Diabetic Macular Edema
Upcoming SlideShare
Loading in...5
×
 

Diabetic Macular Edema

on

  • 314 views

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

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

Statistics

Views

Total Views
314
Views on SlideShare
314
Embed Views
0

Actions

Likes
0
Downloads
27
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

Diabetic Macular Edema Diabetic Macular Edema Presentation Transcript

  • 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 cβ • 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 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
  • 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 • PKCβ – Ruboxistaurin – Oral administration