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1 General aspects (0)   1.1 Epidemiology (10)   1.2 Population genetics (0)   1.3 Pathogenesis (0)   1.4 Quality of life (5)   1.5 Glaucomas as cause of blindness (6)   1.6 Prevention and screening (5) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (7)   2.2 Cornea (15)   2.3 Sclera (4)   2.4 Anterior chamber angle (1)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (3)     2.5.2 Schlemms canal (0)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (2)       2.6.2.1 Trabecular meshwork (1)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (4)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (0)   2.9 Ciliary body (1)   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 (14)   2.14 Optic disc (21)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (0)   2.17 Stem cells (1)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (0)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (1)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (2)     3.4.2 Gene studies (19)   3.5 Molecular biology incl. 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with intraocular tumors (4)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (0)       9.4.10 Glaucomas associated with hemorrhage (1)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (2)       9.4.11.2 Glaucomas in aphakia and pseudophakia (8)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (2)       9.4.11.4 Glaucomas associated with corneal surgery (4)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (0)     9.4.15 Glaucoma in relation to systemic disease (17)     9.4.20 Other (1) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (3) 11 Medical treatment (0)   11.1 General management, indication (8)   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 (3)     11.3.4 Betablocker (7)     11.3.5 Other (0)   11.4 Prostaglandins (16)   11.5 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Without tube implant (8)     12.8.2 With tube implant or other drainage devices (13)     12.8.3 Non-perforating (5)     12.8.4 Using laser (0)     12.8.5 Other (1)     12.8.10 Woundhealing antifibrosis (15)     12.8.11 Complications, endophthalmitis (9)   12.9 Trabeculotomy, goniotomy (0)   12.10 Cyclodestruction (2)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (5)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (1)     12.14.3 Phacoemulsification (8)   12.15 Capsulotomy (0)   12.16 Vitrectomy (0)   12.17 Anesthesia (1)   12.20 Other (4) 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 (7) 15 Miscellaneous (19)

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Abstract #24463 Published in IGR 11-3

Efficacy of topic ocular hipotensive agents after posterior capsulotomy

Minello AA; Prata Junior JA; Mello PA
Arquivos Brasileiros de Oftalmologia 2008; 71: 706-710

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PURPOSE: To analyze and compare the effects on intraocular pressure (IOP) of several topic hypotensive agents after posterior capsulotomy with Nd:YAG laser in non glaucoma patients. METHODS: 145 pseudophakic eyes underwent to Nd:YAG laser posterior capsulotomy. Before capsulotomy. 21 were treated with apraclonidine, 20 with brimonidine, 23 with dorzolamide, 20 with latanoprost, 20 with pilocarpine, and 20 with timolol. Controls (21 eyes) received placebo. IOP measurements (Goldmann applanation tonometry) were taken under masked conditions 1 hour before procedure and after 1 and 2 hours. If postoperative PIO was above 20 mmHg its measurements were extended to 4 and 24 hours. Capsulotomy was performed with Abraham lens, under topic anesthetic, using Nd:YAG laser. Ocular hypertension would be considered if the IOP had suffered an increase of 4 mmHg above the initial. Mean total energy used was 2.1 +/- 1 mJ. RESULTS: The preoperative IOP did not differ statistically among groups. Mean IOPs of treated eyes 1h (11.9 +/- 3.8) and 2h (11.5 +/- 3.0) were statistically lower than IOP compared with control group (12,6 +/- 2,8) (p=0.001). There were no statistically significant differences for the other measurements. Control and pilocarpine had a percentual IOP increase after 2 hours of 8.7 +/- 19.1% (13.5 +/- 3.2 mmHg) and 1.2 +/- 26.3% (12.5 +/- 3.6 mmHg) respectively. Mean percentual postoperative IOP reduction was detected in the apraclonidine group -24.7 +/- 15.5% (9.8 +/- 2.6 mmHg), in the brimonidine group -8.9 +/- 15.5% (10.1 +/- 1.7 mmHg), in the dorzolamide group -6.9 +/- 20.3% (12.1 +/- 2.8 mmHg), in the latanoprost group -0.4 +/- 25.9% (12.1 +/- 2.9 mmHg) and in timolol group -16.2 +/- 14.1% (10.3 +/- 1.7 mmHg). These differences were statistically significant (p=0.001). There was no significant difference between frequencies of hypertension (p=0.148). CONCLUSION: Apraclonidine caused higher hypotensive effect after capsulotomy with YAG laser when compared with brimonidine, dorzolamide, latanoprost, pilocarpine, timolol and control group. LA: Portuguese

Dr. A.A. Minello, Universidade Federal de Sao Paulo, Sao Paulo, Brasil. Aa.minello@uol.com.br

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Classification:

9.4.11.2 Glaucomas in aphakia and pseudophakia (Part of: 9 Clinical forms of glaucomas > 9.4 Glaucomas associated with other ocular and systemic disorders > 9.4.11 Glaucomas following intraocular surgery)
11.1 General management, indication (Part of: 11 Medical treatment)

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