Diabetic retinopathy is a complication of diabetes, caused by high blood sugar levels damaging the back of the eye (retina). It can cause blindness if left undiagnosed and untreated. However, it usually takes several years for diabetic retinopathy to reach a stage where it could threaten your sight.
The retina is the light-sensitive layer of cells at the back of the eye that converts light into electrical signals. The signals are sent to the brain which turns them into the images you see.
The retina needs a constant supply of blood, which it receives through a network of tiny blood vessels. Over time, a persistently high blood sugar level can damage these blood vessels in 3 main stages:
background retinopathy – tiny bulges develop in the blood vessels, which may bleed slightly but don't usually affect your vision
pre-proliferative retinopathy – more severe and widespread changes affect the blood vessels, including more significant bleeding into the eye
proliferative retinopathy – scar tissue and new blood vessels, which are weak and bleed easily, develop on the retina, this can result in some loss of vision
2. What is Retinopathy?
• Retinopathy is due to persistent or acute damage to the
retina of the eye.
• Retinopathy is an ocular manifestation of systemic disease as
seen in diabetes or hypertension.
• Hypertensive retinopathy (HR) is a complication of Htn that
leads to damage to the retina and retinal circulation due to
high BP .Usually they are asymptomatic but may present
with decreased vision.
• Diabetic Retinopathy (DR) is a complication of DM that can
lead to blindness.
3. A map of eye which are affected
by diabetes mellitus (DM).
4. What is diabetic retinopathy?
Diabetic retinopathy is a complication of diabetes
that affects the eyes. It's caused by damage to
the blood vessels of the light sensitive tissue at
the back of the eye (retina).
Diabetic retinopathy can develop in anyone who
has type 1 diabetes or type 2 diabetes.
Diabetic retinopathy has four stages, mild
nonproliferative retinopathy, moderate
nonproliferative retinopathy, severe
nonproliferative retinopathy, and proliferative
retinopathy.
5. Pathophysiology of DR
• Retinopathy happens when high blood sugar damages blood vessels in the
retina. When these blood vessels are damaged, they can leak fluid or bleed.
This causes the retina to swell and form deposits. This is an early form of
diabetic retinopathy called nonproliferative or background retinopathy.
• In a later stage, called proliferative retinopathy, new blood vessels grow on
the surface of the retina. These new blood vessels can lead to serious vision
problems because they can break and bleed into the vitreous, the clear, jelly
like substance that fills the center of the eye. Proliferative retinopathy is a
much more serious form of the disease and can lead to blindness.
• Progressive stages of DR have Mild Nonproliferative Retinopathy, Moderate
Nonproliferative Retinopathy , Severe Nonproliferative Retinopathy, Proliferative
Retinopathy respectively.
.
7. Nonproliferative (NPDR)
Mild Nonproliferative Retinopathy is the earliest stage of Diabetic Retinopathy.
Characterized by the presence of “dot” and
“blot” hemorrhages and “microaneurysms”
in the Retina during your eye examination.
Microaneurysms are areas of balloon like
swelling of the tiny blood vessels in the Retina
caused by the weakening of their structure.
Mild Nonproliferative Retinopathy can be
present without any change in your vision..
Mild Nonproliferative Retinopathy usually does
not require treatment unless it progresses or if
is accompanied by Diabetic Macular Edema.
8. Increased leukocyte adhesion
results in loss of endothelial cells
and breakdown of the blood-
retinal barrier
11. • The blood–retinal barrier, or the BRB, is part of the blood–ocular barrier that
consists of cells that are joined tightly together to prevent certain substances
from entering the tissue of the retina.
• VEGF is a potent vasoactive cytokine that causes increased vascular
permeability. It affects endothelial tight junction proteins, resulting in
extravasation of fluid and retinal edema.
• VEGF induces the phosphorylation of VE-cadherin, occludin, and ZO-1, and
thus causes a disruption of the barrier
• VEGF also stimulates increased leukostasis in the microvessels of the retina,
and the sticky leukocytes release cytokines or may migrate via the
transendothelial route, which causes BRB breakdown.
12. Moderate Nonproliferative Retinopathy
• Moderate Nonproliferative Retinopathy is the second and slightly more severe
stage of Diabetic Retinopathy.
• During this stage, some of the small blood vessels in the Retina may actually
become blocked. The blockage of these tiny blood vessels causes a decrease in
the supply of nutrients and oxygen to certain areas of the Retina.
• blockage of the small blood vessels in the Retina it may be necessary to have a
diagnostic test called a Fluorescein Angiogram (FA). If this is necessary, prior to
starting your Intravenous Fluorescein Angiogram, drops will be placed in your
eyes to dilate your pupils.
• Using the Fluorescein Angiogram, it is possible for the doctor to observe the
circulation and the integrity of the blood vessels in the Retina so that he can
identify any blood vessels that might be blocked.
13. Severe Nonproliferative Retinopathy
• Severe Nonproliferative Retinopathy is the next stage of Diabetic Retinopathy.
• Severe Nonproliferative Retinopathy is characterized by a significant number of
small blood vessels in the Retina actually becoming blocked. As more blood
vessels become blocked, it results in areas of the Retina being deprived of
nourishment and oxygen.
• A lack of sufficient oxygen supply to the Retina results in a condition called
“Retinal Ischemia”. To attempt to compensate for “Retinal Ischemia”, these areas
of the Retina then send signals to the body to stimulate the growth of new blood
vessels in order to try and reestablish the supply of oxygen.
15. • Proliferative Retinopathy is the most severe stage of Diabetic Retinopathy and
carries a significant risk of vision loss.
• Retina responds to a lack of oxygen, or “Retinal Ischemia”, by attempting to
compensate for the reduced circulation by growing new, but abnormal blood
vessels-a process called “neovascularization”.
• Retinal Neovascularization is formed from new blood vessels that are extremely
fragile and tend to break easily and hemorrhage into the Vitreous. If left
untreated, Proliferative Retinopathy may lead to bleeding into the Vitreous and
Retinal Detachment with profound vision loss.
• These new blood vessels are stimulated into growing by the release of a natural
chemical called vascular endothelial growth factor (VEGF). Unfortunately these
blood vessels even though they are formed for the good of the retina, tend to be
very fragile and can leak or haemorrhage. This in turn creates a vicious cycle,
which causes more damage to the retina. Left untreated it can ultimately lead to
blindness.
16. Risk Factors
DURATION OF DM
Type 1 4-5 yrs no DR Type 2 11-13yrs 23% NPDR
3% PDR
5-10yrs 25%-30% 16 yrs 60% NPDR
10-15yrs 75%-95%
20-25yrs PDR in 18%-40
TYPE OF DM
AGE , TOBACCO
BLOOD GLUCOSE LEVRLS
HT
NEUROPATHY
SERUM LIPIDS
ANEMIA
PUBERTY , PREGNENCY ,BMI
17. Diagnosis & Tests
The health care provider can diagnose diabetic retinopathy by dilating your pupils
with eye drops and then carefully examining the retina. A retinal photography or
fluorescein angiography test may also be used.
If you have nonproliferative diabetic retinopathy-
Blood vessels in the eye that are larger in certain spots (called microaneurysms)
Blood vessels that are blocked
Small amounts of bleeding(retinal hemorrhages) and fluid leaking into the retina.
If you have proliferative retinopathy-
New blood vessels starting to grow in the eye that are fragile and can bleed
Small scars developing on the retina and in other parts of the eye (the vitreous)
18. How is diabetic retinopathy treated?
• Intravitreal Anti-VEGF Therapy
• VEGF-A imprortnt factor for angiogenesis (increase vascular permibility) in DR.
• Anti-VEGF drugs prevent neovascularization (New blood vescle formation).
• These are:
1- Lucentis (Ranibizumab)
2- Avastin (bevacizumab)
3- Macugen (Pegaptanib)
Topical Drops : Ocular Corticosteroids :
■ Mecamylamine. ■ Nova63035 (Cortiject).
■ Bromfenac (Bromday) ■ Triamcinolone acetonide (TA).
■ Nepafenac (Nevanac)
19. Vitrectomy: In advanced PDR, the doctor may
recommend a vitrectomy. blood-filled vitreous is
removed and replaced with a clear solution. Vitrectomy
often prevents further bleeding by removing the
abnormal vessels that caused the bleeding. If the retina
is detached, it can be repaired during the vitrectomy
surgery.
Laser surgery: Laser surgery is often recommended for
people with macular edema, PDR, and neovascular
glaucoma. For macular edema, focal or grid laser is
focused on the damaged retina near the macula to
decrease the fluid leakage. This panretinal
photocoagulation treatment causes abnormal new vessels
to shrink and often prevents them from growing in the
future.
20. CONCLUSIONS
• Diabetic Retinopathy happens when high blood sugar damages blood vessels in
the retina.
• Diabetic retinopathy can develop in anyone who has type 1 diabetes or type 2
diabetes. The longer you have diabetes, and the less controlled your blood sugar
is, the more likely you are to develop diabetic retinopathy
• Diabetic retinopathy, eye damage that frequently occurs as a result of diabetes, is
related to the breakdown of the blood–retinal barrier.
• Diabetic retinopathy is characterized by proliferative and nonproliferative.
21. REFERENCES
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vitreoretinopathy and proliferative diabetic retinopathy. Retina 1998;18:546-50.
• Giebel SJ, Menicucci G, McGuire PG, Das A. Matrix metalloproteinases in early diabetic retinopathy and their role in
alteration of the blood-retinal barrier. Lab Invest 2005;85:597-607.
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protein kinase C in vivo and suppressed by an orally effective beta-isoform-selective inhibitor.
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