Continuing Education Activity

Central retinal arterial occlusion is an ophthalmic emergency characterized by the sudden blockage of the central retinal artery, the primary blood vessel supplying the retina. This occlusion leads to rapid and severe vision loss in the affected eye. The most common cause of central retinal arterial occlusion is an embolus that obstructs the artery from the carotid artery or the heart. The sudden interruption of blood flow to the retina results in ischemia, causing damage to the retinal cells. Patients with central retinal arterial occlusion typically experience sudden, painless vision loss, necessitating immediate medical attention to address the underlying cause and attempt to restore blood flow. Unfortunately, the prognosis for visual recovery in central retinal arterial occlusion is limited, making early diagnosis and intervention critical in managing this serious eye condition. 

This activity describes the etiology, epidemiology, clinical presentation, evaluation, and management of central retinal arterial occlusion, providing clinicians with the knowledge and tools to improve patient care. Participating clinicians within emergency medicine, ophthalmology, and related disciplines are equipped to intervene when treating patients with central retinal arterial occlusion.

Objectives:

• Identify the etiology of central retinal arterial occlusion based on patient history and physical examination.

• Determine the prognosis of patients with central retinal arterial occlusion based on monitoring of vision.

• Develop comprehensive care plans for managing central arterial retinal occlusion by assessing patient comorbidities and risk factors.

• Collaborate with interdisciplinary healthcare teams, including ophthalmologists, cardiologists, and primary care physicians, to ensure comprehensive care for patients with central retinal artery occlusion.

Introduction

Central retinal artery occlusion (CRAO) is an ophthalmic emergency that can lead to sudden and severe vision loss.[1] CRAO has been defined as interruption of blood flow through the central retinal artery by thromboembolism or vasospasm with or without retinal ischemia. An embolus from the carotid artery, aortic arch, or heart often causes the condition. Giant cell arteritis is another rare but serious cause of CRAO.[2] The condition is similar to a cerebral ischemic event and is associated with an increased risk of subsequent cerebral stroke and ischemic heart disease.[3][4][5][6] Unfortunately, no established therapies exist to improve visual outcomes in CRAO.[7] Therefore, management should focus on preventing further vascular events, such as cerebral ischemia and cardiovascular death.[8] Although visual prognosis is typically poor, early diagnosis and treatment of CRAO can restore visual acuity in some patients.[9][10]

Etiology

CRAO is classified into nonarteritic CRAO and arteritic CRAO according to the basic pathophysiology.[11] Nonarteritic CRAO comprises more than 90% of cases.[12] An embolism is the most common cause of nonarteritic CRAO.[3] Atherosclerosis of the carotid artery may be noted on the same side in around 70% of patients with CRAO or branch retinal arterial occlusion.[13][14] The emboli may be composed of solid, liquid, or gaseous material and are carried from a distant source through the blood flow in the arteries.[15] The 3 main types of emboli are cholesterol (Hollenhorst plaques), calcium, and platelet-fibrin.[16] The most common type of retinal embolus is composed of cholesterol, accounting for around 46% to 80% of all retinal emboli. Platelet-fibrin is the second most common type, accounting for 6% to 32%. Calcific embolus is less common, accounting for 6% to 16%.[17][18][19][20][21] 

Cholesterol and platelet-fibrin emboli typically arise from atheromas in the carotid arteries, whereas calcium emboli often arise from cardiac valves.[22] On fundoscopy, calcium emboli appear white, cholesterol emboli, also known as Hollenhorst plaques, appear orange, and platelet-fibrin emboli appear dull white.[23] Retinal emboli may comprise other materials, such as talc; malignancy; fat, emboli resulting from long bone fractures; and infectious material commonly observed in patients with septicemia.

In-situ thrombosis may also cause CRAO. Thrombi may arise from various disorders, including atherosclerotic diseases, collagen-vascular disease, inflammatory states, and hypercoagulable states.[24] Predisposing conditions of CRAO include but are not limited to polycythemia vera, sickle cell anemia, multiple myeloma, factor V Leiden, prothrombin III mutation, hyperhomocysteinemia, activated protein C resistance, Behçet disease, pyoderma gangrenosum, and syphilis.[10][25] Cosmetic facial injections or fillers can cause CRAO if the agent is inadvertently injected inside an artery communicating with the central retinal artery.[26]

The causes of arteritic CRAO include giant cell arteritis, systemic lupus erythematosus, polyarteritis nodosa, antiphospholipid syndrome, granulomatosis with polyangiitis, and Takayasu arteritis.[27] Rapid differentiation between thromboembolic and arteritic processes is essential as optimal therapy differs, and the rapid administration of steroids for vasculitic causes of CRAO is associated with improved outcomes. Typically, this is completed by checking for inflammatory markers, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), which are raised in giant cell arteritis.[28]

Hayreh and Zimmerman classified CRAO into 4 groups as follows:

• Nonarteritic CRAO (66%) is caused by a permanent occlusion of the central retinal artery due to an embolus at the narrowest part of its course at its entry into the optic sheath.
• Nonarteritic CRAO with cilioretinal artery sparing (13%).
• Transient nonarteritic CRAO (16%) is a temporary blockage of the central retinal artery lasting from minutes to hours. This transient occlusion can occur due to various factors, including a migrating embolus, increased intraocular pressure, or a transient severe fall of perfusion pressure of the central retinal artery.
• Arteritic CRAO (5%) is caused by the occlusion of the common trunk of the central retinal artery and the posterior ciliary artery, typically due to giant cell arteritis.[2][29]

Epidemiology

The incidence of CRAO is approximately 1 to 1.9 per 100,000 people in the United States, with less than 2% presenting with bilateral involvement.[3][8] The age-standardized incidence of CRAO is 2.53 per 100,000 person-year in Japan, 2.7 per 100,000 person-year in Germany, and 1.8 per 100,000 person-year in Korea.[30][31] The incidence increases with age, with around 10 per 100,000 person-year in adults aged 80 or older.[32] The reported incidence and mean age at presentation may vary according to geographical location, but it typically occurs in individuals aged 60 to 70.[33] However, CRAO can also occur in the pediatric age group related to non-atherosclerotic causes, including trauma, embolism from calcified cardiac valves, and infection.[34] Men have a slightly higher incidence compared to women.[35] Patients diagnosed with CRAO have a life expectancy of 5.5 years compared to 15.4 years for age-matched patients with non-CRAO.[36][37] Risk factors for CRAO are similar to those of other thromboembolic diseases and include hypertension; smoking; hyperlipidemia; diabetes; high body mass index (BMI); dyslipidemia; atrial fibrillation; hypercoagulable states; cardiac disease, including rheumatic heart disease and other cardiac valve diseases; and male gender.[10][25] Approximately 37% to 40% of patients with CRAO have clinically significant ipsilateral carotid artery stenosis.[38][39][40]

Pathophysiology

In the clinical setting where occlusion may be incomplete, the return of vision may be achieved after delays of 8 to 24 hours. Up to 25% of the population receives significant macular collateral circulation from the cilioretinal artery.[41] Patients with this anatomical variant typically have less severe presentations and better long-term prognoses. 

Retinal ganglion cell infarction takes an indeterminate amount of time following total CRAO. However, some experts speculate that the process might be less than 15 minutes. In a study by Hayreh and colleagues, the central retinal artery was clamped in rhesus monkeys with hypertension and atherosclerosis aged 38. The monkeys were evaluated using fundus photo, fluorescein angiography, visual evoked potential, and electroretinography. This study found that the retina did not suffer detectable damage in histopathology, electrophysiology, and morphometric analysis in CRAO of 97 minutes in this experimental model. However, after this critical time, irreversible damage increased as the time of CRAO increased.[42] This experimental model may not be extrapolated directly for CRAO in humans.[43][44] The function of the ischemic brain stops within seconds, and tissue necrosis can occur in the brain within 5 minutes of ceasing the supply of oxygen and glucose.[45] Retinal ganglion cells are also recognized as part of the brain tissue.[46] Thus, the exact time for infarction of the retina after CRAO may need further evaluation. However, incomplete or intermittent forms of CRAO exist that can have a satisfactory visual outcome after prompt diagnosis and therapy.

The retina receives blood from 2 vascular systems. The central retinal artery supplies the inner retina, and choriocapillaris supplies the retinal pigment epithelium and outer retina, typically starting from the outer plexiform layer.[47] Short posterior ciliary arteries supply choriocapillaris. The watershed zone of the 2 systems may vary in individuals due to differences in retinal thickness, light exposure, and specific retinal locations. When the central retinal artery is occluded, the inner retina, specifically the nerve fiber and ganglion cell layer, becomes ischemic and loses transparency.[2]

Histopathology

The central retinal artery is the first intraorbital branch of the ophthalmic artery.[48] The artery enters the optic nerve 1 cm posterior to the globe and supplies blood to the retina.[49] The CRAO results in inner retinal ischemia, vision loss, and eventual necrosis. Acute CRAO results in retinal edema and pyknosis of the ganglion cell nuclei. As ischemia progresses, the retina becomes opacified and takes on a yellow-white appearance.

History and Physical

CRAO typically presents with sudden, painless, monocular vision and visual field loss that occurs over seconds. Patients may report an antecedent transient visual loss, also known as amaurosis fugax, and a history of atherosclerotic disease.[50] In patients with no light perception, ophthalmic artery occlusion, abnormalities in the optic nerve, and occluded short posterior ciliary arteries should be excluded.[51]

Patients with CRAO often present with severe monocular vision loss and an afferent pupillary defect, also known as Marcus Gunn pupil.[52] The relative afferent pupillary defect may not be noticeable if the fellow eye has a damaged retina or optic nerve due to preexisting diseases, including glaucoma. The visual acuity can vary from loss of light perception to finger counting. According to Hayreh and Zimmerman, approximately 75% of patients with CRAO present with vision of finger counting or worse.[29] Occasionally, some patients have visual acuity better than 20/40. The causes of good visual acuity in CRAO may include collateral circulation, sparing of fovea due to patent cilioretinal artery, peripheral retinal arterial occlusion, retrograde blood flow through the central retinal artery, paracentral acute middle maculopathy, individual variability, and incomplete or partial CRAO.[53][54] The evolution of CRAO may progress from mild retinal whitening with hyperreflectivity of the inner nuclear layer, which is only visible on optical coherence tomography (OCT) before the full-fledged fundus appearance is observed.[55] Intraocular pressures, anterior chamber examinations, and extraocular eye movements are within normal limits.

A thorough fundoscopic examination is crucial for accurate diagnosis of CRAO, and a dilated examination should be performed on any patient without contradictions to mydriatic medications who presents with symptoms suggestive of CRAO. The patient may have a normal-looking fundus on a cursory examination. The typical white retina and cherry red spot may take hours to be present on ophthalmoscopy. However, inner retinal hyperreflectivity may be observed on OCT in the early stages of CRAO.[56] Severe sudden onset vision loss and relative afferent pupillary defect in the eye are other indicators. The retina appears diffusely pale on fundoscopy with a cherry red macular spot.[9] The whitening of the retina results from ischemia of the nerve fiber layer around the fovea, which becomes opaque and swollen. A cherry red spot at the macula results from the preserved choroidal circulation (perfused and red vascular choroid) visible beneath the thin fovea with a surrounding white retina that blocks the view of the vascular choroid. The retinal whitening may be more appreciable when comparing the fundus picture of the involved eye with the fellow normal eye. Some cases of CRAO may not show a cherry red spot at the macula.[57] 

Narrowing, boxcarring, also known as cattle-tracking, or slow segmental blood flow in the arterioles or venules may also be observed (see Image. Central Retinal Arterial Occlusion). The blood flow through the retinal artery is slow and can be visualized by the movement of the segments of blood during the slit-lamp biomicroscopic examination using a 90D lens. The slow blood flow through the arterioles is also prominently observed during fluorescein angiography. In this procedure, the dye filling of the arteriole progresses slowly. This observation is better appreciated by comparing early images of the involved eye taken in rapid succession or using video angiography.[58] Retinal arteriolar caliber may be irregularly narrowed. Cilioretinal arteries arising from short posterior ciliary arteries are present in around 15% to 25% of patients, and these typically supply the fovea. Thus, in CRAO with the patent cilioretinal artery (cilioretinal artery sparing), the central vision may be maintained. However, the visual field is severely reduced (see Image. Central Retinal Artery Occlusion with Cilioretinal Artery Sparing). Typically, no retinal hemorrhage of retinal venous dilation and tortuosity occurs, as noted in central retinal venous occlusion. Multiple cotton wool spots characterize transient nonarteritic CRAO and may appear similar to Purtscher retinopathy.[59]

In up to 40% of cases, arteriolar emboli may be visualized.[60] Other conditions, such as commotio retinae, Tay-Sachs disease, and Niemann-Pick disease, may present with a cherry red spot on fundoscopic examinations but can be easily differentiated based on clinical presentation.[61][62] Arteritic CRAO almost always has a pale edematous disc suggestive of arteritic anterior ischemic optic neuropathy with characteristics of CRAO.[63][64][65] Arteritic CRAO should be suspected in older patients with a history of jaw claudication, polymyalgia rheumatica, and scalp tenderness. Ipsilateral carotid artery disease may cause a contralateral motor or sensory deficit.[66] The carotid pulse should be checked.

Evaluation

CRAO is analogous to a cerebral vascular accident involving the retina. As such, the workup for CRAO closely parallels the workup for stroke or transient ischemic attacks.[12] The ophthalmic workup includes a photo of the color fundus and an OCT of the macula. The color fundus photograph typically reveals retinal whitening in the involved eye compared to the contralateral eye. Cherry red spots at the macula may or may not be visible. The OCT of the macula shows inner retinal hyperreflectivity in the acute phase (see Image. Optical Coherence Tomography of Macula in Central Retinal Artery Occlusion). Some cases of CRAO may have paracentral acute middle maculopathy characterized by hyperreflectivity of the inner nuclear layer.[67] Over time, the thinning of the inner retina becomes apparent. A fundus fluorescein angiogram (FFA) is not required for the diagnosis. However, the FFA shows a slow progression of the dye in the arterioles (see Image. Fundus Fluorescein Angiogram in Central Retinal Artery Occlusion). The choroid fills normally in nonarteritic CRAO. An absent or late filling of the retinal arterioles may occur. The choroidal phase may show hypoperfusion in arteritic CRAO or ophthalmic artery occlusion. In some cases of CRAO, the FFA may be normal.[58][68] 

Initial blood work should include point-of-care glucose, a complete blood count with differential, and coagulation assays, including prothrombin time (PT), international normalized ratio (INR), and activated partial thromboplastin time (PTT). An ESR and CRP should be obtained to rule out giant cell arteritis. If inflammatory markers are elevated, and the patient's history and physical examination findings are consistent with giant cell arteritis, high-dose intravenous (IV) steroids should be initiated immediately.[69] Temporal biopsy should be planned in such cases within 2 weeks of the initiation of steroid therapy.[70][71]

If symptom onset occurs within a window of less than 4.5 hours, a computed tomography (CT) head without contrast should be obtained to rule out intracranial hemorrhage and assess the patient's eligibility for thrombolytic therapy.[8] Other tests should be considered based on individual risk factors and medical history. These tests include hemoglobin A1c (glycated hemoglobin), lipid profile, Rh factor (rheumatoid factor), antinuclear antibody, fluorescent treponemal antibody absorption test, hypercoagulability labs, carotid artery imaging, electrocardiogram, echocardiogram, and outpatient Holter monitoring.[72] Carotid artery imaging is a crucial part of systemic evaluation as the most common source of embolus. The imaging modalities include carotid duplex ultrasound, CT, magnetic resonance, and digital subtraction angiography. If carotid imaging is normal, cardiac evaluation should include modalities such as echocardiography. Patients with CRAO require interprofessional collaboration among ophthalmologists, cardiologists, primary care clinicians or internists, and neurologists.

Treatment / Management

The visual prognosis of CRAO remains poor despite treatment, and ongoing research aims to identify evidence-based, effective, and safe therapy. No consensus is available regarding the optimal treatment for CRAO, although early IV thrombolytic administration shows promise.[73] Time is crucial in management, and treatment should be started before the diagnosis is confirmed. Proposed therapies are aimed at restoring retinal perfusion or oxygenation. Basic strategies include vasodilation, causing ocular hypotony so that the thrombus or embolus dislodges, increasing oxygen tension, surgical removal of the clot, or thrombolysis. Lifestyle modification and control of systemic factors are essential for secondary prevention.

Various therapies have been tried with variable success:

• Immediate ocular massage: Ocular massage may induce oscillations of intraocular pressure and dislodge the offending thrombus. The patient is seated on a slit-lamp comfortably. Pressure is applied on the globe with a 3-mirror Goldmann lens for 10 seconds until retinal arterial pulsations are visible. If the pulsations are not visible, cessation of arterial flow should be obtained, followed by the release of pressure for 5 seconds. In the absence of a slit-lamp or Goldmann lens, digital ocular massage may be tried. However, ocular massage is not a standard treatment for CRAO. Research on the effectiveness is limited and inconclusive, although described since the 1880s.

• Drugs to reduce intraocular pressure: IV acetazolamide 500 mg, mannitol (1.5 to 2 g/kg over 30 to 60 min), and topical timolol (0.5%, 1 drop twice daily) may be started to reduce intraocular pressure, which can increase the perfusion pressure (mean arterial pressure or intraocular pressure).

• Anterior chamber paracentesis: Paracentesis is often recommended in conjunction with or after failed digital ocular massage. A 26- or 27-gauge needle is inserted into the anterior chamber anteriorly to the limbus, and around 0.1 to 0.2 mL of aqueous liquid is drained. This action is expected to cause sudden ocular hypotony and possible dilation of retinal arteries. However, anterior chamber paracentesis caused a maximum 20% rise in retinal arterial flow in animal studies. Complications of this procedure include hyphema and endophthalmitis. A study on 74 patients with CRAO found no added benefit of anterior chamber paracentesis compared to conservative treatment. The authors recommended against use in CRAO, considering the risks of ocular injury and infection.[74][75][76]

• Carbogen: A mixture of 95% oxygen and 5% carbon dioxide inhalation is thought to cause vasodilation and increased oxygen supply to the retina. Carbogen is given 10 minutes per 1 hour during waking and 10 minutes per 4 hours during sleep. The therapy is continued for 2 to 3 days. A study involving 89 cases of patients with acute CRAO failed to show the benefit of combined anterior chamber paracentesis with carbogen inhalation compared to no interventions.[77]

• Hyperventilation into a paper bag: Respiratory acidosis and vasodilation are induced by either hyperventilation into a paper bag or by inhaling 10% carbon dioxide.

• Pentoxifylline: The recommended dosage for this hemorheological agent is three 600 mg tablets daily. The hemorheological agent works by increasing erythrocyte flexibility, reducing blood viscosity, and improving perfusion. The medication has been tested in patients with CRAO and shown to increase retinal flow, although studies evaluating this drug have multiple limitations.[78][79]

• Sublingual isosorbide dinitrate: 10 mg of isosorbide dinitrate causes vasodilation and has been utilized in managing CRAO, although comprehensive studies on its efficacy are currently insufficient.[80]

• Supplemental oxygen

• IV methylprednisolone: The mainstay of therapy to manage arteritic CRAO caused by giant cell arteritis is 1 g/d for 1 to 3 days. This dose reduces inflammatory causes and retinal edema.

• IV thrombolysis (fibrinolysis): The most commonly used therapy is the IV infusion of alteplase, also known as tissue plasminogen activator, 0.9 mg/kg. The initial 10% dose is delivered rapidly in 1 minute, and the rest is delivered through slow infusion for 59 minutes. Around 5.8% of patients with CRAO in the United States receive tissue plasminogen activator. A patient-level meta-analysis found that thrombolysis was more beneficial compared to the natural history group when administered within 4.5 hours of onset. Larger randomized controlled trials are necessary to further evaluate the role of IV fibrinolysis in treating patients with CRAO. The American Heart Association recommends considering IV thrombolysis in nonarteritic CRAO within 4.5 hours without any systemic contraindications of IV thrombolysis.[81][82]

• Intra-arterial thrombolysis: In the EAGLE study, a catheter was super selectively inserted into the ophthalmic artery, and a maximum of 50 mg of recombinant tissue plasminogen activator was injected. This study was prematurely stopped due to safety concerns as intra-arterial thrombolysis had similar efficacy but higher adverse events compared to conservative standard treatment. Adverse events of this procedure include dislodgment of atheromatous plaque, arterial dissection, and spasms. The American Heart Association recommends considering intra-arterial thrombolysis in centers with this facility for patients who are not candidates for IV thrombolysis and who have presented within 6 hours.[8][39]

• Hyperbaric oxygen therapy: This therapy aims to increase blood oxygen tension. Typically, 2 to 2.5 atm is administered for 90 minutes within 8 hours of symptom onset.[1][83]

• Neodymium:yttrium-aluminum-garnet laser embolectomy: The neodymium:yttrium-aluminum-garnet laser (1064 nm) is used to lyse the embolus applying power up to 2 mJ. This procedure is performed using a fundus contact lens such as Goldmann 3-mirror or Volk Quadraspheric lens. A meta-analysis noted that although the procedure was associated with visual recovery in most cases, vitreous hemorrhage was frequent. Higher pulse energy may be associated with more vitrectomies and cause subretinal or vitreous hemorrhage.[84][85]

• Pars plana vitrectomy: The procedure with a longitudinal incision over the artery or arteriole and thrombus removal has been reported in a few cases.[79][86][87][88]

Differential Diagnosis

The differential diagnosis of CRAO includes several conditions.

• Ophthalmic artery occlusion: Ophthalmic artery occlusion is characterized by incomplete or complete occlusion of the ophthalmic artery, resulting in severe ischemia or infarction of the globe and surrounding structures. Visual acuity typically means no perception of light, and the cherry red spot at the macula may not be visible due to choroidal ischemia.
• Paracentral acute middle maculopathy: Paracentral acute middle maculopathy is characterized by hyperreflectivity of the inner nuclear layer on the OCT macula. Some cases with aracentral acute middle maculopathy may progress to CRAO, and this may denote a spectrum of ischemic disorders.
• Purtscher retinopathy: Purtscher flecken may simulate cotton wool spots observed in transient nonarteritic CRAO.
• Hypertensive retinopathy: The retinopathy is bilateral with arteriovenous changes, papilledema, cotton wool spots around the optic disc, and subretinal fluid around the disc extending up to the nasal side of the fovea. The blood pressure is raised severely.
• Differential diagnoses of a cherry red spot at the macula include lysosomal storage disorders, commotion retinae, retinitis around the optic disc, and adverse relations of drugs.[9][59]

Prognosis

The visual prognosis of CRAO remains poor despite the recent advances in the medical field. Less than 10% to 20% of patients with CRAO regain functional vision.[82][89] A large study involving 130 patients with CRAO showed that visual improvement was most notable in cases of transient nonarteritic CRAO, with approximately 82% of affected eyes showing improvement from baseline vision of finger counting or worse. Around 67% of eyes with nonarteritic CRAO with patent cilioretinal artery had experienced visual gain compared to 22% with nonarteritic CRAO. The vision typically improved within the first 7 days.[29]

CRAO has been included in the definition of acute ischemic stroke, which encompasses an episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction, as outlined by the American Heart Association.[8] Similar to acute ischemic stroke, CRAO is associated with an increased risk of recurrent vascular events.[90][91] Retinal arterial occlusion may result in higher mortality rates compared to the general population.[92]

Complications

Patients with CRAO eventually develop inner retinal thinning and optic atrophy. Around 20% of cases develop neovascularization of the iris, typically after 30 to 60 days, although this may occur within 1 week. Such cases need panretinal photocoagulation with or without intravitreal anti-vascular endothelial growth factor (anti-VEGF agents) injection.[93] The chances of the other eye involvement are high with arteritic CRAO in giant cells, and arteritis and IV high-dose steroids may prevent the involvement of the other eye.[94] As mentioned, the risk of arterial thromboembolic events and mortality may be high after CRAO, and patients should be informed.

Deterrence and Patient Education

Patients should be aware of the signs and symptoms of CRAO, such as sudden, painless vision loss. The urgency of seeking immediate medical attention in the event of sudden vision loss should be emphasized, along with the recommendation to regularly check their vision by closing alternate eyes to detect any sudden visual decline. Time is critical in preserving vision, and delays may result in irreversible damage. CRAO is a medical emergency, and although no therapy is effective in such cases, early diagnosis and prompt initiation of available treatment may improve visual outcomes.

Common risk factors for CRAO, such as hypertension, diabetes, cardiovascular disease, and hyperlipidemia, should be discussed. Patients should be encouraged to manage and control these risk factors through lifestyle modifications, including avoidance of smoking, and medications. Patients should be advised about the necessity of undergoing a thorough examination by healthcare professionals, including eye specialists and possibly vascular specialists, to determine the underlying cause of CRAO and guide appropriate treatment decisions. The uncertain prognosis for visual recovery in CRAO should be discussed. Although some individuals may experience partial or complete recovery, most of the patients (around 80%) may have permanent vision loss. 

The outcome depends on factors such as the extent of ischemia and the effectiveness of interventions. Follow-up with eye care professionals and other relevant specialists should be emphasized. Regular monitoring is essential to assess the patient's visual function, manage risk factors, and address potential complications. The emotional impact of sudden vision loss should be acknowledged, and information should be provided about available support services, including counseling or support groups, to help patients cope with the psychological aspects of the condition. To reduce the risk of vascular events, the patients should be educated on lifestyle modifications, such as maintaining a healthy diet, exercising regularly, managing blood pressure and cholesterol levels, and refraining from smoking.[95]

Enhancing Healthcare Team Outcomes

Healthcare professionals should promptly refer patients exhibiting signs of CRAO to an ophthalmologist. CRAO is the sudden blockage of the central retinal artery, resulting in retinal hypoperfusion, rapidly progressive cellular damage, and vision loss. Retina survival depends on the degree of collateralization and the duration of retinal ischemia. Prompt diagnosis and early treatment to dislodge or lyse the offending embolus or thrombus is crucial to avoid irreversible retinal damage and blindness.

The prognosis for these patients depends on the timing of diagnosis and initiation of treatment. Individuals treated promptly often regain their sight, but delay can cause some degree of vision loss and, in some cases, permanent blindness. The team treating a patient with CRAO may include ophthalmologists, cardiologists, primary care physicians or internists, neurologists, nurses, and pharmacists. Ophthalmologists help confirm the diagnosis and follow up on the ocular condition. The cardiologists perform a detailed search for the source of the embolus and ensure optimal cardiovascular health. The internists or the primary care clinicians refer to the ophthalmologists urgently without delay and in following up on the patient's systemic condition. Neurologists help exclude cerebrovascular accidents and follow up on such cases. The nursing staff monitors the patient. Pharmacists help patients with medication management. Effective communication and collaboration among team members facilitate a swift response, improving patient care. This holistic approach ensures that the patient receives prompt management, leading to a potentially better outcome that includes preserving vision.[96]