Corneal iron deposition occurs in the normal aging cornea (Hudson-Stahli lines), in pathologic conditions such as keratoconus (Fleischer ring) and pterygia (Stocker-Busacca line), and in filtering blebs (Ferry line). Different shapes of iron deposition may also be evident after refractory corneal procedures such as penetrating keratoplasty (annular line), lamellar keratorefractive surgery (paracentral ring), radial keratotomy (central satellite line), intrastromal corneal ring (mid-peripheral arcuate line), hyperopic photorefractive keratectomy (PRK) (peripheral ring), myopic PRK (central spot), hyperopic laser-assisted in situ keratomeliusis (LASIK) (paracentral ring), myopic LASIK (ring or patch near the margin of the ablated zone), and orthokeratology (ring coinciding with fitting curve). Moreover, such deposits have been reported to be related to the steep central island after myopic PRK and to iatrogenic keratectasia after'myopic LASIK. Here, we report 24 patients who developed a previously undescribed pattern of iron deposition located in the center of the corneal flap after uneventful myopic LASIK.
DISCUSSION
Refractive surgical procedures have become increasingly popular in recent years, leading to published reports of corneal iron deposition. With respect to LASIK procedures, corneal iron rings have been noted in eyes following hyperopic LASIK and in eyes with iatrogenic keratectasia following myopic LASIK. Vongthongsri et al reported that, after myopic LASIK surgery, 35 of 83 eyes (42.2%) displayed a corneal iron line in a ring or patch configuration near the margin of the ablated zone in the overlying corneal flap epithelium. Here, we report that 42 eyes of 24 patients displayed a distinctive central spotty iron deposit after myopic LASIK surgery.
Our observations differ from the previous descriptions in that iron deposition was located centrally in all our patients, rather than near the margin of the ablated zone. However, the observations in the current report are similar to those reported by Seiler and Holschbach. In their study of 193 eyes of 146 patients, central spotty iron deposits occurred within 1 year of myopic PRK in 84% of cases. Similar but stellate-appearing deposits following RK have been described as well. In our experience, we have had difficulty discerning the corneal iron ring after myopic LASIK, as described by Vongthongsri et al. We have yet to determine the reason for this difficulty. It is possible that the iron deposits are in different locations after myopic LASIK because of the influence of different microkeratome and laser settings, different mechanisms of wound healing, or possibly even ethnic factors.
The pathogenesis of corneal iron deposition remains unclear and has been the subject of considerable debate. In 1964, Gass proposed the tear pool hypothesis, which suggests that malposition of the eyelids with respect to the cornea, in regions of altered topography, enables development of a localized tear pool. Iron is sequestered from the thickened tear film and accumulates within the basal epithelial cells that lie beneath the tear pool. The validity of this hypothesis is called into question, though, by the inadequate concentration gradient for iron diffusing through the several layers of epithelial cells to the basal layer, the presence of high iron binding-affinity lactoferin within tears, the presence of the Hudson-Stahli line even in the absence of tear secretion, and Bell phenomenon preventing tear pooling in the Hudson-Stahli zone during sleep.
In 1987, Rose and Lavin suggested an alternative hypothesis, the basal cell migration theory. According to this hypothesis, attrition of superficial epithelium by the lid margins or in the area of the elevated corneal surface leads to a high mitosis rate for basal cells, and thus slows down basal cells migration. These rapidly dividing, nonmigrating and relatively mature basal cells are responsible for the accumulation of iron. In 1993, Assil et al proposed that a combination of the tear desiccation and senescent basal cell mechanisms could uniformly explain the presence of iron deposition in all circumstances. With respect to tear desiccation, iron deposition in areas of initial tear breaks up in patients with an intrastromal corneal ring. The evaporation of aqueous tear may result in an increased concentration of soluble iron, thus creating a concentration gradient favoring uptake of iron by epithelial cells. With respect to senescent basal cell mechanisms, Assil et al note that iron lines are observed in the area of greatest epithelial hyperplasia. This may be the result of a diminished surface cell turnover rate and accumulation of iron in the senescent basal cell layer over time. These senescent basal cells are neither actively migrating nor replicating and are somewhat isolated from the X-Y-Z mechanism of epithelial regulation.
In the current study, our observations suggest that iron deposition is always found in the area of greatest epithelial hyperplasia. Increased central epithelial thickness was noted after myopic LASIK and PRK, whereas increased peripheral epithelial thickness was noted after hyperopic LASIK. The areas of iron deposition after hyperopic LASIK and myopic PRK are consistent with the locations of epithelial hyperplasia. Reinstein et al showed that the epithelium varies in thickness after LASIK and appears able to remodel itself to compensate for underlying stromal surface abnormalities, modulating basal cell mitosis and migration, then promoting epithelial hyperplasia. Corneal topography only provides a graphic representation of the presence and location of irregularities, not any underlying anatomic abnormalities, which may be masked by epithelial hyperplasia. Further study in histopathology and histochemistry may provide more insight into whether the basal cell senescence or other mechanisms are responsible for iron accumulation.
Previous studies have noted a tendency toward increased iron deposition with increases in attempted refractive change after PRK 7 and myopic LASIK. In our study, the spherical equivalents of the achieved correction ranged from 4.0 D to 17.5 D. It appears that iron deposition develops in patients with a wide range of myopic correction after LASIK surgery. The achieved correction was similar in both eyes of patients 4, 7, 11, 13, and 21. There were also no significant differences between the topography of the 2 eyes. However, unilateral iron deposition occurred in these 5 patients. Investigation of other factors and variables that may contribute to iron deposition is therefore warranted.
Most of the patients in our study were incidentally diagnosed with corneal iron deposition when they visited our clinic for other unrelated symptoms. This fact lends credence to our belief that central spotty iron deposition after LASIK surgery is a relatively common occurrence. However, it may take 6 months or more for the pigmentation to become visible at slit lamp.7 Therefore, because of the relative short postoperative follow-up period after uncomplicated and satisfactory LASIK surgery, it could easily be missed. Furthermore, fine, spotty iron deposition does not disturb visual function, so the condition will typically remain undiagnosed until a visit to an ophthalmologist for relief of other ocular symptoms. For this reason, it is likely that the true incidence of corneal iron deposition is higher than hitherto suspected and difficult to determine. A more detailed analysis of a larger prospective and longitudinal study of a patient population that has undergone myopic LASIK would help to verify the incidence and course of iron deposition. Michaeli-Cohen et al described 2 patients who underwent penetrating keratoplasty, performed by surgeons who did not know that the donor eyes had previously had LASIK. If the incidence of iron deposition after myopic LASIK is high, central iron deposition may be helpful for eye bank screening, as the increased popularity of LASIK threatens the donor cornea pool.
In summary, we report a new type of iron deposition that comprises a central spot in the corneal flap after uneventful myopic LASIK. Whereas the condition seems to have no impact on visual function, it may usefully serve as an indicator of previous refractive surgery. Further study of the mechanism of the location and pattern of corneal deposits in refractive surgeries may lead to a better understanding of tear film dynamics and epithelial wound healing.
Conclusion:
Spotty corneal iron deposition can develop in the center of the corneal flap after myopic LASIK surgery. Because it is asymptomatic, the condition may have been hitherto underestimated in patient populations.
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