Philip Cheng is an experienced practitioner in orthokeratology and myopia control in Australia and clinical director of the Myopia Clinic Melbourne. As an industry leader in myopia care, Philip is a regular presenter and writer on myopia management, consults with industry and educational providers, a mentor for fellow optometrists and students, and a committee board member of the Orthokeratology Society of Oceania.
In the feature article, Philip Cheng examined the dose-dependent response that is being reported across a number of myopia control interventions. Here he discusses how to apply the evidence base, including consideration of those results, to clinical practice.
How can we apply the results of research in clinical practice
First, start the discussion about myopia management early. Planting the seed of available treatment options can help with later discussions when interventions are indicated. Review high genetic risk and pre-myopic kids more frequently so that early changes from hyperopia to myopia can be detected. The CLEERE study found that less than +0.75D of hyperopia in first grade children was a reliable risk factor for predicting future myopia.1 Baseline measurements of axial length can help detect rapid eye growth that is known to precede the imminent onset of myopia.
Act as soon as a child is diagnosed with myopia. The greatest determinant of progression to high myopia is the age of myopia onset. It would be unwise to delay interventions or dissuade young children from trying contact lenses, given that contact lenses are an effective and safe option. In fact, younger children may be safer contact lens wearers than adults.2 The ROMIO study suggested the most beneficial time to commence orthokeratology is at age 7-8, the age group that tends to show the fastest axial elongation.3 Early intervention for fast progressors is paramount to preventing high myopia.
Once a decision has been made to start myopia management, the clinician’s role is to choose the most appropriate intervention for the child. This means balancing potential therapeutic effect against undesirable side effects and treatment risks. But the difference in a child’s end point level of myopia can be significant if a ‘weak’ treatment is chosen instead of an effective treatment.
Treatment recommendations should be based on careful analysis of the child’s risk factors for progression and individual characteristics. Factors such as, but not limited to, family history, level of parental myopia, current age, age of myopia onset, progression history, refractive error, axial length, current optical correction, near work habits, binocular vision, near fixation disparity, and pupil size all need consideration.
Spectacle lenses
The prescribing of progressive addition spectacle lenses (PALs) for children with myopia has long been common practice in optometry. But the evidence to support prescribing PALs is weak. The COMET study showed only a 0.20D difference in myopia progression over 3 years between the PAL group (prescribed with +2.00D near add) and single vision (SV) lens group – a statistically significant but not clinically meaningful outcome.4 While PALs may benefit a subgroup of children with near esophoria and accommodative lag, reinvestigation of these children in the COMET 2 study found only a small, clinically insignificant effect.5
Furthermore, if PALs with +2.00D add are not clinically effective in most cases, there is arguably no place for low add lenses (such as anti-fatigue lenses and occupational-type lenses, typically with less than +1.00D add) in evidence-based myopia management.
Executive bifocal lenses, cosmetic considerations aside, are an evidence-based option according to a 3-year study;6 the larger area of peripheral defocus on the superior retina cast from the near segment of a bifocal, as well as easier access to the reading portion for near work, may contribute to its greater myopia control effect compared to PALs.
Of the commercially available spectacle lenses currently on the market, the Defocus Incorporated Multiple Segments (DIMS) lenses, manufactured by Hoya, with a 52% reduction in myopia progression and 62% less axial elongation compared to SV spectacle lenses over 2 years,7 show the highest reported efficacy in retarding myopia progression. DIMS lenses, with a central 9mm optical zone for correcting distance refraction surrounded by about 400 multiple defocus segments, each 1.03mm in diameter and creating +3.50D of myopic defocus, were developed to provide simultaneous defocus while maintaining good distance vision.
Multifocal soft contact lenses (MFSCLs)
If prescribing soft contact lenses for myopia management, the lens with the strongest clinical evidence to date is the CooperVision MiSight® 1 day. Its 3-year randomised controlled trial demonstrated a myopia control efficacy of 59% in slowing refractive error progression and 52% in slowing axial elongation.8 The VTI NaturalVue® Multifocal 1 Day provides a wider power range, to up -12.25D, and has demonstrated myopia control efficacy in a retrospective case series analysis.9 When prescribing MFSCLs where a choice of near add is required, a high add should be chosen over a medium or low add. For example, while the +2.50D add Biofinity Multifocal – shown to slow myopia progression by 43% and axial length change by 36% over 3 years10 – appears less effective than the FDA-approved MiSight, it may serve as an alternative for ‘off-label’ prescribing in some cases. Examples of this could include its use in practices and countries where MiSight is not available, or when the patient’s prescription falls outside of MiSight’s power range of -0.25 to -6.00D. A practical consideration from an earlier paper by the BLINK study group is that an over-refraction of -0.50 to -0.75D is typically required to optimise visual acuity with +2.50D high add lenses.
Atropine
Although 0.01% atropine remains a popular choice of treatment among ophthalmologists and optometrists, due to the much-publicised earlier ATOM 2 study,11 the newer LAMP study suggests the use of more potent concentrations of low-dose atropine (0.025 and 0.05%) for more effective control of axial elongation.12 Atropine treatments up to 0.05% are generally well tolerated, but binocular vision and glare symptoms should be evaluated and managed appropriately. It is worth remembering that some children are poor responders to atropine. Indeed, in the LAMP study 9% of children receiving 0.05% atropine progressed more than 2D in 2 years, while a previous study found that 12% of children continued to progress even on high-dose (1%) atropine.13 It has been suggested that poor responders to atropine are generally younger children and those with higher myopia at baseline and two myopic parents.14
Orthokeratology (OK)
OK has been shown to be effective in slowing axial elongation in moderate to high myopes,15 in astigmatic myopes,16 as well as in high myopia with partial-reduction OK and glasses for residual refractive correction.17 However, for children with low baseline myopia, with OK offering less multifocality on the cornea, it might not be the best option. Other interventions such as MFSCL, where the multifocality is inherent in the lens design and independent of refractive error correction, may be more effective in low myopia. Pupil size can affect treatment efficacy, hence baseline pupil size measurement is important when assessing patient suitability for OK. Further research is needed on whether customising OK lens designs with increased compression factors ,18 smaller optic zone sizes and aspheric base curves, which could increase the amount of induced HOAs and spherical aberrations, may improve OK treatment efficacy. OK practitioners should ideally use axial length as the metric to monitor myopia progression, given that refractive error cannot be readily and reliably measured during treatment.
Combined atropine with orthokeratology
There is emerging evidence to support combining atropine with orthokeratology as a more effective myopia management strategy. The recently published results from the AOK study has shown an additive effect when combining 0.01% atropine with orthokeratology over 1 year, with 0.09mm less axial elongation in the atropine-plus-OK group compared to OK treatment alone (0.07mm vs 0.16mm progression, respectively).19 Interestingly, the enhanced treatment effect was only observed in the first 6 months, and not in the second half of the year.
A study on Japanese children also demonstrated an additive effect with the combined 0.01% atropine with OK treatment over 2 years.20 The axial length change in the combined group of 0.29mm was 0.11mm less than the OK monotherapy group, thus slowing axial elongation by 28% more than OK treatment alone. But similar to the AOK study, the enhanced effect was only apparent in the initial treatment period of 6-12 months, after which both groups demonstrated similar rates of progression.
The Kinoshita study20 indicated the additional effect of 0.01% atropine was more evident in younger children and those with lower myopia, with less apparent effect as the baseline refractive error increased. It is possible these two variables are linked; younger children may presumably be those with lower myopia, who would benefit more from adding atropine to their OK treatment.
As 0.01% atropine alone has insignificant direct pharmacological effect on eye growth, it is believed the primary effect of adding 0.01% atropine to OK is the increase in pupil size (photopic pupil diameter increased by 0.49mm with 0.01% atropine in the LAMP study), thereby enhancing the optical effect of OK. This supports an earlier study which showed larger pupil sizes with OK was associated with slower progression.21 Larger pupils are believed to help facilitate the transmission of OK-induced peripheral myopic defocus rays through the pupils onto the retina. Higher-order ocular aberrations are also a function of pupil size; OK-induced elevation in spherical aberrations is significantly greater in eyes with enlarged pupils.
Combined treatment showing a greater effect in low myopia may be due to the dose-response relationship associated with OK treatment; OK for low myopia generates less peripheral defocus and less elevation of spherical aberrations. Whereas the optical effect of OK in moderate or high myopia may already reach a threshold level necessary to slow axial elongation, its effect in low myopia may be insufficient as a monotherapy treatment. Therefore, children with low myopia commencing OK may benefit from a combined treatment strategy with 0.01% atropine from the onset.
In addition, it is worth considering that as the pharmacological effect of atropine is concentration-dependent, 0.025% or 0.05% atropine with OK might be more effective than 0.01% atropine with OK, although these combinations have not yet been specifically studied. This is another treatment variable we have in our toolkit for children who demonstrate continued progression. There is also opportunity to combine various concentrations of low-dose atropine with other optical interventions.
Conclusion
Go early – start myopia management as early as possible. Go hard – choose the more potent treatment options over the weaker ones. Especially for younger children, those demonstrating fast progression, or those with additional risk factors such as long baseline axial length and parental high myopia. Find the right dose required; if one intervention doesn’t show enough effect, be agile to change to a different intervention or use a combined treatment strategy to achieve the optimal outcome for the child in your chair. As the practitioner, the child’s myopia future depends on the choices you make today.
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