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

Donders’s push-up method of measuring accommodative amplitude becomes instead a method of measuring the effective depth of focus of the eye, with any contribution due to true accommodation being impossible to distinguish. Similarly, adding minus lenses until blur occurs is simply a measure of depth of focus, not of accommodation.

Infrared objective optometers have been used in attempts to measure accommodation after surgery for presbyopia, but without success (5). Caution must be observed in using these instruments, however, because some of them use only small portions of the pupil for the refractive measurement, and small changes in alignment can yield variable results in the presence of irregular or multifocal optics.

G. WAVEFRONT ANALYSIS

Wavefront analysis methods of measuring the refractive state across the pupil will be able to determine the refractive state of the multifocal zones in the altered crystalline lenses observed by retinoscopy. These new methods will also be able to detect whether or not any true optical changes occur with attempted accommodation (6). To my knowledge, these instruments have not yet been used to measure accommodation after surgery for presbyopia. I look forward to the results.

H. CONCLUSION

Whatever the mechanism of refractive change produced by surgical procedures for presbyopia, there is no question that a close focus can be created under certain conditions. Whether these beneficial effects will prove to be reproducible and stable and whether they will provide acceptable visual acuity and contrast remains to be seen.

REFERENCES

1.Jackson E. Skiascopy and Its Practical Application to the Study of Refraction. Philadelphia: Edwards and Docker Co., 1895:86–88.

2.Guyton DL, O’Connor GM. Dynamic retinoscopy. Curr Opin Ophthalmol 1991; 2:78–80.

3.Rutstein RP, Fuhr PD, Swiatocha J. Comparing the amplitude of accommodation determined objectively and subjectively. Optom Vis Sci 1993; 70:496–500.

4.Rosenfield M, Portello JK, Blustein GH, Jang C. Comparison of clinical techniques to assess the near accommodative response. Optom Vis Sci 1996; 73:382–388.

5.Mathews S. Scleral expansion surgery does not restore accommodation in human presbyopia. Ophthalmology 1999; 106:873–877.

6.Gray GP, Campin JA, Pettit GH, Liedel KK. Use of wavefront technology for measuring accommodation and corresponding changes in higher order aberrations (abstr). Invest Ophthalmol Vis Sci 2001; 42:S26.

to decentration are evident in higher hyperopic corrections. There are other potential complications of H-PRK (Table 1). For example, PRK produces large (9.5-mm) epithelial defects, leading to prolonged healing time, and an increased risk of infection while the cornea is healing. Recurrent corneal erosions are a bothersome potential complication of PRK. Haze and scar formation may also occur. Postoperative glare may be a nuisance, particularly for patients with larger pupils.

Table 1 Complications of PRK for Correction of Spherical Primary Hyperopia

9.4-mm peripheral zone/6.5-mm optical zone

a. Ablation Zone Decentration

A hyperopic correction, which produces a steepening of the central cornea, is less forgiving of decentration. And yet centration is more difficult during hyperopic corrective surgery because hyperopic eyes tend to be smaller, with smaller corneas, and because the ablation zone must be large. In addition, H-PRK takes up to three times longer than a comparable myopic PRK procedure; thus the risk of decentration is higher. Decentration is the H- PRK complication that is most likely to cause loss of BCVA or irregular astigmatism.

Decentration, with either H-PRK or H-LASIK, may occur either due to a decentered treatment throughout the ablation (shift) or due to intraoperative drift. Shift can be secondary to poor patient fixation or to the surgeon’s error. Drift occurs secondary to involuntary intraoperative eye movement or to a surgeon’s attempt to correct apparent decentration during treatment.

Decentration is difficult to treat. Theoretically, one can lift the flap and retreat the patient with decentration of the treatment in the opposite direction to the previous ablation. An alternative solution is to use miotics to constrict the pupillary axis and to minimize optical aberrations. Finally, a hard contact lens may neutralize optical aberrations resulting from irregular astigmatism (13).

Techniques to avoid decentration include (1) the creation of larger optical (5-mm) and ablation (9.0–9.5 mm) zones, (2) the use of faster laser pulses to decrease the ablation time, and (3) more sophisticated eye-tracking devices. Finally, performing the ablation under the lowest illumination possible can improve patient fixation.

b. Regression

Regression of effect after H-PRK remains one of the limitations of this procedure. It has been observed that “aggressive healers,” patients with severe corneal haze and marked scarring in the region of ablation, had significant regression of their refractive correction. This observation supports the theory that the mechanisms associated with regression are the subepithelial deposition of collagen and glycosaminoglycans which occurs during wound healing and produces a filling in of the ablation and loss of effect (12,14–15). Some ophthalmologists have given topical corticosteroids after PRK in an attempt to inhibit regression. Studies consistently show that while topical corticosteroids (fluorometholone or dexamethasone) inhibit some regression when used during the first 3 to 6 postoperative months, this effect is negated approximately 3 months after cessation of steroids (4,14–17). The development of new strategies to reduce aggressive wound healing and haze after PRK may prevent post-PRK regression.

c. Haze

One potential post-PRK complication is the development of haze. Fortunately, haze is less of an issue with H-PRK than it is for myopic PRK. This is because the stromal haze is most dense at the border of the ablated zone, which is in the peripheral (rather than central) cornea of eyes treated for hyperopia (Fig. 2). Nevertheless, haze can contribute to regression of effect, as mentioned above. Therefore, it is best to try to prevent haze formation. Risk factors for haze include small ablation diameters with steep transition zones, UV exposure, acute systemic viral illness, and ocular surface disorders such as dry eyes (18–20).

Haze may be prevented by maintaining a good tear film layer with nonpreserved tears or punctal plugs if necessary. One can encourage patients to decrease exposure to

Figure 2 Midperipheral ring of corneal haze, characteristic of the haze seen after PRK for hyperopia. (From Ref. 10.)

UV radiation by using sunglasses and a hat for 1 year after PRK is performed. Some authors suggest preventing formation of the corneal haze with a single intraoperative treatment of mitomycin C to suppress proliferation of keratocytes. Studies in rabbits have proven this to be very effective (21). A less aggressive approach is to wait and see if haze occurs and then to apply mitomycin C to treat corneal haze and reduce the regression that often accompanies the haze (22). One can treat stromal haze that persists beyond 6 months with excimer laser retreatment or a transepithelial PRK followed by PRK retreatment.

2. Hyperopic-Laser in situ Keratomileusis (H-LASIK)

Although early trials of hyperopic LASIK (H-LASIK) reported unsatisfactory results with a high rate of BCVA loss and significant regression, H-LASIK is now supplanting H- PRK as the refractive procedure of choice for hyperopia (23,24). H-LASIK is associated with a faster recovery time with less postoperative pain than H-PRK. Initially, H-LASIK was limited by small outer-zone ablations: microkeratomes that could create only small flaps as well as unrefined excimer laser algorithms contributed to the poor results of early H-LASIK. With the development of keratomes that are able to create 9.5-mm rather than the older 8.5-mm flaps, H-LASIK has become safer. In addition, better algorithms and nomograms are being developed as we accrue more experience with H-LASIK.

Limitations of LASIK for the treatment of hyperopia include problems with predictability, regression, and difficulty treating hyperopia greater than 4 D. Complications of H-LASIK can be divided into three groups. First are the complications specific to the surgical correction of hyperopia itself. As discussed above, these include the older age of the patients and the length of time of the procedure. Second, there may be intraoperative complications, including flap complications and ablation-related complications. Finally, postoperative complications include infection, flap complications, striae, diffuse lamellar keratitis, epithelial ingrowth, decentration, corneal ectasia, and, rarely, retinal complications (Table 2).

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Table 2 Complications of LASIK for Correction of Spherical Primary Hyperopia

Table 2 Continued

a. Flap Complications

Intraoperative complications include free flaps, incomplete flaps, buttonholes, small flaps, and thin flaps. Free flaps, thin flaps, or incomplete flaps are more likely to occur in patients with flat ( 41.00-D) and large ( 11.5-mm) corneas. Unusually steep ( 48.00-D) and small ( 11.5-mm) corneas are more conducive to buttonholes or large flaps.

The larger ablation areas necessary for H-LASIK require larger flaps. Extra care must be taken with the larger flaps because a large flap may be more prone to wrinkles

or misalignment, which may lead to irregular astigmatism. When pannus exists, a large flap may cause bleeding, which must be cleared from the bed prior to ablation.

Appropriate preoperative examinations can help one identify and discourage patients at greater risk for flap complications. Preplaced surgical landmarks that straddle the flap edge will help with accurate repositioning of the flap in the operative and postoperative period. In addition, the newer microkeratomes and suction rings create fewer flap complications.

b. Epithelial Ingrowth

To achieve successful H-LASIK results, the diameter of the corneal flap must be large enough. Epithelial ingrowth can result from laser energy to the periphery of the flap, or it may occur secondary to wound edge instability with migration of epithelial cells under the flap (Fig. 3). Epithelial ingrowth can progress to involve the visual axis, creating irregular astigmatism and even melting of the overlying flap (13,36).

If epithelial cells under the flap progress toward the visual axis or induce stromal melting, the flap should be lifted, the stromal bed and flap undersurface should be thoroughly irrigated and scraped, and the flap should then be repositioned (37).

With larger flaps of 9 to 10 mm, the risk of epithelial ingrowth is greatly reduced, most likely because this avoids ablation of epithelium beyond the edge of the flap (38). Other measures one may take to prevent epithelial ingrowth include using dedicated instruments exclusively for interface manipulation, so that these instruments do not come in contact with the surrounding epithelium. Also, one should be careful to avoid flap folds, as these may provide a conduit for cell infiltration (13).

c. Decentration

Decentration or small optical zones may lead to irregular astigmatism, causing loss of BCVA, glare, monocular diplopia or halos, and halo effects. The same principles of decentration described above for PRK apply here. For example, whether with PRK or LASIK, a larger optical zone is more forgiving of a slight decentration. More sophisticated LASIK ablation profiles may also diminish the risk of decentration: a more gradual transition zone between ablated and unablated tissue helps minimize epithelial and stromal regeneration, with its subsequent regression.

Figure 3 Epithelial ingrowth after LASIK. (A) Stable epithelial ingrowth at the LASIK interface.

(B) Retroillumination used to view the same area of epithelial ingrowth. (From Ref. 13.)

Figure 4 Diffuse lamellar keratitis following LASIK. (A) Diffuse lamellar keratitis 2 days after LASIK. (B) Diffuse lamellar keratitis, 5 days after LASIK, with central coalescence, scarring, and stromal melt. (From Ref. 13.)

d. Diffuse Lamellar Keratitis

Although diffuse lamellar keratitis (DLK) is a recently described syndrome, not yet documented after H-LASIK, it has been reported in approximately 0.2 to 3.2% of cases of myopic LASIK (13,39–42). DLK is characterized by a proliferation of inflammatory cells at the LASIK interface (Fig. 4). It can lead to loss of BCVA due to irregular astigmatism and may also cause stromal corneal melting with induced hyperopia or hyperopic astigmatism.

The cause of DLK is still unclear; thus, prevention remains a challenge. When present, however, DLK must be treated immediately with hourly topical prednisolone actate 1% and broad-spectrum topical antibiotic coverage. It has been observed that if the DLK is not resolved by the fifth postoperative day, there is typically central coalescence of the inflammatory cells, which may lead to central stromal melting and scarring. Thus, if inflammation progresses despite the steroid/antibiotic treatment, the flap should be lifted, scraped, and irrigated by the fourth postoperative day at the latest (13). The use of topical intrastromal steroid during LASIK has been proposed as a way of reducing the incidence and severity of DLK (43).

e. Late Flap Dislocation

One rare, potential H-LASIK complication is traumatic flap dislocation, occasionally seen months or years after LASIK (44,45). One might expect a slightly greater risk of flap dislocation in H-LASIK because the flap tends to be wider than that created for myopic LASIK. For this reason, it would be wise to avoid performing H-LASIK on high-risk patients, such as boxers. One should also encourage patients to wear safety glasses when engaging in high-risk sports activities after H-LASIK.

f. Corneal Ectasia

Corneal ectasia is a rare complication. For example, in one of the largest studies of H- LASIK, Suarez et al. performed LASIK on 154 eyes of patients with simple hyperopia of between 1.00 and 8.50 D with astigmatism of less than 0.75 D. Suarez et al. had only two cases of postoperative corneal ectasia, both occurring in patients with high levels of hyperopia. Keratectasia is most likely due to the mechanical uncoupling of the posterior