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Up Front | Sep 2007

Central Toxic Keratopathy

Although the cause is unknown, this condition may occur after PRK or femtosecond laser-created flaps.

Central toxic keratopathy (CTK) is a noninflammatory opacification of the central corneal stroma following laser refractive surgery. Striae and hyperopic refractive shift are the common accompanying signs of this syndrome.1

Corneal clouding after laser refractive surgery is uncommon. Patients with corneal opacification within 1 week after laser surgery have previously been reported.2-4 Fraenkel and associates2 described the first report as an inflammatory opacification with hyperopic shift 1 week following LASIK. They treated four eyes with topical steroids. Parolini and associates3 reported a similar condition after LASIK, this time starting in postoperative day 1 and accompanying with severe pain. Lyle and Jin4 described a central interface haze that improved over time but was associated with striae and hyperopic shift. They called this condition central lamellar keratitis, implying an inflammatory etiology. Linebarger and associates5 also believed that this condition had an inflammatory nature; they described it as severe interface inflammation and proposed a classification system for diffuse lamellar keratitis (DLK).

Although clinical descriptions of this condition overlap, differences exist in terms of understanding the (1) inciting factor, (2) nature of pathology, and (3) way to treat it. We believe that this condition (ie, CTK) is different from severe DLK, although CTK is usually preceded by it. Recently, we studied 23 eyes (14 patients) to elucidate the clinical spectrum of this syndrome.1

OPACIFICATION IS CENTRAL
CTK usually starts within 3 to 9 days after laser refractive surgery. The inciting procedure may be PRK, LASIK, or intra-LASIK. This is an important feature. In our series, four eyes (two patients) developed CTK within 3 to 4 days after PRK.4 The opacification is typically central, and it extends posteriorly into the corneal stroma (Figure 1). In both LASIK and PRK cases, the opacification may be associated with striae. Striae were observed in 17 of 23 eyes, one of which interestingly developed post-PRK striae in the corneal stroma after PRK.

Hyperopic shift is a common feature of this syndrome. Postoperatively, 12 of 23 eyes had hyperopia more than 2.00 D. The maximum hyperopic spherical equivalent was 7.25 D in a LASIK eye and 12.00 D in a post-PRK eye. The opacity cleared gradually—usually within 12 to 18 months. It is rare for the opacity to persist beyond 18 months. After LASIK and intra-LASIK, laser enhancements for residual hyperopia may be performed as flap lift and retreatment. If the previous treatment was surface ablation, the choice of hyperopic correction should be repeat PRK with mitomycin C. We did not observe recurrence of CTK after enhancement surgeries.1

Two well-known noninfectious causes for the loss of corneal clarity after laser refractive surgery are DLK and post-PRK haze, which occur after LASIK and surface treatments, respectively. These conditions should be differentiated from CTK. The onset of haze after surface treatments usually occurs approximately 1 month postoperative, and the intensity peaks in 3 to 6 months. This haze is noninflammatory and subepithelial. It is mainly confined to the central cornea and may resolve within months to years. Reablation with mitomycin C is the choice of treatment for persistent cases. DLK, on the other hand, is as its name implies, is an inflammatory condition that starts on the first or second day after LASIK. There are mild-to-moderate inflammatory cells within the central or peripheral flap interface. DLK usually resolves in 1 week. There is no hyperopic shift.

DLK usually precedes CTK. The DLK resolves, leaving the opacification, which persists. Mild-to-severe DLK coexisted in 18 of 23 eyes of our patients. Thus, topical steroids should be limited to inducing resolution of any coexisting DLK. A prolonged course of topical steroids is inadvisable, since CTK is noninflammatory, and there could be additional morbidity from side effects (eg, glaucoma, cataract). We also do not recommend irrigation of the flap interface. We have found that the stroma in CTK is gel-like from necrosis. Irrigating or scraping may remove the central stroma, worsening hyperopic shift.

Linebarger and colleagues5 have called this condition stage IV DLK. We believe this is not the preferred term, because CTK is a distinct entity for several reasons. First, DLK is confined to the interface, whereas CTK extends anteriorly or posteriorly to the interface. Second, DLK resolves in 5 to 7 days, whereas CTK persists for months. Third, CTK may occur in the absence of DLK and can occur after PRK, whereas DLK cannot.

The cause of CTK is unknown, although we hypothesize that photoactivation of some substance—possibly povidone-iodine—by the laser induces keratocyte apoptosis and stromal necrosis. The inciting factor, however, is not the microkeratome itself; this condition can happen after PRK and also after femtosecond laser-created flaps.1 Could this reaction be an intrinsic patient response to laser ablation? This is also unlikely since it does not recur after enhancements.

Robert K. Maloney, MD, is Director of the Maloney Vision Institute, in Los Angeles. Dr. Maloney states that he has no financial interest in the products or companies mentioned. He may be reached at +1 310 208 3937; rm@maloneyvision.com.

Baris Sonmez, MD, is Assistant Professor of Ophthalmology at the Ondokuzmayis University Samsun, in Turkey. Dr. Sonmez states that he has no financial interest in the products or companies mentioned. He may be reached at drbarissonmez@gmail.com.

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