The postoperative course of a patient who underwent retinal detachment repair using perfluoro-n-octane (PFO) and perfluoropropane (C3F8) gas endotamponade is described in which midlenticular optic opacification of a hydrophobic acrylic intraocular lens was noted. Mechanisms for optic opacification are proposed, which include dystrophic calcification and PFO-induced optic degeneration. The case presents a novel case of midlenticular intraocular lens optic opacification in the setting of retained perfluorocarbon liquid following retinal detachment repair.
Midlenticular Optic Opacification af a Hydrophobic Acrylic Intraocular Lens in Association with Retained Perfluorocarbon Liquid Following Vitreoretinal Surgery
From the Department of Ophthalmology and Jules Stein Eye Institute, University of California, Los Angeles, California.
Supported by the Frederic G. Rappaport Fellowship Award to Scott C. N. Oliver, MD.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Christine R. Gonzales, MD, Jules Stein Eye Institute and Department of Ophthalmology, David Geffen School of Medicine at UCLA, 100 Stein Plaza, Los Angeles, CA 90095-7000.
Accepted: January 13, 2009
Posted Online: March 09, 2010
Post operative opacification of intraocular lenses (IOLs) has been reported in a variety of clinical settings and with various IOL types.1 In most cases, IOL opacification occurs on the anterior and posterior optic surfaces. Optic opacification following vitreoretinal surgery has been reported once previously,2 however to our knowledge there have been no cases reported in the Medline-indexed English literature of midlenticular optic opacification in single-piece AcrySof acrylic (SA60AT, Alcon) IOLs. We present a case of midlenticular optic opacification of a single-piece hydrophobic acrylic IOL in the setting of retained perfluorocarbon liquid following retinal detachment surgery.
A 57-year-old man with an AcySof acrylic SA60AT IOL and a prior history of retinal detachment repair with vitrectomy, scleral buckle encirclement, and perfluoropropane (C3F8) gas endotamponade presented 18 months postoperatively with a recurrent rhegmatogenous retinal detachment. He underwent 25-gauge pars plana vitrectomy using perfluoro-n-octane (PFO), air-fluid exchange and 14% C3F8 gas tamponade. One week after surgery, a non-buoyant fluid bubble thought to be PFO was noted to fill 75% of the anterior chamber. Anterior chamber paracentesis was performed on postoperative weeks 1 and 2 to remove the retained PFO. Anterior segment examination at postoperative week 4 revealed numerous small, white, crystalline midlenticular optic opacities in the IOL (Fig. 1) and a collection of emulsified PFO bubbles in the inferior anterior chamber. The lenticular opacities were unchanged at postoperative month 3 and no residual PFO was noted in the anterior chamber.
Figure 1. Anterior Segment Photograph Demonstrating Small White, Crystalline Opacities (white Arrow) Within the Substance of the Hydrophobic Acrylic Intraocular Lens Optic Associated with Retained Perfluorocarbon Liquid Following Vitreoretinal Surgery. The Larger Brown Pigment Opacities (arrowhead) are Located on the Anterior and Posterior Optic Surfaces.
To our knowledge, postoperative IOL midlenticular optic opacification has not been reported in hydrophobic acrylic SA60AT IOLs. Surface optic opacification following vitreoretinal surgery with this type of IOL has been reported, in which an unknown proteinaceous deposit was identified on IOL removal and postulated to be related to the postoperative presence of suspended hemocyte components.2 However, postoperative vitreous or anterior segment hemorrhage did not occur in our patient. Optic opacification caused by hydroxyapatite deposition has been reported with hydrophilic IOLs (SB60B-OUV, MDR Inc.) however these opacities generally occur 12 to 24 months after implantation.3
A number of mechanisms may explain the opacification noted in this case. One possibility is that the retained PFO catalyzed dystrophic calcification within the optic, although such a degenerative process would be unusual over the short timeframe of this case. Intraoperative and postoperative medications, such as topical steroids and beta-blockers, and those containing phosphorous compounds, such as some glaucoma medications, have been hypothesized to promote IOL opacification.4 This is unlikely in our case since no special intraoperative medications were used and the patient’s routine post-operative medications were rapidly tapered. Diabetes has also been suggested as a risk factor for IOL opacification,5 however our patient had no known history of diabetes. A final potential mechanism is that the retained PFO penetrated the substance of the optic, promoting degeneration of the optic material.
To our knowledge, this is the first reported case of midlenticular optic opacification of a hydrophobic acrylic IOL. The development of this complication in the setting of retained PFO suggests a potential role of PFO in premature IOL opacification. Should IOL removal become necessary in this patient, histopathologic and spectroscopic analysis of the IOL may aid in determining the nature of the lens opacities.
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