Diabetic retinopathy is a complication of diabetes that affects the eyes. It can progress from mild non-proliferative retinopathy to more severe proliferative retinopathy. Risk factors include duration of diabetes, poor blood sugar control, pregnancy, hypertension, and nephropathy. Symptoms may include blurred vision, floaters, and vision loss. Signs seen on eye exam include microaneurysms, hemorrhages, hard exudates, cotton wool spots, venous beading, neovascularization, and macular edema. Treatment depends on severity but may include improved blood sugar control, laser therapy, anti-VEGF injections, and vitrectomy surgery in advanced cases. Regular eye

1. Diabetic Retinopathy
Priyanshu Kumar

2. Retinopathy is the most important ocular
complication of diabetes. DR is more
common in type 1 DM than type 2 DM.
 Proliferative Diabetic Retinopathy (PDR)
affects 5-10% of diabetic population. Type 1
Diabetes are at particular risks, with an
incidence of upto 90% after 30 years.

3. RISK FACTORS ofDR
Duration of diabetes
-Most important
• Patient diagnosed before age 30 years
• 50% DR after 10 years
• 90% DR after 30 years
Poor metabolic control
• Less important, but relevant to development and
progression of DR
• Increased HbA1c associated with increased risk.

4.  Pregnancy
• Associated with rapid progression of DR
• Predicating factors : poor pre-pregnancy control
of DM, too rapid control during the early stages
of pregnancy, pre-eclampsia and fluid imbalance.
 Hypertension
• Very common in patients with DM type 2
• Should strictly control (<140/80 mmHg)

5.  Nephropathy
• Associated with worsening of DR
• Renal transplantation may be ass with
improvement of DR and better response to
photocoagulation
 Other
• Obesity, increased BMI, high waist-to-hip
ratio
• Hyperlipidemia
• Anemia

6. Pathogenesis
 Here microangiopathy occurs and it
leads to:
Microvascular occlusion
Microvascular leakage

7. Hyperglycemia
Intracellular sorbitol accumulation
Free radicals
Glycated end products
Disruption of ion channel function
Protein kinase C activation
Direct effect
on retinal cells
Microangiopathy
(damage to capillary wall)
Hematological &
Rheological changes
Intra retinal
Hemorrhages
Edema
Exudates
Microvascular Occlusion causes
Ischemia
IRMA
Neovascularization
Fibrosis
hemorrhage
Traction

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

10. SIGNS OF DIABETIC
RETINOPATHY
 Microaeurysm
 Retinal hemorrhage
 Hard exudates
 Cotton wool spot
 Venous beading
 Intraretinal microvascular
abnormalities (IRMA)
 Macular oedema

11. Microaneurysm
 Localized saccular outpouchings of capillary wall red dots
• Focal dilatation of capillary wall where pericytes are absent
• Fusion of 2 arms of capillary loop
 Usually seen in relation to areas of capillary non-perfusion
• at the posterior pole in temporal to fovea
 It is the earliest signs of DR

13. Scattered hyperfluorescent
Microaneurysms may leak plasma
constituents into the retina

14. Retinal Hemorrhage
 Capillary or microaneurysm is weakened rupture intraretinal
hemorrhages
 Dot & blot hemorrhages
• Deep hemorrhage - inner nuclear layer or outer plexiform layer
• Usually round or oval
• Dot hemorrhages - bright red dots (same size as large microaneurysms)
• Blot hemorrhages - larger lesions
 Flame-shape or splinter hemorrhages
• More superficial - in nerve fiber layer
• Absorbed slowly after several weeks
• Indistinguishable from hemorrhage in hypertensive retinopathy
• May have co-existence of systemic hypertension BP must be checked

15. Dot & blot VS splinter
hemorrhage

18. Hard exudate
 Intra-retinal lipid exudates
 Yellow deposits of lipid and protein within the retina
 Accumulations of lipids leak from surrounding capillaries and
microaneuryisms
 May form a circinate pattern
 Hyperlipidemia may correlate with the development of hard
exudates

20. Cotton Wool Spot
 White fluffy lesions in nerve fiber layer
 Result from occlusion of retinal pre-capillary arterioles
supplying the nerve fiber layer with concomitant swelling of
local nerve fiber axons
 Also called "soft exudates" or "nerve fiber layer infarctions“
 Fluorescein angiography shows no capillary perfusion in the
area of the soft exudate
 Very common in DR, specially if patient with hypertension.

22. Hard Exudate VS Cotton Wool
Spot

24. Venous beading
 Dilatation and beading of retinal vein
 Appearance resembling sausage-shaped dilatation of the
retinal veins
 Sign of severe NPDR

25. Intraretinal microvascular abnormalities
(IRMA)
 Abnormal dilated retinal capillaries or may represent
intraretinal neovacularization which has not breached the
internal limiting membrane of the retina.
 Severe NPDR indicate rapidly progress to PDR

26. Diabetic maculopathy
 Macular ischemia
• Retinal capillary non-perfusion
• Progressive NPDR
 Macular edema
Focal or diffuse or mixed
Increased retinal vascular permeability
Seen in both NPDR and PDR
Cause of visual loss in DR
Important in planning for treatment

28. Focal macular edema
Diffuse macular edema

29. Macular ischemia

30. Clinical Significant Macular
Edema
(CSME)
Retinal edema
within 500 microns
of centre fovea
Hard exudates within
500 microns of fovea
if ass with adjacent
retinal thickening
Retinal edema > 1 disc
diameter, any part is
within 1 disc diameter
of centre of fovea

31. CLASSIFICATION
 Non-proliferative Diabetic Retinopathy (NPDR):
• No DR
• Very Mild NPDR
• Mild NPDR
• Moderate NPDR
• Severe NPDR
• VerySevereNPDR
 Proliferative Diabetic Retinopathy (PDR):
• Mild to Moderate PDR
• High Risk PDR

32. Nonproliferative diabetic retinopathy
 Very Mild :
Indicated by the presence of at
least 1micro aneurysm.
 Mild :
Microaneurysms, retinal
haemorrhage, exudates, cotton
wool spots.

33.  Moderate:
• Includes the presence of
hemorrhages(1-3 quadrants), micro -
aneurysms, hardexudates and
Cotton woolspot. Microaneurysm
Exudate
Cotton wool

34.  Severe:
The (4-2-1) rule; one or more of:
• Hemorrhages and microaneurysms
in 4 quadrants.
• Venous beading in at least 2
quadrants.
• Intraretinal microvascular
abnormalities in at least 1 quadrant
IRMA
Beading

35. Proliferative diabetic
retinopathy
 5% of DM pt.
 Findings-
• Neovascularization : NVD, NVE
• Vitreous changes
 Advanced diabetic eye disease
• Final stage of Uncontrolled PRD
• Glaucoma (neovascularization)
• Blindness from persistent vitreous hemorrhage,tractional
retinal detachment, opaque membrane formation.

38. Rubeosis iridis
(neovascularisation of
the iris)
Neovascular glaucoma

39. Diagnostic Testing
 Fundus FluoresceinAngiography:
To guide treatment of CSME
To identify Ischemic maculopathy
Intraretinal microvascular
abnormalities vs Neovascularization
It can be evaluation in hazy media
It is not a screening modality
It is not a routine investigation

41.  Fundus Photography:
• For documentation purpose

42.  Optical Coherence Tomography(OCT):
Non contact
Non invasive
Micron resolution
Cross-sectional study of retina
Correlates very well with the retinal histology

43. Optical Coherence Tomography(OCT)
 Qualitative analysis:
Description by location
Description of form and structure
Identification of anomalous structures
Observation of the reflective qualities of
the retina
 Quantitative analysis:
Retinal thickness and volume
Nerve fiber layer thickness.

44. Retinal Anatomy Compared to OCT
 The vitreous - black space on the top of the image
 Fovea - normal depression
 Umbo- central hyper reflective dot within foveola
 The nerve fiber layer (NFL) and the retinal pigment epithelium (RPE)
• highly reflective than the other layers of the retina ( red – yellow)
 Retinal nerve fiber layer – thicker on nasal side of macula
 Areas of minimal signals ( blue – black)
 Outer nuclear layer – thickest portion

47.  Ultrasonography ( B- scan) :
• When opaque media preclude retinal examination.
• Useful in ruling out-
• Retinal detachment
• Traction threatening
macular detachment
• Vitreous hemorrhage.

48. Diabeticretinopathy
Normal
Comparison between Normal Retina &DR

49. Screening for DR
Patients withType 1 diabetes should have an
ophthalmologic examination within 5 years
after onset.
Patients with Type 2 DM should have an
ophthalmologic examination at the time of the
diabetes diagnosis.
If there is no DR then one annual examination
required.
If any level of DR, progression and sight
threatening, then examination will be required
more frequently

50. Screening for DR
Women with pre existing type 1 or type 2 DM
who are planning pregnancy or pregnant
should be counseled on risk of development &/
or progression of DR.
Eye examinations should be started from 1st
trimster and monitored every trimster and for 1
year of postpartum period.

51. Management
 Medical treatment .
 Observation.
 Laser therapy.
 Anti VEGF Agents
 Vitrectomy.

52. Medical treatment:
 Glucose control :
 controlling diabetes.
 maintaining the HbA1Clevel in the 6-7%range.
 Level of activity :
Maintaining a healthy lifestyle with regular exercise can
help reduce the complication of diabetes and DR.
 Blood pressurecontrol.
 Lipid-lowering therapy.

53. Laser therapy
 Panretinal photocoagulation (PRP)
High-risk PDR (3/4)
○ Vitreous or preretinal hemorrhage
○ New vessels on optic disc or within 1,500 microns
from optic disc rim
○ Large new vessels
Iris or angle neovascularization
CSME

54.  Focal or Grid laser
o CSME in both NPDR and PDR
Inducing involution of new vessels
Preventing vitreous hemorrhage and preventing visual
loss
Limitations :
○ Patient must have clear lens and vitreous
○ If cataract treat before laser PRP
○ If vitreous hemorrhage vitrectomy + laser
photocoagulation

55. (a) before and (b) after focal laser photocoagulation.
(b)
(a)

56. Focal
laser
Before After

57. Intravitreal Anti VEGF Agents
 Bevacizumab
 Ranibizumab
 Aflibercept

58. Surgery
 Pars plana vitrectomy (PPV)
Inications-
○ Severe persistent vitreous hemorrhage
○ Progressive tractional RD (threatening or involving
macula)
○ Combined tractional and rhegmatogenous RD
○ Premacular subhyaloid hemorrhage
○ Recurrent vitreous hemorrhage after laser PRP

59.  Vitrectomy:
 Removes blood
 Removes Traction
 Allows PRP

60. Vitrectomy

61. Aspirin indiabetic eye
 Aspirin use did not alter progression of diabetic
retinopathy.
 Aspirin use did not increase riskof vitreous
hemorrhage.
 Aspirin use did not affect visual acuity.
 Aspirin reducesriskof cardiovascular morbidity
and mortality.

62.  Follow up:
Retinalfinding Suggestedfollow-up
Normal Annually
Mild NPDR 1 year
Moderate NPDR 6 months-1year or referto
ophthalmologist.
Sever NPDR Every 4months
DME Every 2-4months
PDR Every 2-3months