Lacquer Cracks in Pathological Myopia: Signs and Impact

Pathological myopia is a severe form of nearsightedness that leads to progressive and often irreversible eye damage. Unlike typical myopia, which can be corrected with lenses, pathological myopia involves structural changes in the retina and choroid, increasing the risk of vision-threatening complications.

One such complication is the formation of lacquer cracks—breaks in Bruch’s membrane that contribute to retinal damage. Understanding their characteristics, detection methods, and potential visual consequences is essential for early intervention and management.

Structural Changes in Pathological Myopia

Pathological myopia profoundly alters the eye’s structural integrity, primarily affecting the sclera, choroid, and retina. As axial elongation progresses, the sclera thins and loses biomechanical stability, leading to excessive stretching of the posterior segment. This elongation distorts the eye’s normal curvature and compromises the vascular supply to the outer retina, increasing susceptibility to degenerative changes. Studies using optical coherence tomography (OCT) and histological analysis show that scleral thinning in highly myopic eyes can reduce thickness to less than 50% of that in emmetropic eyes, exacerbating mechanical stress on adjacent tissues (Ohno-Matsui et al., Progress in Retinal and Eye Research, 2017).

The choroid, which supplies oxygen and nutrients to the outer retina, undergoes significant atrophy as myopia advances. Choroidal thinning is a hallmark of pathological myopia, with research indicating that subfoveal choroidal thickness can decrease to below 100 µm in highly myopic individuals, compared to 250–300 µm in normal eyes (Ikuno, American Journal of Ophthalmology, 2019). This reduction in vascular support impairs metabolic exchange between the choroid and the retinal pigment epithelium (RPE), accelerating degenerative processes such as chorioretinal atrophy and myopic maculopathy. The loss of choroidal vasculature also predisposes the retina to ischemic stress, which can trigger complications like neovascularization and fibrotic scarring.

Retinal changes in pathological myopia are particularly pronounced in the macular region. Progressive stretching leads to posterior staphylomas—outpouchings of the posterior pole that distort retinal architecture. These staphylomas increase the risk of foveoschisis, where retinal layers separate due to mechanical traction. High-resolution OCT imaging shows that myopic foveoschisis can occur in up to 30% of eyes with posterior staphylomas, often progressing to full-thickness macular holes if untreated (Takano & Kishi, Ophthalmology, 2018). Mechanical stress on Bruch’s membrane contributes to lacquer crack formation, which can allow choroidal neovascularization to develop, further worsening vision loss.

Characteristics of Lacquer Cracks

Lacquer cracks in pathological myopia appear as irregular, yellowish linear breaks in Bruch’s membrane, typically in the macular region. These disruptions result from excessive mechanical stress due to axial elongation. Unlike age-related Bruch’s membrane changes, lacquer cracks follow distinct patterns, often appearing in parallel or branching configurations. Histopathological studies confirm that these disruptions extend through the RPE, exposing the underlying choroid and increasing the risk of choroidal neovascularization (CNV) (Spaide, Retina, 2018). Their presence signals advanced myopic degeneration and a heightened risk of vision-threatening complications.

Lacquer cracks evolve over time, with early lesions appearing as fine, barely discernible breaks that gradually widen. Longitudinal imaging studies using fundus autofluorescence and indocyanine green angiography show that these lesions expand over months to years, reflecting the progressive nature of scleral and retinal stretching (Ohno-Matsui et al., Progress in Retinal and Eye Research, 2020). As cracks enlarge, they contribute to localized atrophy of the RPE and choriocapillaris, further weakening metabolic support to the outer retina and fostering an environment conducive to secondary complications, including abnormal blood vessel infiltration.

The distribution of lacquer cracks varies among individuals but predominantly occurs in the posterior pole, where biomechanical stress is greatest. Clinical observations indicate that these lesions are more common in eyes with pronounced posterior staphylomas, suggesting that localized curvature changes intensify strain on Bruch’s membrane (Ikuno, American Journal of Ophthalmology, 2019). Advanced imaging modalities such as optical coherence tomography angiography (OCTA) reveal that lacquer cracks often coincide with focal RPE disruptions and choroidal thinning, highlighting their structural impact.

Imaging Techniques for Detection

Detecting lacquer cracks in pathological myopia requires advanced imaging capable of capturing subtle structural disruptions. Conventional fundus photography provides an initial assessment, revealing lacquer cracks as fine, yellowish lines in the posterior pole. However, due to its limited resolution, this method often fails to detect early-stage lesions. Fluorescein angiography (FA) enhances visualization by highlighting areas of hyperfluorescence where the RPE is compromised, making it particularly useful for assessing complications like choroidal neovascularization (CNV). However, FA’s invasive nature and potential for adverse reactions to contrast dye make non-invasive alternatives preferable.

Optical coherence tomography (OCT) is the gold standard for detecting and monitoring lacquer cracks due to its ability to produce high-resolution cross-sectional images of retinal and choroidal structures. Swept-source OCT (SS-OCT) offers enhanced penetration, allowing precise visualization of Bruch’s membrane integrity and choroidal thinning. Studies using SS-OCT show that lacquer cracks appear as hyperreflective interruptions in Bruch’s membrane, often with localized RPE irregularities (Kamoi et al., Retina, 2021). These findings help differentiate lacquer cracks from other myopic degenerative changes, ensuring accurate diagnosis and risk assessment.

Optical coherence tomography angiography (OCTA) provides critical insights into vascular alterations associated with lacquer cracks. By capturing motion contrast within blood vessels, OCTA enables non-invasive evaluation of choriocapillaris perfusion, which is often diminished in areas surrounding lacquer cracks. The ability to detect early microvascular changes before CNV development makes OCTA particularly valuable for identifying patients at higher risk of vision loss. Comparative studies show that eyes with lacquer cracks exhibit significantly reduced choriocapillaris flow density, reinforcing the importance of vascular assessment in disease monitoring (Zhao et al., American Journal of Ophthalmology, 2022).

Visual Effects and Symptoms

Lacquer cracks in pathological myopia can significantly impact vision, particularly as they expand and disrupt retinal layers. While some individuals remain asymptomatic in the early stages, many experience a gradual decline in visual acuity due to progressive RPE atrophy, which compromises photoreceptor function. Patients commonly report difficulty with fine detail perception, especially in low-contrast environments, as the macula’s structural integrity deteriorates. The extent of visual impairment depends on the location and number of lacquer cracks, with those affecting the fovea posing the greatest threat to central vision.

As cracks widen, they create pathways for abnormal vascular growth, increasing the risk of CNV. CNV often leads to sudden-onset metamorphopsia, where straight lines appear distorted or wavy. This distortion is particularly noticeable when reading or focusing on geometric patterns, as irregularities in Bruch’s membrane alter retinal signal processing. In some cases, CNV results in subretinal hemorrhages, further exacerbating vision loss by introducing localized blind spots in the visual field. These changes interfere with everyday tasks such as recognizing faces or navigating unfamiliar environments.

Associated Ocular Conditions

Lacquer cracks in pathological myopia often signal broader degenerative changes, contributing to progressive visual deterioration. These structural disruptions weaken the posterior segment, fostering additional complications. Among the most concerning is choroidal neovascularization (CNV), which results from abnormal blood vessel growth through the compromised Bruch’s membrane. CNV can rapidly lead to exudative changes, including subretinal fluid accumulation and hemorrhages, significantly impairing central vision. Without timely intervention, such as anti-vascular endothelial growth factor (anti-VEGF) therapy, CNV can progress to macular scarring, causing irreversible photoreceptor damage and permanent vision loss. Studies indicate that up to 10% of individuals with lacquer cracks develop CNV, underscoring the need for vigilant monitoring (Ophthalmology, 2019).

Macular atrophy is another significant concern, as chronic tissue stretching leads to progressive RPE and choriocapillaris thinning. As these support structures deteriorate, affected individuals experience a gradual decline in central vision, often struggling with contrast sensitivity and night vision. Unlike CNV, which may present with sudden vision changes, macular atrophy progresses insidiously, making early detection challenging. OCT studies reveal that areas surrounding lacquer cracks often exhibit localized RPE loss, serving as a precursor to widespread atrophy. The presence of posterior staphylomas, frequently seen in eyes with lacquer cracks, exacerbates these degenerative processes. The combined impact of these conditions places individuals with pathological myopia at a high risk of severe visual impairment, emphasizing the need for long-term ophthalmic surveillance.