Ocular Abnormality- Macular Degeneration

5 mm

4mm temporal

0.8mm inferior to the disc

Macula region

11%

28%

• Smoking

• Diet

• Aspirin

• Race- whites>blacks

• Gender- F >M

• Age

• Hypertension

• Sun

• Nutrition

• Refractive error

• Len opactities

• Aphakia

• Non- exudative/ atrophic DRY

• Exudative WET

• Most common (85-90%)

• Geographic atrophy

• Usually Bilateral, slower

• Choriocapillaris, RPE, Photoreceptors

• Neo-vascularisation

• Causes more devastating and sudden vision “loss”’ aggressive, more quickly

• Choroidal NV ,Serous or haemorrhagic neurosensory or RPE detachment

• Genetic predispositions

• Lipofuscinogenesis (with its linkage to oxidative stress)

• Drusogenesis

• Inflammation

• Neovascularization (wet form)

• Age-related thickening of Bruch’s membrane

• Interferes with photoreceptor/RPE metabolism

• Causing deposition of metabolites / formation of drusen

• Damage to overlying RPE/photoreceptors and underlying choriocapillaris

• Further disruption of RPE/photoreceptor metabolism

• Cause variable amount of depigmentation and eventually atrophy of overlying RPE

• Small: <63 µ (usually Hard)

• Intermediate: 63-124 µ (usually soft)

• Large: >125 µ

• 63-175 µ

• Pale, shallow appearing drusen

• About 250 µ

• Solid appearing drusen

• >500 µ

• Serous fluid

• Blister like appearance

Confident drusen

Calcified drusen

• sharply demarcated, glistening, refractile lesions associated with RPE atrophy.

•Focal areas of hypo- and hyper- pigmentation (‘stippling’)

•Leads to neurosensory atrophy revealing underlying choriocapillaris

Geographic atrophy

• Soft drusen present in early stages (significant risk factor for GA – due to RPE detachment)

• Decreased retinal thickness and increased visualisation of choroidal vessels

• Sharply demarcated pale area

• Choroidal vessels sometimes white

Gradual mild to moderate impairment over months or years

• Slow/progressive atrophy of RPE and photoreceptors or

• Collapse of an RPE detachment overlying soft drusen

Exudative AMD

•Choroidal neo-vascularisation

•Exudative detachment of RPE and/or retina

•Disciform scar

• Proliferations of fibrovascular tissue from choriocapillaris through defects in Bruch’s membrane

• Formation of a subretinal/choroidal neovascular membrane (SRNVM/CNVM)

• Fibrous tissue proliferation – scar development (Disciform scar) - Permanent vision loss

Tendency to leak

• Serous and blood

• Distorted or blurred vision

• Red if sub-retinal, darker if sub-RPE

• Rarely vitreous haemorrhage

closest point to the foveal avascular zone (FAZ)

• Subfoveal: under the centre of FAZ

• Juxtafoveal: 1-199 µm from the centre of FAZ

• Extrafoveal: >200 µm & <2500 µm from the centre of FAZ

Classic – Early leakage from edge of membrane

Occult type 1 - fibrovascular.

Occult type 2- Undetermined leakage

Exudative AMD Ocult CNVM Type I Fibrovascular

Exudative AMD Ocult CNVM Type II late leakage of undetermined source

Wet disciform AMD

To evaluate the effect of high-dose vitamins C and E, beta-carotene and zinc formulations on age-related macular degeneration (AMD) progression and visual acuity.

Antiangiogenic drugs (VEGF)

• A naturally occurring protein

• Stimulates angiogenesis

• Proinflammatory

• Stimulates angiogenesis of choroidal blood vessels into the retina beneath the macula.

• Angiogenesis begins with vasodilatation and increases in vascular permeability, followed by activation and proliferation of vascular endothelial cells.

reduce the growth of new blood vessels, decrease the leakage through them.

• Bevacizumab (Avastin)

• Ranibizumab (Lucentis)

• Pegaptanib sodium (Macugen)

• Aflibercept (Eylea)

• Anecortave acetate (Retaane)

- (modified steroid)