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1 General aspects (0)   1.1 Epidemiology (2)   1.2 Population genetics (1)   1.3 Pathogenesis (0)   1.4 Quality of life (4)   1.5 Glaucomas as cause of blindness (0)   1.6 Prevention and screening (3) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (0)   2.2 Cornea (3)   2.3 Sclera (0)   2.4 Anterior chamber angle (1)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (10)     2.5.2 Schlemms canal (0)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (1)     2.6.1 Production (0)     2.6.2 Outflow (1)       2.6.2.1 Trabecular meshwork (0)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (2)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (0)   2.9 Ciliary body (0)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (0)   2.13 Retina and retinal nerve fibre layer (12)   2.14 Optic disc (9)   2.15 Optic nerve (4)   2.16 Chiasma and retrochiasmal central nervous system (2)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (5)   3.1 Microscopy (0)   3.2 Electron microscopy (2)   3.3 Immunohistochemistry (3)   3.4 Molecular genetics (1)     3.4.1 Linkage studies (9)     3.4.2 Gene studies (5)   3.5 Molecular biology incl. 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with intraocular tumors (0)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (0)       9.4.10 Glaucomas associated with hemorrhage (0)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (1)       9.4.11.2 Glaucomas in aphakia and pseudophakia (0)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (2)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (0)     9.4.15 Glaucoma in relation to systemic disease (9)     9.4.20 Other (0) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (3) 11 Medical treatment (0)   11.1 General management, indication (9)   11.2 Cholinergic drugs (1)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (0)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (5)     11.3.4 Betablocker (10)     11.3.5 Other (0)   11.4 Prostaglandins (28)   11.5 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Without tube implant (4)     12.8.2 With tube implant or other drainage devices (11)     12.8.3 Non-perforating (11)     12.8.4 Using laser (0)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (9)     12.8.11 Complications, endophthalmitis (10)   12.9 Trabeculotomy, goniotomy (3)   12.10 Cyclodestruction (8)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (1)     12.12.3 Phacoemulsification (5)   12.14 Combined cataract extraction and glaucoma surgery (1)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (3)   12.15 Capsulotomy (1)   12.16 Vitrectomy (1)   12.17 Anesthesia (1)   12.20 Other (2) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (0)   13.2 Outcome (0)     13.2.1 IOP (0)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (2) 15 Miscellaneous (3)

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Abstract #10580 Published in IGR 6-2

Cystoid macular edema in a low-risk patient after switching from latanoprost to bimatoprost

Carrillo MM; Nicolela MT
American Journal of Ophthalmology 2004; 137: 966-8

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PURPOSE: To report a case of angiographically documented cystoid macula edema occurring after switching a pseudophakic patient from latanoprost to bimatoprost. DESIGN: Observational case report. METHODS: A 68-year-old man developed intense conjunctival hyperemia and cystoid macula edema after switching from latanoprost to bimatoprost 9 months after cataract surgery in an eye at low-risk for this cystoid macular edema. RESULTS: Bimatoprost was discontinued and diclofenac initiated. After 2 months, visual acuity and ocular hyperemia returned to baseline levels. Fundus examination revealed resolution of cystoid macula edema. CONCLUSION: It is possible that pseudophakic eyes that develop intense conjunctival hyperemia associated with ocular hypotensive lipids might be at higher risk for developing cystoid macula edema.

Department of Ophthalmology, Dalhousie University, 1278 Tower Road, Halifax, Nova Scotia B3H 2Y9, Canada.

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Classification:

11.4 Prostaglandins (Part of: 11 Medical treatment)

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