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Nonexudative ARMD Clinical Presentation

  • Author: Raj K Maturi, MD; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Apr 24, 2014
 

History

Patients with age-related macular degeneration (ARMD) usually report a family history of decreased vision late in life.

  • They often report difficulty with night vision and with changing light conditions. Specifically, patients report changes in Amsler grid self-evaluation and trouble with reading.
  • Commonly, ARMD patients report visual fluctuation (ie, days when vision is poor and other days when it appears improved).
  • Patients report difficulty with reading and making out faces.
  • Metamorphopsia is not a major complaint, but it may be present as the atrophy slowly progresses.
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Physical

Funduscopic examination in age-related macular degeneration (ARMD) is significant for drusen in the early stages of disease. These drusen usually are confluent with significant pigment changes and accumulation of pigment in the posterior pole. RPE often appears atrophic with an easier visualization of the underlying choroidal plexus.

  • In advanced stages of dry ARMD, these focal islands of atrophy coalesce and form large zones of atrophy with severely affected vision.
  • Other signs of choroidal neovascularization include RPE elevation, exudate, or subretinal fluid. The presence of these symptoms may indicate that neovascularization is occurring and that fluorescein angiography may be indicated to evaluate the retina.
  • The periphery of patients with ARMD often has areas of drusen, as well as RPE mottling and atrophy.
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Causes

Oxidative stress is believed to play a major role in the pathogenesis of age-related macular degeneration (ARMD) because of combined exposures of the retina to light and oxygen. Additionally, ARMD is now widely accepted as a genetically inherited disorder with late onset.

Groundbreaking studies in the genetics of ARMD have changed the way in which most specialists perceive the disease. Specifically, a majority of the risk of developing ARMD is determined by variations in 3 specific genes, as follows:

  • CFH gene (chromosome 1)
  • BF (complement factor B) gene and C2 (complement component 2) gene (chromosome 6)
  • LOC gene (chromosome 10)

Maller and others showed that polymorphisms in the above 3 genes independently raise the risk of ARMD.[12] The above genetic factors contribute to approximately 50% of the sibling risk of developing ARMD.

  • Smoking and a higher body mass index are 2 of the most common other environmental factors that contribute independently to the increase in the risk of developing ARMD. Smoking has been clearly identified as increasing the risk of ARMD by 2 times.
  • Large studies have not shown hypertension or heart disease to increase the odds of developing ARMD.
  • Serum lipids were extensively studied in regard to their relationship with ARMD in the National Eye Institute–sponsored AREDS. One report suggests dietary total omega-3 long-chain polyunsaturated fatty acid (LCPUFA) intake was inversely associated with the development of neovascular ARMD (although not nonexudative ARMD). [13] Similarly, individuals with higher fish consumption had a slightly lower incidence of developing neovascular ARMD.
  • A study looking at whether the regular consumption of omega-3 fatty acids and fish may affect the onset of ARMD in women found that incidence of the disease was significantly decreased among women who ate 1 or more servings of fish per week. [14]
  • Studying twins with ARMD, Seddon and others arrived at some interesting conclusions. [15] Current cigarette smoking increased the risk of developing ARMD by 1.9-fold, and past smoking still increased the risk by 1.7-fold. Increased consumption of fish (>2 servings of fish per week) and a higher intake of omega-3 fatty acids both were protective and reduced the odds of developing ARMD by 0.55-fold.

These studies have generally been performed in individuals from the United States of European descent. Thus, the results may not apply to individuals of other races.

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Contributor Information and Disclosures
Author

Raj K Maturi, MD Private Practice in Vitreoretinal Diseases, Surgery, and Uveitis; Volunteer Clinical Associate Professor, Department of Ophthalmology, Indiana University School of Medicine

Raj K Maturi, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Society of Heed Fellows, Indianapolis Ophthalmological Society, Indiana Academy of Ophthalmology

Disclosure: Received grant/research funds from Allergan for consulting; Received consulting fee from DRCR/National Eye Institute, NIH for consulting; Received grant/research funds from LUX, Inc for consulting; Received grant/research funds from DRCR/JAEB for none; Received consulting fee from ALIMERA for consulting; Received consulting fee from ALCON for consulting; Received consulting fee from GLAXOSMITHKLINE for consulting; Received consulting fee from QUARK PHARMACEUTICALS for consulting; Received consul.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Steve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Macula Society, Retina Society, Club Jules Gonin

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Brian A Phillpotts, MD, MD 

Brian A Phillpotts, MD, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, National Medical Association

Disclosure: Nothing to disclose.

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A normal-appearing macula of the left eye. Note the even pigmentation of the retinal pigment epithelium and the absence of any yellow excrescences (drusen) in the fovea. The optic nerve has unrelated changes.
In angiography, fluorescein dye is passed through a peripheral vein and transmits through the vascular system. The dye fluoresces in the vasculature, as seen here. No vascular prominences are seen in the macula or in any areas of dye pooling or staining. The abnormal vessels in the optic nerve, however, do show dye leakage.
Moderate nonexudative age-related macular degeneration is shown with the presence of drusen (yellow deposits) in the macular region.
Staining of drusen. Drusen absorb dye and, in the late frames of the angiogram, show hyperfluorescence. This staining is distinguished from the leakage that occurs when the dye spreads outside the boundary of the lesion.
A more advanced case of nonexudative age-related macular degeneration (ARMD). This image shows drusen that are larger, more confluent, and soft. Soft drusen are defined as drusen that have indistinct borders. Such drusen are more likely to convert to wet ARMD. A few areas of atrophy are noted, where the retinal pigment epithelium (RPE) has lost pigmentation. The retinal cells overlying atrophic RPE are generally nonfunctional and result in a scotoma.
The atrophic retinal pigment epithelium (RPE) demonstrates staining of the underlying choroidal vasculature. Normally, the intact RPE masks the presence of choroidal fluorescence. However, when the RPE atrophies, the underlying dye appears as an area of hyperfluorescence in the early stages of angiography. In the late stages, the drusen lose fluorescence in concert with (or with a small time lag) the rest of the retinal layers.
A more advanced case of dry age-related macular degeneration. Several areas of atrophy are present, as are areas of significant pigment mottling in the macula. The large drusen inferior to fixation are poorly distinguished from each other.
The atrophic areas are easily distinguished by the hyperfluorescence of the retinal pigment epithelium (RPE) in the mid phase of the angiogram. Hypofluorescence of dye, due to masking caused by the increased pigmentation, is seen. No areas of frank dye leakage or exudative age-related macular degeneration (ARMD) are apparent. A "hot cross bun" pattern of dry ARMD-related pigment changes is evident near the fovea.
High-definition optical coherence tomography scan of a 67-year-old woman showing retinal pigment epithelium mottling and pigment epithelial detachments temporal to fixation consistent with dry macular degeneration.
Fundus photo showing drusen in a 67-year-old woman with dry age-related macular degeneration.
Fluorescein angiogram 4 minutes after injection of dye on 67-year-old woman showing pigment epithelial detachments.
A later frame of the angiogram demonstrating the absence of dye leakage outside the lesion, with staining of the areas of atrophy (window defects) in the macular region.
High definition optical coherence tomography right eye demonstrating retinal pigment epithelium atrophy and changes in the deeper layers of retina. The absence of intraretinal cysts, subretinal fluid, or sub-retinal pigment epithelium fluid indicates the absence of wet age-related macular degeneration.
 
 
 
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