Acute Secondary Optic Neuropathy as a Complication of a Single Episode of Acutely Raised Intraocular Pressure: A Case Series

Abstract

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.

Survival analysis of phacomorphic glaucoma at a tertiary hospital in North India

“…This has been validated by previous studies where a rise in IOP was found to reduce the perfusion pressure of the ONH from compression of vessels in the prelaminar region leading to NAION. [ 32 33 34 ]…”

Nonarteritic Anterior Ischemic Optic Neuropathy After Intravitreal Aflibercept for Age-Related Macular Degeneration

“…The blood supply to the optic nerve may be compromised in the setting of high IOP and NAION has been reported in patients with an acute rise in IOP including those with Posner-Schlossman syndrome, hypertensive uveitis, acute angle-closure glaucoma, and cataract surgery. 2,3 The mean peak IOP immediately postintravitreal injection has been reported to be as high as 42.6 mmHg, with up to 11.6% of patients having sustained IOP elevation for two consecutive visits or longer than 30 days post-injection? 4 Moreover, scleral rigidity, globe dimensions, and reduced outflow facility can result in even small injected volumes (0.05 mL) increasing IOP in the acute period.…”

Low expression of TGF‐β2 and matrilin2 in human aqueous humour with acute primary angle closure

“…Eyes with APAC usually have a narrow anterior chamber angle and forward bowing of the peripheral iris. This abnormal anatomy obstructs aqueous humour (AH) outflow and results in a sudden elevation in intraocular pressure (IOP) and acute optic nerve damage, manifesting as abruptly reduced vision, afferent pupillary defects, optic disc oedema and disc haemorrhages, which are similar to those with ischemia injury 1–4 . Without timely treatment, it can lead to iris synechia, angle dysfunction, higher IOP and irreversible optic nerve damage.…”