Myopia Control


Introduction

Myopia is a commonly seen condition and is the most important cause of distance vision impairment. Data from many East Asian countries show a consistent rise in the prevalence of myopia from approximately 20–30% in the 1940s to 70% and above today ( ). Although the prevalence is not as high in many other countries, a similar trend to rising prevalence has been observed ( ). To provide some further context, it is estimated that by the year 2050 every 1 of 2 people will be myopic, with a large proportion of this rise in prevalence expected in countries that are rapidly urbanizing ( ).

The burden of myopia on affected individuals, their families and the society is significant. Uncorrected myopia as low as −1.50 D is considered to result in moderate visual impairment ( ). For the year 2015 alone the productivity loss resulting from vision impairment and blindness due to uncorrected myopia was estimated at US$250 billion ( ). In addition to vision impairment resulting from uncorrected or under-corrected myopia, there is the risk of myopia- related complications. Although any level of myopia increases the risk of pathological and sight-threatening complications, higher levels of myopia, especially in older individuals, increase the risk of sight-threatening complications such as myopic macular degeneration (MMD), retinal detachment, posterior staphyloma and glaucoma ( ).

With the rising prevalence of myopia, there were will be a concurrent but disproportionately higher increase in the prevalence of high myopia, with approximately 1 in 10 people likely to be highly myopic by the year 2050 ( ). MMD is already one of the major causes of blindness in studies in Japan and Taiwan ( ). Unless there are attempts to manage the rising epidemic, it is anticipated that the risk of myopia related complications and related visual impairment will rise in the future ( ).

Myopia is multifactorial, with both genetic and environmental factors at play in the onset and progression of the condition. However, it is regarded that the rapid rise in the prevalence of myopia observed in the recent decades is not compatible with a purely genetic involvement and that environmental factors play a significant role ( ).

Support for environmental influence is from data that indicates that visual feedback regulates eye growth and from observations that demonstrate that visual conditions that affect eye growth can be used to precisely influence eye growth. For example, in animal models, compensation to optical defocus (both plus and minus lenses creating myopic and hyperopic defocus) occurs in a highly regulated manner involving both direction and magnitude ( ). Additional support for environmental influence is from data that demonstrate an association of myopia with urbanization, the greater amount of time on near based activities and less time outdoors ( ).

To slow the rising burden, there have been significant efforts over the past couple of decades directed to slowing the onset and progression of myopia with optical, pharmaceutical and environmental strategies. There is a large and growing base of evidence confirming the efficacy of such strategies, and a number of these are available for the practitioner to manage myopia ( ). This chapter presents the current understanding on the risk factors for progression, the various approaches developed so far using contact lenses to manage the progression of myopia, and discusses the selection and fitting of individuals into these lenses. Methods of myopia control by fitting and reshaping the cornea with orthokeratology lenses are presented in detail in Chapter 30 .

Risk Factors for Progression

Myopia commonly onsets in children anywhere from ages 6 to 12 years and is commonly progressive through childhood with stabilization in late adolescence; however, it is difficult to determine the age at which myopia will stabilize for a given individual eye. Furthermore, there is some recent evidence indicating that in certain eyes, progression may continue even until early adulthood ( ) and especially if they are highly myopic ( ). Additionally, there is increasing evidence of myopia onsetting at a younger age than before; thus a greater number of years are likely to be spent in progression mode resulting in a higher net myopia.

It may be inferred from the above that any myope who presents during childhood and early adulthood may be a candidate for a myopia control contact lens. However, certain individuals may be at greater risk of progression and/or developing high myopia, and therefore identification of the ‘at risk’ group helps tailor interventions to suit the individual. Fig. 31.1 lists the various risk factors associated with the progression of myopia and the strength of relationships based on the evidence.

Fig. 31.1, Risk factors for myopia progression

Of the many factors considered to influence progression, age is a significant factor and independent of other factors such as ethnicity, parental myopia, gender and lifestyle-related factors such as outdoor time ( ). Younger age is associated with a faster progression. In addition to age, ethnicity significantly influences the progression of myopia.

Children of Asian ethnicity show a faster progression rate compared to a predominantly European or Caucasian children ( ). For a child with myopia with an estimated mean age of 9.3 years, the estimated annual progression was −0.82 D/year for children of Asian descent and −0.55 D/year for children of European descent ( ).

A number of studies have reported the prevalence of myopia to be higher in females ( ), but others failed to find such an association ( ). Faster progression was also reported in females ( ). Based on a meta-analysis of progression data from spectacle wearers, for a baseline age of 8.8 years, the estimated annual progression was −0.80 D/year for females and −0.71 D/year for males ( ). The reasons for this higher progression rate in females are not understood but suggested that girls may have a more myopiagenic activity pattern (increased near work and less outdoor time) compared to boys ( ).

Other than age and ethnicity, parental myopia was also found to influence the progression of myopia. In a group of nonmyopic children, grouped by parental history of myopia, those with two parents myopic showed a more myopic shift in refraction over 1 year compared to those with only one parent or no myopic parents ( ). Other studies have also found that parental myopia was a significant risk factor ( ) with analyses showing myopic children with two parents myopic progressing faster compared to those with only one parent myopic or those with no parental myopia ( ). However, there have also been studies to the contrary with few studies failing to demonstrate the effect of parental myopia on development and progression ( ).

In addition to the patient-related factors, certain eye-related factors were considered to promote progression. Eyes exhibiting peripheral retinal hyperopic defocus were considered to be at greater risk of progression ( ). Relative peripheral hyperopia is commonly found in myopic eyes ( ) but was only weakly linked ( ) or not linked to progression ( ). It was also suggested that near phorias especially esophoria ( ), esofixation disparity, high AC/A ratio ( ) and lag of accommodation ( ) have a role to play but other studies have not found a correlation between lag and progression ( ). The role of esophoria and high AC/A ratio on progression also remains uncertain.

Lifestyle-related risk factors such as outdoor time, near distances and activities have long been considered to play a role in the aetiology of myopia. Support for regulation of progression with lifestyle-related factors is from data that indicates that there is less progression in summer than winter months ( ). Groups such as young school-age children, university graduates, occupations requiring close and near work activities such as microscopists were considered to be at higher risk of progression ( ).

A strong evidence base exists for the role of outdoor time being protective for myopia from school-based intervention trials as well as systematic meta-analysis; however, it appears that whilst time outdoors may be protective for the onset of myopia, the evidence on whether it slows the progression of myopia remains equivocal ( ). Similarly, the evidence for the role of near work in myopia progression is conflicting. Whilst some studies found no association ( ), other studies find an association.

A recent report found that examination of visual behaviour data of a large cohort found that near work distance of >30 cm, continuous near work without breaks of ≤30 min and more outdoor time during school recess was associated with a reduced myopic shift ( ). A greater near workload and a shorter reading distance were also found to be a risk factor for progression in other studies ( ). More recently, sleeping late was found to be a risk factor for progression over 24 months in a prospective evaluation of a large cohort of children and was independent of age, gender and urban-rural location. It was suggested that children sleeping late might be spending more time on myopigenic activities ( ).

Myopia Management With Contact Lenses

Of the various contact lens-based approaches considered for myopia management, it is established that single vision contact lenses, that is both rigid and soft contact lenses correct for the myopic refractive error but do not slow the progression of myopia. On the other hand, multifocal and extended depth of focus (EDOF) contact lenses has proven to slow the progression of myopia. Table 31.1 presents the efficacy data from published clinical trials for the various contact lens approaches and their role is discussed below.

Table 31.1
Summary of Evidence for Various Types of Contact Lenses in Slowing Myopia
Study Sample Size Test Control Duration of Study % Slowing Sph Eqv % Slowing Axial Elongation Age Range (years) Myopia Range (D)
428 RGP Spectacle 2 −4.0 −6.3 6–12 −1.00 to −4.00, Astig ≤2.00
116 RGP Soft CL 3 30.8 −6.5 8–11 −0.75 to −4.00, Astig <1.50
175 SV soft spectacles 3 −21.0 11–14 >−0.75, Astig <1.00
484 SV soft Specs 3 −17.0 −6.8 8–11 −1.00 to −6.00, Astig <1.00D
54 Multifocal SV CL 2 50.5 29.3 8–11 −1.00 to −6.00, Astig <1.00
Aller (2016) 79 Multifocal SV CL 1 77.2 79.2 8–18 −1.00 to −6.00, Astig ≤1.00
294 Multifocal SVCL 3 +1.50:15.2+2.50:43.8 +1.50:10.6+2.50:34.8 7–11 −0.75 to −5.00, Astig <1.00D
82 Perip plus Specs 1 35.7 38.5 7–14 −0.75 to −3.50 D, Astig ≤1.00D
Anstice et al. (2011) 70 Dual focus SV CL 10 m 36.2 50 11–14 Sph eqv: −1.25 to −4.50D
128 Dual focus Soft CL 2 25.3 32.4 8–13 −1.00 to −5.00, Astig ≤1.00D
109 Spherical aberration SV CL 2 20.6 38.9 8–11 −0.75 to −4.00, Astig ≤1.00D
Ruiz- 89 MiSight Specs 2 39.3 36.0 8–13 −0.75 to −4.00, Astig <1.00D
24 Decentred plus Cross over CL 2 26.2 25.0 10–16 −0.75 to −3.50, Astig ≤1.00
71 Gradient peripheral plus Specs 2 42.9 26.9 9–16 −0.75 to −7.00, Astig <1.25
Chamberlain (2019) 144 MiSight SV CL 3 59% 52% 8–12 −0.75 to −4.00, Astig <1.00D
Sankaridurg (2019) 508 Central and peripheral plus; EDOF SVCL 2 24–32% 22–32% 7–13 −0.75 to −3.50 D, Astig ≤0.75
Astig , Astigmatism; CL , contact lens; RGP , rigid gas permeable; Sph Eqv , spherical equivalent; SV , single vision.

Refractive Correction With Single-Vision Contact Lenses

Rigid Gas Permeables

Early studies from the 1990s suggested that wear of rigid gas permeable (RGP) lenses resulted in less progression; the observed reduction in progression could not be fully explained by the corneal flattening suggesting that there may be other factors related to RGP lens wear responsible for the slowing of myopia ( ). However, subsequent large-scale trials for up to 2 years of lens wear found no evidence of reduced progression ( ). A later 3-year trial found a slower spherical equivalent change with RGP compared to soft CL but was not consistent with the axial length change and was thought to may have resulted from RGP related corneal flattening (spherical equivalent −1.56±0.95 D with RGP versus −2.19±0.89 D with SCL) ( ).

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