Consider the following scenario. Your patient, mid-40s, long-term myope, moderately high prescription, has been wearing glasses since childhood and attending routine eye checks for years. You’ve been monitoring them carefully. But when they develop new distortion or a sudden shower of floaters, the question of how urgently they need a retinal opinion, and what’s really going on in the back of that elongated eye, can become genuinely complex.

I completed my PhD in myopia research, examining how the condition affects populations, how early it strikes, and why some people seem far more susceptible to its consequences than others. That background shapes how I think about myopia, not just as a refractive inconvenience but as a structural disease with lifelong implications, particularly for the retina. And with the cohort of heavily myopic patients who emerged in the 1980s and 1990s now well into their 40s and 50s, those implications are becoming increasingly urgent for everyone in the eye care team – including me as a fellow myope in that cohort!

WHY THE MYOPIC RETINA IS DIFFERENT

Myopia is fundamentally a structural problem. As the eye elongates beyond its optical ideal, the outer coat, sclera, choroid, Bruch’s membrane, and retinal pigment epithelium (RPE), must stretch to accommodate a larger posterior globe. That process is not benign. The choroid thins progressively, blood supply to the RPE and photoreceptors decreases, Bruch’s membrane develops mechanical stress and eventually breaks, and the retina is stretched more thinly across a greater surface area. In very high myopes, the axial length can exceed 30 mm, nearly a third longer than a normal eye, and the consequences of that elongation accumulate over decades.

From my own research into myopia prevalence and progression, one thing is striking: the current adult generation of high myopes is larger than any that has come before. In East Asian populations, rates of high myopia, defined as -6.00D or more, or an axial length exceeding 26 mm, have reached epidemic proportions.1 The generation of children who developed high myopia in school during the 1980s and 1990s is now squarely in the age range where retinal complications begin to manifest. We are only beginning to see the full clinical burden of this.

The figures are sobering. A large-scale epidemiological study from 2023 found that the incidence rate of rhegmatogenous retinal detachment (RRD) in phakic high myopes was 39 times higher than in non-myopes.2 For myopes in general, even moderate prescriptions, it was three times higher. Globally, myopic macular degeneration is already the leading cause of irreversible visual impairment in some Asian populations, and a significant cause of visual loss in working-age adults across the developed world.3 In Australia and New Zealand, where high myopia is increasingly prevalent, this isn’t a distant public health concern. It’s already sitting in your consulting chair.

STRUCTURAL CHANGES: WHAT ELONGATION DOES TO THE RETINA

Understanding what you’re looking for requires understanding why the eye changes the way it does.

As axial length increases, the posterior pole undergoes progressive structural remodelling. The choroid thins, sometimes dramatically so, reducing oxygen and nutrient delivery to the outer retina. Bruch’s membrane, the critical structural layer between the choroid and RPE, stretches and can develop linear breaks known as lacquer cracks. The RPE itself thins, becomes less functional, and in some areas atrophies entirely. Vitreous liquefaction occurs earlier and more extensively in myopic eyes, leading to earlier posterior vitreous detachment (PVD) and the tractional complications that follow.

In the periphery, the stretching of the outer eye wall creates areas of retinal thinning prone to specific degenerative changes. Lattice degeneration, a thinning of the peripheral retina with firm vitreoretinal adhesions at its margins, is the lesion most strongly associated with future retinal detachment. White without pressure, a more common but less dangerous finding, reflects areas of retinal thinning and altered vitreoretinal interface. Both become substantially more prevalent as axial length increases.

A useful approach to risk stratification is by axial length rather than refraction alone. Recent studies show that peripheral retinal abnormalities are present in about 17% of myopic eyes with axial length of 24 mm or less, rising to nearly 48% of those between 24 and 27 mm, and exceeding 80% in eyes with axial length above 27 mm.4 For optometrists with access to biometry, axial length is a more reliable marker of structural risk than the number on the prescription card.

THE SPECTRUM OF MYOPIC MACULOPATHY

Macular disease in myopia can be classified using the ATN system, which categorises changes into atrophic (A), tractional (T), and neovascular (N) components. This is worth knowing because a patient’s maculopathy can involve any combination of these three processes simultaneously, and each requires different monitoring and management.

Figure 1. A widefield fundus image in a pathological myope (-23D!) – demonstrating patchy macula and peripheral chorioretinal atrophy but still preserving 6/9 vision.

Figure 2: Posterior staphyloma in a pathological myope, with areas of peripheral traction (2B).

Figure 3. A macular OCT for a pathological myope with a dome-shaped macula and posterior staphyloma at the disc, and secondary CNVM with adjacent subretinal and intraretinal fluid.

Atrophic Changes

These progress along a well-defined spectrum. The earliest visible sign is tessellation, a tiling appearance to the fundus where choroidal vessels become visible through a thinning RPE. Many of your younger high myopes will have this. It doesn’t require referral, but it signals structural change and warrants regular monitoring. Beyond tessellation, diffuse chorioretinal atrophy represents more widespread RPE and choroidal loss. Patchy atrophy, with discrete, pale, well-demarcated areas, is a more advanced stage and carries higher risk of choroidal neovascular membrane (CNVM) development (Figure 1). At the severe end, macular atrophy with central scotoma represents end-stage loss. While there are trials, there is no current cure for this progressive atrophy.

The landmark of structural vulnerability is the lacquer crack: a fine, irregular, yellowish line in the posterior pole representing a full-thickness break in Bruch’s membrane. These appear in roughly 4% of eyes with axial length above 26.5 mm. Their clinical importance lies not in what they are, but in what they predict: patients with lacquer cracks have approximately a 30% lifetime risk of developing choroidal neovascularisation at that site. Finding a lacquer crack on fundoscopy or optical coherence tomography (OCT) should prompt serious counselling about warning symptoms and more frequent surveillance.

Posterior Staphyloma

Posterior staphyloma, an outpouching of the posterior globe, is estimated to occur in up to 35% of highly myopic eyes and is considered a hallmark of pathologic myopia. It’s often difficult to appreciate fully on slit-lamp biomicroscopy, but OCT will reveal the curvature change, and B-scan ultrasound can be helpful in very high myopes (Figure 2). Eyes with a posterior staphyloma are at elevated risk of virtually all the major myopic macular complications: traction, atrophy, choroidal neovascularisation membranes (CNVM), and macular hole. The staphyloma doesn’t stay stable either; in some patients it progresses significantly over years, driving further structural deterioration.

Choroidal Neovascularisation: Small Lesion, Big Consequences

Myopic choroidal neovascularisation membranes (mCNVM) are one of the most sight-threatening complications of high myopia, and one I would particularly like non-retinal specialists to have front-of-mind when dealing with a high myope. The prevalence among highly myopic eyes ranges from five to 11%, but the timing makes it particularly dangerous: around 62% of patients develop their first mCNVM episode before the age of 50. This is not a disease of the very old. It affects working-age adults, often at the height of their productive years.

Before the anti-VEGF era, the natural history of mCNVM was grim; around 90% of untreated patients had visual acuity below 6/60 within five years. Fortunately, intravitreal anti-VEGF treatment has transformed outcomes. Unlike age-related macular degeneration, mCNVM tends to respond with relatively few injections, often just one to three, and most patients show significant improvement at 12 months. But outcomes depend critically on early treatment. Vision lost to macular atrophy after chronic or untreated mCNVM is not recoverable.

The diagnostic challenge is that mCNVM can be very subtle. On fundoscopy, you may see a small grey-green membrane, a tiny area of subretinal haemorrhage, or nothing at all. The classic dark spot many patients report is Fuchs’ spot, a hyperplastic RPE response to a regressed CNVM, which signals that CNVM has already occurred and resolved, often with irreversible central damage. By the time a Fuchs’ spot is visible, the opportunity for anti-VEGF treatment has passed.

This is why OCT is so valuable in high myopes presenting with new central symptoms. A subretinal hyperreflective lesion, even small and with minimal fluid, in the context of a high myope with lacquer cracks or patchy atrophy, should be treated as active CNVM until proven otherwise. OCT angiography (OCT-A) has emerged as a particularly useful tool here, allowing direct visualisation of neovascularisation without the need for fluorescein dye. If there is doubt about whether mCNVM is active in a patient you are considering referring, OCT-A is a tool that can help (Figure 3).

The fellow-eye risk is also important to communicate clearly. A history of mCNVM in one eye increases the risk of developing it in the other eye to around 35%. These patients need close bilateral surveillance.

Myopic Tractional Maculopathy: The OCT Diagnosis

Myopic tractional maculopathy (MTM), sometimes called myopic foveoschisis, is a condition I suspect is underdiagnosed in many practices, simply because it isn’t visible on clinical examination without OCT. The fundus appearance in these patients is dominated by the myopic atrophic background, and the schisis is virtually invisible without cross-sectional imaging.

MTM occurs in nine to 34% of highly myopic eyes with posterior staphyloma. As the staphyloma progresses, it pulls the posterior globe away from the vitreous cavity. Structures that resist this pull: the internal limiting membrane, epiretinal membranes, retinal vessels, and cortical vitreous, create tangential traction that progressively splits the retinal layers. The result on OCT is a characteristic appearance of the neurosensory retina separated into multiple layers, with a distinctive bridging structure spanning the schisis cavities.

Many of these patients retain surprisingly good visual acuity for years, which is one reason the condition can go undetected. But MTM progresses in roughly 10–15% of cases, with serious outcomes including full-thickness macular hole formation or foveal retinal detachment, both requiring vitreoretinal surgery. Risk factors for progression include more severe retinoschisis, epiretinal membrane, and greater staphyloma height.

The key message for optometrists: any high myope complaining of progressive metamorphopsia or gradual central visual decline deserves OCT. You may be the first to detect MTM on routine imaging, and early detection, before foveal detachment, is associated with significantly better surgical outcomes.

Figure 4. Peripheral widefield imaging of a high myope with recent new haemorrhagic posterior vitreous detachment, and a temporal fresh retinal tear. Laser retinopexy has been applied, and an old inferior retinal tear and laser. Patients need to be forever vigilant of symptoms.

Figure 5. Peripheral lattice degeneration in a patient with past detachment in the other eye – prophylactic laser is often warranted in such patients.

Peripheral Retinal Disease and Retinal Detachment Risk

The peripheral retina in high myopia deserves as much clinical attention as the macula, and arguably more in terms of risk of sudden vision-threatening events (Figures 4 and 5).

Lattice degeneration is found in roughly 12– 16% of myopic eyes overall, and considerably more in high myopes. The critical risk is not the lattice itself but the firm vitreoretinal adhesion at its margins. When PVD occurs, and in high myopes this can happen decades earlier than in the general population, that adhesion creates a zone of traction that can tear the retina at the edge of the lattice. The resulting horseshoe tear, if undetected, can progress to rhegmatogenous retinal detachment. Myopia was present in over 80% of phakic patients under 50 who developed RRD in one large study.5

Other peripheral findings worth knowing include white without pressure, the most common peripheral finding in myopia, present in around 25% of myopic eyes in recent data,6 and snail-track degeneration. White without pressure is generally considered a benign marker of retinal thinning rather than a direct detachment risk, but its presence in a symptomatic myope warrants full dilated examination. Retinal holes or tears were found in around 2.4% of myopic eyes with white without pressure in recent prospective data.7

Figure 6. A pathological myope with past right retinal detachment, scarring from past 360º laser retinopexy, and circumferential buckle.

The practical implication: every pathological or high myope in your practice needs a dilated peripheral retinal examination, ideally with scleral indentation, or at minimum a thorough wide-field dilated view, at least annually, and urgently whenever they report new floaters, photopsias, or visual field changes. This is not optional and it is not something to defer.

A point about PVD in myopic patients: because vitreous liquefaction and PVD occur earlier in myopes, your patients may present with acute PVD symptoms at a much younger age than you might expect. A 35-year-old high myope reporting a sudden shower of new floaters is not reassuring until you have excluded a retinal tear. The three-month post-PVD window is the period of highest tear risk, and any myopic patient with a fresh PVD should be seen promptly.

WHAT YOU SHOULD LOOK FOR IN THE CONSULTING CHAIR

Good examination of a high myope requires deliberate, systematic effort. Here is what to look for and elicit.

History

Ask specifically about new photopsias, new floaters, a curtain or shadow in vision, central distortion, or change in central colour perception. These symptoms require same-day or urgent assessment. Always ask whether symptoms are monocular; patients often cover one eye only after prompting.

Anterior Segment

Look for early nuclear or posterior subcapsular cataract – high myopes develop cataracts significantly earlier than emmetropes, sometimes a decade ahead. This matters for counselling and for setting pre-operative expectations.

Posterior Pole

Look for peripapillary and temporal crescents around the disc, tilted disc appearance, and any evidence of peripapillary atrophy. In the macula this could be tessellation, diffuse atrophy, patchy atrophy, lacquer cracks (fine linear streaks in the posterior pole), Fuchs’ spot (dark pigmented lesion), and subretinal haemorrhage. Note staphyloma if visible: a characteristic crescentic shadow, displaced vascular patterns, and difficulty keeping the macula in focus as you sweep across the posterior pole.

Peripheral Retina

Dilate fully. Examine to the equator with a 78D or 90D lens. In high-risk patients, or those with symptoms, scleral indentation to the ora serrata is the standard of care, though referral for this is appropriate if it cannot be performed confidently.

Optic Nerve

High myopes are at elevated risk of normal-tension glaucoma, and disc assessment is complicated by tilting, crescents, and peripapillary atrophy. Disc haemorrhages, progressive retinal nerve fibre layer (RNFL) loss on OCT, and corresponding visual field defects may be present, even at normal IOP. Standard normative OCT databases perform poorly in highly myopic eyes; interpret RNFL results with appropriate caution and a low threshold for specialist referral.

Imaging and Monitoring

OCT has transformed myopic macular disease management and is now an essential tool for any optometrist monitoring high myopes.

The information you can extract from a well-performed macular OCT, including CNVM presence, choroidal thickness, presence of schisis, subretinal fluid, and subretinal hyperreflective lesions, simply cannot be obtained by clinical examination alone.

Serial OCT is particularly valuable for patients with early atrophic maculopathy where documenting stability over time is the main clinical goal. For patients with lacquer cracks or patchy atrophy, OCT every six to 12 months – with close attention to any new subretinal hyperreflective material or fluid – is appropriate baseline surveillance.

Fundus autofluorescence (FAF) is useful for mapping atrophic lesions and identifying hyperautofluorescent margins, suggesting active atrophy progression. It is particularly helpful for documenting baseline status in patients with established maculopathy and for monitoring progression objectively.

Widefield imaging systems, whether true ultrawidefield or extended field fundus photography, have vastly improved the documentation and detection of peripheral retinal pathology. A widefield fundus image at each visit for high myopes is worth the time for many practices with a large volume of high myope patients: it establishes baseline, documents new lesions, and provides a record for any colleague who might see the patient acutely.

OCT-A is becoming a useful tool for the diagnosis and monitoring of mCNVM. The ability to directly visualise a neovascular network without dye injection makes it genuinely useful, particularly for monitoring known mCNVM patients or evaluating new central symptoms in patients with high-risk features such as lacquer cracks.

WHEN TO REASSURE, MONITOR, OR REFER

This is where clinical nuance matters most.

Routine annual monitoring. Appropriate for high myopes with tessellated fundus only,

stable peripheral findings without breaks, and no macular symptoms. OCT should be performed at least annually.

Increased monitoring. Monitoring every six months with OCT is appropriate for patients with diffuse chorioretinal atrophy, lacquer cracks, patchy atrophy (without active CNVM signs), stable MTM, or known peripheral degeneration (lattice, snail-track) without breaks and in the absence of symptoms.

Urgent referral within one week. This is warranted for new central visual distortion or metamorphopsia in a high myope with known maculopathy; new small subretinal haemorrhage; new subretinal hyperreflective lesion on OCT suggestive of mCNVM; new or progressive MTM with declining vision; or peripheral retinal breaks without detachment where laser retinopexy is indicated.

Same-day or immediate referral. This is required for suspected retinal detachment (curtain, shadow, field loss), macula-threatening symptomatic retinal tear (superior break, large break, symptoms of acute PVD with tear), or any break associated with a macula-threatening detachment.

A point worth emphasising: a macula-on retinal detachment has far better visual outcomes than a macula-off detachment. The difference in time to surgery – hours to days – can mean the difference between 6/6 and 6/60. Your role in triaging these patients promptly is genuinely sight saving.

TALKING TO YOUR PATIENTS

One finding from my research and clinical experience that I find particularly striking is how unaware many myopic patients are of their retinal risks. In a recent prospective study,8 more than half of myopic patients were unaware that myopia could cause serious retinal disease. Only 48.8% knew the importance of regular retinal examinations, this in a group with established myopia and an active eye care provider.9 This is a communication opportunity we should not be wasting.9

Explain that refractive surgery – laser-assisted in situ keratomileusis (LASIK), photorefractive keratectomy (PRK) – corrects the optics of the eye, but does not address the underlying structural myopia. Patients who have had refractive surgery and no longer wear glasses are sometimes under the impression their myopic risk has resolved. It has not. The stretched retina, the peripheral degeneration, the lacquer cracks – all of it remains. This is an important and commonly missed counselling point.

When patients ask whether their prescription will “cause problems”, the honest answer is that higher prescriptions carry higher risk, but that most high myopes do not develop sight-threatening complications, and those who do are very often treatable if caught early. Frame the monitoring as proactive, not alarming.

Explain warning signs clearly and specifically: sudden increase in floaters, new flashes of light, a shadow or curtain in vision, or new blurring or distortion in the centre. Instruct patients to cover each eye in turn if they notice anything, to determine which eye is affected. And advise them to contact your practice or an emergency service rather than wait for a scheduled appointment.

For bilateral high myopes, always discuss the fellow-eye risk. A patient who has had a retinal detachment in one eye has significant lifetime risk in the other. This should be explicitly acknowledged and documented.

CONCLUSION

Myopia in the adult eye is a structural disease with lifelong retinal consequences, not a refraction to be corrected and otherwise set aside (Figure 6). The generation of high myopes currently moving through their 40s and 50s represents a cohort with a scale of retinal risk unlike anything our profession has previously managed. The good news is that most myopic retinal disease is treatable, but only if detected, and only if managed promptly.

Associate Professor Abhishek Sharma MBBS DPhil (Oxon) FRANZCO is a vitreoretinal specialist at the Queensland Eye Institute in Woolloongabba, and BrisEye Surgeons in Chermside, Brisbane. He is an Associate Professor with the School of Medicine, University of Queensland.

Assoc Prof Sharma’s clinical interests include retinal surgery, macular disease, and the retinal complications of myopia. He holds a PhD in myopia research and is co-author of Mindmaps in Ophthalmology (CRC Press).

References available at mivision.com.au.