Retinal artery occlusion (RAO) usually presents as painless loss of monocular vision.[1, 2] Ocular stroke commonly is caused by embolism of the retinal artery, although emboli may travel to distal branches of the retinal artery, causing loss of only a section of the visual field. Retinal artery occlusion represents an ophthalmologic emergency, and delay in treatment may result in permanent loss of vision.[3]
Immediate intervention improves chances of visual recovery, but, even then, prognosis is poor, with only 21-35% of eyes retaining useful vision. Although restoration of vision is of immediate concern, RAO is a harbinger for other systemic diseases that must be evaluated immediately.
Blood supply to the retina originates from the ophthalmic artery, the first intracranial branch of the internal carotid artery that supplies the eye via the central retinal and the ciliary arteries. The central retinal artery supplies the retina as it branches into smaller segments upon leaving the optic disc. The ciliary arteries supply the choroid and the anterior portion of the globe via the rectus muscles (each rectus muscle has 2 ciliary arteries except the lateral rectus, which has 1).
Anatomic variants include cilioretinal branches from the short posterior ciliary artery, giving additional supply to part of the macular retina. A cilioretinal artery occurs in approximately 14% of the population.
Typical funduscopic findings of a pale retina with a cherry red macula (ie, the cherry red spot) result from obstruction of blood flow to the retina from the retinal artery, causing pallor, and continued supply of blood to the choroid from the ciliary artery, resulting in a bright red coloration at the thinnest part of the retina (ie, macula). These findings do not develop until an hour or more after embolism, and they resolve within days of the acute event. By this time, vision loss is permanent and primary optic atrophy has developed. In those with a cilioretinal artery supplying the macula, a cherry red spot is not observed.[3]
View Image
The cherry red spot of central retinal artery occlusion.
An embolism, atherosclerotic changes, inflammatory endarteritis, angiospasm, or hydrostatic arterial occlusion may occlude the retinal artery. The mechanism of obstruction may be obvious from comorbid systemic disease or physical findings. Atrial fibrillation and ipsilateral carotid stenosis are more commonly associated with prolonged visual disturbances.[3]
Animal studies have shown that a retina with completely occluded circulation has irreversible ischemic damage at 105 minutes but may recover at 97 minutes. Complete occlusion of retinal artery circulation in humans is rare with retinal artery disease; thus, retinal recovery is possible even after days of ischemia.
Branch retinal artery occlusion (BRAO) occurs when the embolus lodges in a more distal branch of the retinal artery.[1, 4] Branch retinal artery occlusion typically involves the temporal retinal vessels and usually does not require ocular therapeutics unless perifoveolar vessels are threatened. The central retinal artery is affected in 57% of occlusions, the branch retinal artery is involved in 38% of occlusions, and cilioretinal artery obstructions occur in 5% of occlusions.[5]
Estimates put the incidence of RAO at 0.85 per 100,000 per year, with a 10-year cumulative incidence of retinal emboli of 1.5%.[6]
A retrospective cohort study from South Korea explored the epidemiology of RAO from 2002 to 2018.[7] It identified 51,326 patients with RAO, predominantly male (56.2%), with an average age of 63.6 years at diagnosis. The nationwide incidence of RAO was reported as 7.38 per 100,000 person-years. Specifically, the incidence rate of noncentral RAO was 5.12 per 100,000 person-years, more than double that of central retinal artery occlusion (CRAO) at 2.25 per 100,000 person-years.
Mortality/Morbidity
Mortality rates associated with RAO vary significantly across studies, reflecting inconsistencies due to small sample sizes and varying follow-up durations. For example, individual studies have reported mortality rates ranging from 5.4% to 29.6% over periods from 2.2 to 11 years, while a pooled analysis from two population-based cohort studies over a decade reported a 56% mortality rate among RAO patients, nearly double that of non-RAO individuals. A comprehensive nationwide study observed a 13.8% mortality rate among 51,326 patients with newly diagnosed RAO over 14 years, with a standardized mortality ratio (SMR) of 7.33, indicating significantly higher mortality compared to the general population. This SMR was higher for CRAO than for noncentral RAO, and notably higher in women than in men, with younger patients under 50 years showing exceptionally high SMRs.
The primary causes of death in RAO patients are cardiovascular or cerebrovascular diseases, with acute myocardial infarction being the most frequent. This underscores the strong link between RAO and systemic cardiovascular conditions, further supported by the high prevalence of cardiovascular diseases at diagnosis. The association with risk factors such as hypertension, diabetes, and dyslipidemia underscores the need for comprehensive cardiovascular evaluation and management in RAO patients to address immediate risks and mitigate long-term cardiovascular complications.[8, 9] Additionally, RAO is linked to smoking and significantly increases the risk for stroke, affecting both eyes equally with bilateral involvement in 1-2% of cases, highlighting the severe prognosis associated with CRAO compared to noncentral RAO.[7]
Sex
Men are affected slightly more frequently than women.
Age
The mean age of presentation of RAO is early in the seventh decade of life, although a few cases have been reported in patients younger than 30 years.[10]
The etiology of occlusion changes, depending on the age at presentation.
The recovery of useful vision is closely linked to the speed of intervention and the initial visual acuity at presentation.
Research indicates that 21% of patients experienced an improvement of six levels in visual acuity, 35% improved by three levels, and 26% showed no improvement at all.[11] Patients who improved typically had an initial visual acuity of counting fingers and experienced vision loss for an average of 21.1 hours. In contrast, those who did not improve had an initial visual acuity of hand movement and experienced vision loss for an average of 58.6 hours.
The maximum delay in treatment that still resulted in significant visual recovery is documented to be approximately 72 hours. The presence of a cilioretinal artery with foveolar sparing is associated with better outcomes in visual acuity.
Branch retinal artery occlusions (BRAOs) generally have a higher likelihood of recovery, with 80% of cases improving to 20/40 vision or better. In contrast, CRAOs often result in severe vision loss, which remains profound despite treatment. Once retinal infarction sets in, which can occur as quickly as 90 minutes after the occlusion, the vision loss becomes permanent.[1]
Prompt diagnosis and treatment of underlying giant cell arteritis can protect vision in the unaffected eye and potentially restore some vision in the affected eye.
Patients must understand that the prognosis for visual recovery is poor and that the visual changes are usually a result of a systemic process that needs treatment.
Retinal artery occlusion (RAO) manifests as sudden, painless, and severe unilateral vision loss or visual field defect. The primary symptom reported is an acute and persistent loss of vision.[3, 12, 13] Central retinal artery occlusion (CRAO) typically results in profound central vision loss, whereas branch retinal artery occlusion (BRAO) may cause a peripheral visual field defect that could remain unnoticed. A complete visual field defect is indicative of CRAO, whereas a sectional visual field defect, often altitudinal and affecting either the upper or lower hemifield without crossing the vertical axis, suggests BRAO.
A medical history revealing hypertension or diabetes mellitus is common in patients with CRAO, present in 67% and 25% of cases, respectively. It is crucial to assess for conditions predisposing to embolism, such as atrial fibrillation, endocarditis, coagulopathies, or atherosclerotic disease. CRAO also may occur following prolonged direct pressure on the globe, as seen in drug-induced stupor or improper surgical positioning.
During the physical examination, it is crucial to assess for a relative afferent pupillary defect, which is characterized by a diminished pupillary response to direct light but brisk constriction when light is shone on the contralateral eye. This defect may be observed within seconds of the occlusive event. The fundus examination should be conducted acutely and may reveal a pale, opaque fundus with a cherry-red spot at the fovea.[3, 12, 13] The arteries might appear attenuated or completely bloodless, and an embolus, such as a cholesterol embolus (Hollenhorst plaque), may be visible. If the occlusion is localized to a major branch of the artery, the resulting fundus abnormalities and vision loss will be restricted to that specific sector of the retina.
For patients over 55 years old presenting with symptoms like headache, a tender and palpable temporal artery, jaw claudication, and fatigue, giant cell arteritis should be considered in the differential diagnosis. This condition demands prompt recognition and management to avert further complications.
Assess the degree of vision loss, which can range from no light perception to the ability to count fingers or detect hand movements. Documenting the ability to detect hand movements, count fingers, and assess visual fields at a standard distance of 1 to 3 feet is essential. This documentation aids in clear communication with consultants and ensures consistency in repeated examinations.
Additionally, the physical examination should include an evaluation for murmurs, carotid bruits, or other signs of cardiovascular disease.
Funduscopic Examination
A dilated funduscopic examination is necessary to observe the pathological signs of RAO. Initial findings may include a cherry-red spot and a ground-glass appearance of the retina, which are classic but may take hours to develop. Over days to weeks following the acute event, these funduscopic findings typically resolve, potentially leaving a pale optic disc as the only residual physical sign.
In cases of BRAO, retinal whitening along the distribution of the occluded vessel is observed, along with boxcar segmentation of the blood column, which indicates severe occlusion and slowed circulation. Emboli are detectable in approximately 20% of patients with CRAO.
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.
Embolism
Embolism usually is 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 RAOs.
Embolus from the heart is the most common cause of CRAO in patients younger than 40 years.
Amaurosis fugax preceding persistent loss of vision suggests BRAO or temporal arteritis and may represent emboli causing temporary occlusion of the retinal artery. (See Transient Vision Loss (TVL) and Amaurosis Fugax)
Coagulopathies from sickle cell anemia or antiphospholipid antibodies are common etiologies for CRAO in patients younger than 30 years.
Atherosclerotic changes
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.
Central artery spasm is an additional cause that can lead to occlusion of the vessel.
Inflammatory endarteritis
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
Migraines are rare causes of CRAO but are most common in patients younger than 30 years.
Central retinal artery occlusion (CRAO) typically presents as a sudden, painless loss of both visual acuity and peripheral vision in one eye.[4] The degree of vision loss can vary significantly; over 80% of patients initially present with visual acuity of "count fingers" or worse, though vision may be nearly normal if a cilioretinal artery is present. Color vision impairment correlates directly with the extent of visual acuity loss. Most patients exhibit an ipsilateral relative afferent pupillary defect unless there is contralateral optic neuropathy, which might mask this defect. Funduscopic examination often reveals retinal edema characterized by retinal whitening and a distinct cherry red spot due to preserved choroidal circulation beneath the fovea surrounded by pale, ischemic retina.
Other common findings include slow, segmental blood flow or 'boxcarring' in the attenuated retinal arteries, typically with a normal-appearing optic disc. Visible retinal emboli in the branch retinal arteries occur in less than 10% of cases, and emboli in the central retinal artery itself are even rarer due to its mostly retrobulbar course. The presence of optic disc edema alongside acute CRAO may indicate a rare co-occurrence of arteritic anterior ischemic optic neuropathy (AION) and inner retinal ischemia, suggesting underlying vasculitis. CRAO should be particularly suspected in patients over 50 with systemic symptoms like jaw claudication, polymyalgia rheumatica, or new-onset headache, among others, and elevated inflammatory markers should prompt further investigation.
For patients who exhibit symptoms that may suggest central retinal artery occlusion (CRAO), particularly those over age 50 years or those with systemic symptoms that could indicate vasculitis, conducting laboratory tests is essential.[4] Elevated levels of inflammatory markers may point to an underlying condition such as giant cell arteritis. Important tests in this context include the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), which are used to evaluate the level of inflammation potentially contributing to the occlusion.
Although laboratory studies are useful for identifying the cause of CRAO, they do not influence the emergency department (ED) treatment directly. These tests can include:
A complete blood count (CBC) to check for anemia, polycythemia, and platelet disorders.
Erythrocyte sedimentation rate (ESR) to detect inflammatory endarteritis when no other cause is evident.
Tests for coagulopathies, such as fibrinogen level, antiphospholipid antibodies, prothrombin time (PT), activated partial thromboplastin time (aPTT), and serum protein levels.
Cholesterol, triglycerides, and a full lipid panel to assess for atherosclerotic disease.
Blood cultures to identify bacterial endocarditis and septic emboli.
Additionally, sickle cell disease can also lead to retinal artery occlusion and may require specific tests for those considered at risk.
Imaging techniques are crucial for confirming a diagnosis of central retinal artery occlusion (CRAO).[4] Optical coherence tomography (OCT) is particularly valuable for identifying retinal edema in the early stages of the condition.[14] Fluorescein angiography, though more time-intensive, provides comprehensive images that reveal delayed or absent retinal perfusion and can identify specific locations of retinal arterial branch occlusions. These imaging methods are vital for accurately diagnosing CRAO and excluding other causes of vision loss.
Although imaging studies are important for understanding the cause of CRAO, they do not typically influence the treatment provided in emergency departments (EDs) and do not need to be conducted urgently in the ED setting.
For cases that do not require immediate emergency intervention, color fundus photography and fluorescein angiography should be used. Further investigations for potential sources of emboli can be carried out using Doppler ultrasonography and echocardiography. Additionally, carotid Doppler ultrasonography, magnetic resonance angiography (MRA), or computed tomography angiography should be used to check for atherosclerotic disease. Although not commonly performed in the ED, echocardiography can be useful for evaluating valvular disease, wall motion abnormalities, mural thrombi, and vegetations that may cause septic emboli.
Patients experiencing acute thromboembolic events should be urgently referred to a specialized stroke center for appropriate care.[1]
A comprehensive ophthalmologic evaluation is necessary for anyone suspected of having CRAO. This includes a dilated funduscopic examination or a nonmydriatic color fundus photograph to exclude other causes of acute vision loss such as vitreous and chorioretinal hemorrhage, retinal detachment, or acute optic neuropathy. In situations where an eye care specialist is not available, ocular fundus photography can be shared via telemedicine for expert confirmation. Further guidance on the clinical diagnosis of CRAO and related conditions is available in the American Academy of Ophthalmology’s Preferred Practice Pattern on Retinal and Ophthalmic Artery Occlusions.[15]
Perform an ECG to evaluate for possible atrial fibrillation (24-hour Holter monitor may be necessary if arrhythmia is suspected but not detected on ECG testing).
Systems are being developed to quickly identify and treat patients with central retinal artery occlusion (CRAO), which is essential for making treatments widely available and for successful enrollment in clinical trials.[4] The use of stroke code systems facilitates the rapid assessment of hemorrhage risk factors. In CRAO cases, it is necessary to add a funduscopic examination to confirm the diagnosis and rule out other causes such as vitreal or retinal hemorrhage, and to screen for arteritis. Although the effectiveness of thrombolysis in arteritic CRAO has not been assessed, early screening and immediate steroid therapy are recommended to protect vision in the other eye.[1, 15]
Given the narrow window for effective CRAO treatment and the high incidence of serious associated illnesses, immediate triage to an emergency department is crucial upon diagnosis in any medical setting. Stroke centers should collaborate with community eye care professionals to streamline patient transfers, potentially allowing more patients to receive timely treatment with tissue plasminogen activator (tPA).[4, 13, 15, 16, 17, 18, 19, 20, 21, 22, 23] Public awareness campaigns should highlight sudden, painless, monocular vision loss as a stroke symptom, similar to sudden unilateral weakness, facial droop, and speech difficulties.
In the emergency department, the treatment protocol for CRAO should start with an urgent ophthalmologic exam alongside a structured neurological evaluation and a brain CT scan without contrast. If coagulopathy is suspected, relevant blood tests should be conducted. For patients suspected of having giant cell arteritis (GCA), testing for erythrocyte sedimentation rate and C-reactive protein is advisable before deciding on tPA administration.[4, 13, 15, 16, 17, 18, 19, 20, 21, 22, 23] Following these assessments, if a patient is deemed suitable, an expedited inpatient workup should be initiated.
No specific prehospital treatment is available for retinal artery occlusion. The prognosis for visual recovery is related directly to the promptness in treatment; thus, rapid transport to the ED is essential.
There are 2 phases of care for patients with RAO. The first phase occurs in the ED and involves rapid detection and treatment of visual loss.
The second phase involves a thorough investigation for the cause of visual loss. No randomized controlled trials to support 1 treatment modality over any others are underway, but anecdotal reports and case series have suggested many modalities of treatment with varying success. Nonetheless, recent data suggest that these therapies may not be beneficial.[16, 24] In fact, Schrag et al (2015) suggest that classic treatments such as ocular massage and paracentesis may be harmful.[16]
Ocular massage
Apply direct pressure for 5-15 seconds, then release. Repeat several times.
Increased IOP causes a reflexive dilation of retinal arterioles by 16%.
A sudden drop in IOP with release increases the volume of flow by 86%.
Ocular massage dislodges the embolus to a point further down the arterial circulation and improves retinal perfusion.
Anterior chamber paracentesis
Advocated when visual loss has been present for less than 24 hours[25]
Early paracentesis is associated with increased visual recovery.
Slit-lamp removal of 0.1-0.4 mL of aqueous humor via tuberculin syringe and a 27-gauge needle may decrease IOP to 3 mm Hg.
Decrease in IOP is thought to allow greater perfusion, pushing emboli further down the vascular tree.
Other treatments
See Medication for details and mechanisms of action for medications.
Start timolol early in the treatment of CRAO, as this is readily available in most emergency departments. Acetazolamide and mannitol also should be used when CRAO is suspected because there are few downsides to starting these medications early.
In carbogen therapy (5% carbon dioxide, 95% oxygen), carbon dioxide dilates retinal arterioles, and oxygen increases oxygen delivery to ischemic tissues.[26]
Hyperbaric oxygen (HBO) therapy may be beneficial if initiated within 2-12 hours of symptom onset. Institute treatment with other interventions first; transport to a chamber may usurp precious time.[27, 28, 29, 30] Results from noncontrolled studies have been mixed. A 2001 controlled study in Israel showed a benefit in the treatment group.[27, 28] In this study, all patients were treated within 8 hours of symptom onset.
Thrombolytics may be useful, but they may not be much help if the embolus is cholesterol, talc, or calcific. Whereas some evidence suggests intra-arterial thrombolytics may be helpful, a 2015 meta-analysis suggests that systemic thrombolytics may be beneficial if given within 4.5 hours of onset.[16] Research is evaluating the role of thrombolytics in RAO.
Immediate evaluation is imperative for any patient with acute CRAO.
Ophthalmologists can decide with which further treatment (eg, thrombolytics, hyperbaric oxygen, retrobulbar block) to proceed.
Early treatment (< 2 h from onset of symptoms) with HBO may be associated with increased visual recovery, but HBO can be considered if the duration of visual loss is less than 12 hours. Inhalation of 100% oxygen at 2 atm can provide an arterial pO2 of 1000-1200 mm Hg, resulting in a 3-fold increase in oxygen diffusion distance through ischemic retinal tissues. Some studies show a 40% improvement of 2 or more levels of visual acuity.
In patients older than 50 years, there should be a high suspicion for giant cell arteritis (GCA).[15] If GCA is diagnosed or highly suspected, urgent systemic corticosteroid therapy should be considered. This treatment aims to preserve or restore vision in the affected eye and protect vision in the opposite eye.
The following organizations have released guidelines for the management of retinal artery occlusion (RAO). Key diagnostic and treatment recommendations have been reviewed and integrated throughout the article.
American Academy of Ophthalmology (2024): Preferred practice pattern on retinal and ophthalhmic artery occlusions.[15]
Medical therapy for retinal artery occlusion is directed toward lowering IOP, increasing retinal perfusion, and increasing oxygen delivery to hypoxic tissues. The first goal is accomplished by using the same drugs that are used in acute closed-angle glaucoma. Retinal perfusion may be increased by vasodilatory drugs, increasing arterial pCO2, or by giving peripheral thrombolytics to remove the offending embolus. Oxygen delivery is improved by breathing higher concentrations of oxygen or with hyperbaric oxygen.
Clinical Context:
Reduces rate of aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP. Used most frequently as single diuretic agent in acute management of CRAO. Other diuretics may be added if sufficient decrease in IOP not attained.
Clinical Context:
Used concomitantly with other topical ophthalmic drug products to lower IOP. If more than one ophthalmic drug is being used, administer the drugs at least 10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubules and increases renal excretion of sodium, potassium bicarbonate, and water to decrease production of aqueous humor.
Carbonic anhydrase (CA) is an enzyme found in many tissues of the body, including the eye. The reversible reaction it catalyzes involves the hydration of carbon dioxide and the dehydration of carbonic acid.
By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit CA in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP.
Clinical Context:
Reduces elevated IOP when the pressure cannot be lowered by other means.
Initially assess for adequate renal function in adults by administering test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h.
In children, assess for adequate renal function by administering test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 1 mL/h over 1-3 h.
Clinical Context:
Used in glaucoma to interrupt acute attacks. Oral osmotic agent for reducing IOP. Able to increase tonicity of blood until finally metabolized and eliminated by kidneys. Maximum reduction of IOP usually occurs 1 h of glycerin administration. Effect usually lasts approximately 5 h.
Clinical Context:
Reduces elevated (and normal) IOP, whether accompanied by glaucoma or not. Apraclonidine is a relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.
Clinical Context:
Converted to epinephrine in eye by enzymatic hydrolysis. Appears to act by decreasing aqueous production and enhancing outflow facility. Has same therapeutic effect as epinephrine with fewer local and systemic adverse effects. May be used as initial therapy or as adjunct with other antiglaucoma agents for control of IOP.
Lower IOP mainly by increasing outflow and reducing the production of aqueous humor. The combination of a miotic and a sympathomimetic has additive effects in lowering IOP. Each may be added in rotation after 5-minute intervals until target IOP is reached.
Clinical Context:
Directly stimulates cholinergic receptors in the eye, decreasing resistance to aqueous humor outflow.
Instillation frequency and concentration are determined by patient's response.
If other glaucoma medication also is being used, at bedtime, use gtt at least 5 min before gel.
Patients may be treated with pilocarpine as long as IOP is controlled and no deterioration in the visual fields occurs.
May use alone or in combination with other miotics, beta-adrenergic blocking agents, epinephrine, carbonic anhydrase inhibitors, or hyperosmotic agents to decrease IOP.
These direct-acting agents used to be considered the first step in the treatment of glaucoma; however, they have now yielded to the beta-blockers. DOC in this category is pilocarpine; a useful adjunctive agent that is additive to the effects of beta-blockers, carbonic anhydrase inhibitors, or sympathomimetics. Individualize dosage and frequency of administration. Patients with darkly pigmented irides may require higher strengths of pilocarpine.
Clinical Context:
Useful in the treatment of inflammatory and allergic reactions. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Lower IOP by decreasing the rate of aqueous humor production and possibly outflow. May be more effective than pilocarpine or epinephrine alone and have the advantage of not affecting pupil size or accommodation.
What is retinal artery occlusion (RAO)?What is the pathophysiology of retinal artery occlusion (RAO)?What is the prevalence of retinal artery occlusion (RAO) in the US?What is the mortality and morbidity associated with retinal artery occlusion (RAO)?What is the sexual predilection of retinal artery occlusion (RAO)?Which age group has the highest prevalence of retinal artery occlusion (RAO)?What is the prognosis of retinal artery occlusion (RAO)?What is included in patient education about retinal artery occlusion (RAO)?Which clinical history findings are characteristic of retinal artery occlusion (RAO)?What is included in the physical exam for retinal artery occlusion (RAO)?Which findings on funduscopic exam are characteristic of retinal artery occlusion (RAO)?What causes retinal artery occlusion (RAO)?What is the role of migraines in the etiology of retinal artery occlusion (RAO)?What is the role of embolism in retinal artery occlusion (RAO)?What is the role of atherosclerotic disease in the etiology of retinal artery occlusion (RAO)?What is the role of inflammatory endarteritis in the etiology of retinal artery occlusion (RAO)?What is the role of increased intraocular pressure in the etiology of retinal artery occlusion (RAO)?Which conditions are associated with retinal artery occlusion (RAO)?What are the possible complications of retinal artery occlusion (RAO)?What are the differential diagnoses for Retinal Artery Occlusion (RAO)?Which lab tests are performed in the workup of retinal artery occlusion (RAO)?What is the role of imaging studies in the workup of retinal artery occlusion (RAO)?What is the role of ECG in the workup of retinal artery occlusion (RAO)?What is the prehospital care for retinal artery occlusion (RAO)?What are the phases of care for retinal artery occlusion (RAO)?What is the role of ocular massage in the treatment of retinal artery occlusion (RAO)?What is the role of anterior chamber paracentesis in the treatment of retinal artery occlusion (RAO)?Which medications are used in the emergency department (ED) treatment of retinal artery occlusion (RAO)?What is the role of an ophthalmologist in the treatment of retinal artery occlusion (RAO)?How is retinal artery occlusion (RAO) prevented?What is included in the long-term monitoring of patients with retinal artery occlusion (RAO)?When is inpatient care indicated for the treatment of retinal artery occlusion (RAO)?When is patient transfer indicated for the treatment of retinal artery occlusion (RAO)?What are the goals of medical therapy for retinal artery occlusion (RAO)?Which medications in the drug class Beta-adrenergic blocking agents are used in the treatment of Retinal Artery Occlusion (RAO)?Which medications in the drug class Corticosteroids are used in the treatment of Retinal Artery Occlusion (RAO)?Which medications in the drug class Cholinergic/miotic agents are used in the treatment of Retinal Artery Occlusion (RAO)?Which medications in the drug class Sympathomimetics are used in the treatment of Retinal Artery Occlusion (RAO)?Which medications in the drug class Hyperosmotic diuretics are used in the treatment of Retinal Artery Occlusion (RAO)?Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Retinal Artery Occlusion (RAO)?
Benjamin Feldman, MD, Associate Partner, Emergency Medicine Physician, The Permanente Medical Group; Clinical Professor, Touro University College of Osteopathic Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Pascal SC Juang, MD, Medical Director, ED Information Systems, Department of Emergency Medicine, Hoag Memorial Hospital Presbyterian
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
Bruce M Lo, CPE, MD, MBA, RDMS, FACEP, FAAEM, FACHE, FAAPL, Chief, Department of Emergency Medicine, Sentara Norfolk General Hospital; Medical Director, Sentara Transfer Center; Professor and Assistant Program Director, Core Academic Faculty, Department of Emergency Medicine, Old Dominion University; Board Member, American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Assaad J Sayah, MD, FACEP, President and Chief Executive Officer, Cambridge Health Alliance
Disclosure: Nothing to disclose.
Neil Jain, MD, Staff Physician, Yale University School of Medicine, Department of Surgery, Section of Emergency Medicine
Disclosure: Nothing to disclose.
Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Disclosure: Nothing to disclose.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Kilbourn Gordon III, MD, and Enoch Huang, MD, to the development and writing of this article.
References
Mehta S. Central Retinal Artery Occlusion and Branch Retinal Artery Occlusion (Retinal Artery Occlusion). Porter RE. The Merck Manual of Diagnosis and Therapy. Rahway, NJ: Merck & Co Inc; Reviewed/Revised Apr 2024 | Modified Sept 2024.
Brown GC. Retinal artery obstructive disease. Ryan SJ, ed. Retina. St. Louis: Mosby; 1994. Vol 2: 1361-77.
AAO. Retinal and Ophthalmic Artery Occlusions PPP 2024. American Academy of Ophthalmology. Available at https://www.aao.org/education/preferred-practice-pattern/retinal-ophthalmic-artery-occlusions-ppp. February 2025; Accessed: March 25, 2025.
Dagra A, Lucke-Wold B, McGrath K, et al. Central Retinal Artery Occlusion: A Review of Pathophysiological Features and Management. S:VIN. 15 August 2023. 4(1):
Miyake Y, Horiguchi M, Matsuura M, et al. Hyperbaric oxygen therapy in 72 eyes with retinal arterial occlusion. 9th International Symposium on Underwater and Hyperbaric Physiology. 1987. 949-53.
The cherry red spot of central retinal artery occlusion.
The cherry red spot of central retinal artery occlusion.
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