Central Retinal Artery Occlusion Clinical Presentation
- Author: Robert H Graham, MD; Chief Editor: Hampton Roy, Sr, MD more...
The most common presenting complaint is an acute, persistent, painless loss of vision in the range of counting fingers to light perception in 90% of patients. Consider ophthalmic artery occlusion if visual acuity is worse.
Some patients may reveal a history of amaurosis fugax involving transient loss of vision lasting seconds to minutes but which may last up to 2 hours. The vision usually returns to baseline after an episode of amaurosis fugax.
Ask about symptoms of temporal arteritis in the older population. Patients complain of sudden, painless, nonprogressive vision loss in one eye. History of headaches, jaw claudication, scalp tenderness, proximal muscle and joint aches, anorexia, weight loss, or fever may be elicited.
Ask about any medical problems that could predispose to embolus formation (eg, atrial fibrillation, endocarditis, coagulopathies, atherosclerotic disease, hypercoagulable state).
Prolonged direct pressure to the globe during drug-induced stupor or improper positioning during surgery may lead to CRAO.
Ask about drug history.
Determine the degree of vision loss (eg, no light perception, hand movement, counting fingers).
Ocular examination includes the following:
Check for afferent pupillary defect.
Perform an optic nerve examination to look for signs of temporal arteritis. Critical signs include afferent pupillary defect and pale/swollen optic nerve with splinter hemorrhages.
Cherry-red spot and a ground-glass retina may take hours to develop.
The funduscopic findings typically resolve within days to weeks of the acute event, sometimes leaving a pale optic disc as the only physical finding.
Emboli can be seen in about 20% of patients with CRAO.
Boxcar segmentation can be seen in both arteries and veins. This is a sign of severe obstruction.
Perform a cardiovascular examination for murmurs or carotid bruits.
Perform a systemic examination for temporal tenderness, jaw claudication, muscle weakness, and fever to evaluate for temporal arteritis.
Causes of CRAO vary depending on the age of the patient. A detailed analysis of comorbid disease is necessary to elucidate the cause of the acute visual loss.
Systemic hypertension seen in two thirds of patients
Cardiac valvular disease seen in one fourth of patients
Cardiac anomalies, such as patent foramen ovale
- This is most commonly cholesterol but can be calcific, bacterial, or talc from intravenous drug abuse.
- This is associated with poorer visual acuity and higher morbidity and mortality.
- Emboli from the heart are the most common cause of CRAO in patients younger than 40 years.
- Amaurosis fugax preceding persistent loss of vision suggests branch retinal artery occlusion (BRAO) or temporal arteritis and may represent emboli causing temporary occlusion of the retinal artery.
- Coagulopathies from sickle cell anemia or antiphospholipid antibodies are more common etiologies for CRAO in patients younger than 30 years.
- Carotid atherosclerosis is seen in 45% of cases of CRAO, with 60% or greater stenosis in 20% of cases.
- Atherosclerotic disease is the leading cause of CRAO in patients aged 40-60 years.
- Chang et al have found an increased risk of acute coronary syndrome (indicative of coronary atherosclerosis) in patients with retinal arterial occlusions.
Giant cell arteritis
- Giant cell arteritis should be considered in patients older than 65 years, but do not ignore in younger patients.
- Giant cell arteritis may produce CRAO or ischemic optic neuropathy.
- Giant cell arteritis needs to be treated to preserve vision in the fellow eye.
Collagen vascular disease
Consider in younger patients
Increased intraocular pressure from glaucoma or prolonged direct pressure to the globe in unconscious patients
Hydrostatic arterial occlusion
Iatrogenic: With the increasing popularity of cosmetic facial filler injections, Chen et al and Carle et al report that these injections are a cause of retinal artery occlusions. [3, 4]
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