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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
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 protocolFocal Grid
Spot size 50-100 u <200u
Exposure time 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 lensAvoid argon blue-green (488 nm)Follow up after 4 weeks, if lesions missed then treat after 4 monthsSpacing 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