Age-related Macular Degeneration with the longevity of the population increase and with increased exposure to oxidants in the food, and environment; exposure to UV rays, blue light in LEDs (lights, mobile screens, TV screens) etc, the prevalence of macular degeneration is increasing.
There is a normal process of degeneration within the pigment epithelial cells of the Retina. In the case of AMD, this process is hastened leading to the accumulation of lipofuscin debris (drusens in the Bruch’s 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 the fovea, there is visual diminution. Early stages, wherein there is only an accumulation of yellow, refractile bodies (drusens), are known as NON-NEOVASCULAR/ Dry Age-related macular degeneration.
In advanced cases, with deterioration of Bruch’s 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, is NEOVASCULAR/WET AMD. These new vessels are leaky and cause pigment epithelial (PED) or Neurosensory (NSD) detachment causing falls in vision. The vessels may also bleed and cause subretinal/submacular hemorrhage which can be very damaging to the existing photoreceptors.
Early stages may have no symptoms. In advancing cases,
Doctors typically perform surgical intervention for significant submacular hemorrhages, as the iron from red blood cells has the potential to harm 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 bleeding faster.
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