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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 #10836 Published in IGR 6-2

Influence of non-penetrating glaucoma surgery on aqueous outflow facility in isolated porcine eyes

Shaarawy T; Wu R; Mermoud A; Flammer J; Haefliger IO
British Journal of Ophthalmology 2004; 88: 950-2

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PURPOSE: To investigate, in vitro, the influence of non-penetrating glaucoma surgery (NPGS) and the influence of tightly suturing the superficial scleral flap on the aqueous outflow facility of isolated porcine eyes. MATERIALS AND METHODS: The anterior chambers of 12 enucleated porcine cadaver eyes were cannulated and perfused. NPGS was performed by the same surgeon. The overall ocular aqueous outflow facilities were assessed before and after the surgical interventions of NPGS, as well as after scleral flap closure. RESULTS: The mean (SD) aqueous outflow facility, which was 0.164 (0.014) μl/min/mmHg before surgery, increased significantly after NPGS to 1.584 (0.217) μl/min/mmHg, p<0.001. When the superficial flap was closed, the aqueous outflow facility significantly decreased (0.754 (0.107) μl/min/mmHg, p<0.001) but remained significantly higher than preoperatively (p<0.01). After suturing the superficial flap, the overall resistance increased to 1.625 (0.210) μl/min/mmHg. The difference in the resistance to outflow before and after flap closure was 0.848 (0.169) μl/min/mmHg. CONCLUSION: After NPGS suturing the scleral flap can modulate aqueous outflow resistance. The experimental set up described might provide an efficient model for the technical training of glaucoma surgeries.

University Eye Hospital, Basel, Switzerland. shaarawy@glaucoma-surgery.com

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Classification:

12.8.3 Non-perforating (Part of: 12 Surgical treatment > 12.8 Filtering surgery)

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