Eyes on Diabetics:

How to Avoid Blindness in Diabetic

Patient

Rova Virgana
FK Unpad
Pusat Mata Nasional RS Mata Cicendo
Bandung Eye Center (Hospital and Clinic)

PIT IDI Jabar 2018

 Keys Facts from WHO
• The number of people with diabetes has risen from
108 million in 1980 to 422 million in 2014
• The global prevalence of diabetes* among adults
over 18 years of age has risen from 4.7% in 1980 to
8.5% in 2014
• Diabetes prevalence has been rising more rapidly in
middle- and low-income countries
• Diabetes is a major cause of BLINDNESS, kidney
failure, heart attacks, stroke and lower limb
amputation
What are effects of Diabetes Mellitus
on Eyes
 Effects of DM on Eyes
• Dry eyes
• Refraction changes
• Cataract
• Retinopathy Figure 3: Normal Vision

• Papilopathy
• CN disturbances
• Glaucoma
Figure 4: How vision may
be affected by diabetic retinopathy
 Diabetic Retinopathy (DR)
Definition
• Progressive dysfunction of the retinal blood
vessels caused by chronic hyperglycemia.
• DR can be a complication of diabetes type 1
or diabetes type 2.
• Initially, DR is asymptomatic, if not treated
though it can cause low vision and blindness.
 Anatomy of The Eye
The retina – senses light &
transmits images to the
brain

The macula – central part of

the retina used to read and see
fine details clearly

The vitreous – clear gel fills

the back of the eye and sits in
front of the retina
RETINA
Healthy Retina Diabetic Retinopathy
 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.

http://www.who.int/bulletin/volumes/82/11/en/844.pdf
http://www.ncbi.nlm.nih.gov/pubmed/19896746
http://www.who.int/bulletin/volumes/82/11/en/844.pdf
 Prevalence
• Blindness is 25 more common in diabetics
than non diabetics.
• Prevalence of PDR is much more in type I than
type II.
• Diabetic retinopathy more sever in type I than
type II.
 Prevalence
• Macular edema :
NPDR : 2 -6 %
PDR : 20-63 %
• Macular edema :
20.1 % in younger onset group.
25.4 % in older onset group taking insulin
13.9 % in older onset group not taking insulin
 Prevalence
• The 25-year cumulative rate of progression of DR
in Type I was:
- progression of DR was 83%.
- progression to PDR was 42%.
- macular edema was 26%.

( WESDR Ophthalmology. 2008 Nov;115(11):1859-68 (

 RISK FACTORS
1. The duration of diabetes :
• is the most important factor.
• In patients diagnosed as having diabetes
before the age of 30 years, the incidence of
DR :
- after 10 years is 50%
- after 30 years is 90%
 RISK FACTORS
• It is extremely rare for DR to develop within 5
years of the onset of diabetes.

• about 5% of Type II have NPDR at presentation

perhaps due to the lag between onset and
diagnosis.
 RISK FACTORS
2 . Glycemic control :
• Good metabolic control of diabetes will not
prevent DR, although it may delay its development
by a few years.
• increased severity of diabetic retinopathy is
associated with poorer glucose control.
• insulin treatment is associated with a decreased
risk of either the development or progression of
diabetic retinopathy in patients with type 1
diabetes.
 RISK FACTORS
• With strict control of DM:
- risk of developing retinopathy was
reduced by 75% .
- 50% reduction in the rate of progression of
retinopathy in existing retinopathy
- early worsening of retinopathy is unlikely to
threaten vision .

Diabetes Control and Complications Trial Research Group N Engl J Med 1993; 329:977-986.
 RISK FACTORS
3 . Miscellaneous factors :
- pregnancy (Hormonal changes )
- systemic hypertension
- renal disease
- anaemia ( ↓oxygen )
- elevated serum lipid
- carotid artery occlusive disease
- obesity
- barriers to care
 Ocular Risk Factors
 PVD :
• due to degenerative changes in the vitreous.
• significantly more common in diabetic
subjects.
• complete PVD may prevent the development
of PDR because the hyaloid is needed as a
scaffold for retinal neovascularization.
• attached posterior hyaloid has also been
associated with an increased risk for DME
 Ocular Risk Factors
 High myopia :
• choroidal degeneration and extensive old
chorioretinopathy protect against DR.
• believed to act in the same manner as pan
retinal photocoagulation by reducing the
metabolic needs of the retina
 Ocular Risk Factors
• Removal of cataract :
• DR may progress after cataract surgery.
• Patient who have CSME, SNPDR or PDR should
undergo photocoagulation if the media is
sufficiently clear.
• If the cataract preclude retina evaluation and
treatment, prompt postoperative retinal
evaluation and treatment should considered.
 Diabetic retinopathy symptoms
Diabetic retinopathy is 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
HOW DIABETES CAUSES VISION LOSS
How diabetes cause vision loss

Macular Clinical
significant
edema
macular edema

Preclinical Background Vision

Diabetes changes DR loss

Vitreous hemorrhage
Preproliferative Proliferative and/or Retinal
DR DR detachment and/or
neovascular glaucoma
 Microvascular
Occlusion

Ischemia

Infarction

Increased VEFG

Cotton – wool spot

Neovascularization

Vitreous Neovascular
Fibrovascular bands
hemorrhage glaucoma

Tractional retinal
detachment Retina in systemic disease : a color manual of
ophthalmoscopy / Homayoun Tabandeh, Morton F.
Goldberg 2009
 Microvascular Leakage

Retinal
Edema Hard exudates
hemorrhage

Retina in systemic disease : a color manual of ophthalmoscopy / Homayoun Tabandeh, Morton F. Goldberg 2009.
RECOMMENDED
DiabeticEYE EXAMINATION
Eye Disease
SCHEDULE Key Points
Diabetes Type Recommended Time of Recommended Follow-
First Examination up*

Type 1 3-5 years after Yearly

diagnosis

Type 2 At time of diagnosis Yearly

Prior to pregnancy • Treatments

Prior exist but workNobest
to conception retinopathy to mild
(type 1 or type 2) and early in the first moderate NPDR every
before vision
trimesteris lost 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
 International Clinical Diabetic Retinopathy Disease Severity
Scale
Findings Observable upon Dilated
Proposed Disease Severity Level Ophthalmoscopy
Findings Obsd
No apparent retinopathy No abnormalities

Mild nonproliferative diabetic retinopathy Microaneurysms only

More than just microaneurysms but less than severe NPDR

Moderate nonproliferative diabetic retinopathy

Any of the following:

Severe nonproliferative diabetic retinopathy
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.

One or both of the following:

Proliferative diabetic retinopathy Neovascularization
Vitreous/preretinal hemorrhage

Proposed international clinical diabetic retinopathy and diabetic macular edema disease severity scales
Ophthalmology Volume 110, Number 9, September 2003
No retinopathy
MILD NONPROLIFERATIVE DIABETIC
RETINOPATHY

Microaneurysms
Moderate Nonproliferative Diabetic
Retinopathy (NPDR)

Microaneurysm

Hard exudates

Flamed shaped
hemorrhage
Severe Nonproliferative Diabetic Retinopathy
(NPDR)

Venous
beading
PROLIFERATIVE
DIABETIC
RETINOPATHY Cotton-wool
spot

Neovascularization

Neovascularization Hard exudate

Blot hemorrhage
 PREVENTION

90 percent of diabetic eye disease can

be prevented simply by proper regular
examinations, treatment and by
controlling blood sugar.

http://www.aao.org/newsroom/release/20091030.cfm
Primary prevention
Strict glycemic control
Blood pressure control

Secondary prevention
Annual eye exams

Tertiary prevention
Retinal Laser photocoagulation
Vitrectomy
DIABETIC RETINOPATHY TREATMENT

The best measure for prevention of

loss of vision from diabetic
retinopathy is strict glycemic control
 Laser Photocoagulation
Laser Photocoagulation is recommended for eyes
with:
• Clinical significant macular edema CSME
• High risk Proliferative diabetic retinopathy
 DIABETIC RETINOPATHY TREATMENT
Once DR threatens vision treatments can include:

Laser therapy to seal leaking blood

vessels (focal laser)

Laser therapy to reduce retinal oxygen

demand (scatter laser)

Surgical removal of blood from the eye

(vitrectomy)
 DIABETIC RETINOPATHY TREATMENT
NEWER DEVELOPMENTS:

The use of anti-vascular endothelial growth

factor antibodies has been shown to be
useful in the treatment of DR

Anti-VEGF antibody treatment appears

to be useful for both macular edema and
proliferative retinopathy

Studies to determine the exact role of

anti-VEGF treatment in relation to laser
treatment in specific situations are
underway.

http://drcrnet.jaeb.org
 Diabetic Macular Edema
• Most common cause of decreased VA in DR
• Can occur in any DR stage
• Diabetic retinopathy occurs in 1 out of 3
people with diabetes, with reported rates of
DME reaching 7% in this group of patients
• In fact, DME is the leading cause of visual loss
and legal blindness in people with diabetes
Meta analysis and review on the effect on bevacizumab id diabetic macular edema
Graefes Arch Clin Exp Ophthalmol(2011) 249:15-27
Why is Diabetic macular edema so important?
• 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
Normal Macular Edema
 Pathogenesis of DME
• Vascular endothelial growth factor (VEGF) is believed to be a key mediator

• It promotes angiogenesis and causes a breakdown in the BRB by damaging

the tight junctions between retinal endothelial cells

• These tight junctions are critical to the function and regulation of the BRB

• The breakdown of BRB then results in accumulation of plasma proteins

such as albumin which exert a high oncotic pressure in the neural
interstitium, leading to interstitial edema.

• Other comorbidities such as chronic hyperglycemia, hypertension, and

hyperlipidemia are also implicated in the development of DME
 Treatment of DME
• The various treatment modalities for DME can
be divided into
– ocular
– systemic
 Ocular Treatment of DME
• Laser Therapy (focal and grid)
• Intravitreal anti-VEGF therapy
– Bevacizumab, Ranibizumab, Aflibercept
• Intravitreal steroid therapy
– TCA, Dexamethasone, Fluocinolone acetonide
• Intravitreal NSAID therapy
– Na Diclofenac
• Vitrectomy
• Novel therapy
– Pharmacological / non pharmacological
 Systemic Treatment of DME
• Fenofibric Acid Therapy
– Addition to simvastatin lower progression of 40%
• Systemic Erythropoietin Therapy
– Anemia in ESRF
– Subcutaneous injection
• ACE Inhibitor Therapy
 Negative effects to DME
• GlitazoneTherapy
• Insulin Therapy
• Blood Glucose Levels
• Anaemia
• Hypertension
• Dyslipidaemia
• Kidney Disease
• Pregnancy
 Take home message
• DR and DME has an increasing prevalence
• PREVENTION is the KEY (timely diagnosis,
early finding, controlling risk factors, regular
screening)
• DO FUNDUSCOPIC EXAMINATION in DM
• SYSTEMIC PROBLEMS should be closely
MONITORED and CONTROLLED
• PROMT TREATMENT
Thank you