Age-Related Macular Degeneration

• It is the leading cause of irreversible blindness in developed countries.
• Complex multifactoral progressive disease with genetic and environmental influences.

PATHOGENESIS:
Not well understood but it is believed that oxidative stress is the key component of retinal pigment epithelial (RPE) degeneration. Progressive diffuse thickening of the Bruch's membrane (retinal layer that provides nourishment and oxygen to the RPE and the outer layers of retina, including the rod and cone cells) causes hypoxia----> choroidal neovascularisation---->weak new vessels leak serous fluid/blood---->distort central vision and reduce clarity of central vision.
Alternatively death and atrophy of RPE also occurs.

DRUSEN BODIES: visualized clinically as yellow deposits situated within Bruch's membrane. Vary in size and shape/maybe discrete or confluent. Either collagen-based or granular lipid rich.


ESSENTIALS OF DIAGNOSIS:
Older age group (>55year)
Gradual progressive simultaneous or sudden sequential deterioration of central vision in both eyes affecting reading and recognising faces.
Distortion or abnormal size of images (demonstrated by Amsler chart)
No pain or redness.
Macular abnormalities seen by ophthalmoscope.

Suggested Associated Risk Factors:
famale sex
smoking history
family history
hypertension
hypercholestrolemia
history of exposure to UV light
hypermetropia
cataract surgery

Dry ARMD/ Atrophic Degeneration 85%:
Gradual progressive bilateral visual loss of moderate severity.
Atrophy and degeneration of outer retina and RPE.
Variable and may result in severe visual impairment over a span of 5-10 years.
In advanced stages it is possible to see underlying choroidal vessels.

Treatment: No specific treatment but patients benefit from visual rehabilitation (refraction and low vision assessment). Peripheral fields and hence navigational vision are always maintained.

Wet ARMD/ Exudative Degeneration 15%:
Aggressive form of the disease.
Rapid clinical course and 75% of the patients have marked reduction in vision over 3 years.
Disease characterized by choroidal neovascularisation----> fluid leakage and bleeding in the macular region.

Treatment: is aimed at closing off blood flow through the area of choroidal neovascularisation to allow resolution of exudative changes. It is based on which of the following categories (as seen in Fundus Fuorescien Angiography) the disease falls in:
Classic only- neovascularisation fully delineated
Predominantly classic with little occult- ≥50% classic with some occult
Minimally classic- ≤ 50% but >0% classic
Occult only- full extent of neovascularisation not visible

Laser Photocoagulation: occludes neovascular regions of retina
Done for classic-extrafovealand juxtafoveal conditions but also causes considerable to adjacent retina.

Photodynamic Therapy: light activated agent, verteporfin, is given IV. Laser is then used at a particular wavelength to activate the photosensitizer which causes local vessel occlusion without damage to nearby retina. Needs to be repeated every 12 weeks.
This too is used for the subfoveal type of the classic lesion.

Antiangiogenic Agents:
Inhibitors of vascular endothelial growth factor(eg synthetic steriods) which would reverse neovascularisation.
Have to be administered every 4-6 weeks with risks of intraocular infection, inflammation and retinal detachment.
These can be used for both classic and occult.

Submacular Surgery:
Microsurgical viterectomy + retinal incision and then removal of vessels.
Suitable for selected cases.

Macular Rotation:
Macular region of retina is physically moved to overlie another place where the RPE is healthy followed by strabismus surgery. The procedure is complicated and carried significant risk.