Retinal breaks: Authors’ reply

Letters to the Editor Norman Byer (Ophthalmology 1998; 105:1045–9), Drs. Folk and Boldt state that there were selected guidelines that might be useful to the clinician evaluating patients with retinal breaks. Their second guideline stated that “only operculated retinal holes in a patient with acute symptoms generally should be treated.” The authors imply that they have information supporting this concept or that such information existed in one of the three references that were provided. I am unaware of any report in the literature in which a documented operculated retinal hole, unassociated with a persistent vitreoretinal adhesion in the region of the break, such as on a nearby retinal vessel, was responsible for a subsequent clinical retinal detachment. References 1 and 3, which were provided by these authors, contain examples of these very unusual cases. Although I congratulate the authors on their attempt to summarize appropriately conservative guidelines for the management of retinal breaks, I believe they should provide more specific supportive evidence for the value of therapy in the management of symptomatic operculated retinal holes. C.P. WILKINSON, MD Baltimore, Maryland Authors’ reply Dear Editor: Everything that Dr. Wilkinson stated in his letter is fair and correct. Dr. Byer also took exception, prior to the publication of the Discussion, with our recommendation that operculated retinal holes in a patient with acute symptoms should be treated. We therefore put a lot of thought into these recommendations. The teaching at The University of Iowa for many years has been to carefully examine the retina around an operculated retinal break. Indeed, in patients who are symptomatic, there is often persistent vitreous traction around the break. We have treated a moderate number of patients over the years whose only and causative break for a retinal detachment was an operculated hole. We are not sure whether this operculated hole may have originally been a flap tear that caused the detachment and then became operculated, but it is hard to imagine that this was the pathogenesis in every case. We have also seen a few cases in which a symptomatic operculated hole was not treated and then the retina detached. We admit this is very uncommon. Part of our disagreement with Dr. Wilkinson may be that vitreous traction, like most biologic phenomena, exists on a continuum that resists being placed into defined boxes of “recommended treatments.” Certainly there are different types or appearances to operculated holes. On one extreme is the patient who had symptoms that then resolved and on examination has a hole in which the operculum rests on the PVD far above the retinal surface. We don’t treat these patients. On the other hand, there are also patients who continue to have symptoms, including photopsias, who on examination have an operculum that rests just off the retinal surface and appears to have restricted mobility as if tethered to the area around the hole by vitreous traction. There is also

often vitreous traction to the retina surrounding the hole. We are reluctant to not treat these patients, especially when the entire treatment consists of a few rows of laser spots placed under topical anesthesia. JAMES C. FOLK, MD H. CULVER BOLDT, MD Iowa City, Iowa

Cyclosporine and Neovascularization Dear Editor: We read with interest the article “Intravitreal Sustainedrelease Cyclosporine in the Treatment of Experimental Uveitis” by Jaffe GJ et al (Ophthalmology 1998; 105:46 –56). The authors commented on the suppression of corneal neovascularization by cyclosporine that they noted in their model and speculated as to the mechanism. We previously demonstrated the efficacy of cyclosporine in the suppression of experimentally induced corneal neovascularization in mice.1 It is our belief that cyclosporine acts via T-cell suppression to inhibit immunologically mediated neovascularization. Perhaps this would also explain the suppression of neovascularization noted in the model described by Jaffe and associates. RANDY J. EPSTEIN, MD ROBERT L. HENDRICKS, PHD RICHARD M. LIPMAN, MD Chicago, Illinois Reference 1. Lipman RM, Epstein RJ, Hendricks RL. Suppression of corneal neovascularization by cyclosporine. Arch Ophthalmol 1992;110:405–7.

Authors’ reply Dear Editor: In our model of uveitis, a subcutaneous tuberculin antigen was administered followed by an intravitreal tuberculin challenge approximately 2 weeks later. We believe that the tuberculin antigen initiates an immunologically driven inflammatory response followed by a secondary nonspecific inflammatory response composed of inflammatory cells and soluble inflammatory mediators (e.g., cytokines). Our study did not specifically address the mechanism by which cyclosporine caused corneal neovascularization to regress. However, we believe that the corneal neovascularization most likely resulted from the secondary nonspecific inflammatory response. Cyclosporine could inhibit neovascularization by suppressing the initiating immune-driven inflammatory response. Accordingly, corneal neovascularization is inhibited because the secondary nonspecific inflammatory response is eliminated. Epstein and associates made the interesting observation that systemic cyclosporine inhibited corneal neovascularization initiated by intrastromal IL-2 injection. Similarly, it is likely that cyclosporine inhibited corneal neovascularization induced by nonspecific T-cell inflammatory infiltrate caused by corneal alkali burns (RD Hawkins and associates, 1996, unpublished results). Epstein and colleagues speculated that cyclosporine suppressed T cells to

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