Myopia progression in children
Myopia incidence and prevalence is increasing worldwide. As the age of onset has lowered, the incidence of pathological myopia has increased. Together this has led to a greater burden of eye disease and a significant public health issue.
Understanding how the eye changes in myopic children is now more readily assessable with improved biometry technology. In this thesis, myopic optic nerve parameters were accessed with different measurement techniques and technology correlated to age, axial length and spherical equivalent. Paediatric disc tilt was also measured by adapting a novel technique to assess disc tilt at different meridians. The statistically significant parameters were spherical equivalent, axial length, and average retinal nerve fibre layer thickness in both eyes. The consistent correlation between spherical equivalent and axial length confirmed the link between myopic spherical equivalent and axial length growth. Retinal nerve fibre layer thinning was noted with increased axial length and myopic spherical equivalent but not age. The meridional measurement correlated maximum disc tilt with axial length in the right eye and weakly in the left. This method may prove helpful in delineating disc morphology changes associated with myopia progression.
Research in myopia progression intervention includes refractive and pharmacological methods. A refractive dual focus lens was investigated in a randomised clinical trial. Despite the significant trial limitations and low patient numbers, the current results suggested that the lens design does not provide a therapeutic reduction in myopia progression measured by axial length and spherical equivalent parameters. This finding has been validated with a subsequent Japanese trial.
Atropine 0.01% has widely been reported to reduce myopia progression to varying degrees. There is no clear consensus on when to treat, when to stop and how to best monitor treated patients. This study in the clinical setting was conducted to test the hypothesis that fast and slow myopic progressors could be distinguished using serial baseline axial length measurements. Fast progressors then commenced atropine 0.01% drops, axial length and refraction were monitored at six-month intervals to assess treatment response. The use of atropine 0.01% was well tolerated and slowed myopic progression in fast axial length progressors. A statistically significant reduction in myopic dioptric change and axial elongation was documented. The response to the atropine drops was maintained over time, and axial length accurately measured the treatment effect. The group of children assessed to be slow progressors (using serial baseline axial length measurements) were monitored and not treated with atropine 0.01% and did not progress significantly in either spherical equivalent or axial length.
Finally, myopic ocular biometry in children ages 6 to 15 was analysed at baseline and over time. The results were analysed to determine if a subgroup of patients on atropine 0.01% affected the biometry measured. No clinically significant correlation between corneal or retinal parameters was associated with either axial length or spherical equivalent. No significant change was noted in central corneal thickness, astigmatism or macular thickness over a 12–18-month period. There was progression in retinal fibre nerve layer thinning over the study period, which correlated with spherical equivalent both at baseline and over time. There is no significant effect on ocular parameters with atropine use other than axial length.
Further patient recruitment and greater longitudinal follow up are planned to verify and strengthen the myopic ocular biometry findings and correlations.