AAO 2019-2020

DIABETIK RETINOPATI
Dr. Delfi, Mked(Oph), SpM(K)
Diabetes Association (ADA) classifies
◦ Diabetes mellitus type 1 :
 β-cell destructionabsolute insulin
deficiencyidiopathic or immune
mediated. (under 30 years old)
◦ Diabetes mellitus Type 2 :
 insulin resistant with relative insulin
deficiency to one that is
predominantly an insulin secretory
defect (more than 30 years old)
 The Classification Of Diabetic Retinopathy is
based upon clinical features :
◦ NPDR refers to the presence of intraretinal
vascular changes prior no to the development
of extraretinal fibrovascular tissue; it is staged
as mild, moderate, or severe.
◦ CSME is defined as macular edema that meets
certain minimal severity criteria for size and
location by OCT
◦ PDR is defined by the presence of
neovascularization. PDR is staged as early or
with high-risk characteristics.
Epidemiologi
 Diabetes mellitus is a growing global epidemic that is
expected to affect 642 million individuals by the year 2040
 1/3 of the global population of individuals with diabetes
mellitus is estimated to have diabetic retinopathy.
 Wisconsin Epidemiologic Study of Diabetic Retinopathy
(WESDR) cohort, after 20 years of diabetes mellitus, nearly
99% of patients with type 1 and 60% with type 2 disease
demonstrated some degree of diabetic retinopathy.
 PDR was found in 50% of type 1 patients who had 20 years’
duration of disease and in 25% of type 2 patients who had
25 years’ duration of disease.
WESDR  in 2011, visual impairment was
20.7% for black participants, 17.1% for white
participants, and 15.6% for Hispanic
participants.

The prevalence rate for retinopathy for all

adults with diabetes aged 40 and older in the
United States is 28.5% (4.2 million people);
worldwide, the prevalence rate has been
estimated at 34.6% (93 million people)
Patogenesis DR
Perisyte loss,
and Endotelial
Damage

stress
oxidative,
Protein C
Kinase, AGEs
 HIGH RISK FOR DIABETIC
RETINOPATHY
 Duration Of Diabetic
 Bad Control Diabetic
 Hipertension
 Nephropathy
 Obesity And Hiperlypidemia
 Smoking
 Pregnant
SIGN AND SYMPTOM

 Early  No Symptoms  RAPD May (+)

 Floater  Rubeosis Iris

 Bad Night Vision  Retinal Detach

 Fluctuation Vision  Vitreous Haemorage

 Refraction Disorder  Ocular Hipertension

 Dischromatopsia (Neovascular Glaucoma

 Bilateral Vision Loss

Visual Impairment Causal
Macular edema
Signs of severe NPDR (extensive retinal
hemorrhages/microaneurysms, venous beading,
and IRMA)
Optic nerve head neovascularization and/or
neovascularization elsewhere
Vitreous or preretinal hemorrhage
Examination and
Follow Up For
DIABETIC
RETINOPATHY
WHAT SHOULD WE DO ?
ANAMNESE
STATUS GENERALISATA
VISUS
GONIOSKOPI*
TIO
RAPD
• AMSLER GRID
VISUALFIELD* • OCT
EYE MOVEMENT
• OCTA or FFA
SEGMEN ANTERIOR
SEGMEN POSTERIOR
Numerous hematologic and biochemical
abnormalities Correlate with the
prevalence and severity of Retinopathy:
◦ Increased platelet adhesiveness
◦ Increased erythrocyte aggregation
◦ Abnormal levels of serum lipids
◦ Defective fibrinolysis
◦ Abnormal levels of growth hormone
◦ Upregulation of vascular endothelial growth
factor (Vegf)
◦ Abnormalities in serum and whole-blood
viscositylocal and systemic inflammation
 ◂ Diabetic retinopathy
◂ No retinopathy

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Non Proliferative Diabetic
Retinophaty (NPDR)
 Abrreviated Early Treatment Diabetic Retinopathy Study (ETDRS)
Classification of Diabetic Retinopathy

Very Microaneurysms
Mild only
NPDR
Mild Any or all of Microaneurysms

NPDR Microaneurysms,
retinal hemorrhages,
exudates, cotton
wool spots, up to the
level of moderate
NPDR. No Internal
Microvascular IRMA
Anomalies (IRMA) or
significant beading
 Microaneurysm

Hard
exudates

Hemorrhages

Moderate • Severe retinal hemorrhages in 1-3

NPDR quadrants or mild IRMA
• Significant venous beading can be
present in no more than 1 quadrant
• Cotton wool spot commonly present
Severe NPDR The 4-2-1 rule; one or more of:
• Severe hemorrhages in all 4 quadrants
• Significant venous beading in 2 or more
quadrants
• Moderate IRMA in 1 or more quadrants

Very Severe Two or more of the criteria for severe NPDR

NPDR
TREATMENT NPDR

Observation :
Systemic control of blood glucose, lipids, and
hypertensionRefered Internist
Education : Stop Smoking, Weight Loss, Diet,
Stress treatment, physical excercise

Early treatment with panretinal photocoagulation

should be considered for patients with severe NPDR or
worse
 DIABETIC MACULAR EDEMA

• DME may manifest as focal or diffuse retinal

thickening, with or without exudates.
• Focal macular edema is characterized by areas of
focal fluorescein leakage from capillary lesions,
such as microaneurysms
• Diffuse macular edema is characterized by
extensive retinal capillary leakage and widespread
breakdown of the blood–retina barrier, often
accumulating in a cystoid configuration in the
perifoveal macula (cystoid macular edema)
DIABETIC MACULAR EDEMA (DME)
 CSME

Retinal
thickening
located at or
within 500 μm of
the Center of the
macula.

Hard exudates at
or within 500 μm
of the center if
Associated with
thickening of
adjacent retina

A zone of
thickening larger
than 1 disc area
if Located within
1 disc diameter
of the center of
the Macula
Treatment Focal Photocoagulation
for CSME
1. Focal photocoagulation for DME decreased risk of moderate vision loss
(doubling of initial visual angle).
2. Focal photocoagulation for DME increased chance of moderate vision gain
(halving of initial visual angle).
3. Focal photocoagulation for DME reduced retinal thickening.

Early scatter photocoagulation results:

1. Early scatter photocoagulation resulted in a small reduction in the risk of severe vision
loss (<5/200 for at least 4 months).
2. Early scatter photocoagulation is not indicated for eyes with mild to moderate diabetic
retinopathy.
3. Early scatter photocoagulation may be most effective in patients with type 2 diabetes
mellitus.
 PDR
PDR is graded as early, high-risk.
PDR  Neovascular proliferation (NVD, NVE)
High-risk PDR  having any 1 of the following :
• Mild NVD with vitreous hemorrhage
• Moderate To Severe NVD with or without vitreous
hemorrhage (≥DRS standard 10A, showing one-
fourth to one-third disc area of NVD)
• Moderate (one-half disc area) NVE with vitreous
hemorrhage.
Proliferative Diabetic Retinopathy

• Neovascularization
• Vitreous/preretinal
hemorrhage
Mild- New vessels on the disc (NVD) or
Moderate new vessels elsewhere (NVE),
PDR but extent insufficient to meet
the high risk criteria

High-risk • New vessels on the disc (NVD)

PDR about 1/3 disc area
• Any NVD with vitreous
hemorrhage
• NVE greater than ½ disc area
with vitreous hemorrhage
New vessels at the disc (NVD)  neovascularization on or within one disc
diameter of the optic nerve head

MILD SEVERE

Disc New Vessels

 New vessels everywhere (NVE)  further away from the disc; it may be
associated with fibrosis if long-standing

Associate
Mild Severe d with
fibrosis

New Vessels Everywhere

COMPLICATIONS

Neovascularization of the iris or anterior chamber angle

Vitreous hemmorhage

Tractional retinal detachment

Diabetic macular edema

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New vessels on the iris (NVI)  also known as rubeosis iridis, carry a high likelihood
of progression to neovascular glaucoma

New Vessels on the Iris

 Diabetic
Macular
Edema

Associated with
hard exudates,
which are
precipitans of
plasma
lipoproteins

Fluid Hyperglycem
extravasation ia-induced
from retinal
vessels into the
breakdown of
surrounding the blood
neural retina retina barrier

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Common cause of vision loss in
diabetic patients is central subfield-
involved DME that affects the fovea

Even eyes with mild NPDR can have

substantial vision loss from highly
thickened retinas
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MANAGEMENT

Control ischemia Anti-VEGF drugs or with

and reduce ablation of ischemic
ocular VEGF retina via laser
photocoagulation and
Vitrectomy if indicated
Thank You………………..