Lacquer Cracks in the Retina: Causes and Symptoms

Lacquer cracks are tiny breaks in a thin but critical layer at the back of the eye called Bruch’s membrane, and they occur almost exclusively in people with severe (pathological) myopia. The name comes from their appearance during eye exams, where they look like the fine, branching fractures you see on old lacquerware or a cracked porcelain glaze. While the cracks themselves often cause no symptoms at all, they signal that the structural fabric of the retina is under serious mechanical strain and can set the stage for complications that threaten vision permanently.

What Bruch’s Membrane Is and Why It Breaks

Bruch’s membrane is a thin, five-layered sheet that sits between the retina and the choroid, the blood-vessel-rich layer beneath it. It acts as a filter and a structural scaffold, helping nutrients pass from choroidal blood vessels into the retinal pigment epithelium while keeping the layers properly separated. In a normally shaped eye, the membrane handles everyday mechanical forces without trouble. In pathological myopia, the eyeball grows excessively long from front to back, and this elongation stretches Bruch’s membrane beyond its limits. The result is physical ruptures, the lacquer cracks, that expose the layers beneath.¹

The fundamental driver is the abnormal elongation of the eye’s axial length. As the eyeball stretches, the tissue at the back of the eye, especially around the macula, is subjected to increasing mechanical stress. The fundus layers thin out, choroidal blood flow diminishes, and Bruch’s membrane, which has very little elasticity to spare, cracks under the tension.² These aren’t sudden catastrophic tears. They tend to form gradually, sometimes growing wider or longer over months or years, and sometimes giving rise to entirely new cracks in areas that were previously intact.

Changes in the Eye Wall That Set the Stage

The sclera, the tough white outer shell of the eye, also plays a role. In highly myopic eyes the sclera becomes abnormally thin, especially at the back. Research in animal models has shown that scleral collagen production drops significantly in eyes undergoing myopic elongation, while collagen breakdown speeds up. In myopic eyes, the production of type I collagen, the main structural protein of the sclera, fell by roughly a fifth, and the balance between different collagen types shifted in ways that weakened the tissue.³ A thinner, weaker sclera means the eyeball stretches more easily, which means more mechanical stress on Bruch’s membrane, which means more cracks. The scleral thinning and the Bruch’s membrane breaks are really two faces of the same degenerative process.

Who Gets Lacquer Cracks

Lacquer cracks appear almost exclusively in people with high or pathological myopia, typically those with prescriptions stronger than about minus six diopters. But not every highly myopic person develops them. Several factors shift the odds.

A study of highly myopic patients found that higher myopia, being male, and having a particular eye-shape feature called a narrow macular staphyloma (a localized outward bulge of the eye wall near the macula) were all independently linked to greater risk. Patients whose prescriptions exceeded roughly minus twelve diopters had about seven times the odds of developing lacquer cracks compared with less severely myopic eyes. Men had roughly three times the odds of women overall, and a narrow staphyloma tripled the risk as well. Interestingly, older age was associated with a slightly lower risk of new lacquer cracks, though the relationship is more nuanced than it sounds: in older men, the sex-related risk was especially pronounced, while in younger patients a narrow staphyloma was a stronger predictor.⁴

The age finding can be confusing at first glance. It does not mean that aging protects the eye. Rather, lacquer cracks tend to form during periods of active eye elongation, which is more vigorous in younger people. By older age, the eye may have already passed through the window of rapid stretching. In eyes that have already developed extensive atrophy, the tissue may have degraded past the stage where cracks are the dominant finding; instead, broader patches of tissue loss take over.

Where in the Eye They Form

Lacquer cracks are not randomly scattered across the back of the eye. They strongly favor the central macula, the area responsible for sharp, detailed vision. One study found that about half of all lacquer cracks appeared in the central macula, with the nasal side accounting for about a fifth and the temporal, inferior, and superior zones each contributing smaller shares.⁵ This central concentration is one reason lacquer cracks are clinically important despite their small size: they sit right where the eye does its most precise work.

Symptoms, or the Lack of Them

Here is the frustrating part for patients: lacquer cracks themselves usually produce no noticeable symptoms. Most people with early lacquer cracks have no idea they exist until an ophthalmologist spots them during a dilated eye exam. The cracks are too small and too deep in the retinal architecture to cause the kind of distortion or blurriness a person would notice at home. They are generally considered relatively innocuous lesions on their own.¹

Symptoms tend to appear only when something goes wrong at the site of a crack. The two main complications that bring symptoms are subretinal hemorrhage and choroidal neovascularization, both discussed below. When these occur, a person might notice a sudden dark spot in the central vision, distortion of straight lines (metamorphopsia), or a general blurriness that doesn’t correct with glasses. Any of these in a highly myopic eye warrants urgent evaluation.

How Lacquer Cracks Are Detected

Because patients rarely feel anything, detection relies on imaging. During a standard dilated fundus exam, lacquer cracks appear as fine yellowish or whitish lines against the darker background of the retina. They branch and meander, sometimes forming a network. But traditional examination and even standard color photography can miss thinner or less distinct cracks, especially when they are overlaid by pigment changes.

Fluorescein angiography, in which a dye is injected into a vein and photographed as it circulates through the eye, shows lacquer cracks as bright (hyperfluorescent) lines. But a different dye-based technique, indocyanine green (ICG) angiography, has proven more sensitive. In a study of 37 eyes with lacquer cracks, ICG angiography revealed longer cracks and detected more individual cracks than fluorescein angiography in a large proportion of cases.⁶ With ICG, the cracks appear as dark (hypofluorescent) lines, reflecting the disruption of the pigment epithelium and choroid beneath them. The practical implication is that when a clinician suspects lacquer cracks, ICG angiography can reveal cracks that fluorescein alone would miss.

Optical coherence tomography (OCT), a non-invasive scan that creates cross-sectional images of the retina, has become the workhorse for monitoring these eyes over time. OCT can show the physical discontinuity in Bruch’s membrane and track changes in the overlying retinal layers without requiring dye injection. It’s particularly useful for spotting early signs of complications like fluid buildup from new blood vessel growth.

How Lacquer Cracks Progress

Lacquer cracks are not a static, one-time event. They tend to evolve. A long-term study of natural progression in myopic eyes found a recurring sequence: eyes first develop a tessellated (mottled) appearance, then progress to diffuse thinning and lacquer cracks. From there, many eyes develop broader patches of atrophy as cracks widen and the tissue around them degrades further. Eventually these patches can enlarge and merge.⁷

In the Beijing Eye Study, which followed highly myopic eyes over a decade, about one in five eyes showed either new lacquer cracks or enlargement of existing ones over the study period. Some eyes progressed from having isolated cracks to developing patchy chorioretinal atrophy, a more advanced and vision-threatening stage.⁸ The progression is not inevitable for every eye, but clinicians treat lacquer cracks as an early warning signal that the disease is on a trajectory toward more serious damage.

Subretinal Bleeding as a Warning Sign

One of the more dramatic early complications is subretinal hemorrhage: a small bleed that occurs beneath the retina, right at or near a lacquer crack. In many cases, this bleeding actually marks the moment a new crack is forming. Bruch’s membrane ruptures, tiny choroidal blood vessels are disrupted, and blood leaks into the subretinal space. A study of 22 eyes with this type of bleed found that in the majority, a visible lacquer crack appeared at the bleeding site within two to six months, averaging about four months.⁹

These bleeds are usually small and self-limiting, and many resolve on their own. A patient might notice a sudden dark smudge in their central vision that slowly fades over weeks. The bleed itself isn’t typically the major threat; what matters is what it signals about the integrity of Bruch’s membrane. Once the membrane has ruptured, the door is open for abnormal blood vessels to grow through the gap.

Choroidal Neovascularization and the Real Threat to Vision

The complication that clinicians worry about most is myopic choroidal neovascularization (CNV). This is when new, fragile blood vessels sprout from the choroid, push through the break in Bruch’s membrane, and grow beneath or into the retina. These abnormal vessels leak fluid and blood, causing rapid and sometimes permanent damage to central vision.

Lacquer cracks are one of the strongest predictors of this happening. In one long-term study, CNV developed in about 29% of eyes that had lacquer cracks, compared with 20% of eyes with patchy atrophy and under 4% of eyes with only diffuse thinning.¹⁰ A systematic review and meta-analysis found that highly myopic eyes with CNV had roughly three times the odds of having lacquer cracks compared with highly myopic eyes without CNV.¹¹

The mechanism makes intuitive sense: the crack in Bruch’s membrane provides a physical gap through which new vessels can sprout. Add in the fact that these eyes already have a thinned choroid and elevated growth factors in the fluid inside the eye, and the environment is primed for abnormal vessel growth.

Treatment When Complications Develop

Lacquer cracks by themselves don’t have a direct treatment. You cannot patch or glue Bruch’s membrane back together. The focus of management is monitoring and early intervention if complications arise.

When myopic CNV does develop, the standard treatment is intravitreal injection of anti-VEGF (vascular endothelial growth factor) drugs. These medications block the chemical signal that drives abnormal blood vessel growth. Multiple clinical trials, including large randomized controlled studies, have established that anti-VEGF injections are effective at improving or stabilizing vision in myopic CNV.¹² These injections are now considered first-line therapy for myopic CNV, having largely replaced older treatments like laser photocoagulation and photodynamic therapy, which could themselves damage the retina.¹³

One notable difference between myopic CNV and the more common age-related form is that myopic CNV often responds well to fewer injections. Many patients need only one or a small number of treatments rather than the long-running monthly or bimonthly injection schedules typical for age-related macular degeneration. This is partly because the CNV lesions in myopic eyes tend to be smaller and the underlying growth-factor environment is different.¹⁴

Long-Term Visual Outlook

Eyes with lacquer cracks alone generally maintain better vision than eyes that have already progressed to patchy atrophy or CNV. A ten-year follow-up study confirmed that visual outcomes were considerably worse in eyes with patchy atrophy and choroidal neovascularization compared with eyes where lacquer cracks were the only macular finding.¹⁵ In other words, the cracks are an early marker. If you catch them and monitor closely, there is a meaningful window to intervene before irreversible damage sets in.

That said, lacquer cracks do indicate that the degenerative process is underway, and there is no proven way to halt axial elongation in an already adult eye. For younger patients whose myopia is still progressing, strategies aimed at slowing myopic progression (low-dose atropine eye drops, specialized contact lenses, increased outdoor time) may indirectly reduce the risk of future Bruch’s membrane breaks by limiting how much the eye continues to stretch. These interventions don’t reverse existing cracks, but they address the upstream cause.

What Highly Myopic Patients Should Watch For

Because lacquer cracks are silent until complications hit, the most important practical step for anyone with high myopia is regular dilated eye exams. The exact frequency depends on the degree of myopia and whether other degenerative changes are already present, but annual exams are a common recommendation for people in the pathological range. Some specialists follow patients every six months when cracks or early atrophy have been documented.

Between exams, an Amsler grid, a simple printed grid of straight lines, can be used at home to check for new distortion. If the lines suddenly appear wavy, bent, or if a dark spot appears in the center of the grid, that could signal fluid or bleeding from new vessel growth and is a reason to see an eye doctor promptly rather than waiting for the next scheduled visit. The speed of intervention matters: the sooner CNV is identified and treated, the better the chance of preserving useful central vision.

It is also worth noting that lacquer cracks can appear in both eyes, though they don’t always develop symmetrically or at the same time. A person who has cracks documented in one eye should assume the other eye is at elevated risk as well, particularly if both eyes are similarly myopic. Monitoring both eyes carefully remains the most effective strategy available.