Diabetic macular edema (DME) is the leading cause of visual loss in diabetes, with various clinical associations including severity of diabetic retinopathy and glycemic control. The pathophysiology involves capillary damage, increased permeability, and fluid accumulation leading to progressive vision loss. Treatment options include laser photocoagulation, anti-VEGF therapy, and corticosteroids, each with specific protocols and potential complications.

1. DIABETIC MACULAR EDEMA

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

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

4. ANATOMY

5. ANATOMY

6. PATHOPHYSIOLOGY
• ALDOSE REDUCTASE
• VASOPROLFERATIVE FACTORS
• PLATELET DYSFUNCTION

7. 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 cβ
• Microaneurysms
• IRMAs

9. PATHOPHYSIOLOGY
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Extracellular fluid accumulation
Cystoid spaces in the outer plexiform layer
May occupy entire thickness
Tissue disorganisation
Atrophic changes

10. PATHOPHYSIOLOGY
• Hard exudates (HE):
– Lipoproteinaceous deposits
– Transudation
– Outer plexiform layer
• Subretinal fluid
• Subretinal fibrosis

11. 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

12. EXAMINATION
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Clinically best detected by 60 D, 78 D lenses
Decreased translucency
Loss of foveolar reflex
Patterns :
– Diffuse
– Focal; circinate pattern
– Ischemic
– Mixed

14. EXAMINATION
• Stereoscopic fundus photography
• Fluorescein angiography
– Macular perfusion
– Extent and location of capillary leakage
• OCT
– Documenting macular thickness
– Monitoring progression

15. 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

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

17. 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)

18. 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

19. ETDRS protocol
Focal
Spot size
Exposure time
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
1
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

20. LASER photocoagulation
• Adverse effects
– Foveal burns
– Subretinal hemorrhage
– Vitreous hemorrhage
– RPE creep
– CNV
– Paradoxically increased HE

21. TRIANCINOLONE ACETONIDE
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Intravitreal route
Needs repeated injections
Duration of effect : 2-3 months with 4mg
Complications
– Raised iop
– Endophthalmitis
– Cataracts
• Peribulbar route

22. ANTI-VEGF therapy
• Bevacizumab (Avastin)
• Ranibizumab (Lucentis)
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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

23. PROTEIN KINASE C Inhibitors
• PKCβ
– Ruboxistaurin
– Oral administration