Diabetic Retinopathy 2

Diabetic Retinopathy
Dr. Winnie
MS Ophthalmology
• Retinopathy is the most important ocular
complication of diabetes
• more common in T1DM
• Proliferative DR (PDR) affects 5-10% of
diabetic population
• T1DM are at higher risk-incidence 90% after
3o years
RISK FACTORS of DR
 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.
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)
 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
Pathogenesis
 Here microangiopathy occurs and it
leads to:
Microvascular occlusion
Microvascular leakage
Hyperglycemia
Intracellular sorbitol accumulation

Free radicals
Glycated end products
Disruption of ion channel function
Protein kinase C activation
Direct effect Microangiopathy Hematological &

on retinal cells (damage to capillary wall) Rheological changes
Intra retinal Edema Microvascular Occlusion causes

Hemorrhages Exudates Ischemia
IRMA
Neovascularization hemorrhage
Fibrosis Traction
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
SIGNS OF DIABETIC RETINOPATHY
 Microaeurysm
 Retinal hemorrhage
 Hard exudates
 Cotton wool spot
 Venous beading
 Intraretinal microvascular
abnormalities (IRMA)
 Macular oedema
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

Scattered hyperfluorescent
Microaneurysms may leak plasma
constituents into the retina
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
Dot & blot VS splinter hemorrhage
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
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.

Hard Exudate VS Cotton Wool Spot
Venous beading
 Dilatation and beading of retinal vein
 Appearance resembling sausage-shaped dilatation of the retinal

veins
 Sign of severe NPDR

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
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
Focal macular edema
Diffuse macular edema

Macular ischemia
Clinical Significant Macula
Edema-CSME
Retinal edema Hard exudates within Retinal edema > 1 disc

within 500 microns 500 microns of fovea diameter, any part is
of centre fovea if ass with adjacent within 1 disc diameter
retinal thickening of centre of fovea
CLASSIFICATION
 Non-proliferative Diabetic Retinopathy (NPDR):
• No DR
• Very Mild NPDR
• Mild NPDR
• Moderate NPDR
• Severe NPDR
• Very Severe NPDR
 Proliferative Diabetic Retinopathy (PDR):

• Mild to Moderate PDR
• High Risk PDR
Nonproliferative diabetic retinopathy
 Very Mild :
Indicated by the presence of at
least 1 micro aneurysm.
 Mild :
Microaneurysms, retinal
haemorrhage, exudates, cotton
wool spots.
 Moderate:
Exudate
• Includes the presence of
hemorrhages(1-3 quadrants), micro -
aneurysms, hard exudates and
Cotton wool spot. Microaneurys
m
Cotton
wool
 Severe:
The (4-2-1) rule; one or more of:
• Hemorrhages and microaneurysms
in 4 quadrants.
• Venous beading in at least 2 Beading
quadrants.
• Intraretinal microvascular
abnormalities in at least 1 quadrant IRMA
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.
Rubeosis iridis Neovascular glaucoma
(neovascularisation of
the iris)
Diagnostic Testing
Fundus Fluorescein Angiography:
– 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
 Fundus Photography:
• For documentation purpose
Optical Coherence Tomography(OCT):
– Non contact
– Non invasive
– Micron resolution
– Cross-sectional study of retina
– Correlates very well with the retinal histology
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.
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

 Ultrasonography ( B- scan) :
• When opaque media preclude retinal examination.
• Useful in ruling out-
• Retinal detachment
• Traction threatening
macular detachment
• Vitreous hemorrhage.
Comparison between Normal Retina & DR
Normal
Diabetic
retinopathy
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
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.
Management
 Medical
treatment .
 Observation.
 Laser therapy .
 Anti VEGF
Agents
 Vitrectomy.
 Medical treatment:
 Glucose control :
 controlling diabetes.
 maintaining the HbA1C level 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 pressure control.
 Lipid-lowering therapy.
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
 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
(b)
(a)
(a) before and (b) after focal laser photocoagulation.

Focal laser
Before After
Intravitreal Anti VEGF Agents
 Bevacizuma
b
 Ranibizumab
 Aflibercept
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
 Vitrectomy:
 Removes blood
 Removes Traction
 Allows PRP
Vitrectomy
Aspirin in diabetic eye
 Aspirin use did not alter progression of
diabetic retinopathy.
 Aspirin use did not increase risk of

vitreous hemorrhage.
 Aspirin use did not affect visual acuity.
 Aspirin reduces risk of cardiovascular morbidity

and mortality.
 Follow up:
Retinal finding Suggested follow-up
Normal Annually
Mild NPDR 1 year
Moderate NPDR 6 months - 1yearor refer to

ophthalmologist.
Sever NPDR Every 4 months
DME Every 2-4 months
PDR Every 2-3 months

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Diabetic Retinopathy

 Poor metabolic control

Intracellular sorbitol accumulation

Direct effect Microangiopathy Hematological &

Intra retinal Edema Microvascular Occlusion causes

 Usually seen in relation to areas of capillary non-perfusion

 It is the earliest signs of DR

 Dot & blot hemorrhages

 Flame-shape or splinter hemorrhages

 Yellow deposits of lipid and protein within the retina

 Accumulations of lipids leak from surrounding capillaries and

 May form a circinate pattern

 Hyperlipidemia may correlate with the development of hard

 Result from occlusion of retinal pre-capillary arterioles

 Also called "soft exudates" or "nerve fiber layer infarctions“

 Fluorescein angiography shows no capillary perfusion in the

 Very common in DR, specially if patient with hypertension.

 Appearance resembling sausage-shaped dilatation of the retinal

 Sign of severe NPDR

Diffuse macular edema

Retinal edema Hard exudates within Retinal edema > 1 disc

 Proliferative Diabetic Retinopathy (PDR):

 Advanced diabetic eye disease

Fundus Fluorescein Angiography:

– To guide treatment of CSME

 Fovea - normal depression

 Umbo- central hyper reflective dot within foveola

 Retinal nerve fiber layer – thicker on nasal side of macula

 Areas of minimal signals ( blue – black)

 Outer nuclear layer – thickest portion

• Patients withType 1 diabetes should have an

• Eye examinations should be started from 1st trimster

 Blood pressure control.

– Inducing involution of new vessels

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

 Aspirin use did not increase risk of

 Aspirin use did not affect visual acuity.

 Aspirin reduces risk of cardiovascular morbidity

Retinal finding Suggested follow-up

Mild NPDR 1 year

Moderate NPDR 6 months - 1yearor refer to

DME Every 2-4 months

PDR Every 2-3 months

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