Acute retinal arterial ischemia

Abstract

Acute retinal arterial ischemia, which includes transient monocular vision loss (TMVL), branch retinal artery occlusion (BRAO), central retinal artery occlusion (CRAO) and ophthalmic artery occlusion (OAO), is most commonly the consequence of an embolic phenomenon from the ipsilateral carotid artery, heart or aortic arch, leading to partial or complete occlusion of the central retinal artery (CRA) or its branches. Acute retinal arterial ischemia is the ocular equivalent of acute cerebral ischemia and is an ophthalmic and medical emergency. Patients with acute retinal arterial ischemia are at a high risk of having further vascular events, such as subsequent strokes and myocardial infarctions (MIs). Therefore, prompt diagnosis and urgent referral to appropriate specialists and centers is necessary for further work-up (such as brain magnetic resonance imaging with diffusion weighted imaging, vascular imaging, and cardiac monitoring and imaging) and potential treatment of an urgent etiology (e.g., carotid dissection or critical carotid artery stenosis). Since there are no proven, effective treatments to improve visual outcome following permanent retinal arterial ischemia (central or branch retinal artery occlusion), treatment must focus on secondary prevention measures to decrease the likelihood of subsequent ischemic events.

Hyperbaric Oxygen Therapy in Retinal Arterial Occlusion: Epidemiology, Clinical Approach, and Visual Outcomes

“…is is based on the main pathophysiological mechanism of an early HBOT, in case of RAO, of the hyperbaric oxygen evolution of systemic vascular pathologies, thus implying a timely medical articulation with Internal Medicine, Cardiology and/or Neurology. e prevalence of vascular risk factors in our study is consistent with other studies, highlighting the arterial hypertension, dyslipidemia, and brain and cardiovascular diseases [3,23,24].…”

“…Retinal artery occlusion (RAO) is a rare ophthalmological emergency, with embolism being the most common aetiology [1][2][3][4]. It is manifested by acute painless monocular vision loss and a meaningful visual improvement (three lines in Snellen chart) is expected only in 10% of the cases [1][2][3][4][5][6][7]. e time of ischemia is classically the critical prognosis factor for the visual outcome, considering that the retina is the tissue of the human body with the highest oxygen consumption, being therefore very sensitive to variations in oxygen [1,4,8,9].…”

Intermittent Hypoxia Promotes Functional Neuroprotection from Retinal Ischemia in Untreated First-Generation Offspring: Proteomic Mechanistic Insights

“…To test the hypothesis that this type of cytoprotective intergenerational inheritance occurs in the central nervous system of mammals, we used a well-established mouse model of transient, unilateral retinal ischemia. The worldwide incidence of ischemic retinopathies, including nonproliferative diabetic retinopathy, glaucoma, age-related macular degeneration, and acute ischemia secondary to branch and central retinal artery occlusion, is significant 21 – 24 ; however, efficacious therapies designed to protect the retina against their consequent blindness and related visual morbidities have yet to be developed. To ensure rigor, we quantified postischemic retinal function by electroretinography in large cohorts.…”

Intermittent hypoxia promotes functional neuroprotection from retinal ischemia in untreated first-generation offspring

“…To test the hypothesis that intergenerational epigenetic inheritance occurs in the central nervous system of mammals, we used a well-established mouse model of transient, unilateral retinal ischemia. The world-wide incidence of ischemic retinopathies, including nonproliferative diabetic retinopathy, glaucoma, age-related macular degeneration, and acute ischemia secondary to branch and central retinal artery occlusion, is significant (21)(22)(23)(24); however, efficacious therapies designed to protect the retina against the consequent blindness and related visual morbidities have yet to be developed. To ensure rigor, we quantified postischemic retinal function by electroretinography in large cohorts.…”