Journal Article•
Acute retinal arterial occlusive disorders
01 Oct 2013-Medical Journal of Dr. D.Y. Patil University (Medknow Publications)-Vol. 6, Iss: 4, pp 424
TL;DR: The initial section deals with basic sciences; among the various topics briefly discussed are the anatomical features of ophthalmic, central retinal and cilioretinal arteries which may play a role in acute retinal arterial ischemic disorders.
Abstract: The initial section deals with basic sciences; among the various topics briefly discussed are the anatomical features of ophthalmic, central retinal and cilioretinal arteries which may play a role in acute retinal arterial ischemic disorders. Crucial information required in the management of central retinal artery occlusion (CRAO) is the length of time the retina can survive following that. An experimental study shows that CRAO for 97min produces no detectable permanent retinal damage but there is a progressive ischemic damage thereafter, and by 4h the retina has suffered irreversible damage. In the clinical section, I discuss at length various controversies on acute retinal arterial ischemic disorders. Classification of acute retinal arterial ischemic disorders: These are of 4 types: CRAO, branch retinal artery occlusion (BRAO), cotton wool spots and amaurosis fugax. Both CRAO and BRAO further comprise multiple clinical entities. Contrary to the universal belief, pathogenetically, clinically and for management, CRAO is not one clinical entity but 4 distinct clinical entities - non-arteritic CRAO, non-arteritic CRAO with cilioretinal artery sparing, arteritic CRAO associated with giant cell arteritis (GCA) and transient non-arteritic CRAO. Similarly, BRAO comprises permanent BRAO, transient BRAO and cilioretinal artery occlusion (CLRAO), and the latter further consists of 3 distinct clinical entities - non-arteritic CLRAO alone, non-arteritic CLRAO associated with central retinal vein occlusion and arteritic CLRAO associated with GCA. Understanding these classifications is essential to comprehend fully various aspects of these disorders. Central retinal artery occlusion: The pathogeneses, clinical features and management of the various types of CRAO are discussed in detail. Contrary to the prevalent belief, spontaneous improvement in both visual acuity and visual fields does occur, mainly during the first 7 days. The incidence of spontaneous visual acuity improvement during the first 7 days differs significantly (p<0.001) among the 4 types of CRAO; among them, in eyes with initial visual acuity of counting finger or worse, visual acuity improved, remained stable or deteriorated in non-arteritic CRAO in 22%, 66% and 12% respectively; in non-arteritic CRAO with cilioretinal artery sparing in 67%, 33% and none respectively; and in transient non-arteritic CRAO in 82%, 18% and none respectively. Arteritic CRAO shows no change. Recent studies have shown that administration of local intra-arterial thrombolytic agent not only has no beneficial effect but also can be harmful. Prevalent multiple misconceptions on CRAO are discussed. Branch retinal artery occlusion: Pathogeneses, clinical features and management of various types of BRAO are discussed at length. The natural history of visual acuity outcome shows a final visual acuity of 20/40 or better in 89% of permanent BRAO cases, 100% of transient BRAO and 100% of non-arteritic CLRAO alone. Cotton wools spots: These are common, non-specific acute focal retinal ischemic lesions, seen in many retinopathies. Their pathogenesis and clinical features are discussed in detail. Amaurosis fugax: Its pathogenesis, clinical features and management are described.
Citations
More filters
TL;DR: The pathophysiology, epidemiology, and clinical features of CRAO are described, current and future treatments are discussed, including the use of tissue plasminogen activator (tPA) in further clinical trials.
Abstract: Central retinal artery occlusion (CRAO) is an ophthalmic emergency and the ocular analogue of cerebral stroke. Best evidence reflects that over three-quarters of patients suffer profound acute visual loss with a visual acuity of 20/400 or worse. This results in a reduced functional capacity and quality of life. There is also an increased risk of subsequent cerebral stroke and ischaemic heart disease. There are no current guideline-endorsed therapies, although the use of tissue plasminogen activator (tPA) has been investigated in two randomized controlled trials. This review will describe the pathophysiology, epidemiology, and clinical features of CRAO, and discuss current and future treatments, including the use of tPA in further clinical trials.
265 citations
TL;DR: Measurements made with two of the principal methods used to study O2 in the retina are discussed, focusing on measurements of PO2 with oxygen-sensitive microelectrodes in vivo in animals with a retinal circulation similar to that of humans, and oximetry, which can be used non-invasively in both animals and humans to measure O2 concentration in retinal vessels.
157 citations
Cites background from "Acute retinal arterial occlusive di..."
...Central or branch retinal artery occlusion is a condition for which there is no accepted treatment (Hayreh, 2011), but where O2 could probably play a larger role....
[...]
...Central or branch retinal artery occlusion is a condition for which there is no accepted treatment (Hayreh, 2011), but where O2 could probably play a larger role....
[...]
TL;DR: The concept of preconditioning with ischemia or hypoxia demonstrates the capacity of the retina to activate endogenous survival mechanisms, which may protect cells against a following noxious insult and erythropoietin has gained strong interest as potential therapeutic factor for retinal degenerative diseases.
127 citations
TL;DR: While CRAO is a disease that does not have a treatment, nevertheless it needs to follow the same principles of treatment as any other vascular end organ ischaemic disease, to attempt to reperfuse ischemic tissue as quickly as possible and to institute secondary prevention early.
Abstract: Central retinal artery occlusion (CRAO) is an ocular emergency and is the ocular analogue of cerebral stroke. It results in profound, usually monocular vision loss, and is associated with significant functional morbidity. The risk factors for CRAO are the same atherosclerotic risk factors as for stroke and heart disease. As such, individuals with CRAO may be at risk of ischemic end organ damage such as a cerebral stroke. Therefore, the management of CRAO is not only to restore vision, but at the same time to manage risk factors that may lead to other vascular conditions. There are a number of therapies that has been used in the treatment of CRAO in the past. These include carbogen inhalation, acetazolamide infusion, ocular massage and paracentesis, as well as various vasodilators such as intravenous glyceryl trinitrate. None of these “standard agents” have been shown to alter the natural history of disease definitively. There has been recent interest shown in the use of thrombolytic therapy, delivered either intravenously or intra-arterially by direct catheterisation of the ophthalmic artery. Whilst a number of observational series have shown that the recovery of vision can be quite dramatic, two recent randomised controlled trials have not demonstrated efficacy. On the contrary, intra-arterial delivery of thrombolytic may result in an increased risk of intracranial and systemic haemorrhage, while the intravenous use of tissue plasminogen activator (tPA) was not shown to be efficacious within 24 h of symptom onset. Nevertheless, both of these studies have shown one thing in common, and that is for treatment to be effective in CRAO, it must be deployed within a short time window, probably within 6 h of symptom onset. Therefore, while CRAO is a disease that does not have a treatment, nevertheless it needs to follow the same principles of treatment as any other vascular end organ ischaemic disease. That is, to attempt to reperfuse ischemic tissue as quickly as possible and to institute secondary prevention early.
116 citations
TL;DR: Paracentral acute middle maculopathy refers to characteristic hyper-reflective spectral-domain OCT lesions involving the middle layers of the retina at the level of the inner nuclear layer that may develop in response to ischemia of the intermediate and deep capillary plexuses.
109 citations
References
More filters
TL;DR: It is suggested that nocturnal hypotension, in the presence of other vascular risk factors, may reduce the optic nerve head blood flow below a critical level, and thereby may play a role in the pathogenesis of anterior ischemic optic neuropathy and glaucomatous optic Neuropathy; that is, nocturn hypotension may be the final insult in a multifactorial situation.
790 citations
TL;DR: The recent introduction of fluorescence angiography has made a significant contribution to the subject because it enables us to study the microcirculation in vivo.
Abstract: The blood supply of the optic disc is an important and a fascinating subject in ophthalmology. Since the time of Haller (I754) and Zinn (I755) it has remained the centre of controversy. The literature on the subject has recently been reviewed in detail by Hayreh (i963a), Fransois and Neetens (I966), and Bonamour, Bregeat, Bonnet, and Juge (I968). The recent introduction of fluorescence angiography has made a significant contribution to the subject because it enables us to study the microcirculation in vivo.
615 citations
TL;DR: In this paper, the authors report ocular manifestations of giant cell arteritis using the strict criterion of a positive temporal artery biopsy for diagnosis of GCA using a prospective study from 1973 to 1995.
538 citations
Book•
10 Jun 1975
TL;DR: The clinical features of anterior ischemic optic neuropathy are reviewed and its pathogenesis and treatment are discussed.
Abstract: Though anterior ischemic optic neuropathy (AION) has been widely reported, it is not fully appreciated as one of the commonest causes of impaired vision in persons past middle age. These patients are not infrequently suspected of having an intracranial tumor. This article reviews the clinical features of AION and discusses its pathogenesis and treatment.
509 citations