Geographic Atrophy
Also known as: GA, Advanced dry AMD, Atrophic AMD
Overview
Geographic atrophy (GA) is the advanced form of non-neovascular (dry) age-related macular degeneration, defined by sharply demarcated areas of loss of the retinal pigment epithelium, photoreceptors, and choriocapillaris. It causes progressive, irreversible loss of central vision, often sparing the fovea until late and producing dense scotomas that impair reading and face recognition. Complement inhibitors are the first therapies shown to slow GA lesion growth, though none restore vision already lost.
- Affects
- Macula (RPE and photoreceptors)
- Category
- Advanced non-neovascular AMD
- Key imaging
- Fundus autofluorescence, OCT
- Therapy
- Intravitreal complement inhibitors
Key clinical points
- GA is advanced dry AMD, distinct from neovascular (wet) AMD, though the two can coexist.
- Fundus autofluorescence best delineates lesion borders and monitors enlargement over time.
- OCT shows RPE loss, outer retinal thinning, and choroidal signal hypertransmission.
- Complement inhibitors (pegcetacoplan, avacincaptad pegol) slow lesion growth but do not improve vision.
- Foveal involvement drives central vision loss; low-vision rehabilitation is essential.
Pathophysiology and risk
GA reflects the end stage of the atrophic AMD pathway, with dysregulation of the complement system contributing to RPE and photoreceptor death. Lesions typically begin parafoveally and expand, coalescing over time. Age, smoking, genetic variants in the complement pathway, and the presence of GA or advanced AMD in the fellow eye all increase risk.
Progression rates vary widely between patients; lesion configuration and autofluorescence patterns at the lesion margin help predict the speed of enlargement.
Diagnosis and imaging
Fundus autofluorescence is the reference standard for measuring lesion area and tracking enlargement, showing hypoautofluorescence in atrophic zones. OCT reveals loss of the RPE and outer retinal bands with increased choroidal signal transmission, and helps exclude concurrent neovascular activity.
OCT angiography and fluorescein angiography are used when there is suspicion of coexisting choroidal neovascularization, since patients with GA remain at risk of converting to wet AMD.
Treatment and management
Intravitreal complement inhibitors—pegcetacoplan (C3) and avacincaptad pegol (C5)—are the first approved therapies to slow the rate of GA lesion growth. Benefits accrue over time and must be weighed against injection burden and a small increased risk of conversion to neovascular AMD.
AREDS2 supplementation remains appropriate to reduce broader AMD progression risk, and low-vision rehabilitation, home monitoring, and smoking cessation are core to comprehensive care.
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Frequently asked questions
- Is geographic atrophy the same as macular degeneration?
- Geographic atrophy is the advanced form of dry (non-neovascular) age-related macular degeneration. It is one type of advanced AMD; the other is neovascular (wet) AMD.
- Can geographic atrophy be treated?
- Intravitreal complement inhibitors such as pegcetacoplan and avacincaptad pegol can slow the enlargement of GA lesions, but no therapy currently restores vision already lost to atrophy.
- How is geographic atrophy monitored?
- Fundus autofluorescence is the preferred method for measuring lesion size and tracking growth over time, supported by OCT to assess retinal structure and rule out neovascular activity.
References & further reading
Related conditions
Age-Related Macular Degeneration
Age-related macular degeneration (AMD) is a progressive disease of the central retina and a leading cause of irreversible central vision loss in people over 50. It is divided into non-neovascular (dry) disease, marked by drusen and, in advanced form, geographic atrophy, and neovascular (wet) disease, in which choroidal neovascularization threatens rapid vision loss. Anti-VEGF therapy transformed the prognosis of wet AMD.
Clinical overviewRetinaDiabetic Retinopathy
Diabetic retinopathy is a microvascular complication of diabetes mellitus and a leading cause of vision loss among working-age adults. It progresses from non-proliferative changes—microaneurysms, hemorrhages, and exudates—to proliferative disease with neovascularization that risks vitreous hemorrhage and tractional detachment. Glycemic and blood pressure control plus timely screening are the foundation of prevention.
Clinical overviewRetinaRetinal Vein Occlusion
Retinal vein occlusion (RVO) is one of the most common retinal vascular disorders, caused by thrombotic obstruction of a retinal vein that leads to hemorrhage, macular edema, and, in ischemic cases, neovascularization. It is classified as branch or central depending on the site of occlusion. Vision loss most often results from macular edema, which is treated effectively with anti-VEGF therapy.
Clinical overview