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RetinopathyRidwan Hadinata Salim
(I11109037)
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Definition
General term that refers to some form of
non-inflammatory damage to the retina of the
eye.
Frequently, retinopathy is an ocular
manifestation of systemic disease.
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DIABETIC RETINOPATHY
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Definition
Progressive dysfunction of the retinal blood
vessels caused by chronic hyperglycemia.
Diabetic Retinopathy can be a complication of
diabetes type 1 or diabetes type 2.
Initially, Diabetic Retinopathy is asymptomatic,
if not treated though it can cause low vision and
blindness.
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Diabetic retinopathy symptoms
Diabetic retinopathy is asymptomatic in early stages of thedisease
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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Risk factors
Duration of diabetes
Poor Blood Sugar control Hypertension
Hyperlipidemia
Barriers to care
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Risk factors Diabetic Retinopathy
Duration of diabetes is a major riskfactor associated with the development
of diabetic retinopathy
The severity of hyperglycemia is the key
alterable risk factor associated with thedevelopment of diabetic retinopathy
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How diabetes cause vision loss
HOW DIABETES CAUSES VISION LOSS
Preclinical
changes
Macular
edema
ProliferativeDR
DiabetesBackground
DR
Clinical
significant
macular edema
Vitreous hemorrhage
and/or Retinaldetachment and/or
neovascular glaucoma
PreproliferativeDR
Vision
loss
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Pathophysiology
Diabetic Retinopathy is a microvasculopathy
that causes:
Retinal capillary occlusion
Retinal capillary leakage
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Microvascular Occlusion
Microvascular occlusion is caused by:
Thickening of capillary basement membranes
Abnormal proliferation of capillary endothelium
Increased platelet adhesion Increased blood viscosity
Defective fibrinolysis
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Cottonwool spot
Neovascularization
Ischemia
Neovascular
glaucoma
Microvascular
Occlusion
Fibrovascular bandsVitreous
hemorrhage
Increased VEFG
Tractional retinal
detachment
Infarction
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Microvascular leakage
Microvascular leakage is caused by:
Impairment of endothelial tight junctions
Loss of pericytes
Weakening of capillary walls Elevated levels of vascular endothelial growth factor (VEGF)
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EdemaRetinal
hemorrhageHard exudates
Microvascular Leakage
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Classification of diabetic retinopathy
A useful classification according to the types oflesions detected on fundoscopy is as follows:
Non-proliferative diabetic retinopathy (NPDR)
Proliferative diabetic retinopathy
Maculopathy
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No retinopathy
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MILD NONPROLIFERATIVE DIABETIC
RETINOPATHY
Characteristics
Microaneurysms only
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Microaneurysms
Retinal microaneurysms are focal dilatations of retinal
capillaries, 10 to 100 microns in diameter, and appear as reddots. They are usually seen at the posterior pole, especiallytemporal to the fovea. They may apparently disappear whilstnew lesions appear at the edge of areas of widening capillarynon-perfusion. Microaneurysms are the first
ophthalmoscopically detectable change in diabeticretinopathy.
Beginning as dilatations in areas in the capillary wall wherepericytes are absent, microaneurysms are initially thin-walled.Later, endothelial cells proliferate and lay down layers ofbasement membrane material around themselves.
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Fibrin and erythrocytes may accumulate within the aneurysm.
Despite multiple layers of basement membrane, they are
permeable to water and large molecules, allowing the
accumulation of water and lipid in the retina. Since
fluorescein passes easily through them, many moremicroaneurysms are usually seen on fluorescein angiography
than are apparent on ophthalmoscopy
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MILD NONPROLIFERATIVE DIABETIC
RETINOPATHY
Microaneurysms
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Moderate Nonproliferative Diabetic
Retinopathy (NPDR)
Characteristics
More than just microaneurysms but less than severe NPDR
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Moderate Nonproliferative Diabetic
Retinopathy (NPDR)
Hard exudates
Flamed shaped
hemorrhage
Microaneurysm
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Moderate Nonproliferative Diabetic
Retinopathy (NPDR)
Hard exudates
microaneurysm
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Severe Nonproliferative Diabetic
Retinopathy (NPDR)
Any of the following:
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
No signs of proliferative retinopathy
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Severe Nonproliferative Diabetic Retinopathy
(NPDR)
Venous beading
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Proliferative Diabetic Retinopathy (PDR)
Characteristics
Neovascularization
Vitreous/preretinal
hemorrhage
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PROLIFERATIVE
DIABETIC
RETINOPATHY
Neovascularization
Hard exudate
Cotton-wool
spot
Blot hemorrhage
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High-Risk Proliferative diabetic retinopathy
At risk for serious vision loss
Any combination of three of the following four findings
Presence of vitreous or preretinal hemorrhage.
Presence of new vessels (neovascularization, NV) Location of NV on or near the optic disc.
Moderate to severe extent of new vessels.
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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 withproliferative diabetic retinopathy.
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Meta analysis and review on the effect on bevacizumab id diabetic macular edema
Graefes Arch Clin Exp Ophthalmol(2011) 249:15-27
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Why is Diabetic macular edema so important?
The macula is responsible for central vision.
Diabetic macular edema may be asymptomatic atfirst. As the edema moves in to the fovea (the centerof the macula) the patient will notice blurry centralvision. The ability to read and recognize faces will becompromised.
Macula
Fovea
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Normal Macular Edema
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Clinically significant macular edema
(CSME)
Thickening of the retina at or within 500 m of the
center of the macula.
Hard exudates at or within 500 m of the center of
the macula, if associated with thickening of theadjacent retina.
Area of retinal thickening 1 disc area or larger, within
1 disc diameter of the center of the macula.
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International Clinical Diabetic Macular Edema
Disease Severity Scale
Proposed disease severity level Findings observable upon dilated
ophthalmoscopy
DME apparently absent
DME apparently present
DME present
No apparent retinal thickening or hard exudates in
posterior pole
Some apparent retinal thickening or hard exudatesin posterior pole
Mild DME (some retinal thickening or hard exudates
in posterior pole but distant from the center of the
macula)
Moderate DME (retinal thickening or hard
exudates approaching the center of the macula but
not involving the center)
Severe DME (retinal thickening or hard exudates
involving the center of the macula)Proposed International Clinical DiabeticRetinopathy and Diabetic Macular Edema
Disease Severity Scales
Ophthalmology Volume 110, Number 9, September 2003
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DIABETIC RETINOPATHY TREATMENT
The best measure for prevention of
loss of vision from diabetic
retinopathy is strict glycemiccontrol
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Laser Photocoagulation
Laser Photocoagulation is recommended for eyes with:
Clinical significant macular edema CSME
High risk Proliferative diabetic retinopathy
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DIABETIC RETINOPATHY TREATMENT
Once DR threatens vision treatments can include:
Laser therapy to seal leaking bloodvessels (focal laser)
Laser therapy to reduce retinal oxygendemand (scatter laser)
Surgical removal of blood from the eye(vitrectomy)
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DIABETIC RETINOPATHY TREATMENT
NEWER DEVELOPMENTS:
The use of anti-vascular endothelial
growth factor antibodies has beenshown to be useful in the treatment ofDR
Anti-VEGF antibody treatment appearsto be useful for both macular edema andproliferative retinopathy
Studies to determine the exact role ofanti-VEGF treatment in relation to lasertreatment in specific situations areunderway.
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CONCLUSIONS
Diabetic Retinopathy is
preventable through strict
glycemic control and annual
dilated eye exams by an
ophthalmologist.
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HYPERTENSIVE
RETINOPATHY
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Hipertensive Retinopathy
A condition characterized by a spectrum of
retinal vascular signs in people with elevated
blood pressure.
Arterial changes in hypertension are primarily
caused by vasospasm; in arteriosclerosis they
are the result of thickeningof the wall of the
arteriole.
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Pathophysiology
1. Vasoconstrictive stage
2. Sclerotic stage
3. Exudative stage
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Pathophysiology
Vasoconstrictive stage
blood pressure
Retinal arteriol vasoconstrictive
(local autoregulatory mechanisms)
Generalized narrowing of the
retinal arterioles.
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Sclerotic stage
Persistently elevated blood pressure
Intimal thickening, media wallhyperplasia, hyaline degeneration
Changes in the arteriolar andvenular junction (arteriovenous
nicking or nipping)
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Exudative stage
Disruption of the bloodretina barrier
Necrosis of the smooth muscles andendothelial cells exudation of blood
and lipids, and retinal ischemia
Microaneurysms, hemorrhages, hard
exudates, and cotton-wool spots.
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Classifications
Arteriolar Sclerosis Aging causes thickening and sclerosis of the
arterioles
Prolonged systemic hypertension (usually diastolicpressure greater than100 mm Hg).
The amount of arteriolar sclerosis depends on
duration and severity of the hypertension and
may reflection the condition of the arterioleselsewhere in the body.
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Elevated Blood Pressure
A moderate acute rise in blood pressure results inconstriction of the arterioles.
A severe acute rise in blood pressure (usually, diastolic
pressure greater than 120 mmHg) causes fibrinoid
necrosis of the vessel wall, resulting in exudates,cotton-wool spots, flame-shaped hemorrhages, and
sometimes whitish swelling and edema of large
portions of the retina.
In the most severe form of hypertensive retinopathy,malignant hypertension the optic disc swelling that
occurs resembles the swelling seen in papilledema.
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Hypertensive retinopathy: haemorrhages,
cotton-wool spots, exudates, vascular calibre
changes.
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Symptoms
Headaches
Visual disturbances, and sometimes sudden
vision loss
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Treatment
Control of high blood pressure (hypertension)
is the only treatment for hypertensive
retinopathy.
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Thank You
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