Table of Contents  
COMMENTARY
Year : 2013  |  Volume : 6  |  Issue : 4  |  Page : 424-425  

Acute retinal arterial occlusive disorders


Department of Ophthalmology and Visual Sciences, College of Medicine, University of Iowa, Iowa City, USA

Date of Web Publication17-Sep-2013

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How to cite this article:
Hayreh SS. Acute retinal arterial occlusive disorders. Med J DY Patil Univ 2013;6:424-5

How to cite this URL:
Hayreh SS. Acute retinal arterial occlusive disorders. Med J DY Patil Univ [serial online] 2013 [cited 2024 Mar 28];6:424-5. Available from: https://journals.lww.com/mjdy/pages/default.aspx/text.asp?2013/6/4/424/118270

Acute retinal arterial occlusive disorders together comprise one of the major causes of acute visual loss. Central retinal artery occlusion (CRAO) results in sudden, catastrophic visual loss and is therefore one of the most important topics in ophthalmology. Similarly, branch retinal arteriolar occlusion (BRAO) and cilioretinal artery occlusion cause sudden segmental visual loss. I have discussed various aspects of acute retinal arterial occlusive disorders at length elsewhere.[1] Amaurosis fugax is a common transient acute retinal ischemic condition; in our study it precedes the development of CRAO in 12% and in BRAO in 14%. [2] The most common cause is embolism into the retinal arterial circulation. The source of embolus is usually either the carotid arteries or the heart. These emboli may not only cause acute retinal occlusive disorders but also have the potential to produce stroke, if they go to the brain. Therefore, in acute retinal arterial occlusive disorders, it is of paramount importance to investigate these patients for the source of embolism to prevent more serious complications. That also applies to the presence of asymptomatic emboli in the retinal arteries. We investigated the carotid artery and cardiac abnormalities in 249 CRAO and 190 BRAO.[3] Plaque in the carotid artery is the major source of embolism because in the ipsilateral internal carotid artery, plaques were seen in 71% of CRAO and 66% of BRAO. Compared to the plaque, carotid artery stenosis is much less likely to cause embolism. Echocardiography in CRAO showed valvular lesions in 52% - these were mitral valve lesions (calcified valve in 57%, mitral valve prolapse in 17% or other types of lesions in 26%) and/or aortic valve lesions (calcified valve in 78% or other types of lesions in 22%). Echocardiography in BRAO showed valvular lesions in 42% - these were mitral valve lesions (calcified valve in 70%, mitral valve prolapse in 4% or other types of lesions in 26%) and/or aortic valve lesions (calcified valve in 68% or other types of lesions 32%). Patent foramen ovale was detected in 2% in both CRAO and BRAO.

The clinical pictures of various types of acute retinal arterial occlusive disorders are typical and the diagnoses are easy. Our experimental study[4] on CRAO in rhesus monkeys showed that if retinal circulation is restored to normal within 100 minutes, the retina recovers normal function; however, if it lasts longer than that, there is progressive, irreversible retinal damage, so that by about 4 hours, the retina suffers irreversible damage.

In the management of any disease, the first essential is to know the natural history the disease, so that spontaneous recovery is not attributed to the beneficial effect of a treatment. Our prospective studies showed that a significant visual improvement can occur without treatment in both CRAO[5] and BRAO;[6] that has erroneously been attributed to various advocated treatments. A whole host of treatment modalities have been advocated and tried for resuscitation of visual function, and enthusiastic success has been claimed for treatment after treatment, but none has stood the test of the time. The most popular treatment recently has been thrombolysis in CRAO; however, the most recent prospective study[7] has shown that local intra-arterial fibrinolysis in CRAO not only has no beneficial effect on visual outcome on the treated versus the untreated groups, but also carries a significantly higher rate of adverse reactions in the treated group (37%) than the control group (4%). Thus, so far, we have no effective treatment for CRAO and BRAO.

 
  References Top

1.Hayreh SS. Acute retinal arterial occlusive disorders. Prog Retin Eye Res 2011;30:359-94.   Back to cited text no. 1
[PUBMED]    
2.Hayreh SS, Zimmerman MB. Amaurosis fugax in ocular vascular occlusive disorders: Prevalence and pathogeneses. Retina 2013 Apr 29. [Epub ahead of print].   Back to cited text no. 2
    
3.Hayreh SS, Podhajsky PA, Zimmerman MB. Retinal artery occlusion: Associated systemic and ophthalmic abnormalities. Ophthalmology 2009;116:1928-36.   Back to cited text no. 3
[PUBMED]    
4.Hayreh SS, Zimmerman MB, Kimura A, Sanon A. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004;78:723-36.   Back to cited text no. 4
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5.Hayreh SS, Zimmerman B. Central Retinal Artery Occlusion: Visual Outcome. Am J Ophthalmol 2005;140:376-91.   Back to cited text no. 5
    
6.Hayreh SS, Podhajsky PA, Zimmerman MB. Branch retinal artery occlusion: Natural history of visual outcome. Ophthalmology 2009;116:1188-94.   Back to cited text no. 6
[PUBMED]    
7.Schumacher M, Schmidt D, Jurklies B, Gall C, Wanke I, Schmoor C, et al. Central retinal artery occlusion: Local intra-arterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology 2010;117:1367-75.  Back to cited text no. 7
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