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Mechanism for corneal reshaping in hyperopic orthokeratology
Paul Gifford1, Vivien Au, Barney Hon
1FAAO School of Optometry and Vision Science, University of New South Wales, Sydney, New South Wales, Australia.
Purpose:
To investigate the mechanism underlying hyperopic orthokeratology (OK) by comparing the short-term clinical effect of lenses before and after central lens fenestration.
Methods:
Twelve subjects (age 21 to 24 years) were fitted with rigid hyperopic OK lenses (BE Enterprises/Capricornia) in one eye only. The fellow eye acted as a non-lens wearing control. Lens specifications were matched to provide the same post lens tear film profile in all subjects. Non-fenestrated lenses were worn in the open eye for 1 h and in the closed eye for four nights. Subjective spherical equivalent refraction and corneal topography (Medmont E300) were measured at baseline, after 1 h of lens wear, and within 1 h of waking on days 1 and 4 of overnight lens wear. The lenses were then sent for three 0.75 mm fenestrations within the central optic zone, and lens wearing and measurement procedures were repeated.
Results:
There was a statistically significant change from baseline in all variables at all visits in lens wearing eyes. Refraction changed after 1 h of lens wear, with greater effect after overnight wear. Para-central corneal flattening was apparent after 1 h of lens wear, with greater flattening after overnight wear. Central corneal steepening was only statistically significant after overnight wear. Central fenestrations did not lead to a difference in clinical effect in any variables. However, a correlation between apical corneal curvature change and refractive change became apparent only after lens fenestration.
Conclusion:
A hyperopic OK effect was established after 1 h with increased effect with longer lens wearing time. Central fenestrations did not affect the clinical outcomes, indicating that corneal compression by the lens in the para-central region as opposed to central post lens tear film suction may be the primary mechanism behind the hyperopic OK clinical effect.
