EyeWorld is the official news magazine of the American Society of Cataract & Refractive Surgery.
Issue link: https://digital.eyeworld.org/i/422211
EW CATARACT 22 December 2014 by Steven G. Safran, MD toxic keratopathy (CTK). While most commonly seen after LASIK, Maloney et al reported several after PRK. 1 Etiology unknown, not particularly inflammatory, steroids tend not to help much. "Having said that, I'd still treat with steroids in case there is some inflammatory component, although I'm not sure how much good they do. Then I'd wait. The haze tends to improve, as does the central flat- tening/induced hyperopia. It may take 6–12 months, but it usually improves significantly." nomogram, use topical intraoper- ative mitomycin, and follow very closely postoperatively." My thought process was very similar to Dr. Doane's. I have seen haze and thinning develop in corneas but never so quickly. I was concerned about the possibility of infection at first but ruled that out and decided not to pursue that path. I had the feeling that something different and unique was at play here given that both eyes looked so similar and things had developed so quickly. Dr. Rapuano said: "I think this a form of what has been called central D r. Doane commented: "I have never seen a case where there was normal re-epithelialization in 3–5 days that went on to have haze like this patient. I have, on the other hand, seen personal patients and cases in consultation that had delayed healing greater than 7 days with maximum of up to 5–6 weeks that did result in subepithelial haze. None of these cases had confirmed bacterial infection, and I never suspected bacterial infection, yet treated them with broad-spectrum coverage. In all of these cases I felt it was an inflammatory reaction with collagenolytic activity with thinning of stroma and subsequent new colla- gen deposition with haze formation. Invariably these cases have induced hyperopic astigmatism from target with both regular and irregular components of astigmatism. "The best corrected vision loss is due to opacity and irregular sur- face. The quantification of irregular astigmatism best vision loss can be determined by rigid gas permeable (RGP) over refraction. The lost lines of best vision with RGP in place are due to opacity. In cases like this I would always be reminded to check corneal sensation and never forget underlying undiagnosed herpetic eye disease. So what to do in this case of tissue loss and corneal haze after PRK? From my perspective, do not surgically intervene too soon. I would slowly taper the topical corticosteroid. I would postpone any further surgery for as long as possible (i.e., 9–12 months). Many cases can resolve to tolerable but not perfect. My apprehension for further treatment is some of these cases will confirm 'the enemy of good is better' in that the typical nomogram for refraction obtained does not get the patient to plano sphere, and the uncorrected vision can be worse than prior to the second surgery. Additionally, some patients are apprehensive with additional surgery as their first experience was not ideal. If I did have to treat, I would treat with extreme caution, likely undertreat from my normal When PRK becomes a 4-letter word Figures 1 and 2. OD and OS on day 4 after both eyes have completely epithelialized and the contact lenses have been removed. The eyes are white and quiet, but there is central haze with thinning in both corneas. Figures 3 and 4. Anterior segment OCT images of OD and OS taken on day 5 postop. Note stromal thinning and opacification associated with compensatory epithelial hyperplasia. continued on page 24 Anterior segment grand rounds December 2014 T his is a case of a 24-year-old male who had PRK for 5.5 D of myopia OD and 6.0 D OS. He had no significant ocular surface issues, no systemic disease and was on no systemic medication. CustomVue PRK with a VISX S4 (Abbott Medical Optics, Abbott Park, Ill.) was performed after alcohol-assisted removal of the epithelium. Mitomycin-C 0.2 mg/ml was used for 20 seconds OU topically. He was placed on a regimen of topical steroids (prednisolone acetate 1%) QID, topical nonsteroidal (bromfenac) BID, and topical antibiotics (moxifloxacin) QID with frequent lubrication with bandage contact lenses placed OU. On day 1 he seemed to be healing nicely with about a 40–50% reduction in the surface area of his epithelial defect, and his bandage contact lenses were changed for new ones. I kept in touch with him by phone over the weekend. He was seen 3 days later, and I removed the contact lenses. Although he was completely epithelialized without any fluorescein staining of the cornea, he was found to have significant central subepithelial haze/ opacification and thinning of the cornea with decreased vision. Uncorrected vision was 20/40 minus in each eye and did not improve with refraction. Figures 1 and 2 are slit lamp images of the cornea OD and OS. Note the complete epithelialization in the quiet eye with central haze. Although cornea haze and thinning can develop with prolonged course of healing due to exposure, ocular surface disease, or neurotrophic issues, none of those problems were present in this case. This patient had normal sensation, a white and quiet eye OU, and no staining or ocular surface issues. I presented this case to John Doane, MD, Christopher Rapuano, MD, Parag Majmudar, MD, and Robert Maloney, MD, for comments. Steven G. Safran, MD, ASGR editor