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Terrien’s Marginal Degeneration: Clinical Characteristics and Outcomes
Randall Ulate, MD (Presenting Author); Yakov Goldich, MD; Mauricio A. Perez, MD; David S. Rootman, MD, FRCSC; Clara C. Chan, MD, FRCSC; Mario J. Saldanha, FRCS, FRCOphth The authors have no financial interest to disclosure
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PURPOSE To describe clinical characteristics of patients with Terrien’s marginal degeneration (TMD). METHODS: DESIGN: Retrospective case series. Database search of patients with Terrien’s marginal degeneration was conducted. The charts of 25 patients (43 eyes) seen over 10 years ( ) at a specialty cornea clinic at the Toronto Western Hospital were reviewed. Outcome measures included patient demographics, location and laterality of disease, topographical astigmatism, visual acuity, coexisting ocular disease, and surgical treatment.
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Terrien’s Marginal Degeneration
Clinical hallmarks of TMD include ectasia and furrowing of the peripheral cornea with associated lipid deposition, and vascularization. Initial findings present as fine, white-yellow punctate stromal opacification that appear similar to arcus senilis. Subsequent stromal thinning is heralded by the formation of a circumferential, gutter-like cavitation parallel to the limbus. In later stages, lipid deposition, visible as a solid white line, develops along the anterior edge. This leading edge is steeply sloped, in contrast to the gradual slope of the posterior lip. Vascularization stems radially from the limbus, and is located within the anterior stroma. An area of clear cornea can often be visualized between the leading edge of the gutter and the limbus. Pseudopterygia, at positions other than 3 o’clock and 9 o’clock, grow obliquely onto the cornea in approximately 20% of Terrien’s case. These pseudopterygia are thought to be characteristic of TMD, and may occur in the earlier stages of disease, before marked thinning. TMD typically presents bilaterally but can be very asymmetric between the two eyes. The superior cornea is primarily affected, but as the disease progresses, inferior cornea can also be involved.
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Thinning of the peripheral cornea, vascularization and lipid deposition
Intrastromal cyst
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Bilateral Terrien’s marginal degeneration
Advanced disease: Severe vascularization Lipid deposition Severe thinning with spontaneous content perforation
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RESULTS Mean patient age at presentation was 44 years (range, 9 to 82 years) and 14 patients (54%) were male. 18 patients (72%) had bilateral disease. Mean follow up was 30.3 months (range, 0 to 114 months). Mean astigmatism by topography was -5.3 diopters at 85 degrees (range, 0D to -11.3D). Mean acuity at presentation was 20/46 (0.36 logMAR) and 20/48 (0.38 logMAR) at last follow-up. Eyes requiring surgery (18.9%) had mean acuity of 0.71 logMAR at presentation and 0.72 logMAR after surgery. Eyes that perforated (11.6%) had mean acuity of 20/58 (0.46 logMAR) at presentation and decreased to mean 20/87 (0.64 logMAR) after perforation. Three eyes presented with pseudopterygium at oblique angles. Two eyes had intracorneal cysts. Fourteen patients (56%) had ocular inflammation. Ten patients (40%) had Meibomian gland dysfunction and five (20%) patients had rosacea.
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CONCLUSION Terrien’s marginal degeneration is a slow progressing, bilateral, asymmetric, degeneration of the peripheral cornea. Men over the age of 40 are more commonly affected. Stromal thinning, vascularization, lipid deposition, in addition to against-the-rule astigmatism are classic signs. TMD is typically non-inflammatory, but a variant form characterized by prominent inflammation does exist. Surgery (full thickness or lamellar graft) can preserve vision and corneal integrity. Surgery is indicated when conventional options (glasses, contact lenses) fail to maintain vision or if perforation is imminent. Perforations are rare, but can result in significant vision loss; ophthalmologists are reminded to educate patients on proper protection
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