Inferior S hield Ulcers In Atopic Keratoconjunctivitis

1. Inferior Shield Ulcers In Atopic Keratoconjunctivitis A Loh, PY Boey & RS Loh Singapore National Eye Centre World Cornea Congress VI Boston, Massachusetts, April 7-9, 2010 The authors have no financial interests in the subject matter of this poster

2. Introduction • Atopic keratoconjunctivitis (AKC) is a bilateral, chronic inflammation of the conjunctiva and lids associated with atopic dermatitis • There is a male preponderance, with the onset of disease typically in the second to fifth decade • The major symptom is ocular itching which may be seasonal or perennial • Signs include • Lids eczema, blepharitis, meibomianitis & tarsal margin keratinization • Conjunctiva sub-epithelial fibrosis, symblepharon, fornix shortening & giant papillae • Cornea superficial punctate keratitis, neovascularization & persistent epithelial defects • Shield ulcers, as defined as an epithelial defect with intact Bowman’s membrane and an overlying fibrin/mucous plaque, occurring in the superior half of the corneal surface is classically associated with Vernal keratoconjunctivitis (VKC) • In this study we report the incidence of four cases of inferior shield ulcers occurring in atopic keratoconjunctivitis

3. Materials & Methods • IRB review board approval • Retrospective case series in one centre, CGH, from 01/01/05 to 30/12/08 • The diagnosis was based on the history and presentation of ocular surface/corneal findings • The following were assessed - Risk factors - Atopic dermatitis Asthma Allergic rhinitis Examination - Snellen visual acuity Slit-lamp examination Goldman tonometry

4. Results • 27 patients (24 bilateral) with allergic ocular disease were identified in the 4 year study period • AKC was present in 19 of these 27 patients (16 bilateral disease) • Age at onset ranged from 10 to 30 years (mean 18.4 years, median 18). with a male:female ratio of 4.75:1 (females n=4, 21.1%). • Racial preponderance - • Chinese 74.9% (n=15) • Malay 25.1% (n=4) • Follow-up period ranged from 4 to 72 months (median 4 weeks) • Average recurrence rate was 1 per 4.7 months • Number of recurrences ranged from 0 to 5 (median 2)

5. Results • Pre-existing disease at presentation • Asthma 36.8% (n=7) • Eczema 63.2% (n=12) • Allergic rhinitis 42.1% (n=8) • Family history of atopic disease was present in 31.6% (n=6) • Symptoms on presentation • Itch and redness were present in all patients • Mucoid discharge 73.7% (n=14) • Watering 84.2% (n=16)

6. Results • Visual acuity (VA) • Best corrected VA (BCVA) ranged from 20/20 to 20/120 (median 20/30) with final VA on resolution of 20/20 or better. There was no loss in lines of BCVA. • Minimum BCVA ranged from 20/20 to 20/200 (median 20/40) • Slitlamp findings were as follows • Giant papillae 68.4% (n=13) • Limbal follicles 31.6% (n=6) • Shield ulcers 31.6% (n=6) • Corneal scars 26.3% (n=5) • Treatment • All patients were treated with topical mast cell stabilizer/anti-histamine (eg. G Olopatadine 0.1%) and topical steroids (eg. Fluoromethalone 0.5%, Dexamethasone 0.3% and Prednisolone Acetate 1.0%) • Six patients (31.6%) required topical Cyclosporine A (CSA) 0.5% for long term control • There was no incidence of secondary cataract or glaucoma

7. Results • Inferior shield ulcers occurred in 4 patients (21%). This was present in all cases in the left eye, with one having coincident upper shield ulcer in the fellow eye • All patients were males, 3 were of Chinese and 1 of Malay racial origin. Age at presentation ranged from 12 to 19 years • Pre-existing asthma, atopic disease and/or eczema was present in 3 patients • Bilateral disease was present in 3 patients • BCVA was 20/40 to 20/120 at presentation improving to 20/20 in all cases with treatment. All shield ulcers resolved within 4 weeks using a combination of topical Olopatadine 0.1% and Prednisolone Acetate 1.0%. Three patients required topical CSA 0.5% as maintenance therapy • Giant papillae were present in 3 patients, with limbal follicles in one

8. Fig 1. Clinical patterns of inferior shield ulcersa & b – inferior shield with mucous plaque c & d – mucous plaque removed – epithelial defect revealed Fig 1a Fig 1b Fig 1c Fig 1d

9. Fig 2. Other featuresa – inferior pseudogerontoxon b – limbal follicles and meibomiatis c & d – early superior shield ulcer with inferior corneal scar from healed inferior shield ulcer Fig 2a Fig 2b Fig 2d Fig 2c

10. Discussion • This study demonstrates that inferior shield ulcers can occur in atopic eye disease • The pathogenesis of inferior shield ulcers in VKC has been previously described by Buckley • Inferior shield ulcers in AKC may be due to a combination of keratinization of the lid margins, meibomianitis and late presentation for treatment • Visual prognosis in this study group is good • The response to topical anti-histamine/mast cell stabilizers and steroid therapy combination was good although maintenance therapy with topical CSA 0.5% was required in 31% (n=6) of cases. This may partly explain the absence of secondary glaucoma References • Buckley RJ. Vernal keratoconjunctivitis. Int Ophthalmol Clin 1988 28:303-308 • Tuft SJ, Kemeny DM, Dart JK et al. Clinical features of atopic keratoconjunctivitis. Ophthalmology. 1991 Feb;98(2):150-85 • Foster CS, Calonge M. Atopic keratoconjunctivitis. Ophthalmology. 1990 Aug;97(8):992-1000 • Hingorani M, Moodaley L, Calder VL et al. A randomized placebo controlled trial of topical cyclosporin A in steroid-dependent atopic keratoconjunctivitis. Ophthalmology. 1998 Sept;105(9):1715-20 • Anzaaf F, Gallagher MJ, Bhat P et al. Use of systemic T-lymphocyte signal transduction inhibitors in the treatment of atopic keratoconjunctivitis. Cornea 2008 Sep;27(8):884-8