perpendicular to the laser (parallel to the ground)—and that there is no head tilt. Treatment of decentration with topography-guided technology may be effective.

Figure 6-3 Corneal topography findings of a decentered ablation. (Courtesy of Roger F. Steinert, MD.)

Corticosteroid-Induced Complications

The incidence of increased intraocular pressure (IOP) after surface ablation has been reported to range from 11% to 25%. Occasionally, the IOP may be quite high. In 1 study, 2% of patients had IOP greater than 40 mm Hg. The majority of cases of elevated IOP are associated with prolonged topical corticosteroid therapy. Accordingly, postoperative steroid-associated IOP elevations are more likely to occur after surface ablation (after which steroid therapy may be used 2–4 months to prevent postoperative corneal haze) or after complicated LASIK cases. Corticosteroid-induced elevated IOP occurs in 1.5%–3.0% of patients using fluorometholone but in up to 25% of patients using dexamethasone. The increase in IOP is usually controlled with topical IOP-lowering medications and typically normalizes after the corticosteroids are decreased or discontinued. Because of the changes in corneal curvature and/or corneal thickness, Goldmann tonometry readings after myopic surface ablation and LASIK are artifactually reduced (see Glaucoma After Refractive Surgery in Chapter 11). Several alternative techniques of measuring IOP have been suggested, but dynamic contour tonometry is the only technique shown to have sufficient reproducible accuracy in eyes after refractive ablation. Other corticosteroid-associated complications that have been reported after surface ablation are

herpes simplex virus keratitis, ptosis, and cataracts.

Central Toxic Keratopathy

Central toxic keratopathy is a rare, acute, noninflammatory central corneal opacification that can occur within days after uneventful LASIK or PRK (Fig 6-4). The etiology is unknown but may be related to enzymatic degradation of keratocytes.

Figure 6-4 Clinical photograph of central toxic keratopathy, a rare, acute, noninflammatory central corneal opacification that can occur within days after uneventful LASIK or photorefractive keratectomy (PRK). (Courtesy of Parag Majmudar, MD.)

Confocal microscopy has demonstrated activated keratocytes without inflammatory cells, with initial keratocyte loss from the stromal bed and gradual repopulation over time. Central toxic keratopathy has been reported to demonstrate anterior curvature flattening without alteration of posterior curvature in anterior segment tomography; however, some cases do appear to alter all tomographic findings, likely as measurement artifact. The onset is acute without worsening over time, unlike in most other interface entities.

Moshirfar M, Hazin R, Khalifa YM. Central toxic keratopathy. Curr Opin Ophthalmol. 2010; 21(4):274–279.

Thornton IL, Foulks GN, Eiferman RA. Confocal microscopy of central toxic keratopathy. Cornea. 2012;31(8):934–936.

Infectious Keratitis

Infectious keratitis may occur after surface ablation procedures or LASIK, as both types of surgery involve disturbance of the ocular surface, although infections are significantly more common after surface ablation. The risk of infection varies depending on the specific technique. The most common etiologic agents for these infections are gram-positive organisms, including Staphylococcus aureus, methicillin-resistant Staphylococcus aureus (MRSA), Streptococcus pneumoniae, and Streptococcus viridans. Although health care workers and others exposed in hospital and nursing home settings may be at greatest risk for MRSA infection, MRSA infections have been diagnosed in increasing numbers of cases without known risk factors. Atypical mycobacteria, Nocardia asteroides, and fungi have also been reported to cause infectious keratitis after surface ablation and LASIK (Fig 6-5).

Figure 6-5 Slit-beam image of Mycobacterium chelonae interface infection presenting 3 weeks after LASIK; this infection was initially treated as diffuse lamellar keratitis with topical corticosteroids. (Courtesy of Christopher J. Rapuano, MD.)

PRK and other surface ablation techniques involve creation of an iatrogenic corneal epithelial defect that may take 3–5 days to heal. During this time, the risk of postoperative infectious keratitis is greatest because of exposure of the stroma, use of a bandage contact lens, and administration of topical steroid drops, all of which increase the opportunity for eyelid and conjunctival bacterial flora to gain access to the stroma. Treatment of postoperative infectious keratitis consists of culture and sensitivity testing of contact lens and corneal scrapings and institution of appropriate intensive, topical, broad-spectrum antibiotic coverage, being cognizant of the higher prevalence of keratitis secondary to gram-positive organisms. Antibiotics may include a combination of the following:

fourth-generation fluoroquinolones, polymyxin B–trimethoprim, fortified vancomycin or cefazolin, and for tified tobramycin or gentamicin. Fungal keratitis can also occur, especially with concomitant corticosteroid use. With that in mind, cultures should include fungal assays, and treatment for keratitis should include antifungals in suspected cases.

During or shortly after LASIK, which involves creation of a corneal flap, eyelid and conjunctival flora may enter and remain sequestered under the flap. The antimicrobial components in the tears and in topically applied antibiotic drops have difficulty penetrating into the deep stroma to reach the organisms (Fig 6-6). If a post-LASIK infection is suspected, the flap should be lifted and the stromal bed scraped for culture and sensitivity testing. Intensive treatment with topical antibiotic drops, as described previously, should be started pending culture results. If there is lack of clinical progress, additional scrapings may be obtained, the flap may be amputated, and the antibiotic regimen altered.

Figure 6-6 Infectious keratitis in a LASIK flap after recurrent epithelial abrasion. (Courtesy of Jayne S. Weiss, MD.)

Llovet F, de Rojas V, Interlandi E, et al. Infectious keratitis in 204,586 LASIK procedures. Ophthalmology. 2010;117(3):232–238. Epub 2009 Dec 14. Moshirfar M, Welling JD, Feiz V, Holz H, Clinch TE. Infectious and noninfectious keratitis after laser in situ keratomileusis: occurrence, management, and

visual outcomes. J Cataract Refract Surg. 2007;33(3):474–483.

Mozayan A, Madu A, Channa P. Laser in-situ keratomileusis infection: review and update of current practices. Curr Opin Ophthalmol. 2011;22(4):233–237. Solomon R, Donnenfeld ED, Perry HD, et al. Methicillin-resistant Staphylococcus aureus infectious keratitis following refractive surgery. Am J Ophthalmol.

2007;143(4):629–634. Epub 2007 Feb 23.

Wroblewski KJ, Pasternak JF, Bower KS, et al. Infectious keratitis after photorefractive keratectomy in the United States Army and Navy. Ophthalmology. 2006;113(4):520–525. Epub 2006 Feb 17.