Choroidal neovascularization (CNV) is a serious eye condition characterized by the growth of abnormal, fragile blood vessels originating from the choroid, the highly vascular layer beneath the retina. These new vessels break through the natural barriers of the eye and extend toward the light-sensitive retina. If left untreated, the vessels leak blood and fluid, which damages the macula and causes rapid, severe loss of central vision.
Defining Choroidal Neovascularization
The choroid is a dense network of blood vessels located between the retina and the outer white layer of the eye, the sclera. Its function is to supply oxygen and nutrients to the outer layers of the retina, including the photoreceptor cells. This layer is separated from the retina by Bruch’s membrane and the retinal pigment epithelium (RPE), which form a crucial barrier.
CNV occurs when a breakdown in this barrier triggers the formation of new blood vessels, a process called neovascularization. The stimulus is often an overproduction of Vascular Endothelial Growth Factor (VEGF). Conditions like inflammation or low oxygen levels can cause RPE cells to release excessive amounts of VEGF, signaling the need for new blood supply.
The newly formed vessels are structurally weak and highly permeable. They push through Bruch’s membrane, invading the space beneath the retina or the RPE layer. This invasion causes the vessels to leak plasma, fluid, and sometimes blood into the surrounding tissue.
This leakage is damaging because the fluid lifts the retina away from its nourishing support layers, causing tissue swelling and distorting vision. Over time, the body attempts to repair this damage by forming scar tissue, known as a fibrovascular scar. This scar tissue permanently destroys the delicate photoreceptor cells, resulting in irreversible central vision loss.
Conditions That Trigger CNV Development
Age-related Macular Degeneration (AMD) is the most common cause of CNV, often referred to as “wet” AMD. CNV is triggered by the accumulation of fatty deposits and cellular debris, called drusen, beneath the retina. These deposits lead to chronic inflammation and compromise the integrity of Bruch’s membrane, prompting the release of VEGF and the subsequent growth of leaky vessels.
CNV can also affect younger individuals due to other distinct underlying eye conditions. Pathological myopia, a severe form of nearsightedness, is a common non-AMD cause. In highly myopic eyes, the eyeball is excessively elongated, which stretches and thins the choroid and retina. This mechanical stretching can cause linear breaks in Bruch’s membrane, known as lacquer cracks, providing a pathway for vessels to grow through and initiate a neovascular response. The resulting myopic CNV is often less aggressive than wet AMD but can still cause significant vision loss.
Another trigger is Ocular Histoplasmosis Syndrome (OHS), an inflammatory condition resulting from exposure to the Histoplasma capsulatum fungus. The fungus leaves behind small, inactive scars, or “histo spots,” in the choroid. Inflammation surrounding these scars can eventually reactivate and lead to a breach in Bruch’s membrane, stimulating CNV formation.
Other causes include angioid streaks, which are crack-like ruptures in a brittle, calcified Bruch’s membrane. These streaks are often associated with systemic conditions like Pseudoxanthoma Elasticum. Trauma to the eye or other inflammatory disorders of the choroid can also damage the barrier, leading to a local wound-healing response that culminates in the growth of abnormal vessels.
Identifying the Visual Symptoms and Diagnostic Tools
The earliest symptom of CNV is often metamorphopsia, where straight lines appear wavy, bent, or distorted. This occurs because the fluid pooling beneath the macula warps the overlying retinal tissue. Patients may first notice this distortion when looking at door frames, tile grout, or text on a page.
As the condition progresses, a painless decline in central vision occurs, described as blurriness or a dark patch. This blind spot in the center of the visual field is known as a scotoma. Since CNV often begins in one eye, these early changes can sometimes go unnoticed until the unaffected eye is covered.
A simple at-home screening tool is the Amsler Grid, a square chart of evenly spaced horizontal and vertical lines with a dot in the center. By focusing on the central dot and testing each eye individually, any new areas where the lines appear wavy, broken, or missing can be detected. This daily self-test is important for monitoring rapid changes CNV can cause.
To confirm the diagnosis, the eye care specialist relies on advanced imaging techniques, primarily Optical Coherence Tomography (OCT). OCT uses light waves to create high-resolution, cross-sectional images of the retina and underlying layers. It allows the doctor to visualize the pathological signs of active CNV.
Fluorescein Angiography (FA) is another method that involves injecting a fluorescent dye into an arm vein. The dye travels to the blood vessels in the eye, and a specialized camera takes rapid photographs as the dye fills the vasculature. Active CNV is identified by the leakage of the dye from the abnormal vessels, which appears as a bright, spreading area on the images. This test also helps classify the CNV as “classic,” a well-defined and intensely leaking network, or “occult,” which is less distinct and leaks more slowly.
Modern Treatment Approaches
The standard of care for treating active CNV is the use of Anti-Vascular Endothelial Growth Factor (Anti-VEGF) medications. These drugs are administered directly into the vitreous gel of the eye via a precise, in-office injection. The treatment is designed to block the activity of the VEGF protein, which drives the growth and leakage of the abnormal vessels.
By neutralizing VEGF, the medication causes the fragile vessels to regress and shrink, significantly reducing fluid leakage and swelling beneath the retina. This often results in the stabilization of vision, and in many cases, a measurable improvement in visual acuity. Patients typically require a loading phase of monthly injections followed by an individualized schedule of ongoing treatment and monitoring.
Before Anti-VEGF therapy, other treatments were commonly used and are still utilized in select cases.
Photodynamic Therapy (PDT)
PDT involves injecting a light-sensitive drug, such as verteporfin, into the bloodstream. A non-thermal, low-power laser is then directed at the CNV lesion, activating the drug and selectively closing the abnormal vessels while minimizing damage to the surrounding healthy retinal tissue.
Thermal Laser Photocoagulation
This is an older method that uses a high-energy laser beam to directly burn and destroy the new blood vessels. This technique is highly effective at closing the vessels but creates a permanent scar that destroys the overlying retina. Because of this destructive nature, thermal laser treatment is reserved for CNV lesions located far away from the center of the macula, where the resulting blind spot will have a less devastating impact on central vision.