eMedicine Specialties > Ophthalmology > Retina

ARMD, Exudative

Author: Grant M Comer, MD, Vitreoretinal Service, Clinical Ophthalmologist, Kellogg Eye Center, University of Michigan
Coauthor(s): Thomas Ciulla, MD, Associate Professor, Department of Ophthalmology, Indiana University School of Medicine; Mark H Criswell, PhD, Director of Retina Service Research Laboratories, Assistant Research Professor, Department of Ophthalmology, Indiana University School of Medicine; Alon Harris, PhD, Lois Letzter Professor, Director of Glaucoma Research and Diagnostic Center, Department of Ophthalmology, Indiana University School of Medicine
Contributor Information and Disclosures

Updated: Jun 25, 2008

Introduction

Background

Types of macular degeneration

Age-related macular degeneration (AMD) is the leading cause of irreversible vision loss in the industrialized world.1,2,3

Physicians have traditionally recognized two types of macular degeneration: dry and wet. The dry, or nonexudative, form involves both atrophic and hypertrophic changes of the retinal pigment epithelium (RPE) underlying the central macula, as well as drusen deposition beneath the RPE. Patients with nonexudative AMD can progress to the wet, or exudative, form of AMD, in which pathologic choroidal neovascular membranes (CNVM) develop under the retina, leak fluid and blood, and, ultimately, cause a centrally blinding disciform scar over a relatively short time course if left untreated. Approximately 10-20% of patients with nonexudative AMD eventually progress to the exudative form, which is responsible for the majority of the estimated 1.75 million cases of advanced AMD in the United States.4,5

In 1995, the International ARM Epidemiologic Study Group redefined AMD from the traditional wet and dry designations. The criteria for the diagnosis of AMD subsequently became stricter. Patients with minimal or moderate nonexudative age-related changes in the macula were reclassified as having age-related maculopathy (ARM). By definition, advanced RPE atrophy (ie, geographic atrophy) or choroidal neovascularization (CNV) was required to establish a diagnosis of nonexudative AMD and exudative AMD, respectively.6 An alternative classification scheme uses a 9-step severity scale to allow for risk stratification and reproducibility of age-related macular changes.7

As a result of the International ARM Epidemiologic Study Group efforts, patients with ARM account for 85-90% of individuals with age-related macular changes and have only mild drusen, RPE atrophy, and/or RPE hypertrophy. They tend to be asymptomatic or only minimally symptomatic with mild blurred central vision, color and contrast disturbances, and metamorphopsia (waviness). Conversely, the 10-15% of patients with macular changes defined as AMD tend to report painless, progressive, moderate-to-severe blurring of central vision and moderate-to-severe metamorphopsia, which can be acute or insidious in onset.

Pathophysiology

AMD is a degenerative retinal disease, presumably caused by both genetic and environmental factors. While age, race, and family history demonstrate a consistently strong association with AMD in large epidemiological studies, smoking, hypertension, and cataract surgery are also consistently reported modifiable risk factors contributing to the advancement of AMD.8

The exact pathophysiology of AMD is relatively poorly understood; however, recent discoveries in genetics have pointed toward the complement pathway as a primary mechanism. A strong association was discovered between AMD and a single nucleotide polymorphism in the complement factor H (CFH) gene on chromosome 19,10,8,11 and the PLEKHA1 and LOC387715 genes on chromosome 10.12   Conversely, protective effects were reported for polymorphisms in the complement factor B and complement component 2 genes on chromosome 6 and various haplotypes on the CFH gene.13,11

CFH is an inhibitor of the complement pathways; thus, abnormal CFH activity allows for complement cascade activation and subsequent inflammatory response to subretinal tissues.11 Drusen, which are found in AMD, have inflammatory components from the cascade pathway.14 In addition, smoking, which decreases levels of CFH, significantly increases the odds of developing AMD over nonsmokers with the CFH polymorphism.15,16 Similarly, the complement factor B and complement component 2 genes, which are usually involved in the activation of the complement cascade, could limit complement pathway activation with a protective polymorphism and, thus, minimize the degree of chronic inflammation.13

Frequency

United States

AMD is the leading cause of irreversible visual loss in the United States, with variable degrees of age-related macular changes occurring in more than 10% of the population aged 65-74 years and 25% of the population older than 74 years.17

Approximately 10-20% of patients with nonexudative AMD progress to the exudative form.4 As a result, severe vision loss in many of the 1.75 million individuals with advanced AMD is secondary to the effects of CNV from AMD.17,5

As the population of individuals older than 85 years increases an estimated 107% by the year 2020,18 the overall prevalence of advanced AMD (geographic atrophy and/or CNV) is expected to increase from 1.75 million individuals to 2.95 million individuals.5

Mortality/Morbidity

AMD leads to an increase in the rate of depression19,20 and frequent falls.21

Because many activities of daily living require functional central visual acuity, AMD decreases all aspects of the patient's quality of life, including the patient’s ability to drive independently.22

Race

Persons of Caucasian ancestry are far more likely to have late ARM and vision loss from AMD than those of African23 or Hispanic lineage.24 However, studies have failed to show consistent differences between those of Caucasian and Asian descent.25,26

Sex

Data from several large population-based studies, including the Beaver Dam study,27 the Third National Health and Nutrition Examination Survey,28 and the Framingham study29 have suggested that women are at increased risk for AMD compared with men.

Age

According to the International Classification System, AMD cannot be diagnosed in patients younger than 50 years.6 Nearly every large population-based study has shown a positive correlation between the prevalence, incidence, and progression of AMD with increasing age.30,27,31,32,5

Clinical

History

Patients with ARM are often asymptomatic or sometimes notice mild symptoms, including minimally blurred central visual acuity, contrast and color disturbances, and mild metamorphopsia. If geographic atrophy develops in the macular region, patients may notice a scotoma (blind spot), which can slowly enlarge over months to years before eventually stabilizing.

Patients with exudative AMD typically describe painless progressive blurring of their central visual acuity, which can be acute or insidious in onset. Patients who develop subretinal hemorrhage from CNV, for example, typically report an acute onset. Other patients with CNVM may experience insidious blurring secondary to shallow subretinal fluid or pigment epithelial detachments (PEDs). They also report relative or absolute central scotomas, metamorphopsia, and difficulty reading.

The natural history of exudative AMD or occasionally nonexudative AMD results in a stable central scotoma in which the visual acuity falls below the reading level and the legal driving level. However, peripheral visual acuity is usually retained.

Physical

AMD occurs bilaterally, but it is often asymmetric. Visual acuity is variably reduced. Amsler grid testing typically reveals relative central scotomas or metamorphopsia.

The sine qua non of exudative AMD is CNVM. Eyes with exudative AMD present with subretinal fluid, retinal PEDs, subretinal hemorrhage, and, occasionally, subretinal lipid deposits. In addition, RPE hypertrophy, RPE atrophy, and drusen are usually present. The CNV itself may be seen as yellow-green subretinal discoloration and is sometimes surrounded by a pigment ring. Subretinal hemorrhage typically develops at the margins of the CNV and sometimes obscures the entire complex. On occasion, the subretinal hemorrhage can progress and lead to vitreous hemorrhage. Subretinal disciform scarring of the macula is a common end-stage morphology.

Causes

In addition to age (see Age), strong risk factors include the following:  family history,33,10 Caucasian race,8 and a history of tobacco use.34,35

Other risk factors reported fairly consistently include hypertension and cataract surgery.8

More on ARMD, Exudative

Overview: ARMD, Exudative
Differential Diagnoses & Workup: ARMD, Exudative
Treatment & Medication: ARMD, Exudative
Follow-up: ARMD, Exudative
Multimedia: ARMD, Exudative
References
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Further Reading

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Keywords

exudative ARMD, age-related macular degeneration, AMD, age-related maculopathy, ARM, macular degeneration, choroidal neovascularization, choroidal neovascular membrane, CNVM, CNV, vision loss

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Contributor Information and Disclosures

Author

Grant M Comer, MD, Vitreoretinal Service, Clinical Ophthalmologist, Kellogg Eye Center, University of Michigan
Grant M Comer, MD is a member of the following medical societies: American Academy of Ophthalmology, Michigan Society of Eye Physicians & Surgeons, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Thomas Ciulla, MD, Associate Professor, Department of Ophthalmology, Indiana University School of Medicine
Thomas Ciulla, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Mark H Criswell, PhD, Director of Retina Service Research Laboratories, Assistant Research Professor, Department of Ophthalmology, Indiana University School of Medicine
Mark H Criswell, PhD is a member of the following medical societies: Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Alon Harris, PhD, Lois Letzter Professor, Director of Glaucoma Research and Diagnostic Center, Department of Ophthalmology, Indiana University School of Medicine
Alon Harris, PhD is a member of the following medical societies: American College of Sports Medicine, American Physiological Society, American Society for Laser Medicine and Surgery, and New York Academy of Sciences
Disclosure: Nothing to disclose.

Medical Editor

Brian A Phillpotts, MD, Former Vitreo-Retinal Service Director, Former Program Director, Clinical Assistant Professor, Department of Ophthalmology, Howard University College of Medicine
Brian A Phillpotts, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, and National Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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, Club Jules Gonin, Macula Society, and Retina Society
Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Consulting

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

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, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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