A Choroidal Neovascular Membrane (CNVM) is a serious eye condition defined by the growth of abnormal, structurally weak blood vessels beneath the retina. This neovascularization directly threatens the delicate tissue responsible for central vision. The condition requires immediate medical attention because these vessels tend to leak fluid and blood. This leakage can rapidly damage the light-sensitive cells of the retina, potentially leading to severe and permanent central vision loss if not managed promptly.
What is a Choroidal Neovascular Membrane?
A choroidal neovascular membrane is a tangle of fragile new blood vessels that originate in the choroid, the vascular layer situated between the outer white sclera and the light-sensitive retina. The choroid supplies the retina with oxygen and nutrients. The growth of this abnormal membrane breaks through a barrier layer called Bruch’s membrane, invading the space beneath the retina, particularly in the macula.
These new vessels are structurally inferior to normal capillaries, making them inherently leaky. As they grow, they exude fluid and blood into the subretinal space, disrupting the organized layers of the macula. This fluid accumulation physically lifts and damages the photoreceptor cells responsible for sight. Over time, the leaking vessels and resulting inflammation can lead to a scar-like disciform lesion, which permanently destroys the macula’s function.
Conditions That Lead to CNVM
The most frequent underlying cause for CNVM is the “wet” or exudative form of Age-Related Macular Degeneration (AMD). In AMD, the buildup of fatty protein deposits called drusen and chronic inflammation stresses the tissue. This stress leads to the release of Vascular Endothelial Growth Factor (VEGF), which stimulates the growth of abnormal new blood vessels from the choroid.
CNVM can also be a complication of other eye conditions that compromise the integrity of Bruch’s membrane. These include pathological myopia, or extreme nearsightedness, which stretches the retina and choroid, sometimes resulting in cracks that allow neovascular growth. Other causes are inflammatory conditions like presumed ocular histoplasmosis syndrome (POHS), which creates choroidal scars. Physical trauma to the eye, causing a choroidal rupture, also creates a defect where new vessels can proliferate.
How CNVM Affects Vision
The presence of a CNVM in the macula causes changes to central vision. The most common symptom is metamorphopsia, where straight lines appear wavy or distorted. This distortion occurs because the fluid pooling beneath the retina physically pushes the light-sensing cells out of alignment.
Patients may also experience a decline in the sharpness of their central vision, making activities like reading or recognizing faces difficult. As the condition progresses, a central blind spot, known as a scotoma, can develop, appearing as a dark area directly in the center of the visual field. An Amsler grid, a square-gridded monitoring tool, is often given to patients at risk to detect these early distortions at home.
Confirming the Diagnosis
Eye care professionals use advanced imaging techniques to confirm the presence and activity of a choroidal neovascular membrane. Optical Coherence Tomography (OCT) is the non-invasive standard for diagnosis, providing high-resolution, cross-sectional images of the retina. The OCT scan visualizes fluid accumulation, swelling, and membrane structure beneath or within the retina, indicating an active CNVM.
Fluorescein Angiography (FA) is another essential diagnostic procedure. It involves injecting a fluorescent dye into a vein in the arm; as the dye circulates, a specialized camera captures images. The dye highlights the abnormal CNVM, showing the precise location and extent of the vessels and demonstrating the active leakage of fluid. Indocyanine Green Angiography (ICG) is a similar technique that provides a better view of the underlying choroidal circulation, offering additional detail that FA may not capture.
Modern Treatment Options
The current standard of care for CNVM is the use of anti-Vascular Endothelial Growth Factor (anti-VEGF) medications. These drugs, which include ranibizumab (Lucentis), aflibercept (Eylea), and bevacizumab (Avastin), neutralize the VEGF protein that drives the growth and leakage of the abnormal vessels. By blocking this signal, the treatment aims to dry up the fluid, reduce swelling, and stop the progression of vision loss.
The medication is administered directly into the vitreous gel of the eye via an intravitreal injection. The procedure is quick, performed in an outpatient setting, and the eye is thoroughly numbed beforehand. A typical protocol involves an initial series of monthly injections, followed by a variable schedule of ongoing treatment to maintain the vision-preserving effect.
Less common treatments exist, but anti-VEGF therapy is preferred due to its ability to stabilize and often improve vision. Photodynamic Therapy (PDT) uses a cold laser to activate an injected photosensitive drug, which targets and closes the abnormal vessels. However, PDT has been superseded by anti-VEGF agents, which offer superior visual outcomes and are the established first-line treatment for CNVM.