Journal of glaucoma · 2019
Acute Secondary Optic Neuropathy as a Complication of a Single Episode of Acutely Raised Intraocular Pressure: A Case Series.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Garala Pavitra, Bansal Atul
Аннотация
PURPOSE: The purpose of this case series is to report development of acute secondary optic neuropathy due to optic nerve injury associated with single episode of acutely raised intraocular pressure (IOP) of varying etiologies.
PATIENTS AND METHODS: Retrospective review of a series of 3 consecutive cases diagnosed at University hospitals of Coventry and Warwickshire and review of published literature.
RESULTS: Three cases, respectively, with Posner Schlossman syndrome, acute idiopathic hypertensive anterior uveitis, and primary acute angle-closure initially presented with raised IOPs of 38 to 68 mm Hg. All cases were treated initially with medical management and the primary acute angle-closure case had subsequent Nd:YAG laser peripheral iridotomy. All 3 cases developed acute optic nerve injury with reduced vision, an afferent pupillary defect and optic disc swelling which subsequently persisted as optic neuropathy with sectoral optic atrophy and disc pallor.
CONCLUSIONS: This rare cases series highlights the importance of increased awareness of the possibility of developing acute secondary optic neuropathy in patients with acutely raised IOP. On the basis of the acute clinical features, including disc edema with disc hemorrhages and an afferent pupillary defect the most likely pathophysiology of the resultant optic nerve injury is the acute impact of high IOP on optic nerve head perfusion. This appears similar to nonarteritic anterior oschemic optic neuropathy. Other systemic and local risk factors may also contribute. Appropriate timely management to reduce the acutely raised IOP are essential but may not be sufficient in preventing optic neuropathy due to changes at presentation.
PATIENTS AND METHODS: Retrospective review of a series of 3 consecutive cases diagnosed at University hospitals of Coventry and Warwickshire and review of published literature.
RESULTS: Three cases, respectively, with Posner Schlossman syndrome, acute idiopathic hypertensive anterior uveitis, and primary acute angle-closure initially presented with raised IOPs of 38 to 68 mm Hg. All cases were treated initially with medical management and the primary acute angle-closure case had subsequent Nd:YAG laser peripheral iridotomy. All 3 cases developed acute optic nerve injury with reduced vision, an afferent pupillary defect and optic disc swelling which subsequently persisted as optic neuropathy with sectoral optic atrophy and disc pallor.
CONCLUSIONS: This rare cases series highlights the importance of increased awareness of the possibility of developing acute secondary optic neuropathy in patients with acutely raised IOP. On the basis of the acute clinical features, including disc edema with disc hemorrhages and an afferent pupillary defect the most likely pathophysiology of the resultant optic nerve injury is the acute impact of high IOP on optic nerve head perfusion. This appears similar to nonarteritic anterior oschemic optic neuropathy. Other systemic and local risk factors may also contribute. Appropriate timely management to reduce the acutely raised IOP are essential but may not be sufficient in preventing optic neuropathy due to changes at presentation.