Excimer laser photorefractive keratectomy is becoming an increasingly popular method to treat ametropia. The main issue regarding the safety of this procedure has been the postoperative loss of best-corrected visual acuity from various origins, including irregular astigmatism, corneal scarring, and decentered ablations.1 Infection following photorefractive keratectomy is rare; at least 7 patients developed infectious keratitis following excimer laser keratectomy, which in one case progressed to severe endophthalmitis.1,2 We report Staphylococcus aureus keratitis in the early postoperative period following photorefractive keratectomy with the development of severe degenerative keratopathy.
A 27-year-old man was seen for a corneal ulcer in the left eye that had developed 2 days following an uncomplicated photorefractive keratectomy to correct high myopia. A bandage contact lens was placed over the eye that also was treated with topical trimethoprim sulfate–polymyxin B sulfate, fluorometholone, and ketorolac tromethamine. One day postoperatively, the cornea was clear and there was a mild anterior chamber reaction. On the second postoperative day, there was a corneal infiltrate with hypopyon (Figure 1, left). Corneal cultures grew S aureus. The left cornea was treated with topical fortified ciprofloxacin and cefazolin eye drops every half hour and homatropine hydrobromide eye drops twice daily. The hypopyon resolved within 4 days. The ulcer slowly healed during the next 2 months with partial clearing of the central opacity thereafter. Fifteen months later, a chalazion developed in the right upper eyelid from which S aureus was cultured, suggesting that the patient was a carrier of this microorganism. The pinhole visual acuity was 20/100 OS. A substantial ringlike central stromal scar associated with stromal thinning was present (Figure 1, right). Four months later, a penetrating keratoplasty was performed; the graft remained clear 12 months postoperatively.
Left, Two days postoperatively, the cornea shows a ragged, ulcerated appearance in the central treated area with increased opacification around the margin and a hypopyon (H) inferiorly. Right, Nine months later, there is persistent opacification of the treated area, but no evidence of inflammation.
Histopathologic examination of the corneal button revealed several large clusters of eosinophilic material containing occasional cholesterol clefts within the superficial half of the central stroma (Figure 2). These deposits exhibited congophilia with apple-green birefringence and stained positive for amyloid protein by immunohistochemistry and for glycosaminoglycans with the colloidal iron and alcian blue stains (Figure 2). Furthermore, electron microscopy showed clusters of nonbranching fibrils 10 nm in diameter consistent with amyloid. Otherwise, there was irregular thickening of the epithelium of the central cornea overlying an absent Bowman membrane, superficial stromal scarring, and mild endothelial attenuation.
Top, Multiple superficial stromal deposits stain positive with Congo red (original magnification ×250). Bottom, The congophilic material shows apple-green birefringence with polarized light (arrows) in contrast to the normal white birefringence of the collagen lamellae (Congo red, original magnification ×250). Left inset, The deposits also stain positive for glycosaminoglycans (colloidal iron, original magnification ×250). Right inset, Several cholesterol clefts are noted within some of the deposits in adjacent areas (hematoxylin-eosin, original magnification ×250).
The cause of postphotorefractive keratectomy corneal infiltrates may be infectious, toxic, hypersensitivity, or a combination of these processes. An infectious corneal ulcer is a rare but potentially devastating complication of photorefractive keratectomy that may lead to endophthalmitis and to substantial scarring, requiring penetrating keratoplasty, as in our case. Although a rare complication of photorefractive keratectomy, infectious keratitis is of concern, especially since bilateral photorefractive keratectomy is performed frequently in the same surgical intervention.
Our case is an example of secondary amyloid, lipid, and glycosaminoglycan degeneration of the cornea. Amyloid and lipid corneal degenerations are not uncommon sequelae of both infectious and traumatic keratopathies. Glycosaminoglycan deposition has been described as a component of subepithelial opacities following excimer laser photorefractive keratectomy in both human and rabbit corneas3,4 and may be responsible for the late haze following photorefractive keratectomy.5
We thank Merrill D. Benson, MD, professor and chairman, Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, for performing the immunohistochemical stains for amyloid protein.
Corresponding author: Seymour Brownstein, MD, University of Ottawa Eye Institute, 501 Smyth Rd, Room 3818, Ottawa, Ontario, Canada K1H 8L6.
Hill VE, Brownstein S, Jackson WB, Mintsioulis G. Infectious Keratopathy Complicating Photorefractive Keratectomy. Arch Ophthalmol. 1998;116(10):1382–1384. doi: