Diffuse lamellar keratitis (DLK) is a rare noninfectious postoperative complication of laser in situ keratomileusis (LASIK) surgery and usually presents with fine, white inflammatory infiltrates beneath the corneal flap interface. The onset is typically in the immediate postoperative period (1 to 3 days).1 The severity has been classified into 4 stages.2 Stage I presents with peripheral inflammatory infiltrates without central visual axis involvement. As the infiltrates migrate centrally, visual acuity begins to decrease in stage II and III. In stage IV, stromal melting and corneal scarring can cause permanent visual loss. A single cause of DLK has not been clearly identified; however, it has been suggested that epithelial injury can trigger a wound-healing response mediated by interleukin-1 and other epithelial growth factors that might lead to development of DLK.3,4
We report a case of DLK with an onset 14 years after LASIK. This timeline of pathology is rare, with only one other case presenting this late after surgery.5 This delayed presentation is clinically significant because late-onset DLK might not be recognized immediately and delayed treatment can result in serious complications for these patients.
A 45-year-old man with a history of bilateral uneventful LASIK 14 years earlier was referred from the emergency room for ocular irritation and foreign-body sensation in the left eye for 1 day. He denied previous episodes, contact lens use, recent trauma, or infection. In 2012, the patient was seen by an outside provider and diagnosed with a corneal scar. However, a review of the patient's medical record images was consistent with a significant amount of epithelial ingrowth in the left eye rather than scar formation (Figure 1, A).
The initial ophthalmic examination showed a corrected distance visual acuity of 20/60 in the right eye and 20/125 in the left eye. Intraocular pressure measured by tonometry was 21 mm Hg and 25 mm Hg, respectively. No afferent pupillary defect was present. On slitlamp examination, an eyelash was seen in the LASIK flap interface in the left eye and was subsequently removed with a jeweler's forceps, leaving a visible tract (Figure 1, B). In the left eye, conjunctival injection, diffuse stromal edema with increased haze, and infiltrate along the inferior 60 degrees of the LASIK flap, a 1.0 mm central epithelial defect with haze and infiltrate, and an adjacent 0.5 mm staining dendritic-appearing infiltrate were noted. In addition, 2+ mixed cell was observed in the anterior chamber in the left eye. Epithelial ingrowth and temporal haze in LASIK flaps were noted bilaterally in the left eye, greater than in the right eye. The posterior fundoscopic examination was unremarkable. Potassium hydroxide and calcofluor white preparation showed no organisms. Gram stain was likewise negative. Corneal cultures grew 3+ Staphylococcus epidermidis.
The presence of conjunctival injection, anterior chamber reaction along with flap interface infiltrate, epithelial defect, possible dendrite, and stromal haze indicated possible mixed infectious keratitis and DLK. The patient was started on topical fortified vancomycin and tobramycin, acyclovir, and homatropine 5.0%. The following day, the patient presented with worsening corrected distance visual acuity (CDVA) of hand motions in the left eye. Fortified antibiotics and homatropine were discontinued, and topical steroids and moxifloxacin 0.5% (Vigamox) were started.
At 5 days, the CDVA in the left eye had improved to 20/200; however, the diffuse stromal haze showed limited improvement (Figure 1, C). A corneal flap lift and irrigation were performed using alcohol and moxifloxacin. The patient was instructed to continue topical steroids and moxifloxacin 0.5% every hour. The next day, he had residual corneal edema (Figure 1, D). At the 2-week postoperative visit, the CDVA was 20/20 in both eyes with a small corneal opacity and residual epithelial line in the left eye. The topical steroid treatment was tapered and moxifloxacin 0.5% discontinued.
The clinical signs of diffuse stromal haze and response to topical steroids in this patient are consistent with DLK. Diffuse lamellar keratitis is a rare complication of LASIK that usually presents in the immediate postoperative period, with relatively few cases of late-onset DLK being reported.5–9 Furthermore, foreign-body invasion of the LASIK flap interface is rare and is usually associated with obvious trauma.7,10,11 This, to our knowledge, is only the second reported case of an eyelash invading the LASIK flap12 and only the second reported case that presented 14 years or more after LASIK.5
We postulate that incidental trauma from eye rubbing allowed the introduction of an eyelash into the flap interface secondary to epithelial ingrowth, which likely triggered infectious keratitis and DLK. Because the eyelash was only partially in the flap interface, it kept the margin open allowing introduction of conjunctival microbes, forming a wick that allowed access to tears and flora. In addition, the epithelial ingrowth made the interface susceptible to dehiscence from eye rubbing. For large epithelial plaques, the surgical removal by the surgeon might be warranted.
Early recognition and treatment of DLK is vital to preserving vision in patients. Refloating the refloat and flap irrigation should be considered in cases in which visual acuity is affected or there is poor initial response to topical steroids or when progression to stage III DLK is anticipated.1,13 Adequate education about the long-term complications of LASIK might improve early identification of these cases and improve visual outcomes.
In conclusion, our case represents the rare combination of DLK presenting more than a decade after LASIK with foreign-body invasion of the flap interface without identifiable trauma.
None of the authors has a financial or proprietary interest in any material or method mentioned.
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