Friday, November 4, 2011


The patient, usually between the ages of 50 and 80, will present with a sudden, painless, unilateral loss of vision and/or visual field. Acuity may be as low as hand motion. The patient often has significant systemic illness such as hypertension and/or diabetes. There will be a relative afferent pupillary defect in the involved eye.

Ophthalmoscopically, you'll see a pale, milky, edematous retina with attenuated arterioles and a cherry-red macula if the entire central retinal artery is occluded. If a cilioretinal artery is present, there will be an area of perfusion from the optic disc to the macula. An embolus may be visible in the vasculature on the disc. If a branch retinal artery is involved, an embolus will be visible in the vessel with ischemia and infarct appearing distal to the occlusion.

The main cause of retinal arterial occlusions is an embolism lodging in the central retinal artery where it constricts to pass through the lamina cribrosa, or in a smaller branch arteriole. The embolism may be comprised of aggregated fibrin and platelets arising from an ulcerated vessel wall thrombus, cholesterol from an ulcerated carotid artery plaque, or calcium from cardiac valvular disease.

Abnormal cardiac rhythms may allow blood to coagulate and form emboli which may also reach the retinal vasculature. Neovascularization is not common with either central or branch artery occlusions, but if it does occur, it will do so rapidly, with rubeosis forming approximately four weeks after the occlusion. Between two and 10 percent of central retinal artery occlusions are caused by thrombus formation from giant cell arteritis (GCA). If the underlying cause of the central retinal artery occlusion is GCA, there may be a rapid progression to bilateral vision loss if left untreated.

Traditionally, central retinal artery occlusion has been considered an emergency. It was felt that, if the embolus could be dislodged within 90 minutes of occlusion, vision could be potentially salvaged with the retina being re-perfused. To this end, various methods have been employed to reduce resistance on the artery or dilate the artery to induce the embolus to dislodge.

Common methods employed included breathing into a paper bag to increase blood carbon dioxide levels and induce vasodilation, digital globe massage, paracentesis, and carbonic anhydrase inhibitors to reduce intraocular pressure and decrease vascular resistance to flow. Most practitioners would attempt these measures if the occlusion were less than 24 hours old. While there is anecdotal evidence that these measures have sporadically resulted in vision returning, a large study showed that the average final visual outcome in patients with embolic central retinal artery occlusion treated with heroic measures compared to those untreated was only one-quarter line improvement in Snellen acuity.

Patients with arterial occlusion have significant systemic illness, namely hypertension, atherosclerosis or diabetes. These patients are at extreme risk for cardiovascular disease and myocardial infarction. For this reason, these patients need prompt referral to a cardiologist for complete evaluation. Medical testing should include blood pressure evaluation, EKG, fasting blood glucose, lipid and cholesterol levels, and hyperviscosity studies. Patients with central retinal artery occlusion over the age of 60 need an immediate erythrocyte sedimentation rate (ESR) to examine for the possibility of giant cell arteritis. Fluorescein angiography is generally not indicated.


Traditional heroic measures to salvage vision generally do not produce significant changes in the patient's vision.

These patients have a significantly reduced survival rate, and the main cause of mortality is cardiac. Therefore, prompt referral to a cardiologist is indicated.

Central retinal artery occlusion may be caused by GCA; if undetected, the patient can develop severe, bilateral vision loss.

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