Title: Decompensation of chronic open-angle glaucoma following mydriasis-induced pigmentary dispersion into the aqueous humour: a light and electron microscopic study.
Abstract: A patient with well controlled chronic open-angle glaucoma developed after dilatation of both pupils persistent increase in intraocular pressure (IOP) due to extensive pigmentary disper- sion into the aqueous humour.Trabeculectomy specimens obtained from both eyes after 3 and 7 weeks were studied by light and electron microscopy.It seems evident that the initial phase of raised IOP was caused by a clogging mechanism to the outflow channels by melanin and phagocytic cells.The permanent increase in IOP is attributed to the damage induced in the fibrous components of the trabecular sheets as a result of a complete breakdown of their endothelial covering.Dilatation of the pupil occasionally results in an excessive release of pigment into the aqueous humour, sometimes associated with a transient increase in intraocular pressure (IOP).This phenomenon may occur in normal eyes of aged people on instillation of sympathomimetics' but is frequently seen in glaucomatous eyes, especially if pigmentary dispersion and exfoliation syndromes are also present.2-4We report on a patient with well con- trolled primary open-angle glaucoma who, after dilatation of both pupils, developed a marked pigmentary dispersion and a nonresponsive increase in IOP requiring surgery in both eyes.Histological and electron microscopical examination of the trabeculectomy specimens obtained from both eyes disclosed changes that would explain the mechanism which led to the intractable rise in intraocular pressure. Case reportAn 83-year-old woman who was known to have chronic open-angle glaucoma with marked cupping of the optic discs and advanced bilateral visual field loss was finally treated with 0-25 % timolol twice