Age-related macular degeneration (ARMD) is an acquired degeneration of the retina that causes significant central visual impairment through a combination of non-neovascular (drusen and retinal pigment epithelium abnormalities), and neovascular derangement (choroidal neovascular membrane formation). Advanced disease may involve focal areas of retinal pigment epithelium (RPE) loss, subretinal or sub-RPE hemorrhage or serous fluid, as well as subretinal fibrosis.
Eat a diet high in saturated fat (found in foods like meat, butter, and cheese)
Early ARMD: Defined by the presence of numerous small (<63 microns, “hard”) or intermediate (≥63 microns but <125 microns, “soft”) drusen
Dry AMD is when parts of the macula get thinner with age and tiny clumps of protein called drusen grow. You slowly lose central vision. In dry age-related macular degeneration, small white or yellowish deposits, called drusen, form on the retina, beneath the macula, causing it to deteriorate or degenerate over time.
Wet ARMD age-related macular degeneration, abnormal blood vessels under the retina begin to grow toward the macula. Because these new blood vessels are abnormal, they tend to break, bleed, and leak fluid, damaging the macula and causing it to lift up and pull away from its base.
Drusen are a hallmark of ARMD. On histopathology, nodular drusen appear as eosinophilic dome-shaped structures situated between Bruch’s membrane and the displaced, attenuated RPE overlying the drusen.
Serous detachments of the RPE
On histopathology, serous RPE detachments can be associated with thickening of the inner aspect of Bruch’s membrane.
Histopathologically, RPE atrophy may be associated with depigmentation, migration and proliferation of RPE cells into the photoreceptor layer. With progression, RPE degeneration is seen, with loss of adjacent photoreceptors, and juxtaposition of Bruch’s membrane to the inner nuclear layer.
Subretinal or sub-RPE neovascularisation:
Sub-RPE neovascularization is located within Bruch’s membrane, typically between the thickened inner aspect of Bruch’s membrane and the rest of Bruch’s membrane. A sub-RPE neovascular membrane can extend subretinally in areas where Bruch’s membrane is not intact. With discontinuities in Bruch’s membrane, capillary-like choroidal vessels can form a subretinal RPE vascular web that can affect serous or hemorrhagic detachments of the neurosensory retina.
DISCIFORM SCARS OR LESIONS
Fibrous disciform scars are usually results of sub-RPE neovascularization. Fibrous tissue develops within Bruch’s membrane or between the RPE and retina
Subretinalhemorrhage can cause photoreceptor damage as the blood is in contact with the photoreceptors and early treatment is needed. Subretinalhemorrhage may be of varying severity. Massive subretinalhemorrhages are typically thought to be associated with anticoagulation therapy, specifically, warfarin therapy. Surgical management options has been reviewed elsewhere (Management of SubmacularHemorrhage).
Break-through vitreous hemorrhage secondary to neovascular ARMD is a rare complication. Sudden peripheral visual field and central vision loss is noted in these instances, to be distinguished from the central field complaints typically noted with ARMD. Other etiologies, such as retinal tears from hemorrhagic posterior vitreous detachments, retinal vascular diseases such as diabetic retinopathy or vein occlusions should be considered as well.
Diplopia can occur as a result of the choroidal neovascular membrane “dragging” the fovea.