Clinical Pearls & Morning Reports
Published August 4, 2021
In industrialized countries, age-related macular degeneration (AMD) is a leading cause of blindness in adults older than 60 years of age. Read the NEJM Clinical Practice Article here.
Q: Describe some of the epidemiologic features of AMD.
A: AMD is more common in persons of European and North American ancestry than in those of Asian, Hispanic, or African ancestry, although regional differences and genetic predisposition contribute to high variability. The incidence of AMD is similar among women and men. Increasing age is the strongest risk factor. Numerous studies have linked smoking, uncontrolled hypertension, and a body-mass index above 25 to more severe AMD.
Q: How does AMD present?
A: Patients with early or intermediate AMD may be asymptomatic and often receive a diagnosis from their eye care provider at a routine evaluation. Patients who are symptomatic present with blurred or decreased vision in one or both eyes, distortion, blind spots (scotomas) in or around their central vision, and difficulty with visual function and daily activities such as reading and driving, especially in poorly lit settings.
A: AMD is initially characterized by focal or diffuse lipoprotein-rich deposits called drusen, which form underneath the retinal pigment epithelium or by subretinal drusenoid deposits that accumulate under the neurosensory retina. On the basis of the area and size of drusen in the macula, AMD at this stage is classified as either early or intermediate. Longitudinal data from the first and second Age-Related Eye Disease Studies (AREDS and AREDS2) showed that intermediate AMD can progress to advanced disease. Advanced AMD is classified either as neovascular (or “wet”) AMD or as atrophic (or “advanced dry”) AMD. Neovascular AMD is characterized by proliferative neovascularization underneath the neurosensory retina (choroidal neovascularization). Atrophic AMD is characterized by atrophy of the retinal pigment epithelium and the overlying neurosensory retina (geographic atrophy). Although the wet form of AMD accounts for only 10 to 15% of cases, it is responsible for the majority of cases of severe vision loss.
A: AREDS and AREDS2 showed that patients with bilateral intermediate AMD or those with intermediate AMD in one eye and advanced AMD in the other eye may benefit from oral, pill-based micronutrient supplementation. Vascular endothelial growth factor (VEGF)–targeted therapies, which can prevent catastrophic vision loss, have revolutionized care in patients with neovascular AMD. Several antagonists against VEGF-A (a diffusible cytokine that promotes angiogenesis and vascular permeability) are currently used in clinical practice; with all these agents, multiple intravitreal injections are warranted for sustained therapeutic benefit. On average, patients receive seven or eight injections during the initial 12-month period of therapy; whether continued injections are warranted is determined on the basis of clinical examination and by means of optical coherence tomography. Food and Drug Administration (FDA)–approved anti-VEGF agents (ranibizumab, aflibercept, and brolucizumab) and an anti-VEGF agent that is widely used but not approved by the FDA (bevacizumab) have similar efficacy in treating neovascular AMD. Bevacizumab is substantially less expensive than the FDA-approved agents.