Central retinal artery occlusion – rethinking retinal survival time

Abstract

BackgroundThe critical time from onset of complete occlusion of the central retinal artery (CRA) to functionally significant inner retinal infarction represents a window of opportunity for treatment and also has medical-legal implications, particularly when central retinal artery occlusion (CRAO) complicates therapeutic interventions. Here, we review the evidence for time to infarction from complete CRAO and discuss the implications of our findings.MethodsA Medline search was performed using each of the terms “central retinal artery occlusion”, “retinal infarction”, “retinal ischemia”, and “cherry red spot” from 1970 to the present including articles in French and German. All retrieved references as well as their reference lists were screened for relevance. An Internet search using these terms was also performed to look for additional references.ResultsWe find that the experimental evidence showing that inner retinal infarction occurs after 90–240 min of total CRAO, which is the interval generally accepted in the medical literature and practice guidelines, is flawed in important ways. Moreover, the retinal ganglion cells, supplied by the CRA, are part of the central nervous system which undergoes infarction after non-perfusion of 12–15 min or less.ConclusionsRetinal infarction is most likely to occur after only 12–15 min of complete CRAO. This helps to explain why therapeutic maneuvers for CRAO are often ineffective. Nevertheless, many CRAOs are incomplete and may benefit from therapy after longer intervals. To try to avoid retinal infarcton from inadvertent ocular compression by a headrest during prone anesthesia, the eyes should be checked at intervals of less than 15′.

Oxidative Stress and Vascular Dysfunction in the Retina: Therapeutic Strategies

“…Cessation of retinal blood flow as observed in CRAO is known to have a deleterious impact on visual acuity after a short period of time and presents an ophthalmic emergency, because of the risk of permanent vision loss and other ocular complications, such as retinal or vitreous hemorrhage, retinal neovascularization or neovascular glaucoma [ 133 , 134 , 135 , 136 , 137 ]. The ocular ischemic syndrome is typically less acute than CRAO and characterized by a reduced blood supply to both the retinal and choroidal circulation, which is mostly due to a stenosis of the common or internal carotid artery.…”

Hypoxia tolerance in the Norrin-deficient retina and the chronically hypoxic brain studied at single-cell resolution

“…Norrie disease | familial exudative vitreoretinopathy | single-cell RNA-seq | serine synthesis | metabolomics T he mammalian CNS is exquisitely sensitive to hypoxia. When combined with nutrient deprivation, hypoxia in the setting of acute ischemia causes rapid and irreversible cell loss in the brain and retina (1,2). In contrast, mild to moderate hypoxia with continued nutrient delivery-as occurs at high altitude-can be tolerated for days to years (3,4).…”

Central Retinal Artery Occlusion Secondary to Patent Foramen Ovale: The Unexpected Journey of a Paradoxical Embolus

“…CRAO is an ocular vascular occlusive disorder with potentially devastating repercussions regarding visual acuity since the inner two-thirds of the retina lose their blood supply. Therefore, if complete CRAO occurs, a retinal infarction will be installed within 12-15 min while the inner retina is critically dependent on the end-central retinal artery circulation and probably more vulnerable to oxygen deprivation than brain [6].…”