risk Proliferative diabetic retinopathy
At risk for serious vision loss
Any combination of three of the following four findings
◦ NVD <1/4 disc area with vitreous or preretinal hemorrhage.
◦ NVE > 1/2 disc area with vitreous or preretinal hemorrhage.
◦ NVD 1/4 to 1/3 disc area with or without vitreous or
preretinal hemorrhage.
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42. Diabetic macular edema
◦ Diabetic macular edema is the leading cause of
legal blindness in diabetics.
◦ Diabetic macular edema can be present at any
stage of the disease, but is more common in
patients with proliferative diabetic retinopathy.
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43. 43
Meta analysis and review on the effect on bevacizumab in diabetic macular edema
Graefes Arch Clin Exp Ophthalmol(2011) 249:15-27

44. Why is Diabetic macular edema so
important?
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◦ The macula is responsible for
central vision.
◦ Diabetic macular edema may
be asymptomatic at first.
◦ As the edema moves in to
the fovea (the center of the
macula) the patient will
notice blurry central vision.
◦ The ability to read and
recognize faces will be
compromised. Macula
Fovea

45. 45
◦ Normal ◦ Macular Edema

46. Clinically significant Diabetic macular
edema (CSDME)
◦ Thickening of the retina at or
within 500 µm of the center of
the macula.
◦ Hard exudates at or within
500 µm of the center of the
macula, if associated with
thickening of the adjacent
retina.
◦ Area of retinal thickening 1
disc area or larger, within 1
disc diameter of the center of 46

47. 47
Imaging of macular edema with optical
coherence tomography

48. Ischaemic Maculopathy
• Maculopathy in type 1 diabetics
is often due to drop out of the
perifoveal capillaries with non
perfusion.
• Enlargement of the foveal
avascular zone (FAZ) is
frequently seen on fluorescein
angiography.
• Ischaemic maculopathy is not
uncommon in type 2 diabetics
• Maculopathy in this group may
show both changes due to
ischaemia and retinal
thickening.
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49. Advanced diabetic eye Disease
• Persistent vitreous haemorrhage
• Diabetic tractional retinal detachment
• Neovascular Glaucoma
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50. Clinical Stages of Retinopathy
Vitreous hemorrhage

51. Late Complications
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TRACTIONAL RETINAL DETACHMENT

52. Clinical Stages of Retinopathy
New vessel growth

53. Diabetic Eye Disease
Key Points
•Treatments exist but work best
before vision is lost
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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
h ttp://one.aao.org/CE/PracticeGuidelines/PPP_Content.aspx?cid=d0c853d3-219f-487b-a524-326ab3cecd9a

54. Screening for diabetic eye problems
should ideally include the following
• The history of any visual symptoms or changes
in vision
• Measurement of visual acuity
• Iris examination by slit lamp biomicroscopy
prior to pupil mydriasis.
• Pupil mydriasis. ( tropicamide 0.5 %
• Patients should be accompanied by a relative
and instructed not to drive home.
• Examination of the crystalline lens
• Fundus examination
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55. PREVENTION
http://www.aao.org/newsroom/release/20091030.cfm
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90 percent of diabetic eye disease
can be prevented simply by
proper regular examinations,
treatment and by controlling
blood sugar.

56. 56

57. DIABETIC RETINOPATHY TREATMENT
The best measure for prevention of loss
of vision from diabetic retinopathy is
strict glycemic control
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58. Laser Photocoagulation
Laser Photocoagulation is recommended for
eyes with:
◦ Clinical significant macular edema CSME
◦ High risk Proliferative diabetic retinopathy
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59. Treatment

60. Panretinal laser photocoagulation
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61. Anti VEGF Injections
•Aflibercept
•Ranibuzumab
•Bevacizumab
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62. VITRECTOMY
•Remove vitreous
hemorrhage
•Repair retinal
detachment
•Allow treatment
with PRP

63. Treatment

64. CONCLUSIONS
Diabetic Retinopathy is
preventable through strict
glycemic control and annual
dilated eye examination by an
ophthalmologist.
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