Macular Degeneration, Age-Related

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Basics

Description

  • Age-related macular degeneration (ARMD) is the leading cause of irreversible, severe visual loss in persons age >65 years.
  • ARMD can be classified as:
    • Atrophic/nonexudative, such as drusen or macular pigmentary changes
    • Neovascular/exudative

Epidemiology

  • Neovascular/exudative form is rare in blacks and more common in whites.
  • Predominant sex: female

Incidence
  • In the Framingham Eye Study (FES), drusen were noted in 25% of all participants who were ≥52 years of age. ARMD-associated visual loss was noted in 5.7%.
  • Atrophic/nonexudative stage accounts for 20% of cases of severe visual loss.
  • Neovascular/exudative stage accounts for 80% of cases of severe visual loss.
Prevalence

Per FES study:

  • People 65 to 74 years old: 11%
  • People ≥75 years old: 27.9%

Etiology and Pathophysiology

  • Atrophic/nonexudative
    • Visible light can result in the formation and accumulation of metabolic by-products in the retinal pigment epithelium (RPE), a pigment layer underneath the retina that normally helps remove metabolic by-products from the retina. Excess accumulation of these metabolic by-products interferes with the normal metabolic activity of the RPE and can lead to the formation of drusen.
    • Drusen and/or pigmentary changes in the macula. Drusen are deposits of hyaline material between the RPE and Bruch membrane (the limiting membrane between the RPE and the choroid)
    • Most do not progress beyond the atrophic/nonexudative stage; however, those who do are at a greater risk of severe visual loss.
  • Neovascular/exudative
    • Neovascular stage generally arises from the atrophic stage.
      • In type 1 neovascularization, breaks in the Bruch membrane allow choroidal neovascular membranes (CNVMs) to grow in the sub-RPE space. This corresponds to occult CNVMs. Fluid leakage and bleeding can produce a vascularized serous or fibrovascular RPE detachment.
      • In type 2 neovascularization, the CNVM passes through the RPE and is located in the subretinal space. Typically appears as a lacy or gray-green lesion. This corresponds to classic CNVM.
      • Type 3 neovascularization, also known as retinal angiomatous proliferations (RAPS), the neovascularization develops from the deep capillary plexus of retina and grows downward toward the RPE.
      • Polypoidal choroidal vasculopathy is a subtype of exudative ARMD and often presents with multiple, recurrent serosanguineous RPE detachments.

Genetics
  • Genetic susceptibility may be a factor in ARMD: ~25% genetically determined
  • Complement factor H Y402H genotype is an important susceptibility gene for ARMD.
  • Although the development of ARMD may be predicted by specific alleles, the clinical response to antivascular endothelial growth factor (VEGF) is not.

Risk Factors

  • Obesity
  • Ethnicity: non-Hispanic whites
  • Cigarette smoking
  • Chlamydia pneumoniae infection
  • Family history
  • Excess sunlight exposure
  • Blue or light iris color
  • Hyperopia
  • History of cardiovascular disease
  • Short stature
  • High plasma high-density lipoprotein cholesterol levels are associated with an increased risk for ARMD.
  • Physical activity is associated with lower risk of early and late ARMD in white populations.
  • Female sex

General Prevention

  • Ultraviolet (UV) protection for eyes
  • Routine ophthalmologic visits
    • Every 2 to 4 years for patients age 40 to 64 years
    • Every 1 to 2 years after age 65 years

-- To view the remaining sections of this topic, please or --

Basics

Description

  • Age-related macular degeneration (ARMD) is the leading cause of irreversible, severe visual loss in persons age >65 years.
  • ARMD can be classified as:
    • Atrophic/nonexudative, such as drusen or macular pigmentary changes
    • Neovascular/exudative

Epidemiology

  • Neovascular/exudative form is rare in blacks and more common in whites.
  • Predominant sex: female

Incidence
  • In the Framingham Eye Study (FES), drusen were noted in 25% of all participants who were ≥52 years of age. ARMD-associated visual loss was noted in 5.7%.
  • Atrophic/nonexudative stage accounts for 20% of cases of severe visual loss.
  • Neovascular/exudative stage accounts for 80% of cases of severe visual loss.
Prevalence

Per FES study:

  • People 65 to 74 years old: 11%
  • People ≥75 years old: 27.9%

Etiology and Pathophysiology

  • Atrophic/nonexudative
    • Visible light can result in the formation and accumulation of metabolic by-products in the retinal pigment epithelium (RPE), a pigment layer underneath the retina that normally helps remove metabolic by-products from the retina. Excess accumulation of these metabolic by-products interferes with the normal metabolic activity of the RPE and can lead to the formation of drusen.
    • Drusen and/or pigmentary changes in the macula. Drusen are deposits of hyaline material between the RPE and Bruch membrane (the limiting membrane between the RPE and the choroid)
    • Most do not progress beyond the atrophic/nonexudative stage; however, those who do are at a greater risk of severe visual loss.
  • Neovascular/exudative
    • Neovascular stage generally arises from the atrophic stage.
      • In type 1 neovascularization, breaks in the Bruch membrane allow choroidal neovascular membranes (CNVMs) to grow in the sub-RPE space. This corresponds to occult CNVMs. Fluid leakage and bleeding can produce a vascularized serous or fibrovascular RPE detachment.
      • In type 2 neovascularization, the CNVM passes through the RPE and is located in the subretinal space. Typically appears as a lacy or gray-green lesion. This corresponds to classic CNVM.
      • Type 3 neovascularization, also known as retinal angiomatous proliferations (RAPS), the neovascularization develops from the deep capillary plexus of retina and grows downward toward the RPE.
      • Polypoidal choroidal vasculopathy is a subtype of exudative ARMD and often presents with multiple, recurrent serosanguineous RPE detachments.

Genetics
  • Genetic susceptibility may be a factor in ARMD: ~25% genetically determined
  • Complement factor H Y402H genotype is an important susceptibility gene for ARMD.
  • Although the development of ARMD may be predicted by specific alleles, the clinical response to antivascular endothelial growth factor (VEGF) is not.

Risk Factors

  • Obesity
  • Ethnicity: non-Hispanic whites
  • Cigarette smoking
  • Chlamydia pneumoniae infection
  • Family history
  • Excess sunlight exposure
  • Blue or light iris color
  • Hyperopia
  • History of cardiovascular disease
  • Short stature
  • High plasma high-density lipoprotein cholesterol levels are associated with an increased risk for ARMD.
  • Physical activity is associated with lower risk of early and late ARMD in white populations.
  • Female sex

General Prevention

  • Ultraviolet (UV) protection for eyes
  • Routine ophthalmologic visits
    • Every 2 to 4 years for patients age 40 to 64 years
    • Every 1 to 2 years after age 65 years

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