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Ocular ischemic syndrome

From Wikipedia, the free encyclopedia
Lack of blood flow within the eye
Medical condition
Ocular ischemic syndrome
SpecialtyOphthalmology Edit this on Wikidata

Ocular ischemic syndrome is the constellation of ocularsigns andsymptoms secondary to severe, chronicarterial hypoperfusion to theeye.[1]Amaurosis fugax is a form of acutevision loss caused by reduced blood flow to the eye; it may be a warning sign of an impendingstroke, as both stroke andretinal artery occlusion can be caused bythromboembolism due toatherosclerosis elsewhere in the body (such ascoronary artery disease and especiallycarotid atherosclerosis). Retinal artery occlusion is also caused by a left atrial thrombus in patients withatrial fibrillation. Consequently, those with transient blurring of vision are advised to urgently seek medical attention for a thorough evaluation of thecarotid artery.Anterior segment ischemic syndrome is a similar ischemic condition ofanterior segment usually seen in post-surgical cases. Retinal artery occlusion (such ascentral retinal artery occlusion orbranch retinal artery occlusion) leads to rapid death of retinal cells, thereby resulting in severe loss of vision.

Symptoms and signs

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Those with ocular ischemic syndrome are typically between the ages of 50 and 80 (patients over 65);[2][3] twice as many men as women are affected.[3] More than 90% of those presenting with the condition havevision loss.[1] Patients may report a dull, radiating ache over the eye andeyebrow.[1] Those with ocular ischemic syndrome may also present with a history of other systemic diseases includingarterial hypertension,diabetes mellitus,coronary artery disease, previousstroke, andhemodialysis.[4][5]

The condition presents with visual loss secondary to hypoperfusion of the eye structures. The patient presents with intractable pain or ocular angina. On dilated examination, there may be blot retinal hemorrhages along with dilated and beaded retinal veins. The ocular perfusion pressure is decreased.The corneal layers show edema and striae. There is mildanterior uveitis. A cherry-red spot may be seen in the macula, along with cotton-wool spots elsewhere, due to retinal nerve fiber layer hemorrhages. The retinal arteries may show spontaneous pulsations.[citation needed]

Complications

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If carotid occlusive disease results in ophthalmic artery occlusion, general ocular ischemia may result in retinal neovascularization, rubeosis iridis, cells and flare, iris necrosis, and cataract. The condition leads to neovascularization in various eye tissues due to the ischemia. The eye pressure may become high due to associatedneovascular glaucoma. Anischemic optic neuropathy may eventually occur.[citation needed]

Causes

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Severe ipsilateral or bilateralcarotid artery stenosis or occlusion is the most common cause of ocular ischemic syndrome.[1] The syndrome has been associated with occlusion of thecommon carotid artery,internal carotid artery, and less frequently theexternal carotid artery.[6] Other causes include:

Diagnosis

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Differential diagnoses

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Treatment

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Quick determination of the cause may lead to urgent measures to save the eye and life of the patient. High clinical suspicion should be kept for painless vision loss in patients withatherosclerosis,deep venous thrombosis,atrial fibrillation,pulmonary thromboembolism or other previous embolic episodes. Those caused by a carotid arteryembolism or occlusion have the potential for further stroke by detachment of embolus and migration to an end-artery of the brain.[11] Hence, proper steps to prevent such an eventuality need to be taken.[citation needed]

Retinal arterial occlusion is an ophthalmic emergency, and prompt treatment is essential. Completely anoxic retina in animal models causes irreversible damage in about 90 minutes. Nonspecific methods to increase blood flow and dislodge emboli include digital massage, 500 mgIVacetazolamide and 100 mg IVmethylprednisolone (for possible arteritis). Additional measures include paracentesis of aqueous humor to decrease IOP acutely. AnESR should be drawn to detect possible giant cell arteritis. Improvement can be determined by visual acuity,visual field testing, and by ophthalmoscopic examination.[citation needed]

At a later stage, pan-retinal photocoagulation (PRP) with an argon laser appears effective in reducing the neovascular components and their sequelae.[citation needed]

The visual prognosis for ocular ischemic syndrome varies from usually poor to fair, depending on speed and effectiveness of the intervention. However, prompt diagnosis is crucial as the condition may be a presenting sign of serious cerebrovascular and ischemic heart diseases.[5]

In 2009, theUndersea and Hyperbaric Medical Society added "central retinal artery occlusion" to their list of approved indications forhyperbaric oxygen (HBO).[12][13] When used as an adjunctive therapy, the edema reducing properties of HBO, along with down regulation of inflammatorycytokines may contribute to the improvement in vision.[14] Prevention of vision loss requires that certain conditions be met: the treatment be started before irreversible damage has occurred (over 24 hours), the occlusion must not also occur at theophthalmic artery, and treatment must continue until the inner layers of the retina are again oxygenated by the retinal arteries.[15]

References

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  1. ^abcdDe Graeve C, Van de Sompel W, Claes C (1999)."Ocular ischemic syndrome: two case reports of bilateral involvement".Bull Soc Belge Ophtalmol.273:69–74.PMID 10546383.
  2. ^Friedberg MA, Rapuano CJ.The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease, J.B. Lippincott, 1994.
  3. ^ab"Ocular Ischemic Syndrome."Archived 2009-09-27 at theWayback Machine Accessed October 25, 2006.
  4. ^Chen KJ, Chen SN, Kao LY, Ho CL, Chen TL, Lai CC, Wu SC (August 2001). "Ocular ischemic syndrome".Chang Gung Medical Journal.24 (8):483–91.PMID 11601190.
  5. ^abMizener JB, Podhajsky P, Hayreh SS (May 1997). "Ocular ischemic syndrome".Ophthalmology.104 (5):859–64.doi:10.1016/s0161-6420(97)30221-8.PMID 9160035.
  6. ^Alizai AM, Trobe JD, Thompson BG, Izer JD, Cornblath WT, Deveikis JP (December 2005)."Ocular ischemic syndrome after occlusion of both external carotid arteries".Journal of Neuro-Ophthalmology.25 (4):268–72.doi:10.1097/01.wno.0000189831.92504.2d.PMID 16340491.
  7. ^Koz OG, Ates A, Numan Alp M, Gultan E, Karaaslan Y, Kural G (January 2007). "Bilateral ocular ischemic syndrome as an initial manifestation of Takayasu's arteritis associated with carotid steal syndrome".Rheumatology International.27 (3):299–302.doi:10.1007/s00296-006-0194-4.PMID 16944156.
  8. ^Hamed LM, Guy JR, Moster ML, Bosley T (June 1992). "Giant cell arteritis in the ocular ischemic syndrome".American Journal of Ophthalmology.113 (6):702–5.doi:10.1016/s0002-9394(14)74798-1.PMID 1598963.
  9. ^Munch IC, Larsen M (Aug 2005). "[The ocular ischemic syndrome.]".Ugeskrift for Læger.167 (35):3269–73.PMID 16138965.
  10. ^Bigou MA, Bettembourg O, Hebert T, Cochener B (Jan 2006). "[Unilateral ocular ischemic syndrome in a diabetic patient.]".J Fr Ophtalmol.29 (1): e2.doi:10.1016/s0181-5512(06)73751-2.PMID 16465117.
  11. ^Kaiboriboon K, Piriyawat P, Selhorst JB (May 2001). "Light-induced amaurosis fugax".American Journal of Ophthalmology.131 (5):674–6.doi:10.1016/S0002-9394(00)00874-6.PMID 11336956.
  12. ^The Undersea and Hyperbaric Medical Society (UHMS), Hyperbaric Oxygen Therapy Committee. Guidelines: Indications for Hyperbaric Oxygen. Durham, NC: UHMS; 2009.
  13. ^Butler FK, Hagan C, Murphy-Lavoie H (2008)."Hyperbaric oxygen therapy and the eye".Undersea & Hyperbaric Medicine.35 (5):333–87.PMID 19024664. Archived from the original on January 13, 2013. Retrieved2010-11-09.
  14. ^Wright JK, Franklin B, Zant E (2007)."Clinical case report: treatment of a central retinal vein occlusion with hyperbaric oxygen".Undersea and Hyperbaric Medicine.34 (5):315–9.PMID 18019081. Archived from the original on January 13, 2013. Retrieved2009-05-26.
  15. ^Butler Jr, FK (2010). "Hyperbaric oxygen for central retinal artery occlusion".Wound Care & Hyperbaric Medicine.1 (3): 25.

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