Keratitis can be a serious complication of laser in situ keratomileusis (LASIK). We present a case in which post-LASIK keratitis appeared to be a reactivation of adenoviral keratoconjunctivitis.
A healthy 51-year-old man who had a history of adenoviral keratoconjunctivitis had LASIK to correct high myopic errors of −13.00 diopters (D) in the right eye and −14.00 D in the left eye. The best corrected visual acuity (BCVA) was 20/20 in both eyes. The preoperative corneal thickness was 520 μm in the right eye and 523 μm in the left eye. In December 1999, the patient reported acute tearing, a foreign-body sensation, and mucoid discharge in the right eye. He developed lid edema, chemosis, conjunctival hyperemia, mild follicular reaction, and preauricular adenopathy. The left eye was completely normal. The intracytoplasmic basophilic inclusion body was not seen in Giemsa staining of the conjunctival scraping. Adenovirus was not isolated in this case because of the difficulty of isolation and culture techniques. The clinical findings were consistent with an adenoviral infection. A treatment regimen was quickly begun, and the symptoms and findings resolved.
At the last examination before LASIK, there was no abnormal finding. In March 2000, LASIK was performed in the right eye with the Aesculap Meditec MEL 60 excimer laser after a nasally hinged corneal flap was made with the Eye Tech microkeratome. The procedure was uneventful.
On the first postoperative day, minimal conjunctival hyperemia and multiple subepithelial infiltrations consistent with adenoviral keratoconjunctivitis were seen inside the flap region only, not in the peripheral cornea (Figure 1). No other findings were noted. Dexamethasone 0.1% was started topically every 3 hours in addition to antimicrobial treatment. After 14 days, all the lesions in the flap were completely resolved (Figure 2). The treatment was completed in 1 month.
One week postoperatively, a single subepithelial corneal infiltration was noticed in the left eye. The same topical treatment was started in that eye. Laser in situ keratomileusis was delayed because of the active corneal infiltration. The corticosteroid dosage was tapered, and LASIK was performed 1 month later, when the steroid was administered 3 times daily. The patient was treated with a similar postoperative regimen. No reactivation findings were seen after LASIK.
At the last examination, 6 months postoperatively, no active adenovirus keratitis findings were seen in either eye. The BCVA was 20/100 with +0.75 −3.25 × 10 in the right eye and 20/32 with +2.50 +1.25 × 55 in the left eye. The BCVA line loss was thought to be the result of inferior decentralization and macular Fuchs'-like lesions in the right eye and overcorrection in the left eye (Figure 3). The corneal thickness was 391 μm in both eyes.
Post-LASIK keratitis is a serious complication, but a good visual outcome can be achieved following prompt and appropriate treatment. Keratitis in the early postoperative period includes diffuse lamellar keratitis (sands of Sahara syndrome), sterile peripheral keratitis,1 and microbial keratitis.2 The organisms that have been isolated include viral agents,7–9Streptococcus pneumoniae,3Mycobacterium chelonae,4Staphylococcus aureus,5 and Nocardia asteroides.6 In our patient, subepithelial opacities were seen early postoperatively. We thought it was a reactivation of adenoviral keratitis because of the patient's history. Other types of virus, for example Epstein-Barr virus, might produce similar subepithelial opacities, but the absence of systemic symptoms of infectious mononucleosis suggests a greater likelihood of adenovirus being the original infecting agent.7 A recurrence of active herpes simplex keratitis after phototherapeutic keratectomy leading to subepithelial opacities has been reported. This is postulated to result from viral reactivation after exposure to the ultraviolet wavelengths of the excimer laser.9
Although no viral agents were isolated in our case, the clinical findings were consistent with adenoviral infection.10 Adenovirus stromal keratitis is thought to represent a delayed hypersensitivity immune response to viral antigens in the corneal stroma.11 Phototherapeutic keratectomy has been used to treat adenovirus-induced subepithelial corneal opacities.12,13 As reported in a patient with adenoviral keratoconjunctivitis and myopia, PRK has the potential to eliminate central subepithelial corneal opacities and prevent recurrent keratitis within the treated area.11 Excimer laser keratectomy in each eye has removed all central subepithelial corneal opacities and has prevented further inflammation within the treatment zone, suggesting that the source of adenovirus-induced subepithelial infiltration may reside within the postinfectious corneal stroma.
In patients with adenovirus keratitis and high myopia, care should be taken while performing LASIK because of the potential to reactivate the adenoviral infection. As subepithelial opacities were not removed while the partial-thickness corneal flap was created with the microkeratome and the corneal stroma was ablated, the reaction to viral antigens in the operating area can be reactivated. In our patient, subepithelial opacities were located in the treatment area; the peripheral cornea was normal. Although the reactivation of adenoviral keratitis was thought to be due to the LASIK procedure, the reactivation might have occurred without surgery; for example, in any stressful situation.
In conclusion, LASIK successfully corrected high myopia, but unlike with the PRK procedure, the adenoviral keratoconjunctivitis might have been reactivated after LASIK despite the absence of symptomatic and clinical findings before the procedure.
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