Diabetic Retinopathy

Diabetic Retinopathy
Introduction
• It refers to retinal changes seen in patients with
diabetes mellitus.
• With increase in the life expectancy of diabetics,
the incidence of diabetic retinopathy (DR) has
increased.
• In Western countries, it is the leading cause of
blindness
Risk factors
• 1. Duration of diabetes is the most important determining
factor. Roughly 50 percent of patients develop DR after 10
years, 70 percent after 20 years and 90 percent after 30
years of onset of the disease.
• 2. Sex. Incidence is more in females than males (4:3).
• 3. Poor metabolic control
• 4. Heredity
• 5. Pregnancy
• 6. Hypertension
• 7. Others: smoking, obesity and hyperlipidemia.
Pathogenesis
• Essentially, it is a microangiopathy affecting retinal

precapillary arterioles, capillaries and venules
Diabetic retinopathy has been variously classified. Presently
followed classification is as follows:
I. Non-proliferative diabetic retinopathy (NPDR)
• Mild NPDR
• Moderate NPDR
• Severe NPDR
• Very severe NPDR
II. Proliferative diabetic retinopathy (PDR)
III. Diabetic maculopathy
IV. Advanced diabetic eye disease (ADED)
I. Non-proliferative diabetic retinopathy (NPDR)
Ophthalmoscopic features of NPDR include:
• Microaneurysms in the macular area (the earliest
detectable lesion).
• Retinal haemorrhages both deep (dot and blot
haemorrhages) and superficial haemorrhages (flame-
shaped).
Hard exudates-yellowish-white waxy-looking patches are
arranged in clumps or in circinate pattern.
These are commonly seen in the macular area.
• Retinal oedema characterized by retinal thickening.
• Cotton-wool spots (if > 8, there is high risk of
developing PDR).
Venous abnormalities, beading, looping
and dilatation.
• Intraretinal microvascular
abnormalities (IRMA).
• Dark-blot haemorrhages representing
haemorrhagic retinal infarcts.
On the basis of severity of the above findings the NPDR
has been further classified as under:
1. Mild NPDR
• At least one microaneurysm or intraretinal hemorrhage.
2. Moderate NPDR
• Moderate microaneurysms/intraretinal hemorrhage.
• Early mild IRMA.
• Hard/soft exudates may or may not present.
3. Severe NPDR. Any one of the following (4-2-1 Rule):
• Four quadrants of severe microaneurysms/ intraretinal
hemorrhages.
• Two quadrants of venous beading.
• One quadrant of IRMA changes.
4. Very severe NPDR. Any two of the following (4-2-1 Rule):
• Four quadrants of severe microaneurysms/ intraretinal
hemorrhages.
• Two quadrants of venous beading.
• One quadrant of IRMA changes.
Diabetic retinopathy: A, Mild NPDR; B, Moderate NPDR; C, Severe NPDR; D, Very severe NPDR; E, Early PDR; F, High risk PDR; G, Exuda
II. Proliferative diabetic retinopathy (PDR)
❖ Proliferative diabetic retinopathy develops in more
than 50 percent of cases after about 25 years of the
onset of disease.
❖ The hallmark of PDR is the occurrence of
neovascularisation over the changes of very severe
non-proliferative diabetic retinopathy.
❖ It is characterised by proliferation of new vessels from
the capillaries, in the form of neovascularisation at the
optic disc (NVD) and/or elsewhere (NVE)
❖ Vitreous detachment and vitreous haemorrhage may
occur in this stage.
Types:
On the basis of high risk characteristics
(HRCs) described by diabetic
retinopathy study (DRS) group, the PDR
can be further classified as below:
1. PDR without HRCs (Early PDR)
2. PDR with HRCs (Advanced PDR).
1. PDR without HRCs (Early PDR), and
2. PDR with HRCs (Advanced PDR). High risk
characteristics (HRC) of PDR are as follows:
• NVD 1/4 to 1/3 of disc area with or without
vitreous haemorrhage (VH) or pre-retinal
haemorrhage (PRH)
• NVD < 1/4 disc area with VH or PRH
• NVE > 1/2 disc area with VH or PRH
Diabetic retinopathy: E, Early PDR; F, High risk PDR
III. Diabetic maculopathy
Changes in macular region need special
mention, due to their effect on vision.
These changes may be associated with non-
proliferative diabetic retinopathy (NPDR)
or proliferative diabetic retinopathy (PDR).
The diabetic macular edema occurs due to
increased permeability of the retinal
capillaries.
It is termed as clinically significant macular edema (CSME) if one
of the following three criteria are present on slit-lamp
examination with 90D lens:
• Thickening of the retina at or within 500 micron of the centre of
the fovea.
• Hard exudate at or within 500 micron of the centre of fovea
associated with adjacent retinal thickening.
• Development of a zone of retinal thickening one disc diameter
or larger in size, at least a part of which is within one disc
diameter of the foveal centre
Types:Focal exudative type,Diffuse exudative type,Ischemic type,Mixed
IV. Advanced diabetic eye disease
It is the end result of uncontrolled
proliferative diabetic retinopathy. It is
marked by complications such as:
• Persistent vitreous haemorrhage
• Tractional retinal detachment
• Neovascular glaucoma and Rubeosis Iridis
Advanced diabetic eye disease
Investigations
• Urine examination,
• Blood sugar estimation.
• Fundus fluorescein angiography
should be carried out to elucidate areas
of neovascularisation, leakage and
capillary nonperfusion.
Management
I. Screening for diabetic retinopathy
II. Medical treatment
III. Photocoagulation
IV. Surgical treatment
Management
I. Screening for diabetic retinopathy. To prevent visual loss
occurring from diabetic retinopathy a periodic follow-up is
very important for a timely intervention. The
recommendations for periodic fundus examination are as
follows:
• Every year, till there is no diabetic retinopathy or there is
mild NPDR.
• Every 6 months, in moderate NPDR.
• Every 3 months, in severe NPDR.
• Every 2 months, in PDR with no high risk characteristic.
II. Medical treatment. Besides laser and surgery to the eyes (as
indicated and described below), the medical treatment also
plays an essential role. Medical treatment for diabetic
retinopathy can be discussed as:
1. Control of systemic risk factors is known to influence the
occurrence, progression and effect of laser treatment on DR.
The systemic risk factors which need attention are.
• Strict metabolic control of blood sugar,
• Lipid reduction,
• Control of associated anaemia, and
• Control of associated hypoproteinemia
2. Role of pharmacological modulation. Pharmacological
inhibition of certain biochemical pathways involved in the
pathogenesis of retinal changes in diabetes is being evaluated
These include:
• Protein kinase C (PKC) inhbitors(Ruboxitaurin,Sotrastaurin)
• Vascular endothelial growth factors (VEGF) inhibitors,
• Aldose reductase inhibitors(ranirestat,epalestat)and ACE
inhibitors, and Antioxidants such as vitamin E
Anti-VEGF
❖ Antibody against VEGF
Available drugs
❖ Pegabtinib
❖ Bevacizumab
❖ Aflibercept
3. Role of intravitreal steroids in reducing
diabetic macular oedema is also being
stressed recently by following modes of
administration:
• Flucinolone acetonide intravitreal implant
and
• Intravitreal injection of triamcinolone (2 to
4 mg)
III. Photocoagulation.
❖ It remains the mainstay in the
treatment of diabetic retinopathy
and maculopathy.
❖ Either argon(514nm)or
diode(800nm) laser can be used.
The protocol of laser application is different for
macula and rest of the retina as follows:
i. Macular photocoagulation.
• Focal treatment
• Grid treatment
ii. Panretinal photocoagulation (PRP)
i. Macular photocoagulation.
Macula is treated by laser only if there is
clinically significant macular oedema (CSME).
Laser treatment is contraindicated in ischaemic
diabetic maculopathy.
In patients with PDR associated with CSME,
macular photo-coagulation should be
considered first i.e., before PRP since the latter
may worsen macular oedema.
Focal treatment: with argon laser is carried out for
all lesions (microaneurysms, IRMA or short
capillary segments) 500-3000 microns from the
centre of the macula, believed to be leaking and
causing CSME. Spot size of 100-200 µm of 0.1
second duration is used.
Grid treatment: Grid pattern laser burns are applied

in the macular area for diffuse diabetic macular
oedema.
ii. Panretinal photocoagulation (PRP) or scatter laser
consists of 1200-1600 spots, each 500 µm in size and 0.1
sec. duration.
Laser burns are applied 2-3 disc areas from the centre of
the macula extending peripherally to the equator.
In PRP temporal quadrant of retina is first coagulated.
PRP produces destruction of ischaemic retina which is
responsible for the production of vasoformative factors.
Protocols of Laser application in diabetic retinopathy : A, Focal treatment; B, Grid treatment and; C, Panretinal photocoagulation.
Indications for PRP are:
• PDR with HRCs,
• Neovascularization of iris (NVI),
• Severe NPDR associated with:
– Poor compliance for follow up,
– Before cataract surgery/YAG capsulotomy,
– Renal failure,
– One-eyed patient, and
– Pregnancy
IV. Surgical treatment.
❖ It is required in advanced cases of PDR.
❖ Pars plana vitrectomy is indicated for
dense persistent vitreous haemorrhage,
tractional retinal detachment, and
epiretinal membranes.
❖ Associated retinal detachment also
needs surgical repair.
Thank You

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Diabetic Retinopathy

• Essentially, it is a microangiopathy affecting retinal

Grid treatment: Grid pattern laser burns are applied

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