Ординатура / Офтальмология / Английские материалы / Hyperopia and Presbyopia_Tsubota, Boxer Wachler, Azar_2003

Figure 5 Corneal image using ultrasound biomicroscopy.

undergo surgery for enucleation or exenteration, as well as before penetrating keratoplasty, to clarify these potential differences between humans and animal models (21).

Our working hypothesis at the present time is that regression after LASIK or PRK surgery for hyperopia is due to a combination of epithelial hyperplasia and stromal regrowth in the ablation zone. Using confocal microscopy and histological examination in a rabbit model, Hosoda at al. detected subepithelial proliferative changes in the ablated zone that progressed for 1 month after surgery, then decreased by the third month (96). In a similar study by Dierick et al. (11), mean stromal regrowth after 10-D hyperopic PRK was 50% of ablated tissue. Deposition showed a lenticular pattern and could account for up to 5.00 D of regression (11). In addition, the epithelium thickened 20% at the midtransition zone (junction of the optical and ablated zones), contributing to more refractive regression (11).

A key question is whether the epithelial hyperplasia is attributable to an increased wound healing response due to the size of the ablation zone, the altered surface topography associated with steepening the central contour, or a combination of both these factors. With smaller ablation zone diameters that have been tested in the past, rapid regression may have been largely due to abrupt changes in corneal curvature in the midperiphery of the ablation. With wider ablations that allow a more gradual transition than with smaller ablation zones, there is less tendency for regression, suggesting that the influence of this factor has been reduced. Differences in tear pooling and distribution on the corneal surface between smaller and larger ablation zone diameters could play a role. Well-controlled studies of varying ablations with careful measurements of epithelial hyperplasia and stro-

mal regrowth should help to increase our understanding of regression associated with the laser correction of hyperopia.

Other sources of regression may be a greater than average wound-healing response in individual patients or variations in surgery that promote increased healing. For example, a thin flap may be associated with regression, since the stromal wound-healing response and epithelium-modulating modulating growth factor production are more likely to be in proximity to the epithelium (13). This is probably a major factor promoting epithelial hyperplasia. Other factors such as epithelial defects produced by the microkeratome and diffuse interface keratitis may also be associated with a stronger wound-healing response and therefore regression. The rate of enhancement in a recent series was significantly higher (53 versus 16%; p 0.02) following DLK than for eyes that did not have DLK (Wilson and Ambro´sio, unpublished data, 2001). Since the treatment for hyperopia is typically performed in the periphery of the cornea, closer to the limbus, it is likely that a stronger inflammatory reaction will follow those surgeries. A study involving an animal model comparing hyperopic and myopic PRK, using specific antibodies for inflammatory cells as well as cytokines, might be helpful for elucidating this hypothesis.

The higher the level of correction attempted for hyperopia, the more likely regression due to wound healing will occur. In our experience with hyperopic LASIK and PRK, regression is most common in eyes where the attempted correction is over 4 to 5 D.

Intraocular pressure could be a factor in the regression of hyperopic LASIK in some cases with high-pressure increases. A case of acute angle-closure glaucoma was reported by Paciuc et al. 1 year after hyperopic LASIK (100). The glaucoma attack was treated with laser peripheral iridotomy and a prophylactic iridotomy was performed in the fellow eye. Corneal topography was performed 2, 5, and 18 weeks after the acute episode and a myopic shift occurred in the eye that had angle closure. This resolved over 3 months. It is important to consider that the eye blinks over 10,000 times per day (101) at lid velocities up to 30 cm/s (102). Each blink has enough force to raise intraocular pressure 10 to 70 mmHg (103).

Koch and coworkers (21) studied Ho:YAG LTK on three human corneas 1 day before their removal at penetrating keratoplasty in patients with corneal edema secondary to Fuchs endothelial dystrophy (without bullous epithelial changes) and on six New Zealand white rabbit corneas followed for up to 3 months. The pulse radiant energy level was noted to be proportional to the acute tissue injury. In human corneas, changes in the irradiated zones included epithelial cell injury and death, loss of fine filamentous structure in Bowman’s layer, disruption of stromal lamellae, and keratocyte injury and death. A cone-shaped zone of increased stromal hematoxylin uptake extending posteriorly for 90% of stromal thickness was noted in the treatment areas. Special immunohistochemical stains to detect apoptosis were not used, although transmission electron microscopy findings suggested that they might play a role. In the rabbit corneas, similar acute changes were noted. By 3 weeks, epithelial hyperplasia and stromal contraction were present. Wound healing in the rabbits included repair of the epithelial attachment complex, keratocyte activation, synthesis of type I collagen, and partial restoration of stromal keratin sulfate and type VI collagen. There was also a marked endothelial proliferative response in the rabbit corneas. Attempted corrections with LTK of greater than 2 D are associated with significant regression. This is likely related to stromal remodeling, with the keratocytes functioning to repair the altered collagen over time.

D. FUTURE DIRECTIONS AND CONCLUSIONS

The ability to modulate corneal wound healing to achieve better clinical outcomes would be beneficial to extend the efficacy and safety of keratorefractive corrections of hyperopia. Apoptosis is the first detected event in the complex cascade of the corneal wound healing. Differences in this initiator and subsequent events in healing between eyes likely is a major determinant of variation between eyes following laser correction for hyperopia. Development of methods to control this first event may be useful for normalizing the response between patients.

A better understanding of the mechanisms associated with regression, especially differentiating between the key determinants epithelial hyperplasia and stromal remodeling, would provide specific strategies to improve stability.

Corneal implants and inlays may become an option for hyperopic treatment in the future. New alloplastic materials with acceptable permeability for corneal tissue, with refractive indices and clarity equal to those of the cornea, may provide a reversible refractive procedure for hyperopia. Intracorneal lenses with higher refractive indexes than the cornea and therefore intrinsic refractive power would not rely on changing the cornea’s shape. They could attenuate epithelial hyperplasia as a factor in regression.

Corneal surgery for hyperopia has lagged behind that of myopia primarily due to issues related to efficacy, stability, and safety. Several procedures were abandoned during the past decade. Understanding and respecting the limits of the available procedures is key for achieving success with hyperopic patients. Intraocular procedures for hyperopia, such as phakic intraocular lenses and clear lens extraction, may have an important role in treating this group of patients if safety can be improved.

ACKNOWLEDGMENTS

Supported in part by an unrestricted grant from Research to Prevent Blindness, New York, N.Y., and U.S. Public Health Service grant EY 10056 and EYO1730 from the National Eye Institute, National Institutes of Health, Bethesda, Maryland.

PROPRIETARY INTEREST STATEMENT

The authors have no proprietary or financial interest in relation to this manuscript.

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