Secondary Glaucoma: Pathogenesis and Clinical Findings Open-Angle Secondary Glaucoma: • Pre-trabecular defect -> Aqueous outflow is obstructed by a membrane covering the trabeculum • Trabecular defect -> 'Clogging' of the trabecular meshwork by pigmentary particles, RBCs, proteins or pseudoexfoliative material • Post-trabecular defect -> Impairment of aqueous outflow due to increased episcleral venous pressure Closed-Angle Secondary Glaucoma: • Pupillary block -> Impairment of aqueous outflow due to apposition between the peripheral iris and trabeculum with pupillary block • Non-pupillary block -> Impairment of aqueous outflow due to apposition between the peripheral iris and trabeculum without pupillary block => Increased Intraocular Pressure => Secondary glaucoma -> Calcium ion influx and NO in retinal ganglion cells -> Retinal ganglion cell injury -> Astrocyte and glial cell proliferation and alteration in ECM or lamina cribosa -> Optic nerve head remodeling - Direct mechanical damage to optic nerve head - Ischemic damage due to compression of blood vessels supplying the optic nerve -> Decr axoplasmic flow, Decr delivery of nutrients, deprivation or neuronal growth factors, oxidative injury, and initiation of immune mediated damage -> Apoptosis of retinal ganglion cells - RNFL thinning and glaucomatous cupping observed on fundus examination - RNFL thinning and glaucomatous cupping observed on optic disc or peri-papillary RNFL imaging -> Progressive VF defects => End-stage visual field loss with retained small island of central vision #Secondary #Glaucoma #pathophysiology #ophthalmology
