Emmetropization appears to be a rapid process, occurring in the first year of life. Failure to emmetropize leaves about 2 to 8% of children with potentially clinically significant hyperopia after infancy. Uncorrected hyperopia in childhood has a negative impact on distance acuity and the accuracy of the accommodative response for some unknown number of children. The clinical “gray zone” for these problems as judged by distance refractive error alone might begin somewhere around +2.00 to +3.00 D. Use of a refractive correction seems to improve distance acuity and the accuracy of accommodation. Clinicians' reluctance to prescribe hyperopic corrections to children to improve visual performance might be unwarranted. If emmetropization is largely complete, if defocus has only a minor effect on the development of refractive error in infancy or childhood, and if the hyperopic eye is already growing longer but not moving toward emmetropia, then there may be little reason to either wait or be concerned about interfering with emmetropization that may never happen. The immediate visual benefit may outweigh these concerns.

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Hyperopia in childhood presents several clinical challenges. Fortunately, accurate measurement and diagnosis should not be among them. Even mild cycloplegics such as tropicamide are very effective in revealing latent hyperopia with minimal inconvenience to the patient.1–3 The uncertainties about treatment and management begin after diagnosis. The clinician is faced with questions such as how much hyperopia is too much and, if treated, how much correction should be given. This question is complicated by the weight that might be given to a host of associated factors such as the child's symptoms, academic performance, acuity at distance and near, level of astigmatism, accommodative lag, phoria, or AC/A ratio. What is clear is that these uncertainties divide the two professions of optometry and ophthalmology in their approaches to the management of childhood hyperopic refractive error. In 2004, Sean Donahue, MD, PhD, a pediatric and neuro-ophthalmologist from Vanderbilt University, published an article showing how prescribing rates for childhood hyperopia differed significantly between optometrists and ophthalmologists.4 Optometrists in the study sample prescribed refractive corrections more often, after 35% of examinations, compared with a 6% prescription rate for ophthalmologists. The emphasis in the article was that while screenings and examinations in early childhood were typically aimed at amblyopia, a high percentage of children without amblyopia received glasses. Therefore an unknown percentage of children who might be “normal” could end up wearing useless corrections. My concern, expressed in a follow-up Letter to the Editor, was that visual benefits from refractive correction other than those relevant to amblyopia risk were acknowledged but not assessed in the analysis.5 The appropriate question should have been not whether the glasses were necessary to address amblyopia, but whether they did any other good. The number of children helped and the degree of benefit are unknown. As important as I thought that omission was, it seemed equally important that there was a lack of objective evidence or guidelines that could clearly document the level of “good” that was being done. When does refractive correction of childhood hyperopia provide benefit and to what degree? If the optometric approach is correct, can we prove it?

This obvious difference in clinical philosophy seems untenable yet should be a tremendous opportunity for research. It should be unacceptable for two professions, ostensibly with the welfare of the child uppermost in the minds of their practitioners, to manage the same child in such different ways. Evidence from research should be the pathway toward shared guidelines. Such evidence is in short supply however, and hence the research opportunity. Current clinical guidelines are constructed by “consensus and are based solely on professional experience and clinical impressions, because there are no scientifically rigorous published data for guidance” according to the Preferred Practice Pattern, Pediatric Eye Evaluations, produced by the American Academy of Ophthalmology. The 2005 Monroe J. Hirsch Memorial Symposium was organized to explore what these discrepancies in clinical philosophy are and where they originate. What differences in training, literature, and clinical experiences exist that might shape one philosophy or another? What are the appropriate research questions that might elevate clinical practice from very well-informed but essentially seat-of-the-pants personal guidelines to something that is compelling and evidence-based? Speakers presented three perspectives on childhood hyperopia: this one from research, one from a pediatric ophthalmologist (Sean P. Donahue, MD, PhD), and one from a pediatric optometrist (Susan A. Cotter, OD, MS). The perspectives that follow hopefully provide some insight into the issues of where we come from and where we need to go to achieve effective management of childhood hyperopia.

In this research perspective, the data on infants come from the Berkeley Infant Biometry Study (BIBS), a longitudinal evaluation of emmetropization and ocular component development in the first 7 years of life. The Orinda Longitudinal Study of Myopia (OLSM) and its continuation, the Collaborative Longitudinal Evaluation of Ethnicity and Refractive Error (CLEERE) study, follow the ocular component development of school-aged children in an investigation of risk factors for the onset of juvenile myopia. While the specific methods of BIBS and OLSM/CLEERE differ (Table 1), each assessed similar features: refractive error, accommodative response, corneal radius of curvature, crystalline lens radii and power, and axial dimensions consisting of anterior chamber depth, lens thickness, vitreous chamber depth, and axial length. BIBS subjects were seen at 3, 9, 18, 36 months, then again at 4.5 and 6.5 years. OLSM and CLEERE subjects ranged in age from 6 to 14 years, were examined annually, and were recruited from the following clinical centers: Orinda, CA (primarily white); Irvine, CA (primarily Asian American); Houston, TX (primarily Hispanic); Eutaw, AL (primarily African American); and Tucson, AZ (primarily Native American).

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TABLE 1. Tests performed on subjects in BIBS, OLSM, and CLEERE

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One perspective that a clinician might have when facing a young hyperopic patient is that emmetropization may still be active. A decision on whether or not to prescribe might be delayed as the clinician waits to see whether the child will “grow out of it.” Data from BIBS and other work suggest that this will not be an effective strategy because the time course of emmetropization is rapid. The majority of refractive error change appears to take place in the first year of life, thereby reducing the likelihood of substantial refractive change after this early period. This pattern can be seen in BIBS longitudinal data (Fig. 1) and in recent cross-sectional data.6 There is a significant loss of hyperopia and a significant decrease in the variability in refractive error between 3 and 9 to 12 months of age, with little change after that time up to at least 3 years of age.7 Emmetropization shows the expected bi-directional behavior, loss of hyperopia for most infants with a few recovering from low myopic refractive errors.8,9 Most infants' refractive error is in the range of plano to +3.00 D by the age of 18 months. One of the reasons for rapid emmetropization is the rapid growth of the eye during that period. Between 3 and 9 months of age, the average infant eye increases in axial length by 1.20 ± 0.51 mm and decreases in lens power by 3.62 ± 2.13 D to reach values that are 90% of the average axial length and 155% of the average lens power of a child at age 6 years.10

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FIGURE 1. Spherical equivalent refractive error as a function of age (3, 9, 18, and 36 months) in the BIBS study.

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In order for hyperopia to decrease, the dioptric effects of axial growth to reduce hyperopia must exceed the effects of losses in corneal and lens power that would increase hyperopia. In early development during the first year of life, these two processes are highly correlated but sufficiently imbalanced in favor of axial growth to produce a net loss of hyperopia.11 Unfortunately for chances at long-term emmetropization, axial growth and changes in lens power soon reach a balance point where further increases in axial length are ineffective at decreasing hyperopia. Fig. 2 depicts the ratio of change in lens power per millimeter increase in axial length at two different ages: 3 to 9 months when emmetropization is occurring and 9 to 18 months when little emmetropization takes place. At 3 to 9 months, the ratio is in the range of –2.00 to –4.00 D/mm. As the balance point for an eye at this age is about –6.5 D of lens power loss per millimeter of axial growth, the eye loses hyperopia as it grows longer. Rates of refractive change are divided into tertiles, with the slowest change tertile being a loss of 0.38 D of hyperopia or less and the fastest change tertile being a loss of 1.25 D of hyperopia or more. With the eye a little larger between 9 and 18 months, the balance point is closer to –5.8 D of lens power loss per millimeter of axial growth. Each category of refractive change is closer to this balance point (i.e., the open circles are below the filled squares in Fig. 2), resulting in slower rates of refractive change between 9 and 18 months compared to between 3 and 9 months. Two-thirds of the infants (the lower two tertiles) are at this balance point and essentially stable in their refractive error. Two factors work against emmetropizing refractive change after 9 months of age: the slow growth of the eye and the changes in lens power that closely match and offset this slower growth.

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FIGURE 2. The ratio of change in lens power per millimeter change in axial length in the BIBS study. Data along the x-axis are plotted by tertiles of change in spherical equivalent refractive error between 3 and 9 months and between 9 and 18 months of age. Ratios become more negative as the pace of refractive change slows at the later age interval.

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The opportunity for emmetropization does not improve with time, as this balance between growth and power changes continues into childhood. The hyperopic eye is shorter in childhood, but surprisingly its rate of change in axial length and lens power are the same as that of an emmetrope.12 Like a mime walking against the wind, hyperopic and emmetropic eyes make little progress in terms of refractive error change. Myopic changes from axial growth are negated by changes in lens power. The eye is not persistently hyperopic because it is frozen and not growing. Hyperopia is persistent because axial elongation is offset by these changes in lens power. The hyperope unfortunately reaches this balance point with a higher degree of residual refractive error compared to the emmetrope. Similarity in growth produces similar levels of expected change in refractive error, on average equal to –0.16 D per year for all three categories: emmetropes (defined here as between –0.75 and +1.00 D in each meridian, n = 2457), hyperopes (between +1.00 and +2.00 D in each meridian, n = 736), and “high” hyperopes (+2.00 D or more hyperopia in each meridian, n = 186). The expectation would be that it would take 6 years for a high hyperope to undergo a 1.00 D change toward emmetropia. This may occur in some cases, but only infrequently. For example, of 186 children initially classified as highly hyperopic, only 5% achieved emmetropia while under observation in the CLEERE study.

How much hyperopia are we facing clinically? The proportion of children with hyperopia varies by sample, ethnicity, and by level of hyperopia. Studies have reported proportions from about 6% having hyperopic refractive errors >=+1.50 D 13 to nearly 20% with hyperopia >=+2.00 D.14 Data from the CLEERE study also indicate a wide variation in the proportion of hyperopic children depending on criterion level and ethnicity.15 If +2.00 D is taken as the lowest criterion level for clinically significant hyperopia, then between 1.8 and 7.5% of children might be affected (Table 2).

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TABLE 2. Proportion of children with various levels of hyperopia as a function of ethnicity (CLEERE data)15

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Can uncorrected hyperopia affect distance visual acuity in non-amblyopic children? If one considers the referral criterion of worse than 20/30 recommended in Pediatric Eye Evaluations (Preferred Practice Pattern, American Academy of Ophthalmology) then 9% of CLEERE children would fail when their spherical equivalent refractive error is between plano and +2.00 D. The degree of refractive error clearly matters with respect to acuity. The failure rate increases substantially to 31% when the refractive error is more hyperopic than +2.00 D. The visual benefit of correction is depicted in Fig. 3. The first thing to note is that the relationship between refractive error and average corrected distance acuity is relatively flat with only a range of about 0.08 logMAR (four letters) between the best and the worst corrected distance acuity. Uncorrected distance acuity in children who do not wear any habitual correction steadily worsens by about 0.2 logMAR (about two lines) at the highest levels of hyperopia. The curves separate, indicating the beginning of some visual benefit, between +2.00 and +3.00 D. These are, of course, different children in each group. Perhaps the better estimate of visual benefit can be seen by comparing hyperopic children wearing their correction compared with those not wearing their correction. In this case the visual benefit extends across all refractive errors by amounts between 0.05 and 0.15 logMAR (0.5 to 1.5 lines). These data also represent the best-case scenario of a brief measurement time. Acuity testing is not the same task as more sustained viewing such as when looking at the blackboard for long periods. Despite the robust accommodative amplitude of children, uncorrected hyperopic refractive error is detrimental to distance acuity in proportion to the amount of the refractive error. The wearing of a distance hyperopic correction improves distance acuity.

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FIGURE 3. LogMAR visual acuity as a function of spherical equivalent refractive error in the CLEERE study. Groups are children who wore a refractive correction to the study visit tested with that correction (triangles), tested without that correction (squares), and children who wore no refractive correction to the study visit and who were tested without any correction (circles).

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It seems reasonable to assume that the situation would be worse at near. Although CLEERE made no measurements of near acuity, we do have detailed measurements of the monocular accommodative response. These provide estimates of near defocus errors or accommodative lags. Age-adjusted lag values for a 4.0 D stimulus increase as a function of hyperopic refractive error in children who do not wear a refractive correction (Fig. 4). The slope of this function suggests that there will be 0.74 D of increased lag for every 1.0 D of uncorrected hyperopia. It is difficult to pinpoint a threshold value of lag that is clinically significant; the impact of lag as measured by this technique on reading performance has not been evaluated. A lag of 2.0 D might be considered a significant level of defocus and is about twice the average value found using this technique.16 This value for lag would be reached on average at about +3.00 D of uncorrected hyperopia. For refractive errors in the range of +1.50 to +2.50 D, 11% of children (35/322) have this level of lag. This percentage increases with increasing hyperopia, reaching 28% (17/61) if uncorrected hyperopia is between +2.50 and +3.50 D and 52% (11/21) for hyperopia over +3.50 D. Glasses seem to improve this clinical picture. When children wear a correction, there is no significant relationship between refractive error and accommodative lag. Children have 2.00 D or more of accommodative lag even with correction, but only sporadically over the range of refractive errors. These data are limited in that CLEERE is not a randomized clinical trial. The children who wear glasses are different than the ones not wearing a correction. We have no control over spectacle prescriptions provided by doctors in the community, nor do we know why a spectacle prescription was or was not provided to a child. Even with these limitations, however, it seems reasonable to conclude that a hyperopic correction would be effective in reducing accommodative lag given the basic principles underlying accommodative demand and response.

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FIGURE 4. Accommodative lag to a 4.0 D stimulus as a function of hyperopic spherical equivalent refractive error and whether or not a correction was worn. “No correction” means that the child wore no refractive correction to the study visit and was not tested with any correction in place. “With correction” means that the child wore a refractive correction to the study visit and was tested with a correction in place.

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Many clinicians might resist providing a correction to the pediatric hyperope based on recent data from animal experimentation on the visual control of eye growth.17 Recent animal data indicate that clarity at distance is a powerful “stop” signal for eye growth that outweighs the effects of hyperopic defocus in moving the eye toward emmetropia.18,19 A plus correction might interfere with emmetropization and doom the child to persistent hyperopia. Obviously the definitive study has not been done to resolve this question, but there are several perspectives that argue in favor of providing a correction if it is beneficial visually without concern for any undesirable effects on emmetropization. It is not certain that hyperopic defocus is the visual signal driving emmetropization in infancy. Numerous studies indicate that infants from the age of 3 to 6 months can accommodate as accurately and effectively as children over a range of hyperopic refractive errors.20–25 If this is the case, infants would not experience a dose of hyperopic blur in proportion to their hyperopia that would direct eye growth toward emmetropia. It is not clear why an infant with uncorrected refractive error of +4.00 D who accommodates as accurately and effectively as an infant with uncorrected refractive error of +1.00 D would emmetropize while the latter would remain stable. Similar concerns exist as to the influence of hyperopic defocus in childhood myopia. Hyperopic defocus from accommodative lag during prolonged reading has been hypothesized as a risk factor for the onset of myopia and for myopia progression. One study has found an increased accommodative lag in children who go on to develop myopia,26 but our results from CLEERE do not bear this out. Increased accommodative lag only occurred at or after the onset of myopia, not before.16 Our characterization of increased lag in myopes was that it was a symptom rather than a cause of myopia. Recent efforts to reduce myopia progression through the use of bifocals have also had mixed results. Results from such studies have either been not significant or showed modest slowing of progression.27–29 The benefit seems greatest in the first year of treatment and may diminish over time.30 Studies of the effect of correction of hyperopia in infancy have had conflicting results. One found that early correction could interfere with emmetropization,31 while another found no effect.32 The former study can be criticized for basing analyses on compliance and the presence or absence of strabismus. If early correction has a beneficial preventive effect on the development of strabismus (an inconsistent but possible finding),32,33 the exclusion of children who develop strabismus might lead to over-representation of nonemmetropizing, nonstrabismic hyperopic children in the corrected group. Uncorrected children might appear to emmetropize more effectively because the ones who did not emmetropize could have been excluded more often if they developed strabismus more often than corrected children. The study by Atkinson et al.32 concluding that there was no effect of correction on emmetropization was analyzed more appropriately based on the principle of intent-to-treat. This result seems more consistent with the data above on the timing and process of emmetropization. If emmetropization occurs during the first year and if little change in refractive error occurs in hyperopes during childhood, it seems reasonable to conclude that there is little to no emmetropization potential remaining with which to interfere. If emmetropization is complete, refractive error is stable, and the hyperopic eye is growing at a pace equal to emmetropes yet it remains hyperopic, then correction seems unlikely to adversely affect a system that is already stable. Visual benefit perhaps should trump concern over interference with emmetropization when considering correction of the pediatric hyperope.

These perspectives from research are the obvious conclusions. The more difficult research questions are not whether plus corrections for hyperopes can improve distance or near acuity, relieve esophoria, or reduce accommodative lag. The more difficult, unanswered issues are how to quantify these benefits and how to judge their value against the expense of examinations and eyewear. The real issue is finding guidelines that would indicate the cases in which the benefits would likely outweigh the costs. These would be the key pieces of evidence that would be compelling for patients, parents, government, insurers, and eyecare providers. These would also be the pieces of evidence that would lead to the most effective care for the pediatric hyperopic patient.

The BIBS project was supported by NIH/NEI grant R01-11,801. The CLEERE study is supported by NIH/NEI grants U10-EY08893 and R24-EY014792, the Ohio Lions Eye Research Foundation, and the EF Wildermuth Foundation.

The opinions expressed in this work are my own. However, I acknowledge the contributions of my colleagues Sara Frane, OD and Wendy Lin, OD, to the BIBS data presented and those of the CLEERE study Group and its Executive Committee to the CLEERE data presented. The CLEERE Executive Committee includes Susan A. Cotter, OD, MS, Lisa A. Jones, PhD, Robert N. Kleinstein, OD, PhD, Ruth E. Manny, OD, PhD, J. Daniel Twelker, OD, PhD, and Karla Zadnik, OD, PhD.

Donald O. Mutti

The Ohio State University College of Optometry

338 West Tenth Avenue

Columbus, Ohio 43210-1240

e-mail: mutti.2@osu.edu

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Key Words: emmetropization; hyperopia; myopia; development

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Accession Number: 00006324-200702000-00007