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DIABETIC MACULAR EDEMA

OVERVIEW
Most common cause of visual loss in DM
Prevelance 11.1% (2-10%)
Incidence (10 year rate: 20.1%; 25.4%; 13.9%)

CLINICAL ASSOCIATONS

Severity of DR
Duration of diabetes and glycemic control
Proteinuria,
Hypertension,
Dyslipidemia
Pregnancy,
Intraocular surgery
Pan retinal photocoagulation

ANATOMY

ANATOMY

PATHOPHYSIOLOGY
ALDOSE REDUCTASE
VASOPROLFERATIVE FACTORS
PLATELET DYSFUNCTION

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

PATHOPHYSIOLOGY

Extracellular fluid accumulation


Cystoid spaces in the outer plexiform layer
May occupy entire thickness
Tissue disorganisation
Atrophic changes

PATHOPHYSIOLOGY
Hard exudates (HE):
Lipoproteinaceous deposits
Transudation
Outer plexiform layer

Subretinal fluid
Subretinal fibrosis

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

EXAMINATION

Clinically best detected by 60 D, 78 D lenses


Decreased translucency
Loss of foveolar reflex
Patterns :
Diffuse
Focal; circinate pattern
Ischemic
Mixed

EXAMINATION
Stereoscopic fundus photography
Fluorescein angiography
Macular perfusion
Extent and location of capillary leakage

OCT
Documenting macular thickness
Monitoring progression

CSME
Retinal thickening at
the center of macula
Retinal thickening
and/or adjacent hard
exudates at or within
500 u of center of
macula
Retinal thickening 1
disc area, any part of
which is within 1 DD of
the center of macula

THERAPY

Medical
LASER photocoagulation
Triancinolone acetonide
Anti-VEGF therapy
Protein kinase c inhibtion
Vitrectomy

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)

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

ETDRS protocol
Spot size
Exposure time

Focal

Grid

50-100 u

<200u
0.05 0.1 s

Intensity

Whitening/darkening of
microaneurysms (80 - 120
mW)

80 180 mW

Number of burns

Coagulate all leaking foci

All zones of diffuse leakage

Placement

500 3000 u from center sparing papillomacular bundle

Sessions

Argon green laser (514 nm) and Goldmann 3 mirror lens


Avoid argon blue-green (488 nm)
Follow up after 4 weeks, if lesions missed then treat after 4 months
Spacing is one burn width apart

LASER photocoagulation
Adverse effects
Foveal burns
Subretinal hemorrhage
Vitreous hemorrhage
RPE creep
CNV
Paradoxically increased HE

TRIANCINOLONE ACETONIDE

Intravitreal route
Needs repeated injections
Duration of effect : 2-3 months with 4mg
Complications
Raised iop
Endophthalmitis
Cataracts

Peribulbar route

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

PROTEIN KINASE C Inhibitors


PKC
Ruboxistaurin
Oral administration

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