With the longevity of population increase and with increased exposure to oxidants in the food, environment; exposure to UV rays, blue light in LED’s (lights, mobile screens, TV screens) etc, the prevalence of macular degeneration is increasing. In the western world, AMD is one of the main causes of low vision. In India also the cases of AMD are being picked up more day by day.
What is AMD/ARMD?
There is a normal process of degeneration within the pigment epithelial cells of retina. In case of AMD, this process is hastened leading to accumulation of lipofuscin debris (drusens in the bruchs membrane and basal lamina). Excessive accumulation of debris causes the atrophy of RPE cells, in turn leading to dysfunction and death of photoreceptors. When this process is exactly at the site of fovea, there is visual diminution. Early stages, wherein there is only accumulation of yellow, refractile bodies (drusens), is known as NON-NEOVASCULAR/ DRY AMD.
In advanced cases , with deterioration of Bruchs membrane and RPE layer, the barrier activity is lost and new vessels are formed from the choroidal circulation , either under the RPE (type 1) or under the neurosensory retina (type 2). This is called CNVM (choroidal neovascular membrane) and the disease, as NEOVASCULAR/WET AMD. These new vessels are leaky and cause pigment epithelial (PED) or Neurosensory (NSD) detachment causing fall in vision. The vessels may also bleed and cause subretinal/submacular haemorrhage which can be very damaging to the existing photoreceptors.
What are the symptoms of AMD?
Early stages may have no symptoms. In advancing cases,
- Blurring of vision which may be indolent or sudden
- Metamorphopsia (things appearing smaller or bigger than usual, borders of objects appear bent/crooked/wavy)
- Scotomas (black spots in visual field)
- Inability to see in dim light
- Both non-neovascular and neovascular AMD can be detected by simple slit lamp biomicroscopy with 90D lens.
- Fundus Color photograph as a comparative tool.
- OCT can help in quantifying amount of leak and detachment of retina. Also helps in characterising type of PED (serous/hemorrhagic/fibrovascular/drusenoid)
- FFA/ICGA- angiography to delineate the choroidal neovascular membrane (location/type/extent)
- AMSLER Chart Screening
- Dry AMD- presence of only drusens usually needs no treatment. Patient can be educated about healthy diet rich in antioxidants, use of blue light blocker glasses/screen protector. Educate the patient about potential symptoms of worsening and how to catch them using an Amsler chart. In case the patient has soft drusens or large druse or if the other eye has had worsening, then AREDS 2 formula oral medications can be prescribed.
Vitamin E-400IU,Vitamin C-500mg, Copper 2mg, Zinc 80mg,Lutein 10mg,zeaxanthin 2mg
- Wet AMD- in case of a neovascular membrane, the treatment is with Intravitreal AntiVEGF +/- Intravitreal triamcinolone so as to shrink and stabilize the vessels and decrease the ooze.
- Surgical intervention is usually done in case of a large submacular haemorrhage, as the iron from red blood cells can be damaging to the photoreceptors. It involves removing the vitreous and injecting gas along with AntiVEGF and tissue plasminogen activator, so as to displace the blood from the fovea and resolve the bleed faster.