Choroidal neovascularization (CNV) involves the growth of abnormal blood vessels beneath the retina, often leading to rapid and permanent central vision loss. This complication is a primary cause of severe vision impairment worldwide, making early and accurate detection a medical priority. Eye care specialists rely on advanced imaging technology, particularly Optical Coherence Tomography (OCT), to diagnose and manage CNV. OCT provides cross-sectional views of the retina’s internal structure, allowing clinicians to visualize disease activity and guide therapeutic interventions.
Understanding Choroidal Neovascularization
Choroidal neovascularization is defined by the growth of fragile, new blood vessels originating from the choroid, the vascular layer beneath the retina. Normally, the choroid delivers oxygen and nutrients to the outer retina. In CNV, these vessels pathologically break through Bruch’s membrane, a barrier separating the choroid from the retina.
This growth is driven by an overproduction of Vascular Endothelial Growth Factor (VEGF), a protein that stimulates new vessel formation. These abnormal vessels are weak and leaky, allowing fluid and blood components to seep into the subretinal space. This leakage distorts the macula’s light-sensing cells, causing symptoms like blurred vision and metamorphopsia (wavy straight lines). Untreated leakage eventually forms a dense scar, permanently destroying photoreceptors and resulting in a blind spot in the central visual field.
Optical Coherence Tomography: The Imaging Tool
Optical Coherence Tomography (OCT) is a non-invasive imaging technique that uses light waves in the near-infrared spectrum, similar to how ultrasound uses sound waves. The instrument projects a light beam into the eye and measures the intensity and delay of the light reflected back from different retinal layers. This process, called low-coherence interferometry, allows the device to accurately map the precise depth and structure of the tissue.
OCT generates a high-resolution, cross-sectional image, often called a B-scan, providing detailed views of the retina and underlying choroid. Modern OCT devices achieve micrometer resolution, enabling visualization of individual retinal layers and detection of subtle structural changes or fluid accumulation. The speed and non-contact nature of the scan make it an ideal, repeatable tool for both initial diagnosis and ongoing patient monitoring.
Recognizing CNV Indicators on an OCT Scan
The structural OCT scan reveals specific biomarkers indicating the presence and activity of choroidal neovascularization. The most recognizable sign of active disease is fluid, which appears as dark, or hyporeflective, spaces because the fluid does not reflect the light beam. Intraretinal fluid (IRF) is visible as cystic spaces within the retinal layers, indicating leakage and swelling. Subretinal fluid (SRF) is seen as a separation between the neurosensory retina and the retinal pigment epithelium (RPE) layer.
The OCT also helps classify the physical location of the neovascular membrane, which dictates the type of CNV:
CNV Types
Type 1 CNV occurs when new vessels grow beneath the RPE, often causing a dome-shaped elevation known as a Pigment Epithelial Detachment (PED).
Type 2 CNV involves the neovascular complex extending above the RPE into the subretinal space, appearing as hyperreflective tissue.
Type 3 CNV, a less common form, originates from the retina itself and grows downward, typically presenting with severe IRF and a focal PED.
The presence of Subretinal Hyperreflective Material (SHRM), which represents exudates, blood, or the neovascular tissue, also indicates disease activity and severity.
Primary Causes of Choroidal Neovascularization
CNV arises from several distinct underlying eye conditions, although the pathological process is singular. The most frequent cause, accounting for the majority of cases in older individuals, is the progression of Age-related Macular Degeneration (AMD). CNV develops here as a late-stage complication, often triggered by the degradation of Bruch’s membrane.
Another cause is pathological myopia, particularly in younger adults. This form, known as myopic CNV, results from the excessive stretching and elongation of the eyeball. This stretching can mechanically fracture Bruch’s membrane, creating tears called lacquer cracks that allow choroidal vessels to invade the macular space.
Inflammatory conditions, such as the Presumed Ocular Histoplasmosis Syndrome (POHS), are also responsible. Fungal exposure leads to chorioretinal scars that create weak points in Bruch’s membrane, providing an entry site for neovascular growth.
Guiding Treatment Decisions
The information obtained from the OCT scan is the primary determinant for initiating and monitoring anti-VEGF therapy, the standard of care for CNV. Anti-VEGF agents are injected directly into the eye to block the VEGF protein, reducing the leakage and growth of abnormal blood vessels. The presence of retinal fluid (IRF or SRF) on the OCT image is the main criterion for defining active disease and the need for an injection.
OCT monitoring allows specialists to tailor the treatment schedule to the patient’s individual disease activity. Two common protocols are used:
Treatment Protocols
The “Pro Re Nata” (PRN) or “as-needed” regimen involves patients receiving an injection only when the OCT reveals fluid recurrence.
The “Treat-and-Extend” protocol is more common. A monthly injection is given until the macula is dry, then the interval between subsequent injections is gradually extended. This extension continues as long as the OCT confirms the macula remains free of fluid.
This strategy uses the OCT-derived fluid status to balance treatment efficacy with the burden of frequent injections, aiming to maintain a dry macula and preserve vision.