DIABETIC RETINOPATHY

DIABETIC RETINOPATHY
Definition.
Epidemiology.
Risk Factors.
Pathogenesis.
Signs & Symptoms.
Classification.
Investigations.
Complications.
Management.
Diabetic eye disease

refers to a group of eye problems that people

with diabetes may face as a complication of
diabetes. All can cause severe vision loss or
even blindness.

Diabetic retinopathy - most common cause of

blindness between ages 20 and 70 years.
 Diabetes is associated with the
following ocular events :
Corneal abnormalities.
Glaucoma ( rubeotic glaucoma ).
neovascularization.
Cataracts snowflake retinopathy in younger pts and
greater frequency and earlier onset of age related
cataract.
Neuropathies.
Diabetic Retinopathy.
Diabetic retinopathy causes retinal
vascular disease.

Other causes of RVD :

- Hypertensive retinopathy.
- sickle cell retinopathy.
- Retinopathy of prematurity.
- central and branch retinal artery occlusion.
- Central and branch retinal vein occlusion.
- Abnormal retinal blood vessels.
 The Retina
What is Retina?
Structure that lines the inside of the globe behind ora
serrata.

2 major layers:
- Inner neurosensory retina (NSR): transparent, light
sensitive membrane.
- Outer retinal pigment epithelium (RPE).

Retinal blood supply:

From central retinal artery and choroidal circulation.
 Retinal Histology
Sclera Outer
Plexiform layer
Choroid
Bipolar cells
RPE
Inner
Photoreceptor plexiform layer
outer segments
Ganglion cells
Photoreceptor
inner segment Nerve fiber
layer
Retinal Anatomy
 - DM 1 (IDDM) loss of insulin secretion
mostly in young people.. Onset is relatively
acute and retinopathy begins to appear
about 5 years after onset.

- DM 2 (NIDDM) pt may retain some

insulin secretion but develop resistance to
its action. It occurs in older age group.
Bcoz DM2 present several yrs prior to
diagnosis, retinopathy may be found at
predentation.
 RISK FACTORS:
1. Duration of diabetes
2. Poor control of Diabetes
3. Hypertension
4. Nephropathy
6. Obesity and hyperlipidemia
7. Smoking
8. Pregnancy
 Pathogenesis

Microangiopathy which has features

of both microvascular leakage and
occlusion
 Microvascular leakage
Loss of pericytes results in distention of
weak capillary wall producing
microaneurysms which leak.

Blood-retinal barrier breaks down causing

plasma constituents to leak into the retina
retinal oedema, hard exudates
 Microvascular occlusion
Basement membrane thickening,
endothelial cell damage, deformed RBCs,
platelet stickiness and aggregation

Vascular Endothelial Growth Factor

(VEGF) is produced by hypoxic retina

VEGF stimulates the growth of shunt and

new vessels
 Pathogenesis :
Too much sugar in your blood can damage the
tiny blood vessels (capillaries) that nourish the
retina.
This can result in diabetic retinopathy and vision
loss.
Elevated blood sugar levels can also affect the
eyes' lenses. With high levels of sugar over long
periods of time, the lenses can swell, providing
another cause of blurred vision.
 Response to Hypoxia:
More extensive retinal hypoxia triggers compensatory
mechanisms within the eye to provide enough oxygen
to tissues:

Venous caliber abnormalities, such as

venous beading, loops, and dilation.

Intraretinal microvascular abnormalities (IRMA)

represent either new vessel growth or remodeling of
preexisting vessels through endothelial cell
proliferation within the retinal tissues to act as shunts
through areas of nonperfusion.
 Further increases in retinal ischemia trigger the
production of vasoproliferative factors :

neovascularization at border of perfused and

unperfused => fragile &highly permeable vessels
.These delicate vessels are disrupted easily by
vitreous traction, which leads to hemorrhage into
the vitreous cavity or the preretinal space.
Fibrovascular changes & traction => retinal edema,
retinal heterotropia and retinal detachments.
 History symptoms
it's possible to have diabetic retinopathy and not know it. In fact,
it's uncommon to have symptoms in the early stages of diabetic
retinopathy.
As the condition progresses, diabetic retinopathy symptoms may
include:
Spots or dark strings floating in your vision
(floaters)
Blurred vision
Fluctuating vision
Dark or empty areas in your vision
Poor night vision
Impaired color vision
Vision loss
Diabetic retinopathy usually affects both eyes.
Simulation of defective vision as experienced by a
Diabetic whose vision has been affected by Diabetic
retinopathy

Normal Defective
 Signs on Examination:
Microaneurysms (Earliest , red or yellowish
dots).
Earliest clinical sign of diabetic retinopathy
Secondary to capillary wall outpouching due to
pericyte loss
Appear as small red dots in the superficial
retinal layers
Fibrin and RBC accumulation in the
microaneurysm lumen
Rupture produces blot/flame hemorrhages
May appear yellowish in time as endothelial cells
proliferate and produce basement membrane
 Dot and blot hemorrhages
Occur as microaneurysms rupture in the deeper layers of the
retina

(similar to microaneuryms if they are

small, distinguish by fluorescein angio).

Flame-shaped hemorrhages - Splinter

hemorrhages, superficial.
 Retinal edema and hard exudates.
Caused by the breakdown of the blood-retina barrier,
allowing leakage of serum proteins, lipids, and protein
from the vessels.

Cotton-wool spots.
.Nerve fiber layer infarction from occlusion of
precapillary arterioles
.Fluorescein angiography - No capillary perfusion

Intraretinal microvascular abnormalities

Remodeled capillary beds without proliferative
Cotton-wool spots hard exudate
Flame-shape hemorrhage
 Classification of DR
International Clinical DR Disease Severity Scale
No apperant retinopathy.
non-proliferative DR (NPDR)
Mild
Moderate
Severe

Proliferative DR (PDR)
significant macular oedema
- May exist by itself or along with NPDR and PDR
 Mild NPDR
Microaneurisms only
(earliest clinically detectable lesion)
Moderate NPDR
Microaneurysms
and/or dot and blot
hemorrhages in at
least 1 quadrant

Soft exudates
(Cotton wool spots)

Venous beading or
IRMA (intraretinal IRMA
microvascular
abnormalities)
Mild and Moderate Non- proliferative DR
was previously known as Background DR
 Severe NPDR
Any one of the following 3 features is present
Microaneurysms and intraretinal
hemorrhages in all 4 quadrants

Venous beading in 2 or more quadrants

Moderate IRMA in at least 1 quadrant

Known as the 4-2-1 rule

Proliferative DR
(PDR)
Characterized by
Proliferation of
new vessels from
retinal veins

New vessels on
the optic disc

New vessels
elsewhere on the
retina
Proliferative DR

NVD
2. International Clinical Diabetic Macular
Edema (DME) Disease Severity Scale:

DME absent:
No retinal thickening or hard
exudates (HE)present in the
posterior pole.
DME present:
Some retinal thickening or hard
exudates (HE) present in the
posterior pole.
 If DME present, it can be categorized as
follows:
- Mild DME:
Some retinal thickening or HE present in the
posterior pole but distant from the center of
macula.
- Moderate DME:
Retinal thickening or HE approaching the
center of the macula but not involving its
center.
- Severe DME:
Retinal thickening or HE involving the center
of the macula.
Diabetic Macular Edema
 COMPLICATIONS OF DIABETIC
RETINOPATHY
Vitreous hemorrhage

Tractional retinal detachment

Rubeosis Iridis

Glaucoma

Blindness
Vitreous Hemorrhage
SUBHYALOID HEMORRHAGE
Tractional retinal detachment
Rubeosis Iridis
 Neovascular Glaucoma
Complication of rubeosis iridis
New vessels cause angle closure
Mechanical obstruction to aqueous outflow
Intra ocular pressure rises
Pupil gets distorted as iris gets pulled
Eye becomes painful and red
Loss of vision
 Blindness
Non-clearing vitreous hemorrhage

Neovascular glaucoma

Tractional retinal detachment

Macular ischemia
PREVENTION OF COMPLICATIONS

By early institution of appropriate treatment

This requires early detection of DR in its

asymptomatic treatable condition

By routine fundus examination of all

Diabetics (cost effective screening)

And appropriate referral to ophthalmologist

 Screening
Type 1 diabetics:
First screen 5 years after onset, then
annually.

Type 2 diabetics:
First screen upon diagnosis and then
annually.
 Mild and Moderate NPDR

- No specific treatment for retinopathy

- Good metabolic control to delay
progression
- Control of associated Hypertension,
Anemia and Renal failure

Severe and very severe NPDR

Close follow up by Ophthalmologist

Clinically significant macular oedema
- Laser photocoagulation to minimise risk of
visual loss

Proliferative DR
Retinal laser photocoagulation as per the
judgment of ophthalmologist (in high risk eyes)

It converts hypoxic retina (which produces

ANGIOGENIC factors) into anoxic retina (which
cant)
 Referral to Ophthalmologist
Visual Symptoms
Diminished visual acuity
Seeing floaters
Painful eye
Fundus findings
- Macular oedema/hard exudates close to fovea
- Proliferative DR
- Vitreous hemorrhage
- Moderate to severe and very severe NPDR
- Retinal detachment
- Cataract obscuring fundus view
 Referral to Ophthalmologist
Presence of Risk Factors

- Pregnancy
- Nephropathy
DIRECT OPHTHALMOSCOPY
Examination of the fundus of the eye
To screen for Diabetic Retinopathy
After dilatation of both eyes with %0.5
tropicamide
View of the retina through an
ophthalmoscope
Normal fundus views of Right
and left eye
Mild NPDR Microaneurysms, Dot and
Blot hemorrhages
Moderate NPDR
Moderate NPDR with CSME
Circinate retinopathy Hard exudates in a
ring around leaking aneurysms
Age related Macular degeneration: Note the
drusen. Not to be confused with Hard exudates. There
are no microaneurysms or dot/blot hemorrhages.

DRUSEN
Severe NPDR
Cotton wool patches

Hemorrhages - 4 quadrants

With CSME
 Very severe NPDR

-Venous beading
Cotton-wool patches,
- scars of laser spots
venous segmentation
- Absorbing hemorrhages
CSME
in
Different
Stages of
NPDR
Proliferative DR New vessels elsewhere on
the retina along the supero-temporal vessels
PDR New vessels on disc
PDR New vessels on disc and new vessels
elsewhere on retina
PDR with vitreous hemorrhage

Vitreous bleed
Vitreous Hemorrhage
Tractional retinal
detachment Fibro-vascular
proliferation
Thank you!