Diabetic Retinopathy: Dwi Lestari Pohan

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Diabetic Retinopathy

DWI LESTARI POHAN


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 up to
90% after 30 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, 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 as 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
Direct effect Microangiopathy
Protein kinase C activation Hematological &
on retinal cells (damage to capillary Rheological
wall) changes
Intra retinal Edema Microvascular Occlusion
Hemorrhages Exudates causes Ischemia
IRMA
Neovascularizatio hemorrhage
n Fibrosis Traction
SYMPTOM
S
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
 Microaneurysm
 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
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 neovascularization 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 Macular
Edema(CSME)

Retinal edema Hard exudates within Retinal edema > 1 disc


within 500 microns 500 microns of diameter, any part is
of centre fovea fovea if as with within 1 disc diameter
adjacent retinal of centre of fovea
thickening
CLASSIFICATIO
N Diabetic Retinopathy (NPDR):
 Non-proliferative
• 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:

• Includes the presence of Exudate

hemorrhages(1-3 quadrants), micro


- aneurysms, hard exudates and
Cotton wool spot. Microaneurysm

Cotton
wool
 Severe:
The (4-2-1) rule; one or more of:
• Hemorrhages and microaneurysms

in 4 quadrants.

Venous beading in at Beading
least 2 quadrants.
• Intraretinal microvascular
abnormalities in at least 1 quadrant
IRM
A
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


trimester and monitored every trimester 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 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 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
 Bevacizumab

 Ranibizumab

 Aflibercept
Surgery
 Pars plana vitrectomy (PPV)
Indications-
○ 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 - 1year or refer


to ophthalmologist.
Severe NPDR Every 4 months

DME Every 2-4 months

PDR Every 2-3 months

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