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.
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.
- Neovascular stage generally arises from the atrophic stage.
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 log in or purchase a subscription --
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.
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.
- Neovascular stage generally arises from the atrophic stage.
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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