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Emergency and Acute Medicine – Central Retinal Artery Occlusion
Overview
Central retinal artery occlusion (CRAO) is an obstruction of the central retinal artery resulting in sudden, painless, monocular vision loss. It typically affects adults aged 50–70 years and is often described as a “stroke of the eye.” The ophthalmic artery is the first branch of the carotid artery. Risk factors include hypertension, atherosclerosis, carotid artery disease, valvular heart disease, coronary artery disease, vasculitis, lupus, sickle cell disease, and trauma. Incidence is approximately 1–10 per 100,000. Irreversible retinal injury can occur within 90 minutes.
Causative Mechanisms
Embolic causes are most common and include cholesterol or platelet emboli from carotid atherosclerosis, carotid stenosis, valvular heart disease, atrial myxoma, or arterial dissection. Thrombotic causes result from rupture of an atherosclerotic plaque or hypercoagulable states such as sickle cell disease. Inflammatory causes include giant cell arteritis, lupus, and systemic vasculitis. Arterial spasm may be migraine-related. Reduced ocular perfusion may occur with severe hypotension, acute angle-closure glaucoma, or retrobulbar hemorrhage.
Clinical Presentation
Patients present with sudden, painless, unilateral vision loss. Some report prior transient episodes of visual loss lasting seconds to minutes (amaurosis fugax). Visual acuity is markedly reduced. An afferent pupillary defect is usually present. Fundoscopy may reveal emboli within retinal vessels appearing as yellow-white glistening plaques, ischemic retinal edema within 15–20 minutes, and a classic cherry-red spot at the fovea. Retinal arteries may appear empty or show segmented “box-carring.” Within 1–2 hours, the infarcted retina becomes opaque. Partial visual field deficits suggest branch retinal artery involvement.
Essential Evaluation
Immediate assessment includes visual acuity, visual fields, fundoscopic examination, intraocular pressure measurement, and urgent ophthalmology consultation.
Diagnostic Studies
Laboratory evaluation targets underlying causes and includes CBC with platelets, PT/PTT, electrolytes, renal function, glucose, ESR and CRP (especially in patients >55 years for giant cell arteritis), ANA, RF, RPR, hemoglobin electrophoresis, and serum protein electrophoresis. Imaging focuses on embolic sources and includes carotid Doppler ultrasound and echocardiography. Fluorescein angiography or electroretinography may confirm diagnosis.
Differential Considerations
Acute angle-closure glaucoma, central retinal vein occlusion, giant cell arteritis, optic neuritis, and retinal detachment.
Emergency Management Principles
This is a true ophthalmologic emergency. Treatment must begin immediately to attempt retinal salvage. Goals include embolus displacement or dissolution, vasodilation to improve retinal perfusion, and reduction of intraocular pressure to enhance the perfusion gradient.
Emergency Department Interventions
Initiate immediate ocular (global) massage with the patient supine: apply firm pressure on the closed eyelid for 15 seconds, release for 15 seconds, and repeat for five cycles. Administer 100% oxygen via nonrebreather mask and consider hyperbaric oxygen if within 24 hours of onset. Carbogen inhalation may be used if available. Reduce intraocular pressure with IV acetazolamide and topical timolol. Administer aspirin and IV heparin to prevent clot propagation. Obtain emergent ophthalmology consultation for possible anterior chamber paracentesis and consideration of intra-arterial fibrinolysis. If inflammatory arteritis is suspected, begin high-dose systemic corticosteroids immediately.
Medications
First-line options include acetazolamide 500 mg IV or PO, timolol maleate 0.5% ophthalmic drops, IV heparin (80 U/kg bolus then 18 U/kg/hr infusion), and carbogen inhalation. Second-line or adjunctive therapies include aspirin 325 mg PO, methylprednisolone 250 mg IV for suspected arteritis, mannitol, and sublingual nitroglycerin.
Disposition and Follow-Up
Most acute cases require admission for urgent evaluation of embolic, thrombotic, or inflammatory sources. Chronic or remote occlusions without active disease may be evaluated outpatient. All suspected cases require immediate ophthalmology involvement. Carotid imaging is recommended in most patients.
Clinical Insights and Pitfalls
Transient monocular vision loss (amaurosis fugax) is a warning sign for CRAO and systemic stroke and requires urgent evaluation. CRAO is a medical and ophthalmologic emergency with a very narrow therapeutic window. Thorough documentation of visual acuity and fundoscopic findings is essential.
Overview
Central retinal artery occlusion (CRAO) is an obstruction of the central retinal artery resulting in sudden, painless, monocular vision loss. It typically affects adults aged 50–70 years and is often described as a “stroke of the eye.” The ophthalmic artery is the first branch of the carotid artery. Risk factors include hypertension, atherosclerosis, carotid artery disease, valvular heart disease, coronary artery disease, vasculitis, lupus, sickle cell disease, and trauma. Incidence is approximately 1–10 per 100,000. Irreversible retinal injury can occur within 90 minutes.
Causative Mechanisms
Embolic causes are most common and include cholesterol or platelet emboli from carotid atherosclerosis, carotid stenosis, valvular heart disease, atrial myxoma, or arterial dissection. Thrombotic causes result from rupture of an atherosclerotic plaque or hypercoagulable states such as sickle cell disease. Inflammatory causes include giant cell arteritis, lupus, and systemic vasculitis. Arterial spasm may be migraine-related. Reduced ocular perfusion may occur with severe hypotension, acute angle-closure glaucoma, or retrobulbar hemorrhage.
Clinical Presentation
Patients present with sudden, painless, unilateral vision loss. Some report prior transient episodes of visual loss lasting seconds to minutes (amaurosis fugax). Visual acuity is markedly reduced. An afferent pupillary defect is usually present. Fundoscopy may reveal emboli within retinal vessels appearing as yellow-white glistening plaques, ischemic retinal edema within 15–20 minutes, and a classic cherry-red spot at the fovea. Retinal arteries may appear empty or show segmented “box-carring.” Within 1–2 hours, the infarcted retina becomes opaque. Partial visual field deficits suggest branch retinal artery involvement.
Essential Evaluation
Immediate assessment includes visual acuity, visual fields, fundoscopic examination, intraocular pressure measurement, and urgent ophthalmology consultation.
Diagnostic Studies
Laboratory evaluation targets underlying causes and includes CBC with platelets, PT/PTT, electrolytes, renal function, glucose, ESR and CRP (especially in patients >55 years for giant cell arteritis), ANA, RF, RPR, hemoglobin electrophoresis, and serum protein electrophoresis. Imaging focuses on embolic sources and includes carotid Doppler ultrasound and echocardiography. Fluorescein angiography or electroretinography may confirm diagnosis.
Differential Considerations
Acute angle-closure glaucoma, central retinal vein occlusion, giant cell arteritis, optic neuritis, and retinal detachment.
Emergency Management Principles
This is a true ophthalmologic emergency. Treatment must begin immediately to attempt retinal salvage. Goals include embolus displacement or dissolution, vasodilation to improve retinal perfusion, and reduction of intraocular pressure to enhance the perfusion gradient.
Emergency Department Interventions
Initiate immediate ocular (global) massage with the patient supine: apply firm pressure on the closed eyelid for 15 seconds, release for 15 seconds, and repeat for five cycles. Administer 100% oxygen via nonrebreather mask and consider hyperbaric oxygen if within 24 hours of onset. Carbogen inhalation may be used if available. Reduce intraocular pressure with IV acetazolamide and topical timolol. Administer aspirin and IV heparin to prevent clot propagation. Obtain emergent ophthalmology consultation for possible anterior chamber paracentesis and consideration of intra-arterial fibrinolysis. If inflammatory arteritis is suspected, begin high-dose systemic corticosteroids immediately.
Medications
First-line options include acetazolamide 500 mg IV or PO, timolol maleate 0.5% ophthalmic drops, IV heparin (80 U/kg bolus then 18 U/kg/hr infusion), and carbogen inhalation. Second-line or adjunctive therapies include aspirin 325 mg PO, methylprednisolone 250 mg IV for suspected arteritis, mannitol, and sublingual nitroglycerin.
Disposition and Follow-Up
Most acute cases require admission for urgent evaluation of embolic, thrombotic, or inflammatory sources. Chronic or remote occlusions without active disease may be evaluated outpatient. All suspected cases require immediate ophthalmology involvement. Carotid imaging is recommended in most patients.
Clinical Insights and Pitfalls
Transient monocular vision loss (amaurosis fugax) is a warning sign for CRAO and systemic stroke and requires urgent evaluation. CRAO is a medical and ophthalmologic emergency with a very narrow therapeutic window. Thorough documentation of visual acuity and fundoscopic findings is essential.
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