Diabetic Macular Edema

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A concise and brief description of basics and pathophysiology of maculopathy in diabetes mellitus and its management

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Diabetic Macular Edema

  1. 1. DIABETIC MACULAR EDEMA
  2. 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. 3. CLINICAL ASSOCIATONS • • • • • • • • Severity of DR Duration of diabetes and glycemic control Proteinuria, Hypertension, Dyslipidemia Pregnancy, Intraocular surgery Pan retinal photocoagulation
  4. 4. ANATOMY
  5. 5. ANATOMY
  6. 6. PATHOPHYSIOLOGY • ALDOSE REDUCTASE • VASOPROLFERATIVE FACTORS • PLATELET DYSFUNCTION
  7. 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
  8. 8. PATHOPHYSIOLOGY • • • • • Extracellular fluid accumulation Cystoid spaces in the outer plexiform layer May occupy entire thickness Tissue disorganisation Atrophic changes
  9. 9. PATHOPHYSIOLOGY • Hard exudates (HE): – Lipoproteinaceous deposits – Transudation – Outer plexiform layer • Subretinal fluid • Subretinal fibrosis
  10. 10. 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
  11. 11. EXAMINATION • • • • Clinically best detected by 60 D, 78 D lenses Decreased translucency Loss of foveolar reflex Patterns : – Diffuse – Focal; circinate pattern – Ischemic – Mixed
  12. 12. EXAMINATION • Stereoscopic fundus photography • Fluorescein angiography – Macular perfusion – Extent and location of capillary leakage • OCT – Documenting macular thickness – Monitoring progression
  13. 13. 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
  14. 14. THERAPY • • • • • • Medical LASER photocoagulation Triancinolone acetonide Anti-VEGF therapy Protein kinase c inhibtion Vitrectomy
  15. 15. 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)
  16. 16. 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
  17. 17. 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
  18. 18. LASER photocoagulation • Adverse effects – Foveal burns – Subretinal hemorrhage – Vitreous hemorrhage – RPE creep – CNV – Paradoxically increased HE
  19. 19. TRIANCINOLONE ACETONIDE • • • • Intravitreal route Needs repeated injections Duration of effect : 2-3 months with 4mg Complications – Raised iop – Endophthalmitis – Cataracts • Peribulbar route
  20. 20. 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
  21. 21. PROTEIN KINASE C Inhibitors • PKCβ – Ruboxistaurin – Oral administration

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