Drusenoid Pigment Epithelial Detachment (Drusenoid PED) is a specific lesion associated with Age-Related Macular Degeneration (AMD). It is a hallmark of intermediate and advanced dry AMD, indicating a significant accumulation of waste material beneath the retina. A Pigment Epithelial Detachment describes the separation of the retinal pigment epithelium (RPE) layer from its underlying tissue.
Understanding the Pathology: What is Drusenoid PED?
The retina contains the Retinal Pigment Epithelium (RPE), a thin layer of cells sitting on Bruch’s membrane. RPE cells nourish photoreceptors and clear metabolic waste. In AMD, fatty and protein deposits called drusen accumulate.
Drusenoid PED forms when small drusen merge into a large, continuous mound, forcing the RPE layer to detach and lift away from Bruch’s membrane. This creates a smooth, dome-shaped elevation. The lesion is defined as a large drusen when its diameter exceeds 350 to 433 micrometers.
The space created is filled with lipid-rich debris and sometimes calcified nodules. This separation disrupts the metabolic exchange between the RPE and the underlying choroid blood supply. This barrier starves the photoreceptors, leading to cellular stress and dysfunction.
A Drusenoid PED signifies a highly progressed stage of dry AMD. The overlying RPE layer is compromised as it stretches over the dome of material. This mechanical stress creates an unstable environment and marks a high-risk point in the disease’s progression.
Detection and Diagnostic Methods
Drusenoid PED is confirmed using specialized imaging techniques. Optical Coherence Tomography (OCT) is the foundational diagnostic tool, providing a non-invasive, cross-sectional view of the retinal layers. On an OCT scan, the PED appears as a well-defined, smooth, dome-shaped elevation of the hyperreflective RPE layer.
The space beneath the elevated RPE layer is filled with material that appears moderately to highly reflective, distinguishing it from other PED types containing clear fluid. OCT allows doctors to precisely measure the lesion’s height and width to monitor progression. Imaging also identifies subtle complications, such as fluid accumulation beneath the retina or within the PED itself.
Fluorescein Angiography (FA) or Indocyanine Green Angiography (ICGA) may further classify the detachment and rule out active leakage. During FA, a dye is injected into the bloodstream. A Drusenoid PED typically shows hyperfluorescence that increases in intensity but stabilizes without leakage in the late phase, differentiating it from a vascularized PED.
Progression and Risk of Vision Loss
A Drusenoid PED has a high likelihood of progressing to advanced Age-Related Macular Degeneration, which threatens central vision. The primary concern is the potential for the detachment to develop into Choroidal Neovascularization (CNV), known as “wet” AMD. CNV occurs when abnormal blood vessels grow from the choroid beneath the RPE, causing leakage and bleeding that leads to rapid vision loss.
Many eyes with Drusenoid PED progress to late AMD, either through CNV or the development of Geographic Atrophy (GA). GA is the end-stage of dry AMD, where RPE cells and photoreceptors die, leaving a scarred area of vision loss. The sudden collapse of a large Drusenoid PED is associated with a poor visual outcome, often leading directly to GA formation.
Specific features on OCT scans act as predictive markers for high-risk progression. Signs that the lesion is becoming unstable include the appearance of intraretinal hyperreflective foci, which represent migrating RPE cells, or the accumulation of subretinal fluid. Lesions with greater size, particularly in height and diameter, also carry a higher risk of converting to vision-threatening stages.
Current Management Strategies
Management of a non-vascularized Drusenoid PED focuses on intense surveillance and preventative measures, as there is no direct treatment to shrink the lesion. Patients are placed on a frequent monitoring schedule, often involving regular OCT imaging every few months. This close observation allows for the earliest possible detection of conversion to wet AMD, such as new fluid or vascular growth.
For patients at high risk of progression, the Age-Related Eye Disease Study 2 (AREDS2) supplement formulation is recommended. This combination includes high-dose antioxidant vitamins and minerals shown to slow AMD progression:
- Vitamin C
- Vitamin E
- Zinc
- Copper
- Lutein
- Zeaxanthin
Taking these supplements may help stabilize the disease and reduce the risk of vision loss.
If the Drusenoid PED progresses to “wet” AMD with Choroidal Neovascularization, treatment shifts immediately to anti-VEGF therapy. These medications are delivered via injection into the eye. They work by blocking the growth factor that stimulates abnormal blood vessel formation, effectively stopping leakage and stabilizing vision.