Choroidal neovascular membrane (CNVM) is an eye condition where new, abnormal blood vessels grow from the choroid, a blood vessel-rich layer beneath the retina. These vessels extend through Bruch’s membrane, infiltrating the space just below the retina. This process can be compared to weeds pushing up through cracks in a sidewalk, as the abnormal vessels disrupt the normal, flat surface of the retina. The presence of these fragile vessels can lead to fluid leakage or bleeding, which directly affects the macula, the central part of the retina responsible for sharp, detailed vision.
Underlying Causes and Risk Factors
The most frequent cause of choroidal neovascular membrane development is wet age-related macular degeneration (wet AMD). This advanced form of AMD involves the growth of irregular blood vessels from the choroid into the macula, leading to fluid or blood leakage and subsequent vision impairment. Wet AMD accounts for approximately 10-20% of all AMD cases but is responsible for the majority of severe vision loss linked to the condition.
CNVM can also arise from other, less common conditions. Pathologic myopia, a severe form of nearsightedness, can cause the eye to elongate excessively, stretching and stressing the retinal layers. Inflammatory eye conditions, such as uveitis or presumed ocular histoplasmosis syndrome (POHS), can also trigger CNVM formation. Additionally, physical eye trauma, like blunt injuries that rupture Bruch’s membrane, or rare genetic conditions such as angioid streaks (small breaks in the retinal layers) can contribute to CNVM development. Sometimes, no specific underlying cause is identified, and these cases are termed idiopathic CNVM.
Several factors increase the likelihood of developing wet AMD and, consequently, CNVM. Advancing age is the most significant risk factor, with the condition becoming more prevalent in individuals over 50. A family history of AMD also raises the risk, suggesting a genetic predisposition. Lifestyle choices like smoking significantly elevate the risk, making smokers three to four times more likely to develop AMD and potentially accelerating disease onset. Other contributing factors include obesity, cardiovascular disease, and certain nutritional deficiencies.
Symptoms and Diagnosis
The development of a choroidal neovascular membrane can manifest through several noticeable changes in vision. Patients often report a sudden or gradual blurring of their central vision, which can make reading or recognizing faces difficult. A common symptom is metamorphopsia, where straight lines, such as doorframes or telephone poles, appear wavy or distorted. The presence of a dark, gray, or blank spot, known as a scotoma, in the center of the visual field is another indicator, though peripheral vision usually remains unaffected.
Early detection of CNVM is important, and ophthalmologists use specific tests to diagnose the condition. A simple tool for at-home monitoring is the Amsler grid, a square grid with a central dot. If straight lines on the grid appear wavy, broken, or if areas are missing, it can signal macular changes and prompt further evaluation. This allows individuals to track subtle distortions that might indicate new or worsening CNVM.
For a more detailed assessment, ophthalmologists employ advanced imaging techniques. Optical Coherence Tomography (OCT) is a non-invasive test that uses light waves to capture high-resolution cross-sectional images of the retina. This allows the doctor to visualize the retinal layers in detail, detecting fluid accumulation beneath or within the retina, as well as the presence and characteristics of the abnormal membrane itself. Another diagnostic procedure is Fluorescein Angiography (FA), which involves injecting a special dye into a vein in the arm. The dye travels to the blood vessels in the eye, and a specialized camera takes rapid photographs. This highlights leaky, abnormal vessels associated with CNVM, allowing the doctor to pinpoint their location and extent.
Treatment Approaches
The primary treatment for choroidal neovascular membrane, especially when associated with wet AMD, involves anti-VEGF (vascular endothelial growth factor) injections. Vascular endothelial growth factor is a protein naturally produced in the body that plays a significant role in stimulating the growth of new blood vessels and increasing their permeability, leading to leakage. Anti-VEGF drugs work by blocking this protein, thereby inhibiting the formation of new, abnormal vessels and reducing fluid leakage within the retina.
The procedure for administering anti-VEGF injections is typically performed in an ophthalmologist’s office and is quick. The eye is first numbed with anesthetic eye drops to ensure comfort. A small amount of the anti-VEGF medication is then injected directly into the vitreous, the jelly-like substance that fills the center of the eye. Common anti-VEGF medications used include ranibizumab (Lucentis), aflibercept (Eylea), and bevacizumab (Avastin), with newer options like brolucizumab (Beovu) and faricimab also available. These injections are often required on an ongoing basis, with varying frequencies depending on the individual’s response to treatment and the specific medication used.
While anti-VEGF therapy is the current standard, older treatments like photodynamic therapy (PDT) and thermal laser photocoagulation were used previously or are reserved for specific cases. Photodynamic therapy involves injecting a light-sensitive drug, verteporfin, into the bloodstream. After the drug concentrates in the abnormal vessels, a non-thermal laser light is shone into the eye, activating the drug to selectively close off the leaky vessels. Thermal laser photocoagulation uses a focused laser beam to create a microscopic scar that seals off the abnormal blood vessels. This method is typically reserved for CNVMs located away from the very center of the macula, as the laser can cause some damage to surrounding healthy tissue, potentially leading to a permanent blind spot if used centrally.
Prognosis and Management
The primary goal of treating a choroidal neovascular membrane is to stabilize vision and prevent further vision loss. While some patients may experience an improvement in their visual acuity, the main objective of treatment is to halt the progression of the disease and preserve remaining vision. This stabilization often requires consistent and ongoing treatment, typically with anti-VEGF injections.
Regular follow-up appointments with an ophthalmologist or retina specialist are an important part of managing CNVM. These visits allow the doctor to monitor the condition’s activity, assess the effectiveness of treatment, and adjust the injection schedule as needed.
For individuals who experience permanent vision changes despite treatment, various strategies and low-vision aids can help manage daily activities. These include magnifiers, specialized glasses, and assistive technologies like large-print books, talking clocks, or screen magnification software. Adapting to vision changes and utilizing these aids can help maintain independence and quality of life.