Wet Age-related Macular Degeneration (Wet AMD) is a progressive eye disease and a leading cause of vision loss in older adults. This condition involves the growth of abnormal, fragile blood vessels beneath the macula, the central part of the retina responsible for sharp, detailed vision. These vessels leak fluid and blood, which rapidly damages the light-sensing cells. The current standard of care is intraocular injections of anti-Vascular Endothelial Growth Factor (anti-VEGF) drugs, which suppress the disease but do not cure it. Consistency in the injection schedule is necessary to maintain vision and prevent further deterioration, as stopping treatment risks disease reactivation and permanent vision loss.
How Anti-VEGF Injections Stabilize Vision
Wet AMD is driven by an overabundance of a signaling protein called Vascular Endothelial Growth Factor (VEGF). This protein promotes the growth of new, structurally unsound blood vessels, a process known as choroidal neovascularization (CNV). Anti-VEGF medications, such as aflibercept and ranibizumab, bind directly to this protein.
By neutralizing VEGF, the injections remove the signal that causes the abnormal vessels to grow and leak. This reduces fluid and swelling within the macula, stabilizing the retinal environment. The goal of this therapy is to halt disease progression and maintain the patient’s current level of central vision.
The treatment is not curative, so the underlying tendency for the vessels to leak remains. The therapeutic effect of each injection diminishes as the drug is naturally cleared from the eye. Injections must be administered on a regular, ongoing schedule, typically every four to twelve weeks, to maintain a suppressive concentration of the medication.
Immediate Consequences: Disease Reactivation
When anti-VEGF therapy is stopped, the medication concentration drops below the level needed to suppress disease activity. This allows the underlying process of Wet AMD to reactivate, as the unbound VEGF protein is once again free to stimulate the abnormal vessels.
This rebound in VEGF activity causes the fragile vessels to begin leaking fluid and sometimes blood into the macula. This fluid accumulation, or edema, can be detected quickly using imaging tests, such as Optical Coherence Tomography (OCT). Patients may notice symptoms like blurred central vision, distorted straight lines (metamorphopsia), or a central blind spot.
Disease reactivation, often called a “flare-up,” occurs in a significant number of patients following treatment cessation. Recurrence rates can be around 50% within a year, even in previously stable eyes. The timing of this recurrence is variable, often happening within several months, depending on the specific drug used and the patient’s underlying condition.
Long-Term Impact: Irreversible Structural Damage
If leakage from the reactivated disease persists without intervention, the retina will sustain permanent damage. Chronic swelling and inflammation are toxic to the delicate photoreceptor cells in the macula. Persistent fluid accumulation causes the death of these cells and the underlying supporting tissue.
The most severe long-term consequence is the formation of subretinal fibrosis, commonly referred to as disciform scarring. This dense layer of scar tissue replaces the functional retinal layers in the macula. Once this scar tissue forms, the photoreceptors in that area are permanently destroyed.
Vision loss caused by this scarring is typically irreversible, even if anti-VEGF treatment is later resumed. While initial fluid accumulation is often reversible with prompt treatment, the structural damage from chronic, untreated leakage is not. This distinction between temporary fluid and permanent scarring is the most serious risk of stopping the injections.
Outcomes of Resuming Therapy
For patients who experience a disease flare-up after stopping treatment, resuming anti-VEGF injections is the recommended course of action. Restarting therapy can successfully suppress the active leakage, leading to the resolution of fluid and reduction of swelling. This anatomical improvement often results in a recovery of some vision lost during the lapse.
However, vision recovery is often incomplete, especially if treatment was stopped for a prolonged period. Studies show that while the fluid can be cleared, the visual acuity gained back may not reach the level it was before the interruption. The time spent with active, untreated disease contributes to a permanent deficit in visual function.
The goal of resuming therapy after a lapse shifts primarily to preventing further deterioration, rather than achieving a full recovery. Immediate consultation with an ophthalmologist is necessary at the first sign of vision changes or if an injection appointment is missed. Abruptly stopping treatment without medical guidance carries substantial risk of permanent vision loss.