DIABETIC RETINOPATHY

Siti Halida Zoraida Soraya

DISKUSI DIVISI VITREO RETINA

DEPARTEMEN ILMU KESEHATAN MATA – FKUI-RSCM KIRANA
SEPTEMBER 2020
EPIDEMIOLOGY

 Diabetic Retinopathy is responsible for 1.8

million of the 37 million cases of blindness
throughout the world
 In patients diagnosed with DM before the age of
30 years, the incidence of DR after 10 years is
50%, and after 30 years 90%
 decreasing the HbA1c by 1% the microvascular
complications can be reduced by one-third
The American Diabetes Association (ADA) Diabetes Mellitus

Type 1 diabetes mellitus

• formerly known as insulin- dependent diabetes mellitus (IDDM)
• Results from the destruction of pancreatic β-cells
• Absolute insulin deciency.
• Idiopathic or immune-mediated

Type 2 diabetes mellitus, formerly

• non–insulin-dependent diabetes mellitus (NIDDM.
• Insulin resistance that may or may not be accompanied by insulin
deciency.
 Anatomy

 The retina is a multilayered,

light sensitive neural tissue
lining the inner eye ball –
RPE & Neurosensitive retina
 The macula is a highly
sensitive area in the center
of the retina, responsible
for central vision.
Pathogenesis
Pathogenesis
 Pathogenesis

Microvascular Leakage

Retinal
Edema Hard exudates
hemorrhage
Pathogenesis
Diabetic retinopathy
 Non
Proliferative Diabetic
Proliferative
Diabetic Macular
Diabetic
Retinopathy Edema
Retinopathy

DIABETIC RETINOPATHY
Microaneurysm
 localized outpouchings, mainly saccular, of capillary wall
 located in the inner capillary plexus (ganglion cell
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 hemorrhages
MICROANEURYSM
 Hemorrhages
dot-blot

• Intraretinal hemorrhage
• venous end of the capillaries
• compact middle layers of the retina

flame-shaped

• Large more superficial precapillary

arterioles
• follow the course of the retinal
nerve fibre layer
EXUDATE

 Chronic localized retinal edema

 within outer plexiform layer
 Made up of accumulated lipoproteins and lipid-filled macrophage
 The centers of rings of hard exudates usually contain
microaneurysms
 Hard exudates : highly hyperreflective and irregular,
usually located by the outer plexiform layer
HARD EXUDATE

Streaks:, macular star (especially around the fovea)

Hard exudates may migrate and accumulate in the center of

the fovea, forming plaques

inflammatory response → retinal epithelial detachment

with subjacent fibrosis
COTTON-WOOL
SPOTS
 Nerve fiber layer
infarction
 The interruption of
axoplasmic flow caused
by the ischemia,  build-
up of transported material
within the nerve axons,
(white and opaque
appearance of these
lesions)
 OCT: Severe thickening
and reflectivity
enhancement of NFL.
Some vessels are seen
passing through them
 INTRARETINAL MICROVASCULAR ABNORMALITIES
 Dilated, tortuous retinal
capillaries that act as a shunt
between arterioles and venules
 frequently seen adjacent to
areas of capillary closure

Distinguished from NVE:

 intraretinal location
 absence of profuse leakage on
fluorescein angiography
 failure to cross over major
retinal blood vessels
NEOVASCULARIZATIO
N

 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
DIABETIC MACULAR EDEMA

 Diabetic macular edema (DME) is the leading cause of visual impairment in

diabetics.
 DME can be present at any stage of the disease, but is more common in patients
with proliferative diabetic retinopathy.
 DME – retinal thickening. Important observations:
 Location of retinal thickening relative to the foveal center
 Presence and location of exudates
 Presence of cystoid macular edema
 Retinal edema
 Diffuse retinal edema: extensive
capillary leakage
 Localized edema: focal leakage from
microaneurysms and dilated capillary
segments
 located between the outer plexiform
and inner nuclear layers
 Later it may involve the inner plexiform
and nerve fiber layers, until eventually
the entire thickness of the retina may
become edematous
 further accumulation of fluid  cystoid
appearance
 Retinal edema

diffuse diabetic maculopathy

focal diabetic maculopathy
CLINICALLY SIGNIFICANT MACULAR EDEMA (CSME)

Hard exudates at or within

Area of retinal thickening
Thickening of the retina at 500 µm of the center of the
1 disc area or larger,
or within 500 µm of the macula, if associated with
within 1 disc diameter of
center of the macula. thickening of the adjacent
the center of the macula.
retina.
 Hard exudates
Retinal edema within 500 m
within 500 m of centre of
of centre of fovea fovea with adjacent
oedema which may
be outside 500 m
limit

Retinal edema one disc area or larger any

part of which is within one disc diameter
(1500 m) of centre of fovea
 Clinically significant
macular edema (CSME)
focal

• characterised by microaneurysms, haemorrhages, macular oedema and

hard exudates.
• FFA: reveals focal leakage with adequate macular perfusion.

diffuse
• diffuse retinal oedema and thickening throughout the posterior pole
• relatively few hard exudates
• Fluorescein angiography reveals diffuse leakage at the posterior pole
Classification
MILD NPDR MODERATE NPDR
SEVERE NPDR
 MANAGEMENT

Glycemic HbA1c below Control of

Serum lipids
levels 7% blood pressure

Frequent Avoid tobacco

Healthy diet Normal BMI
exercise
 Management

pharmacological modulation
• Involves pharmacological inhibition of certain biochemical
pathways involved in the pathogenesis of DR
• Vascular endothelial growth factors (VEGF) inhibitors
• Bevacizumab (Avastin); Ranibizumab (Lucentis);
 Management

intravitreal steroids
• Diabetic macular oedema reduction
• Endothelial tight junctions stabilization
• Downregulate growth factors that exacerbate vascular permeability
e.g VEGF
• Intravitreal injection of triamcinolone (2 to 4 mg)
• Fluocinolone acetonide intravitreal implant
 Management

Laser Photocoagulation

• depends on the severity of retinopathy and the presence or absence

of CSME
• CSME should be considered for treatment with laser
photocoagulation
• reduces the risk of visual loss by 50%.
 Management
Focal treatment: laser
• laser burns to microaneurysms and microvascular lesions in the centre of
rings of hard exudates located between 500–3000 µm (two disc diameters)
from the center of the fovea.
• spot size: 50– 100 µm
• duration: < 0.10 second
• power : sufficient power to obtain a gentle whitening or darkening of the
microaneurysm.
• Wave length : green – yellow Argon
• Treatment of lesions between 300 and 500 µm from the centre of the fovea
should be considered
• If CSME persists, in spite of previous treatment and,
• If visual acuity is less than 6/12
 Management

Grid treatment: laser

• Burns to macular areas of diffuse retinal thickening

• < 500 µm from the center of the fovea and
• 500 µm from the temporal margin of the optic disc.
• spot size : 50 - 100µm
• exposure time : 0.10 second
• burns should be of very light intensity and one burn width apart.
• Wave length : green – yellow Argon
 Management

Pan-retinal
photocoagulation

• induce involution of new vessels

• prevent vitreous haemorrhage.
• Initial treatment - 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.
 Management

Pan-retinal photocoagulation

Sign of involution
1.regression of neovascularization leaving only 'ghost' vessels or
fibrous tissue
2. decrease in venous dilatation
3.absorption of retinal haemorrhages
4.disc pallor
 Management

Pars plana vitrectomy: indications

• Severe persistent vitreous haemorrhage
• Tractional retinal detachment involving macula
• Combined tractional and rhegmatogenous retinal detachment
• Progressive fibrovascular proliferation
• Dense, persistent, premacular, subhyaloid haemorrhage
• Red Blood Cell-induced glaucoma
• Bilateral vitreous haemorrhage
• Dense cataract associated with vitreous haemorrhage
Severe persistent vitreous Dense, persistent premacular
haemorrhage haemorrhage

Progressive proliferation Retinal detachment involving

despite laser therapy macula
Follow-up
Follow-up
TERIMA KASIH