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Approach to “Visual Loss”
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Aastha Takkar Kapila, Monika Singla, Vivek Lal
Ischemic optic neuropathies (anterior/posterior) ischemic optic neuropathy can be anterior or posterior and often presents with sudden-onset visual deficit, often maximum at onset. Anterior ischemic optic neuropathy (AION) involves ischemic damage to the optic nerve head. It can be non-arteritic (non-arteritic anterior ischemic optic neuropathy [NAION]) or arteritic (A-AION), the latter being associated with giant cell arteritis. While NAION is the most common form of non-glaucomatous optic neuropathy in elderly individuals, arteritic AION is associated with vasculitis and is the most common ophthalmic manifestation of giant cell arteritis (GCA). It is a treatable neuro-ophthalmic emergency, which is exceedingly important to recognize and differentiate from more common NAION. The patients of AION usually have unilateral disc edema (pale disc edema with hemorrhages) and show a “classical” altitudinal horizontal field defect on visual field testing (because of the peculiar blood supply of the optic disc).8,9
Geriatric headache
Published in Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby, Headache in Clinical Practice, 2018
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby
Visual loss is the most feared complication of GCA, occurring in 7–60% of untreated patients, with a pooled incidence of 36% in 819 cases.24 Visual loss is usually sudden and irreversible; however, gradual visual loss and recovery of vision with treatment have been reported.25–29 Visual loss is usually due to ischemic optic neuropathy secondary to arteritis of the short posterior ciliary arteries (the blood vessels that supply the anterior optic nerve).21,25,26,30,31 Visual loss may also occur secondary to posterior ischemic optic neuropathy, central retinal artery occlusion or bilateral occipital lobe infarction.21,24,27,30,31 In untreated cases, monocular visual loss may be followed by loss of vision in the other eye.10,25
The Effect of Acute Hypovolemia on the Eye
Published in Current Eye Research, 2018
Hatice Bilge Araz-Ersan, Nihat Sayin, Sadık Etka Bayramoğlu, Dilara Pirhan, Kamuran Sanli, Necip Kara
Adequate blood supply to the eye is essential for the survival of retinal neurons and the maintenance of visual function. Hypovolemia is a state of decreased blood volume. The reduction in the circulating blood volume reduces tissue perfusion which prevents the metabolic needs of the tissues from being met; consequently, cellular hypoxia and end-organ damage develop. Hypovolemia secondary to various medical conditions including traumatic injuries or surgeries may result in posterior ischemic optic neuropathy, which can cause bilateral and profound visual loss.1 In patients with predisposing anatomy and cardiovascular risk factors, insufficient blood supply can cause non-arteritic anterior ischemic optic neuropathy.2 Furthermore, accumulating evidence suggests that the reduced ocular blood flow and vascular dysregulation underlies different ocular diseases, including glaucoma,3 age-related macular degeneration, diabetic retinopathy,4 and central serous retinopathy.5
Visual impairment by multiple vascular embolization with hydroxyapatite particles
Published in Orbit, 2018
Yayoi Marumo, Miki Hiraoka, Masato Hashimoto, Hiroshi Ohguro
Examining the specifics of each case, in the first case, due to the development of ptosis and anterior segment ischemia, it was concluded, that the occluded vessels were the supraorbital artery and long posterior ciliary artery.11 In the second case, both eyes suffered from total blindness due to the bilateral central retinal artery and short posterior ciliary artery occlusions.8 In the third case, the occluded sites were in the central retinal artery and short and long posterior ciliary arteries.12 In the fourth case, posterior ischemic optic neuropathy developed.13 Although a lack of ophthalmological data in the fifth case makes it difficult to predict the responsible pathology leading to total blindness, central retinal artery occlusion may have been the cause.14 Among the literature, there was no case with permanent central nervous system impairment unlike autologous fat injections. This might be due to the differences of particle sizes and weight of filler materials.
Percutaneous transorbital embolization of a carotid cavernous fistula
Published in Baylor University Medical Center Proceedings, 2019
Lance J. Lyons, Sarah A. Smith, Orlando Diaz, Humberto Diaz, Aroucha Vickers, Claudia Prospero, Andrew G. Lee
CCFs that drain posteriorly into the inferior or superior petrosal sinuses can spare the ophthalmic venous system and produce a white-eyed shunt. Patients with a posterior draining CCF may be asymptomatic or symptomatic (e.g., headache, facial or eye pain, and diplopia—typically from a sixth nerve palsy). However, anterior drainage involving the ophthalmic veins may cause ophthalmic venous hypertension and resultant orbital congestion (“red-eyed shunt”). In the case above, onset of symptoms paralleled angiographic evidence of flow reversal from partial thrombosis. Treatment was initiated after the development of an acute transition from white-eyed to red-eyed shunt, markedly elevated intraocular pressure, and acute visual loss from presumed posterior ischemic optic neuropathy.