Choroidal neovascularization (CNV) is an abnormal growth of new blood vessels that emerge from the choroid, a layer of blood vessels in the eye. These new vessels are fragile and can leak fluid or blood, damaging the retina and leading to vision loss. CNV is a significant cause of vision impairment, particularly affecting central vision.
Understanding Choroidal Neovascularization
The eye’s intricate structure includes the retina, a light-sensitive tissue at the back of the eye, and the macula, a small central area of the retina responsible for sharp, detailed vision. Beneath the retina lies the choroid, a layer rich in blood vessels that supplies oxygen and nutrients to the outer layers of the retina.
CNV occurs when new, abnormal blood vessels grow from the choroid. These vessels extend through Bruch’s membrane, a thin barrier separating the choroid from the retina, and into the subretinal space. The newly formed vessels are often leaky, allowing fluid and blood to accumulate, disrupting the retina’s normal structure. This leakage can damage photoreceptors, leading to impaired vision.
The Process of CNV Formation
CNV development often begins with a compromise in Bruch’s membrane, a critical layer that separates the choroid from the retinal pigment epithelium (RPE), which supports the photoreceptors. This disruption can result from inflammatory or degenerative processes.
Once Bruch’s membrane is compromised, triggers like inflammation or ischemia (insufficient blood flow) can stimulate new vessel growth. Vascular Endothelial Growth Factor (VEGF), a signaling protein that promotes new blood vessel formation, is a major factor. In conditions like age-related macular degeneration, RPE cells, neurons, and other eye cells can produce excessive VEGF.
Elevated VEGF levels encourage choroidal endothelial cells to proliferate and invade the damaged Bruch’s membrane. These new, abnormal vessels then grow into the subretinal space. Their uncontrolled growth and inherent fragility lead to leakage of fluid and blood, causing swelling within the retina. Over time, this leakage can result in the formation of scar tissue, known as subretinal fibrosis, which further damages the delicate retinal tissue and can lead to irreversible vision loss.
Common Causes and Risk Factors
The most frequent cause of CNV is “wet” or exudative Age-related Macular Degeneration (AMD). In wet AMD, the retina produces excess VEGF, triggering the growth of abnormal, leaky vessels.
While AMD is the primary driver, other conditions can also lead to CNV. Pathological myopia, a severe form of nearsightedness, can cause the eye to lengthen, stretching the retina, which can result in CNV formation. Ocular histoplasmosis syndrome, a fungal infection, is another cause of CNV. Angioid streaks, small breaks in Bruch’s membrane, and various inflammatory eye conditions like multifocal choroiditis or punctate inner choroidopathy, can also lead to CNV. Eye trauma can also disrupt the barrier between the retina and choroid, causing CNV to form.
Recognizing the Visual Signs
Individuals developing CNV often experience noticeable vision changes. A common symptom is metamorphopsia, where straight lines appear wavy, bent, or distorted. This distortion can make tasks like reading challenging.
Central vision may become blurred or dim. A central blind spot, known as a scotoma, can also develop, appearing as a dark or blank area in the center of the visual field. Other visual disturbances include changes in the perceived size of objects, a decrease in color intensity, or flickering lights in central vision. These symptoms usually affect one eye first and can progress rapidly.
Diagnosis and Treatment Overview
Diagnosing choroidal neovascularization involves specialized imaging tests to visualize abnormal blood vessels and any associated leakage. Optical Coherence Tomography (OCT) provides cross-sectional views of the retina, allowing doctors to detect fluid accumulation, swelling, and new vessels. Fluorescein angiography (FA) is another diagnostic tool where a dye is injected into the bloodstream, highlighting leaky vessels as it circulates through the eye, making the CNV membrane visible.
The primary treatment for CNV, especially in wet AMD, involves anti-VEGF injections. These medications are administered directly into the eye, blocking Vascular Endothelial Growth Factor (VEGF) to reduce the growth and leakage of abnormal vessels. Anti-VEGF therapy aims to reduce fluid and blood leakage, slow vision loss, and in some cases, improve vision. Other treatments include photodynamic therapy (PDT), which uses a light-activated drug and a laser to target and close abnormal vessels, and laser photocoagulation to seal leaky blood vessels.