using corneal collagen cross-linking in the treatment of keratoconus
TRANSCRIPT
370 Optometry, Vol 82, No 6, June 2011
showed some improvement and the visual field defectresolved, he was educated that the likelihood of recurringoptic neuritis was significant and that separation from theU.S. military was mandatory.
Poster 55
Using Corneal Collagen Cross-Linking in the Treatmentof Keratoconus
Sachie Hase, O.D., and Punit Bhakta, Woolfson EyeInstitute, Atlanta, Georgia
Background: Keratoconus is a disorder that graduallydeteriorates the cornea’s optics and mechanical integrityby thinning and bulging, a process called ectasia. Findingnew treatment options to arrest ectasia is an area of currentand active ophthalmic research, and corneal collagen cross-linking is emerging as the procedure that can preventpatients from progressive vision loss from keratoconus aswell as a treatment for patients with post–laser-assisted insitu keratomileusis (LASIK) ectasia.Case Summary: A 42-year-old male with a history ofprogressive keratoconus presented with symptoms of glare,diplopia, and difficulty driving. He wore rigid gas perme-able (RGP) contact lenses to provide his best correctablevision of 20/32 O.D. and 20/50 O.S. After being qualifiedfor the Food and Drug Administration trial of cornealcollagen cross-linking, the procedure was performed withriboflavin 0.1% solution dosed as 1 drop every 2 minutesfor 30 minutes onto the exposed cornea surface. UltravioletA light at a wavelength of 365 nm was then applied to theexposed surface of the cornea for 30 minutes with addi-tional application of riboflavin every 2 minutes to ensureadequate saturation. Following the treatment, the patientwas placed on topical antibiotic, steroid, nonsteroidal anti-inflammatory drugs, and artificial tears, and therapeuticbandage contact lens to help with healing and comfort. Thepatient was followed closely with 1-day, 1-week, 1-month,6-month, and 1-year follow-up appointments. At the 2-yearfollow-up visit, his uncorrected visual acuities were 20/30O.D. and 20/40 O.S. The Pentacam and topography showedno progression of keratoconus over the preceding 2 yearsfollowing the cross-linking procedure. His refractive errordecreased by approximately 5 diopter spherical equivalentin his left eye. Although his right eye showed no decreasein refractive error, his best-corrected acuity improved.Conclusion: Keratoconus and post-LASIK keratoectasiacause visual symptoms with a decrease in the quality oflife, and sometimes requires corneal transplants to gainadequate vision. With the limited number of treatmentoptions for active keratoconus and no current options todecrease the risk of post-refractive ectasia in higher-riskpatients, corneal collagen cross-linking is likely to becomean attractive treatment option both therapeutically, andperhaps even prophylactically. Understanding cornealcross-linking will better serve patients who may benefitfrom this treatment.
Poster 56
Nutritional Optic Neuropathy as Result of Topiramate-Induced Appetite Suppression
Erica Ittner, O.D., Illinois College of Optometry/IllinoisEye Institute, Chicago, Illinois
Background: Topiramate is an anticonvulsive drug pre-scribed for seizure and migraine prevention. It has recentlybegun to be prescribed as a weight management option forobese patients due to its well-documented side effect ofweight loss secondary to reduced food intake. Opticneuropathy can be caused by a variety of nutritionaldeficiencies resulting in reduced mitochondrial adenosinetriphosphate (ATP) production in the retinal ganglion cellaxons of the papillomacular bundle of the optic nerve. Thisis the first reported case of nutritional optic neuropathycaused by topiramate induced appetite suppression.Case Summary: A 59-year-old black woman presented withsymptoms of bilateral, painless, progressive decreasedvision loss of 4 months duration. Her medical history wassignificant for partial complex epilepsy, which was beingtreated with levetiracetam and topiramate. She had recentlylost a significant amount of weight due to topiramateinduced appetite suppression. Best-corrected visual acuitieswere 20/200 O.D. and 20/400 O.S. External examination,slit lamp examination, ocular motility, and pupil testingwere normal. Fundus examination revealed mild temporalpallor of the optic nerve head of the left eye. Visual fieldtesting noted scattered field defects in each eye. Systemicblood work revealed reduced vitamin B12, folate, andthiamine levels. The patient was treated with a vitamininjection and daily oral vitamin B12, folate, and thiamine.Following treatment, optic nerve head pallor of the left eyeremained unchanged; vision has remained stable at 20/120O.D. and 20/160 O.S.Conclusion: Toxic optic neuropathy secondary to nutri-tional deficiencies can occur in any patient with a reducedappetite. Topiramate use should prompt queries as to recenteating habits or weight loss. Patients should be encouragedto continue regular comprehensive eye examinations and toreport side effects of the medication to their primary carephysician in order to minimize their risk of permanentvision loss.
Poster 57
Chiari I Malformation Presenting as AsymptomaticPapilledema
Erica Ittner, O.D., Wendy Stone, O.D., andBruce Teitelbaum, O.D., Illinois College of Optometry/Illinois Eye Institute, Chicago, Illinois
Background: Chiari I malformation is a congenital brainabnormality with variable presentation. Papilledema is anuncommon ophthalmic complication, which can developsecondary to the tonsilar herniation causing increasedintracranial pressure. This case is significant because it is