Geographic Atrophy Retina OCT: Evolving Clinical Insights

Geographic atrophy (GA) is a progressive form of age-related macular degeneration that leads to irreversible vision loss. As the disease advances, retinal tissue deteriorates, affecting central vision and quality of life. Identifying structural changes early is crucial for monitoring progression and evaluating potential interventions.

Optical coherence tomography (OCT) has become an essential tool in assessing GA by providing high-resolution cross-sectional images of the retina. It allows clinicians to detect subtle alterations in retinal layers and track lesion development over time.

Key Signs In Advanced Retinal Changes

As GA progresses, distinct structural changes emerge, reflecting the degeneration of photoreceptors, retinal pigment epithelium (RPE), and choriocapillaris. A defining feature is the well-demarcated loss of the RPE, which appears as areas of increased hypertransmission on OCT. This occurs due to the absence of the RPE’s natural light-blocking properties, allowing deeper OCT signal penetration into the choroid. The extent of hypertransmission correlates with lesion severity, providing a measurable indicator of disease progression.

Thinning of the outer retinal layers, particularly the ellipsoid zone (EZ) and external limiting membrane (ELM), is another hallmark of advanced GA. The disruption or loss of the EZ, which represents photoreceptor mitochondria integrity, signifies significant functional impairment. Studies have shown that EZ loss precedes complete RPE atrophy, indicating that photoreceptor degeneration begins before structural collapse. This early disruption is often accompanied by reduced retinal sensitivity, as confirmed by microperimetry assessments.

The choriocapillaris, which supplies the outer retina, also undergoes progressive rarefaction. OCT angiography (OCTA) studies reveal a marked decrease in choriocapillaris flow density beneath atrophic regions, indicating perfusion loss that exacerbates retinal degeneration. This vascular insufficiency contributes to lesion expansion, reinforcing the interdependence between retinal and choroidal health. The extent of choriocapillaris loss has been linked to faster lesion growth, highlighting its prognostic significance.

OCT Principles In Retinal Assessment

OCT has transformed retinal evaluation by offering high-resolution imaging that reveals structural alterations at a micrometer scale. In GA, this imaging modality enables precise visualization of retinal layer integrity, facilitating early detection of degenerative changes. Spectral-domain OCT (SD-OCT) and swept-source OCT (SS-OCT) are widely used, with SS-OCT providing enhanced choroidal penetration due to its longer wavelength. This capability is particularly beneficial for assessing GA, as it allows for a more detailed examination of choroidal involvement.

One of OCT’s key advantages in GA assessment is its ability to detect and quantify hypertransmission defects resulting from RPE loss. These defects appear as increased signal penetration into the choroid, serving as a surrogate marker for atrophic expansion. Automated segmentation algorithms measure these hypertransmission areas, providing objective data to track disease progression. Studies indicate that regions with greater hypertransmission expand more rapidly, reinforcing its prognostic value.

Beyond hypertransmission, OCT reveals outer retinal atrophy by detecting thinning or loss of critical layers such as the EZ and ELM. Longitudinal imaging has shown that EZ disruption often precedes overt RPE atrophy, leading to OCT-based staging systems for classifying disease severity. The Classification of Atrophy Meeting (CAM) consensus has proposed specific OCT criteria to define incomplete and complete outer retinal atrophy, aiding in standardized diagnosis and clinical trial enrollment.

OCT angiography (OCTA) has emerged as a valuable tool for evaluating choriocapillaris perfusion in GA. Unlike dye-based angiography, OCTA provides non-invasive, depth-resolved visualization of vascular networks, highlighting capillary loss beneath atrophic lesions. Reduced choriocapillaris flow correlates with lesion expansion rates, suggesting that vascular compromise plays a role in disease progression. Integrating OCTA with traditional OCT data offers a more comprehensive understanding of GA pathophysiology, paving the way for new therapeutic approaches targeting both retinal and choroidal dysfunction.

Visualizing Geographic Atrophy Lesion Features

The structural characteristics of GA lesions vary, reflecting the complexity of disease progression. OCT captures these variations, providing insights into how different retinal layers respond to degeneration. A striking feature in GA is the sharp demarcation between atrophic and preserved retinal areas. This transition zone, known as the junctional zone, contains residual photoreceptors and RPE cells attempting to maintain function before eventual degeneration. Longitudinal imaging shows that junctional zone progression rates differ among patients, with some experiencing slow expansion while others exhibit more aggressive lesion growth.

Within the atrophic core, OCT reveals increased hypertransmission into the choroid due to RPE loss. This provides an indirect measure of tissue loss, with more extensive hypertransmission correlating with greater atrophic severity. The choroidal structures beneath these lesions also undergo secondary changes, including thinning and reduced vascular density, which may further accelerate disease progression. Tracking these changes over time helps refine prognostic assessments.

Another important feature in GA lesions is hyperreflective material at lesion borders. These deposits, composed of degenerating photoreceptor remnants and inflammatory debris, may influence surrounding tissue stability. Some studies suggest that hyperreflective foci predict lesion enlargement, as their presence often precedes further structural breakdown. Additionally, subsidence or collapse of the inner retinal layers is common in advanced disease stages, reflecting the loss of structural support from underlying tissues.

Layer-Specific Characteristics In Atrophic Tissue

The structural consequences of GA extend beyond generalized retinal thinning, with distinct alterations occurring across specific layers. The outer retina, particularly the EZ and ELM, undergoes early disruption before complete atrophy. The EZ, corresponding to photoreceptor mitochondria, gradually fades at lesion margins before disappearing entirely in severely affected regions. This loss of mitochondrial integrity is an early indicator of photoreceptor dysfunction, preceding the collapse of supporting structures such as the RPE. The ELM, which maintains photoreceptor alignment, also becomes fragmented near atrophic zones, contributing to photoreceptor disorganization.

The RPE itself exhibits distinct alterations as GA progresses. In early stages, residual RPE cells may appear as hyperreflective patches before complete loss results in the characteristic hypertransmission signal on OCT. The absence of RPE removes metabolic support for photoreceptors and disrupts nutrient and waste exchange between the retina and choroid. As atrophy advances, residual RPE islands may persist within lesion interiors, sometimes forming hyperreflective clumps indicative of incomplete tissue degradation. These remnants may represent cellular debris or dysfunctional RPE resisting degeneration, though their role in disease progression remains under investigation.