Retinal Artery Occlusion Clinical Presentation
- Author: Benjamin Feldman, MD; Chief Editor: Robert E O'Connor, MD, MPH more...
The most common presenting complaint is an acute persistent painless loss of vision. In central artery occlusions, visual loss is central and dense. In branch artery occlusions, visual loss may go unnoticed if only a section of the peripheral visual field space is affected.
A complete visual field defect suggests central retinal artery occlusion (CRAO).
A sectional visual field defect suggests branch retinal artery occlusion (BRAO) and may be an altitudinal defect affecting the upper or lower hemifield but never respecting a vertical axis.
A history of hypertension or diabetes mellitus is elicited in 67% and 25% of patients with CRAO, respectively.
Prolonged direct pressure to the globe during drug-induced stupor or improper positioning during surgery also may lead to CRAO.
Determine the degree of vision loss (eg, no light perception, hand movement, counting fingers); the prognosis for recovery is directly related to initial visual loss.
Document hand movement, finger counts, and visual fields at a standard distance of 1' to 3'. Documentation of distance will provide concise communication with consultants and for standardization of repeated examinations.
Direct the physical examination to evaluate for murmurs, carotid bruits, or other signs of cardiovascular disease.
An afferent pupillary defect (ie, paradoxical dilatation of the pupil when a light is shined from the unaffected eye to the affected eye) may be observed within seconds of the occlusive event.
The cherry red spot and a ground-glass retina are the classic findings but 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 observed in approximately 20% of patients with CRAO.
A dilated funduscopic examination is required to see the pathological signs of RAO.
BRAO presents with whitening of the retina along the distribution of the occluded vessel.
Boxcar segmentation of the blood column is observed most often in BRAO and is a sign of severe occlusion and slowing of circulation.
Causes of central retinal artery occlusion (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.
Embolism is usually caused by cholesterol, but it can be calcific, bacterial, or talc from IV drug abuse.
It is associated with poorer visual acuity and higher morbidity and mortality than other retinal artery occlusions.
Embolus from the heart is the most common cause of CRAO in patients younger than 40 years.
Coagulopathies from sickle cell anemia or antiphospholipid antibodies are common etiologies for CRAO in patients younger than 30 years.
Carotid atherosclerosis is observed in 45% of CRAO cases, with 60% or more stenosis occurring in 20% of cases.
Atherosclerotic disease is the leading cause of CRAO in patients aged 40-60 years.
Occurrence is rare (only 2% of cases).
Suspect inflammatory endarteritis in elderly patients if no other etiology is observed.
Inflammatory endarteritis can affect the second eye within hours if untreated.
Increased intraocular pressure
Increased intraocular pressure (IOP) from glaucoma or prolonged direct pressure to the globe in unconscious patients can precipitate CRAO.
Low retinal blood pressure from carotid stenosis or severe hypotension may lead to CRAO.
Transection of the retinal artery, transection of the optic nerve, or retrobulbar hemorrhage can cause visual loss.
Migraines are rare causes of CRAO but are most common in patients younger than 30 years.
Other causes of retinal artery occlusion include the following:
- Hydrostatic arterial occlusion
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