Nonexudative age-related macular degeneration (AMD), otherwise known as “dry AMD,” is associated with the presence of small deposits (ie, drusen), under the macula, and areas of retinal pigment epithelium (RPE) loss and outer retinal atrophy in the more advanced stages.¹,⁴

AMD is a leading cause of central vision loss worldwide.⁴

Currently, there is no therapeutic for reversing dry AMD, but results from the AREDS and AREDS 2 clinical trials indicated that increased antioxidant and zinc intake were associated with reduced risk of progression to late-stage AMD.³

Late-stage AMD may progress to neovascular AMD (see Chapter 21) and/or atrophy of photoreceptive layers (ie, geographic atrophy [GA]).

GA is the concurrent atrophy/loss of the RPE, photoreceptors, and choriocapillaris and can cause significant irreversible vision loss.⁵

Decreased choriocapillaris flow has been associated with progression of dry AMD.⁴

With the advent of optical coherence tomography angiography (OCTA), a new entity has been described: neovascular nonexudative AMD. In these eyes, a choroidal neovascular complex is present on OCTA but is quiescent without any evidence of exudation (eg, intraretinal fluid, subretinal fluid).

A hallmark diagnostic feature includes the RPE deflections related to drusen deposits (Figure 21.1). Overall, drusen burden may be a risk factor for progression and may be best documented on optical coherence tomography (OCT).

Early outer retinal attenuation and loss of ellipsoid zone may be identified in eyes overlying drusen or in areas of early atrophy.

Complete GA can be identified by attenuation of the ellipsoid zone (EZ) and loss of the RPE (Figures 21.2 and 21.3). This is associated with increased transmission and “illumination” of the underlying choroid due to the decreased attenuation from the loss of the retinal layers and RPE.