3. DIABETES MELLITUS
Diabetes Mellitus is a group of diseases characterized by high
blood glucose levels. Diabetes results from defects in the
body's ability to produce and/or use insulin.
• Type 1 diabetes is usually diagnosed in children and young
adults. In type 1 diabetes, the body does not produce insulin.
About 10% of people with diabetes have this form of the
disease.
• In Type 2 diabetes, either the body does not produce enough
insulin or the cells ignore the insulin. This is the most
common form of diabetes.
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4. DIABETIC RETINOPATHY (DR)
DEFINITION
• Progressive dysfunction of the retinal
blood vessels caused by chronic
hyperglycemia.
• DR can be a complication of type 1 or type
2 diabetes
• Initially, DR is asymptomatic
• If not treated, it can cause low vision and
blindness.
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5. DIABETIC RETINOPATHY
EPIDEMIOLOGY
• The total number of people with diabetes is
projected to rise from 285 million in 2010
to 439 million in 2030.
• Diabetic retinopathy is responsible for 1.8
million of the 37 million cases of blindness
throughout the world .
• Diabetic retinopathy (DR) is the leading
cause of blindness in people of working
age in industrialized countries.
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6. RISK FACTORS FOR DIABETIC RETINOPATHY
Duration of diabetes is a major risk
factor associated with the development
of diabetic retinopathy
The severity of hyperglycemia is the key
alterable risk factor associated with the
development of diabetic retinopathy
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7. DURATION OF DIABETES
• The best predictor of diabetic retinopathy is
duration of the disease
• After 20 years of diabetes, more than 90% of
patients with type 1 diabetes and 60% with type
2 have some degree on diabetic retinopathy
• 33% of patients with diabetes have signs of
diabetic retinopathy
• People with diabetes are 25 times more likely to
become blind than the general population.
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15. DIABETIC RETINOPATHY
SYMPTOMS
Asymptomatic in early stages of the disease
As the disease progresses symptoms may include
• Blurred vision
• Floaters
• Fluctuating vision
• Distorted vision
• Dark areas in the vision
• Poor night vision
• Impaired color vision
• Partial or total loss of vision
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16. Natural History of Diabetic
Retinopathy
• Mild nonproliferative
diabetic retinopathy (NPDR)
• Moderate NPDR
• Severe NPDR
• Very Severe NPDR
• Proliferative diabetic
retinopathy (PDR)
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17. Findings Obsd
International Clinical Diabetic Retinopathy Disease Severity
Scale
Proposed Disease Severity Level
Findings Observable upon Dilated Ophthalmoscopy
No apparent retinopathy No abnormalities
Mild nonproliferative diabetic retinopathy Microaneurysms only
Moderate nonproliferative diabetic retinopathy
More than just microaneurysms but less than severe
NPDR
Severe nonproliferative diabetic retinopathy
Any of the following:
More than 20 intraretinal hemorrhages in each of
four quadrants
Definite venous beading in two or more quadrants
Prominent IRMA in one or more quadrants
and no signs of proliferative retinopathy.
Proliferative diabetic retinopathy
One or both of the following:
Neovascularization
Vitreous/preretinal hemorrhage 17
20. MICROANEURYSMS
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• Focal dilatations of retinal capillaries
• Appear as red dots.
• Seen at the posterior pole, especially
temporal to the fovea.
• The first ophthalmoscopically detectable
change in diabetic retinopathy.
21. RETINAL HAEMORRHAGES
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Dot haemorrhages
• In the inner nuclear layer or outer plexiform layer
• Bright red dots (same size as large microaneurysms).
Dark Blot/ round haemorrhages
• Larger lesions
• Located within the mid retina
• Extent – marker for neovascularization
Flame Shaped haemorrhages
• Superficial and in the nerve fiber layer
28. LATE NON PROLIFERATIVE CHANGES
Intra-retinal microvascular abnormalities (IRMA)
• Represent intraretinal arteriolar-venular shunts
which have not breached the internal limiting
membrane of the retina.
• Indicate severe non-proliferative diabetic
retinopathy that may rapidly progress to
proliferative retinopathy.
Venous beading
• Focal narrowing and sausage-shaped dilatation
of the retinal veins.
• Sign of severe non proliferative diabetic
retinopathy.
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34. SEVERE NONPROLIFERATIVE DIABETIC
RETINOPATHY (NPDR)
34
Clinical Findings
Any of the following: (4-2-1 Rule)
• More than 20 intraretinal hemorrhages in each of four quadrants
• Definite venous beading in two or more quadrants
• Prominent Intraretinal Microvascular Abnormalities (IRMA) in
one or more quadrants
• And no signs of proliferative retinopathy
35. SEVERE NONPROLIFERATIVE DIABETIC
RETINOPATHY (NPDR)
Management/Treatment
• 3-4 month follow-up
• Color fundus photography
• Possible panretinal photocoagulation
• CSME present: color fundus photography, fluorescein
angiography, focal photocoagulation, 3-4 month follow-up
35
37. 37
• Clinical Findings
• Ischemia induced neovascularization
• at the optic disk (NVD)
• elsewhere in the retina (NVE)
• New vessels on the iris (NVI)
• Vitreous hemorrhage/Pre-retinal
haemorrhage
• Retinal traction, tears, and detachment
Proliferative Diabetic Retinopathy
(PDR)
41. HIGH-RISK PROLIFERATIVE DIABETIC
RETINOPATHY
At risk for serious vision loss
Any combination of three of the following four findings
• NVD <1/4 disc area with vitreous or preretinal hemorrhage.
• NVE > 1/2 disc area with vitreous or preretinal hemorrhage.
• NVD 1/4 to 1/3 disc area with or without vitreous or
preretinal hemorrhage.
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42. DIABETIC MACULAR EDEMA
• Diabetic macular edema is the leading cause of
legal blindness in diabetics.
• Diabetic macular edema can be present at any
stage of the disease, but is more common in
patients with proliferative diabetic retinopathy.
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43. 43
Meta analysis and review on the effect on bevacizumab in diabetic macular edema
Graefes Arch Clin Exp Ophthalmol(2011) 249:15-27
44. WHY IS DIABETIC MACULAR EDEMA
SO IMPORTANT?
44
• The macula is responsible
for central vision.
• Diabetic macular edema
may be asymptomatic at
first.
• As the edema moves in to
the fovea (the center of the
macula) the patient will
notice blurry central vision.
• The ability to read and
recognize faces will be
compromised.
Macula
Fovea
46. CLINICALLY SIGNIFICANT DIABETIC
MACULAR EDEMA (CSDME)
• Thickening of the retina at or
within 500 µm of the center of
the macula.
• Hard exudates at or within
500 µm of the center of the
macula, if associated with
thickening of the adjacent
retina.
• Area of retinal thickening 1
46
50. ISCHAEMIC MACULOPATHY
• Maculopathy in type 1 diabetics
is often due to drop out of the
perifoveal capillaries with non
perfusion.
• Enlargement of the foveal
avascular zone (FAZ) is
frequently seen on fluorescein
angiography.
• Ischaemic maculopathy is not
uncommon in type 2 diabetics
• Maculopathy in this group may
show both changes due to
ischaemia and retinal
thickening.
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55. DIABETIC EYE DISEASE
KEY POINTS
• Treatments exist but work best
before vision is lost
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RECOMMENDED EYE EXAMINATION
SCHEDULE
Diabetes Type Recommended Time of
First Examination
Recommended Follow-
up*
Type 1 3-5 years after
diagnosis
Yearly
Type 2 At time of diagnosis Yearly
Prior to pregnancy
(type 1 or type 2)
Prior to conception and
early in the first
trimester
No retinopathy to mild
moderate NPDR every
3-12 months
Severe NPDR or worse
every 1-3 months.
*Abnormal findings may dictate more frequent follow-up examinations
h ttp://one.aao.org/CE/PracticeGuidelines/PPP_Content.aspx?cid=d0c853d3-219f-487b-a524-326ab3cecd9a
56. SCREENING FOR DIABETIC EYE PROBLEMS
SHOULD IDEALLY INCLUDE THE
FOLLOWING
• The history of any visual symptoms or changes
in vision
• Measurement of visual acuity
• Iris examination by slit lamp biomicroscopy
prior to pupil mydriasis.
• Pupil mydriasis. ( tropicamide 0.5 %
• Patients should be accompanied by a relative
and instructed not to drive home.
• Examination of the crystalline lens
• Fundus examination
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68. PATHOGENESIS
1.Vasoconstriction: It is the primary response of retinal
arterioles to raised blood pressure. It reflects the
severity of hypertension.
2.Atherosclerosis: It mainly occurs in older patients. It
reflects the duration of hypertension.
3.Increased vascular permeability: It results from
hypoxia and may result in retinal edema, exudates
and hemorrhages
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69. KEITH AND WEGNER GRADING
(1939)
• GRADE 1 : Tortuosity (twisting) of retinal arteries with
increased reflectiveness (silver wiring)
• GRADE 2 : Grade 1 + Arteriovenous napping (thickened retinal
arteries pass over retinal veins)
• GRADE 3 : Grade 2 + flamed shape haemorrhage and cotton
wool exudates(due to small infarcts)
• GRADE 4: Grade 3 + Papilledema (blurring of the optic disc
due to swelling )
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71. CLINICAL TYPES
• Hypertension with involutionary (senile) sclerosis: In old age
patients
• Hypertension without sclerosis: In young patients exposed to raised
BP for a short duration
• Hypertension with compensatory arteriolar sclerosis: In young
patients exposed to benign hypertension for a long duration (usually
associated with benign nephrosclerosis; thus called renal retinopathy)
• Malignant hypertension: Rapidly progressive and severe changes in
fundus (marked vasoconstriction, papilloedema, flame shaped
hemorrhage, cotton wool spots is seen; but papilloedema is an essential
feature).
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72. • Acute malignant hypertension will cause
patients to complain of eye pain,
headaches or reduced visual acuity.
• Chronic arteriosclerotic changes from
hypertension will not cause any
symptoms alone.
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73. DIAGNOSIS
• Diagnosis is by history (duration
and severity of hypertension)
and fundoscopy. Sometimes,
fluorescein angiography may be
required.
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74. MANAGEMENT
• By itself, chronic hypertensive retinopathy rarely, if ever, results in
significant loss of vision. Treatment of the underlying systemic
condition can halt the progress of the retinal changes, but
arteriolar narrowing and arteriovenous nicking usually are
permanent.
• Treatment of malignant hypertensive retinopathy consists of
lowering blood pressure in a slow, deliberate, controlled fashion to
prevent end-organ damage.
• Too rapid a decline can lead to ischemia of the optic nerve head,
brain and other vital organs, resulting in permanent damage.
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75. MANAGEMENT
• Drugs that are commonly used in the outpatient setting to reduce
blood pressure include:
• Angiotensin converting enzyme inhibitors,
• Calcium channel blockers, v Diuretics, and V B-adrenergic
blockers.
• Very rarely, If vision loss occurs, treatment of the retinal edema
with laser or with intravitreal injection of corticosteroids or
antivascular endothelial growth factor drugs (eg, ranibizumab,
pegaptanib, bevacizumab) may be useful.
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