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A 65-year-old man with decreased vision OD
Digital Journal of Ophthalmology 2008
Volume 14, Number 11
June 15, 2008
Printer Friendly

Meghomala Das, MRCS | Hairmyres Hospital
Manish Gupta, MRCS | Royal Alexandra Hospital
Robert Harvey, FRCOphth | Royal Alexandra Hospital
Sourjya Kar, MBBS | Huddersfield Royal Infirmary
Diagnosis and Discussion
OIS is defined by a constellation of signs and symptoms and occurs secondary to atherosclerotic carotid artery stenosis of more than 90%, resulting in a 50% reduction in ipsilateral perfusion pressure.(1,2) Both the extra and intracranial portions of the carotid artery can be affected, especially the bifurcation of the common carotid within the neck.

Symptoms of OIS include visual loss, amaurosis fugax, prolonged recovery of vision after exposure to bright light and ocular or periorbital pain.(3) It typically occurs in patients aged 50-80 years; men are more frequently affected than women.

Ocular examination reveals NVI, elevated IOP, uveitis, retinal arteriolar narrowing, dilated retinal venules, characteristic mid-peripheral retinal dot and blot hemorrhages and posterior segment neovascularisation. Fluorescein angiogram can show delayed and patchy choroidal filling, prolongation of the arteriovenous transit time, staining of the retinal vessels, macular edema, retinal capillary nonperfusion, and neovascularization of the disc or elsewhere.(1,2,4,5) OIS may also be associated with neurological symptoms such as stroke, or it may be the sole manifestation of carotid occlusive disease.

Management of patients with suspected OIS involves:

1. Examination of the cardiovascular system and evaluation for hypertension, diabetes and atherosclerotic disease.

2. The carotid artery system can be studied with noninvasive carotid ultrasound, which has an accuracy of around 95% in detecting carotid artery stenosis of 75% or more at the bifurcation.(6) Transcranial Doppler images the ophthalmic artery and documents any reversal of blood flow. Magnetic resonance imaging, magnetic resonance angiography and carotid angiography show the entire extent of the carotid system and its branches and additionally helps to identify intracranial lesions.

3. Treatment of OIS remains difficult and controversial. Since internal carotid artery occlusive disease is the most common cause, carotid endarterectomy (CEA) would seem a logical management; however, the benefit to patients is unknown and controversial.(7) CEA is usually offered if the stenosis is >70%. Intracranial carotid artery disease with stenotic lesions above the second cervical vertebrae (C2) are not amenable to surgical intervention. Carotid artery angioplasty with stenting has shown to improve cerebral perfusion(8) in these cases, resulting in improvement in ophthalmic artery blood flow and FA filling times.

Standard therapy includes treatment of the underlying ischemic stimulus, typically with PRP combined with medical and surgical management of the elevated intraocular pressure. Topical steroids are used to decrease associated inflammation; cycloplegics may be useful to decrease ciliary pain and prevent posterior synechiae. Since perfusion pressure (mean blood pressure minus IOP) in the various ocular vascular beds is diminished, lowering IOP as much as possible is crucial to improve the blood flow and reduce the risk of retinal and optic nerve head ischemic visual loss. In addition, it is important to avoid any drop in systemic blood pressure, particularly nocturnal arterial hypotension, to prevent visual loss.(9,10) For this reason, the use of topical â-blocker eye drops to lower IOP is contraindicated in these eyes because they may produce significant nocturnal arterial hypotension, which can be visually deleterious.(11)

VEGF levels have been shown to be elevated in the vitreous in many pathological conditions that lead to neovascular glaucoma, as well as in the aqueous of patients with active neovascular glaucoma.(12) Anti-VEGF drugs offer the possibility of rapid regression of anterior segment neovascularization in an effort to avoid complete angle closure. There have been several reports of rapid regression of rubeosis following intravitreal bevacizumab in neovascular glaucoma.(13,14,15) However, this is not without potential local and systemic side effects. To date, there is no comprehensive study providing definitive information for long-term control of ocular neovascularization and neovascular glaucoma, and the complications of anti-VEGF therapy. In practice, PRP is still used as standard first line therapy and can be supplemented with intravitreal bevacizumab as a temporizing measure to prevent complete angle closure while awaiting the effect of PRP.

OIS has a poor visual prognosis and is often difficult and frustrating to treat. The ophthalmologist’s diagnosis may be crucial to the health of these patients as OIS may be the presenting sign of serious cerebrovascular and ischemic heart disease. Further studies are required to document role of CEA and anti-VEGF therapy in OIS.