Wet versus Dry Macular Degenerative Changes
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Title: Wet versus Dry Macular Degenerative Changes
Author: Nina Boal, MSIV, Thomas Jefferson University
Photographer: James Gilman, CRA, FOPS
Location: Medical Student Education Outline > II. Anatomical Approach to Eye Disease > RETINA> 2. Wet versus Dry Macular degenerative changes
Overview
Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in industrialized countries among people 50 years or older [1]. It is a degenerative disease of the macula (central portion of the retina), that results in central vision loss. Clinically, it is divided into dry (atrophic) or wet (exudative or neovascular). The risk of progressing from dry AMD to wet AMD is estimated at 1 to 4.7 percent in one year and 13 to 18 percent at three years [2].
Dry age-related Macular Degeneration
Macular changes in dry AMD are characterized by subretinal drusen deposits, atrophy of the retinal pigment epithelium (RPE), pigment epithelial detachments, and subretinal pigment epithelial clumping. There is an absence of neovascularization [3]. Dry AMD affects 85 to 90 percent of everyone with AMD [4].
- Drusen are deposits of extracellular material that appear as bright yellow spots on ophthalmoscopy, seen in figure 1. The risk for progression to wet AMD increases with increasing number and size of drusen and the presence of RPE pigmentary abnormalities. A few, small drusen is typical in people over 50 years old and are considered a normal part of aging [4].
- Retinal pigment epithelium (RPE) atrophy appears appear as clumps of hyperpigmentation or depigmented atrophic areas on ophthalmoscopy. Areas of loss of tissue and thinning can be focal or more widely dispersed on the macula, called geographic atrophy seen in figure 2.
Wet age-related Macular Degeneration
In wet (or neovascular) AMD, abnormal vessels grow into the subretinal space from the choroidal circulation. These vessels can leak and lead to subretinal hemorrhage, seen in figure 3, and subretinal fluid collections, indicating choroidal neovascularization. The goal is to recognize these new vessels before they bleed and cause a hemorrhagic detachment of the retinal pigment epithelium. Wet AMD is less common than dry AMD, affecting only 10 to 15 percent of people with AMD. However, it accounts for more than 80% of patients with severe visual loss or legal blindness [4].
Presentation
The main symptom of AMD is loss of central vision, but initially AMD may be asymptomatic. Patients with dry AMD describe a gradual loss of vision in the center of their visual field. Patients with wet AMD may describe a more acute visual distortion or loss of central vision as fluid or blood accumulates under the retina.
Work-up
- Visual Acuity
- Dilated eye examination
- Amsler grid
- A useful tool, seen in figure 4, to evaluate the functioning of the macula.
- The patient focuses one eye at a time on the center dot of the grid from 1 foot away, and then notes irregularities in the lines.
- This test specifically tests for metamophopsia (distortion of straight lines), an early change in wet AMD [3].
- Fluorescein dye retinal angiography
- Can be helpful to identify neovascularization in wet AMD
- Fluorescein dye is injected intravenously, and a sequence of photographs are taken. Newly formed choroidal neovascular vessels will leak fluorescein as seen in figure 3B.
- Optical coherence tomography (OCT)
- Produces cross sectional images of the retina and can be used to identify drusen, retinal edema, and subretinal fluid.
Treatment of Dry AMD
There is no proven effective treatment for dry AMD, however these patients may eventually develop wet AMD [3]. To prevent this progression, patients can be advised to stop smoking and take a combination of vitamins and minerals that make up the AREDS formula (Age-Related Eye Disease Study). A combination of antioxidant vitamins plus zinc was shown to protect the eye from further damage from AMD in patients who had more extensive dry and wet AMD [5,6].
Treatment of Wet AMD
In addition to the use of antioxidants and zinc, treatment of wet AMD attempts to stop and prevent neovascularization through:
- VEGF inhibitors
- Central to treatment of wet AMD, anti-VEGF therapies such as bevacizumab, ranibizumab, and aflibercept are injected into the vitreous monthly or bimonthly
- VEGF plays an important role in neovascularization. By inhibiting VEGF, the progression of wet AMD is stopped and vision loss can be stabilized or improved [7].
- Photodynamic therapy (PDT)
- Typically used if anti-VEGF therapy is not effective
- Involves intravenous injection of the photosensitization dye verteporfin before treating the eye with a photo-activating laser. The role of this therapy has decreased with the increasing use of anti-VEGF therapy [3].
- Thermal laser photocoagulation
- Use is limited to smaller lesions outside of the central macula due to the risk of scotoma and vision loss [3].
Summary Table
Dry AMD | Wet AMD |
85 to 90% of patients with AMD | 10 to 15% of patients with AMD |
Absence of neovascularization | Choroidal neovascularization– subretinal hemorrhage and subretinal fluid collections |
Drusen, RPE atrophy, pigment epithelial detachments, subretinal pigment epithelial clumping | Drusen, RPE atrophy, pigment epithelial detachments, subretinal pigment epithelial clumping |
Slow progression | Rapid loss of central vision over weeks to months |
Mild to Severe central vision loss | More severe vision loss or legal blindness |
Treatment:
– Monitor progression to wet AMD with Amsler grid – Smoking cessation – AREDS antioxidants and zinc supplements (more effective for extensive dry AMD) |
Treatment:
– Smoking cessation – AREDS antioxidants and zinc supplements – Anti-VEGF therapy – If anti-VEGF therapy does not work consider PDT or thermal laser photocoagulation |
Faculty Reviewer: Griffin Jardine, MD
References:
- Hyman L. Epidemiology of eye disease in the elderly. Eye (Lond) 1987; 1 ( Pt 2):330.
- Bressler NM. Age-related macular degeneration is the leading cause of blindness… JAMA 2004; 291:1900.
- Lietman MW. Manual for eye examination and diagnosis. 9th Hoboken, NJ: John Wiley & Sons Inc.; 2017.
- Jager RD, Mieler WF, Miller JW. Age-related macular degeneration. N Engl J Med 2008; 358:2606.
- Age-Related Eye Disease Study Research Group. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch Ophthalmol 2001; 119:1417.
- Tan JS, Mitchell P, Kifley A, et al. Smoking and the long-term incidence of age-related macular degeneration: the Blue Mountains Eye Study. Arch Ophthalmol 2007; 125:1089.
- Solomon SD, Lindsley K, Vedula SS, et al. Anti-vascular endothelial growth factor for neovascular age-related macular degeneration. Cochrane Database Syst Rev 2014.
Identifier: Moran_CORE_24645