Diabetic Retinopathy

Introduction
Diabetic retinopathy (DR) and diabetic macular edema (DME) are common microvascular complications in patients with diabetes Debilitating impact on visual acuity (VA), eventually leading to blindness

Epidemiology
Epidemic Diabetes proportions: aging population and the rapid increase in obesity The longer patients have diabetes, the higher the prevalence of DR In developed countries, leading cause of blindness in the working-age population (2074 years old) Responsible for 12% of new cases of blindness each year

Patophysiology
Etiology: Hyperglycemia Contributing factor: Hypertension, Hyperlipidemia A hallmark of early DR is the change in the structure and cellular composition of the microvasculature

Endothelial cell
Damage endothelial

Breakdown BloodRetinal Barrier

Increased vascular permeability

Accumalation extravascular fluid

Pericytes function

Regulation retinal perfusion

Altered hemodynamic regulation

Abnormal autoregulation blood flow

Microaneurism formation

Abnormal autoregulation Blood flow

Thickening capillary basement membrane Increased extra cellular matrix deposition

Altered Retinal blood flow

Retinal leukostasis
Leukocytes :
large cell volume, high cytoplasmic rigidity, a natural tendency to adhere to the vascular endothelium, and a capacity to generate toxic superoxide radicals and proteolytic enzymes

Effect of leukostasis
retinal endothelial function, retinal perfusion, angiogenesis, and vascular permeability. Involved in capillary nonperfusion, endothelial cell damage, and vascular leakage in the retinal microcirculation

Main problems (Occluded capilaries)

Retinal ischemia

Neo vascularization

VEGF

Role of sorbitol accumulation

hyperglycemia leads to an increased flux through the polyol pathway intracellular sorbitol disruption osmotic balance cellular damage breakdown Retinal-blood barrier

Role of AGEs
Excessive formation of AGEs another biochemical link between diabetes and the development of microvascular complications AGE-specific receptor perpetuate a proinflammatory signaling process and a proatherosclerotic state in vascular tissues

Role of the PKC- pathway

Diacylglycerol(DAG) an activator of PKC PKC an important role in regulating endothelial cell permeability and is an importantsignaling component for VEGF

Role of oxidative stress

ROS productionthrough glucose auto-oxidation, increased flux through the polyol pathway,and increases in protein glycation ROS may activate aldose reductase, PKC, increase AGE production and DAG formation

Classifiction Diabetic Retinopathy

Non Proliferative Diabetic Retinopathy

Microvascular changes confines of the retina and not extend beyond ILM characterized by the presence of venous dilatation, microaneurysms, retinal hemorrhages, retinal edema, and hard exudates Affect visual function through:
increased intraretinl vascular permeability (macular edema) intraretinal capillary closure (macular ischemia)

Diabetic Macular Edema

Visual consequence of abnormal retinal vascular permeability
Location retinal thickening relative to fovea Presence and Location of exudates Presence of cystoid macular edema

Primarly slit-lamp biomicroscopic diagnosis Gold standard Fluorescein angiography for breakdown blood-retinal barrier

Clinically significant macular edema

Treatment of DME
Argon Laser treatment Side Effect & Complication : Paracentral scotomata, transient decreased vision, choroidal neovascularization, subretinal fibrosis, photocoagulation scar expansion, inadvertent foveolar burns Posterior sub tenon TA, intravitreal steroids Pars plana vitrectomy and detachment of posterior hyaloid

Photocoagulation for CSME

Focal leakage
Applied 500-3000um from centre macula

Diffuse leakage
500 um from centre of macula and 500 um from temporal margin of optic disc

Diabetic retinopathy Neovascularization Hemorrhage

Proliferative Diabetic Retinopathy

Based on extent of proliferations PDR graded into early, high-risk or advanced categories Neovascularization: Disc and Elsewhere High risk PDR (any 1 of the following):
mild NVD + VH moderate-severe NVD VH moderate NVE + VH

High Risk PDR (3 of 4 risk factors):

Vitreous or panretinal hemorrhage Presence of new vessel Location of new vessels on or near the optic disc Moderate to severe extent of new vessel

Diabetic retinopathy Neovascularization

Laser treatment for PDR

High risk PDR Scatter PRP Goal: regression existing neovascular tissue and prevent progressive neovascularization in future 1200 or more, 500 um burns, separated by onehalf burn width at 0,1 second duration

 Contraindicated: prominent fibrovascular membranes, vitreoretinal traction, TRD Contracture fibrovascular resulting recurrent VH, Tractional/rhegmatogenous RD SE: Glare , temporary loss accomodation, photopsia. Decreased night vision, color vision, peripheral vision.

Timetable based on Retinopathy

Retinal Abnormality Normal or rare microaneurysm Mild NPDR Moderate NPDR Severe NPDR Suggested follow-up Annualy Every 9 months Every 6 months Every 2-4 months

CSME
PDR

Every 2-4 months *(careful follow up)

Every 2-3 months *(careful follow-up)

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