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    DIABETIC MACULAR EDEMA

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    OVERVIEW

    Most common cause of visual loss in DM

    Prevelance 11.1% (2-10%)

    Incidence (10 year rate: 20.1%; 25.4%; 13.9%)

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    CLINICAL ASSOCIATONS

    Severity of DR

    Duration of diabetes and glycemic control

    Proteinuria,

    Hypertension,

    Dyslipidemia

    Pregnancy,

    Intraocular surgery

    Pan retinal photocoagulation

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    ANATOMY

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    ANATOMY

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    PATHOPHYSIOLOGY

    ALDOSE REDUCTASE

    VASOPROLFERATIVE FACTORS

    PLATELET DYSFUNCTION

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    PATHOPHYSIOLOGY

    Capillary damage and raised permeability

    (breakdown of inner blood retinal barrier)

    Pericyte loss (oxidative damage and AGEs)

    Disorganisation of tight junctions

    Increased transcelluar endocytosis

    VEGF

    Protein kinase c

    Microaneurysms

    IRMAs

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    PATHOPHYSIOLOGY

    Extracellular fluid accumulation

    Cystoid spaces in the outer plexiform layer

    May occupy entire thickness

    Tissue disorganisation Atrophic changes

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    PATHOPHYSIOLOGY

    Hard exudates (HE):

    Lipoproteinaceous deposits

    Transudation

    Outer plexiform layer

    Subretinal fluid

    Subretinal fibrosis

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    PRESENTATION

    Depends on central macular involvement

    Paracentral scotomas

    Gradual progressive loss of vision (weeks to

    months) Color vision loss

    Metamorphopsia

    Fluctuation of vision

    Contrast sensitivity

    Prolonged adaptation

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    EXAMINATION

    Clinically best detected by 60 D, 78 D lenses

    Decreased translucency

    Loss of foveolar reflex Patterns :

    Diffuse

    Focal; circinate pattern Ischemic

    Mixed

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    CSME

    Retinal thickening atthe center of macula

    Retinal thickeningand/or adjacent hard

    exudates at or within500 u of center ofmacula

    Retinal thickening 1

    disc area, any part ofwhich is within 1 DD ofthe center of macula

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    THERAPY

    Medical

    LASER photocoagulation

    Triancinolone acetonide Anti-VEGF therapy

    Protein kinase c inhibtion

    Vitrectomy

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    LASER photocoagulation

    ETDRS gave conclusive supporting proof

    Focal laser for leaking microaneurysm atleast

    500 u from the fovea

    (aim : closure of leak)

    Grid laser for diffuse retinal thickening/ areas

    of ischemia

    (aim : stimulate retinochoroidal pump)

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    Treatable lesions

    Focal leaks >500 u from center of macula

    causing thickening/exudation

    Focal leaks 300-500 u from center if t/t is not

    likely to damage perifoveal capillary network

    Areas of diffuse leakage

    Abnormal avasular zone

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    ETDRS protocol

    Focal Grid

    Spot size 50-100 u

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    LASER photocoagulation

    Adverse effects

    Foveal burns

    Subretinal hemorrhage

    Vitreous hemorrhage

    RPE creep

    CNV

    Paradoxically increased HE

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    TRIANCINOLONE ACETONIDE

    Intravitreal route

    Needs repeated injections

    Duration of effect : 2-3 months with 4mg Complications

    Raised iop

    Endophthalmitis Cataracts

    Peribulbar route

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    ANTI-VEGF therapy

    Bevacizumab (Avastin)

    Ranibizumab (Lucentis)

    Fusion proteins with human antibody backbone

    Bind all VEGF subtypes

    Intravitreal route

    No definite schedule

    Pegaptinib (Macugen) Engineered RNA fragment

    Specific sites for VEGF binding

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    PROTEIN KINASE C Inhibitors

    PKC

    Ruboxistaurin

    Oral administration