Myopia control is being implemented in clinical practice far more frequently today than just a few years ago, probably due to the proliferation of meaningful research and the increased prevalence of the disease. Yes, myopia is a disease. Because the symptoms can be easily treated using optics instead of a pill, many people—eyecare practitioners included—think of myopia as an adaptation.

If you do an internet search for “define disease,” the first definition is, “a disorder of structure or function in a human, animal, or plant, especially one that produces specific signs or symptoms or that affects a specific location and is not simply a direct result of physical injury.” Myopia is a disorder of structure whereby the optics do not match the length of the eye. The specific sign or symptom of myopia is distance blur. Myopia is genetic and environmental but does not result from injury. Myopia precisely matches the definition of a disease; therefore, as eyecare practitioners, we must do what we can to manage the potential consequences of the disease through treatment that extends beyond symptom relief.

The three most commonly prescribed methods of myopia control are center-distance soft multifocal contact lenses,^1-3 orthokeratology contact lenses,^4,5 and low-concentration atropine.^6,7 There are many research manuscripts, review papers, continuing education lectures, and online seminars that describe the relative abilities of each of these myopia control treatments. Far less often, we receive balanced, evidence-based evaluations of general topics that are important for clinical myopia control. This article will provide perspective—not necessarily answers—for some important questions related to myopia control that will enable practitioners to provide their patients appropriate informed consent and to optimize treatments based on evidence, not speculation.

SHOULD I MEASURE AXIAL LENGTH ON MY MYOPIA CONTROL PATIENTS?

Yes Excessive eye length is the putative cue for sight-threatening morbidities associated with myopia. There is no direct evidence that slowing myopia progression decreases the risk of sight-threatening complications, because they are rare and typically don’t occur until late in life. Sometimes, however, the best evidence available is biological plausibility, and all of these comorbidities can be logically explained by excessive eye length. So, it is a reasonable assumption that if you slow eye growth, you will reduce the risk of vision loss.

Myopia control can be measured only through axial elongation for orthokeratology contact lenses because they temporarily eliminate myopic refractive error, and the return to baseline refractive error is variable and often incomplete. In fact, nearly all studies of myopia control include axial length as a primary outcome, and the U.S. Food and Drug Administration (FDA) requires measurement of axial length in its Phase 3 studies.

Myopia progression is not steady; it tends to be faster in the winter than in the summer^8,9 and can randomly alternate between fast and slow progression. If a child progresses 1.00D after initiation of myopia control, it is unknown whether myopia progression was unchanged by the treatment or whether the child would have progressed 2.00D without myopia control. Measurement of axial length may provide an additional piece of data that helps clinicians understand whether or not the treatment is effective.

No Myopia progression and axial elongation are highly correlated.² Measurement of refractive error is the standard of care, so it is not necessary to collect additional data that will provide very little unique information. Furthermore, myopia progression can be monitored on patients undergoing orthokeratology by over-refracting those who exhibit reduced visual acuity while uncorrected. If they exhibit a “minus over-refraction” with the orthokeratology lens in place, then the myopia progressed, and the base curve radius of the orthokeratology lens should be flattened for appropriate treatment.

Measuring axial elongation is very necessary for myopia control studies that compare the average change over time between two groups because it provides information about the mechanism of the treatment effect. In other words, it tells whether myopia progression may be permanent due to slowed eye growth or temporary due to flattening of the cornea.

Myopia progression is not steady. As mentioned earlier, we know that myopia progression is faster during winter months,^8,9 and eye growth (but not myopia progression) is related to growth spurts.¹⁰ Therefore, when a myopia control patient progresses 0.75D in a year (50% more than average^11-14), it is unknown whether the progression was unaffected by myopia control or whether it was reduced by 50%. If that patient’s eyes grew 0.30mm in a year (50% more than average^11-14), you still don’t know whether the myopia control treatment exhibited an absence of effect or slowed progression by 50%. If a measurement doesn’t actually provide additional information to formulate an optimal treatment plan, then you shouldn’t increase chair time and expense for patients and decrease productivity for staff and the office.

Summary Measuring axial length is imperative for clinical studies, but optional for myopia control in clinical practice. If you believe that measuring axial length informs a more appropriate myopia control management plan, then biometry should be routinely measured on your myopia control patients. If the benefit of measuring axial length is unclear, then you do not need it to implement myopia control in your practice.

WHEN SHOULD I CHANGE MYOPIA CONTROL TREATMENTS?

When Progression Is Too Fast We strive to provide the best treatment for our patients. We owe it to our patients to alter care when it does not meet our standard. Although we may not know how fast an individual patient would progress without myopia control, if we feel that our management plan did not meet our standards or the parents’ standards, then we ought to attempt something different. We can try a different modality to see whether progression is slower, or we can combine pharmacologic and optical treatments. Doing something is always better than doing nothing, even if we are unsure of the ultimate results. Change the treatment when you feel that it is necessary.

Never What is “too fast?” We know that in the United States, the average myopia progression is about 0.50D per year, and the average axial elongation for a myope is about 0.20mm per year.^11-14 This indicates that some people naturally progress or grow slower and some faster. We also know that myopia progression is not steady.^8,9 It is therefore impossible to know whether a myopia control treatment is effective for an individual. Scientifically, we are not yet able to provide individualized treatment for myopia progression, as clinicians and scientists can for some forms of cancer. The genetics of refractive error are extremely complicated; a genome-wide meta-analysis identified 18 single nucleotide polymorphisms that explained only 3.4% of the variation in refractive error.¹⁵ Some people claim protocols that will optimize myopia control, but unfortunately, that level of precision is simply not possible at this time.

As we know little about the actual myopia control effect for an individual, we may switch treatments when the current treatment already provides adequate control and/or we may switch to a treatment that is less effective. The initial determination of the most appropriate myopia control modality should be based on scientific averages (for example, “On average, we expect to reduce your child’s myopia progression by 40%.”) and on the patient’s lifestyle. The myopia control effect may also be dependent on compliance.³ If a treatment is matched to a patient’s lifestyle, then the benefits may improve compliance and, ultimately, the amount of myopia control experienced by the patient.

Summary If you or the parents are uncomfortable with the myopia control effect experienced by a patient, then you may consider changing or combining treatment modalities. Unfortunately, there is no clear evidence to indicate that changing or combining myopia control treatments will result in slower progression beyond the natural slowing of myopia progression. However, trying something new may alleviate strain, and that can be very meaningful to everyone involved.

IS COMBINATION THERAPY BETTER THAN MONOTHERAPY?

Two studies of combination therapies using orthokeratology and low-concentration atropine have been conducted. The study by Kinoshita et al¹⁶ reported one-year eye growth of 0.09mm ± 0.12mm for the combination (0.01% atropine) group and 0.19mm ± 0.15mm for the orthokeratology group (53% slower, p = 0.04). A second study reported by Wan and colleagues¹⁷ concluded that “…combined treatment with atropine and [orthokeratology] lenses achieves a slightly better control of myopia progression.” The researchers based their conclusion on the fact that there was a statistically significant difference in eye growth between those who are using orthokeratology alone and those who are using a combination of orthokeratology and atropine when examining four subgroups based on initial refractive error and atropine concentration. However, the authors failed to notice that where there was the biggest difference in axial elongation between combination and monotherapy, the combination group experienced the fastest eye growth. The last row of Table 1 provides a post-hoc calculation of the eye growth based on sample size-weighted means. The difference in eye growth between the monotherapy and the combination therapy is only 0.02mm when considering the entire sample.

Although the two investigations reported similar conclusions, a thorough examination of the data that were presented leads to conflicting results. Further examination of the question is warranted to provide our patients with evidence-based information regarding combination of optical and pharmacologic treatments for myopia progression.

SHOULD WE APPLY MYOPIA CONTROL TREATMENTS PRIOR TO MYOPIA ONSET?

For every year earlier that myopia onsets, adults are expected to be 0.86D more myopic, or 2.9 times more likely to be a high myope.¹⁸ The progression of myopic children is also 0.39D per year faster for every year younger at onset.¹⁹ These facts indicate that delaying the onset of myopia may have a meaningful effect on the amount of myopia experienced as an adult.

A retrospective chart review conducted in Taiwan compared the onset of myopia and change in refractive error between patients who received 0.025% atropine or nothing before the onset of myopia. The refractive error of those who received atropine shifted 0.14D ± 0.24D, and those who received no treatment shifted 0.58D ± 0.34D (p < 0.0001). The onset of myopia was 8% in the atropine group and 58% in the control group.

More time outdoors can protect against myopia onset.^20-23 A randomized clinical trial showed that just more than six hours per week of additional outdoor time resulted in a reduction of myopia onset over one-year from 17.7% to 8.4% (p = 0.001). These results have been confirmed in a few meta-analyses.^20,24

Although no study has directly examined the hypothesis that delaying the onset of nearsightedness with atropine or outdoor time will ultimately reduce myopic refractive error in adulthood, biological plausibility again indicates that we may consider treating pre-myopes with atropine or suggesting more time spent outdoors to ultimately reduce the risk of high myopia and potential sight-threatening complications. At the very least, studies should be conducted to determine whether outdoor time or atropine before myopia onset can reduce the ultimate myopic refractive error experienced by patients.

CONCLUSION

We have gained significant evidence over the past 10 years to show that myopia control should be considered as a first-line treatment for myopic children. Despite the increased knowledge, many questions remain unanswered. This article presents evidence for eyecare practitioners to weigh when deciding how to implement myopia control in their practice. CLS

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