Epidemiology

AMD is the leading cause of blindness in individuals > 65 years in developed countries.
- Age of onset: usually > 55 years

Etiology

AMD is characterized by progressive degenerative changes in the central part of the retina (macula) → visual impairment.

Dry AMD (∼ 90%)
- Also referred to as nonexudative AMD or atrophic AMD
- Deposition of yellow-whitish material consisting of lipids, vitronectin, and other proteins (drusen) in the retinal pigment epithelium and between it and Bruch membrane → slow progressive atrophy of the local retinal pigment epithelium (centrally or pericentrally)
  - The condition likely results from chronic oxidative damage to the retinal pigment epithelium and choriocapillaris, leading to subretinal inflammation with abnormal extracellular matrix formation (eg, confluent drusen, basement membrane thickening).
Wet AMD (∼ 10%)
- Also referred to as exudative AMD or neovascular AMD
- Choroidal neovascularization (between the retinal pigment epithelium and Bruch’s membrane) → leaking of intravascular serous fluid and blood → sudden localized elevation of the macula and/or detachment of the retinal pigment epithelium
  - Hemorrhages can cause sudden loss of vision.

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Painless central or pericentral visual impairment → reduced visual acuity, difficulty adapting to changes in lighting
- Dry AMD: slow progressive visual impairment (usually over decades) and unilateral or bilateral onset
- Wet AMD: acute or insidious onset (over weeks to months) and usually manifests in one eye first
Metamorphopsia: type of visual distortion in which straight lines appear wavy, which can be tested for using an Amsler grid
Scotoma (blind spot)

Amsler grid: detection of metamorphopsias and scotomas
Fundoscopy
- Dry AMD
  - Drusen
- Wet AMD
  - Subretinal and intraretinal hemorrhage and/or exudate

Treatment of wet AMD
- First-line: injection of VEGF inhibitors (ranibizumab, bevacizumab, pegaptanib) into the vitreous body

Mnemonic

Ranibizumab → bizu 两个眼珠