CRAO Differential Diagnosis: A Comprehensive Guide for Rapid and Accurate Assessment

Central retinal artery occlusion (CRAO) is a critical ophthalmic condition demanding immediate recognition and intervention. Characterized by a sudden and often devastating loss of vision, CRAO occurs when the central retinal artery, the principal vessel supplying blood to the retina, becomes blocked. This blockage leads to retinal ischemia and potentially irreversible damage to retinal cells. Frequently, CRAO is caused by an embolus originating from the carotid arteries or the heart, obstructing the retinal artery. Patients typically present with abrupt, painless vision loss, requiring urgent medical attention to identify the underlying cause and attempt to restore retinal blood flow. Visual recovery in CRAO is often limited, making prompt and accurate diagnosis paramount.

This article serves as an in-depth resource for clinicians, offering a detailed exploration of the differential diagnosis of central retinal artery occlusion. Understanding the nuances of CRAO and its mimics is crucial for effective patient management. This activity will enhance clinicians’ knowledge of the etiology, epidemiology, clinical presentation, evaluation, and, most importantly, the differential diagnosis of CRAO. By participating in this educational endeavor, healthcare professionals in emergency medicine, ophthalmology, and related fields will be better equipped to provide optimal care for patients presenting with suspected central retinal artery occlusion.

Objectives:

• Discern the differential diagnoses of central retinal artery occlusion based on patient history, clinical examination, and diagnostic findings.
• Evaluate the key differentiating factors between CRAO and its mimics to ensure accurate diagnosis and management.
• Formulate appropriate diagnostic and management strategies for patients presenting with symptoms suggestive of CRAO, considering the differential diagnoses.
• Enhance collaboration within interdisciplinary healthcare teams to optimize the diagnostic process and comprehensive care for patients with suspected central retinal artery occlusion and related conditions.

Introduction to CRAO and its Diagnostic Challenges

Central retinal artery occlusion (CRAO) is an ophthalmic emergency marked by sudden, severe vision loss. [1] It results from the interruption of blood flow in the central retinal artery, typically due to thromboembolism or vasospasm, leading to retinal ischemia. Emboli from the carotid artery, aortic arch, or heart are common culprits, while giant cell arteritis represents a rarer but serious arteritic cause. [2] CRAO shares similarities with cerebral ischemic events and is linked to an increased risk of subsequent stroke and ischemic heart disease. [3, 4, 5, 6] Unfortunately, there are no universally effective treatments to guarantee visual recovery in CRAO. [7] Management strategies primarily focus on preventing further vascular complications, such as stroke and cardiovascular events. [8] Although visual outcomes are often poor, timely diagnosis and intervention can improve visual prognosis in some cases. [9, 10]

The diagnostic process for CRAO, especially in the acute setting, necessitates a robust understanding of its differential diagnosis. Several conditions can mimic CRAO, presenting with similar symptoms like sudden vision loss and retinal changes. Accurate differentiation is crucial because the management and prognostic implications vary significantly across these conditions. This article will thoroughly examine the Crao Differential Diagnosis, providing a framework for clinicians to confidently distinguish CRAO from its mimics and ensure appropriate patient care.

Etiology and Classification of CRAO: Key to Differential Diagnosis

To effectively approach the differential diagnosis of CRAO, it is essential to understand its underlying etiologies and classifications. CRAO is broadly categorized into nonarteritic and arteritic forms based on pathophysiology. [11] Nonarteritic CRAO accounts for over 90% of cases. [12] Embolism is the most frequent cause of nonarteritic CRAO. [3] A significant proportion of patients, around 70%, with CRAO or branch retinal artery occlusion exhibit atherosclerosis of the ipsilateral carotid artery. [13, 14] Emboli can be solid, liquid, or gaseous, originating from distant sources and traveling through arterial blood flow. [15] The three main types of emboli are cholesterol (Hollenhorst plaques), calcium, and platelet-fibrin. [16] Cholesterol emboli are the most common, comprising 46% to 80% of retinal emboli, followed by platelet-fibrin emboli (6% to 32%) and less frequent calcific emboli (6% to 16%). [17, 18, 19, 20, 21]

Cholesterol and platelet-fibrin emboli usually arise from carotid artery atheromas, whereas calcium emboli often originate from cardiac valves. [22] Fundoscopy reveals distinct appearances: calcium emboli are white, cholesterol emboli (Hollenhorst plaques) are orange, and platelet-fibrin emboli are dull white. [23] Other less common embolic materials include talc, malignant cells, fat (from long bone fractures), and infectious agents, particularly in septicemia.

Table

Common sources of emboli include the internal or common carotid artery and, less frequently, the brachiocephalic artery or aorta.

In-situ thrombosis can also cause CRAO, arising from conditions like atherosclerotic diseases, collagen-vascular diseases, inflammatory conditions, and hypercoagulable states. [24] Predisposing conditions include 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 can also lead to CRAO if injected into arteries communicating with the central retinal artery. [26]

Arteritic CRAO is associated with giant cell arteritis and other inflammatory conditions such as systemic lupus erythematosus, polyarteritis nodosa, antiphospholipid syndrome, granulomatosis with polyangiitis, and Takayasu arteritis. [27] Differentiating between thromboembolic and arteritic CRAO is critical due to differing optimal therapies. Rapid steroid administration for arteritic causes is crucial for better outcomes. Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are typical in giant cell arteritis and aid in differentiation. [28]

Hayreh and Zimmerman’s classification further categorizes CRAO into four groups:

• Nonarteritic CRAO (66%): Permanent occlusion due to embolus at the narrowest point of the central retinal artery at its entry into the optic sheath.
• Nonarteritic CRAO with cilioretinal artery sparing (13%).
• Transient nonarteritic CRAO (16%): Temporary blockage lasting minutes to hours, due to migrating emboli, increased intraocular pressure, or transient hypotension.
• Arteritic CRAO (5%): Occlusion of the common trunk of the central retinal artery and posterior ciliary artery, typically due to giant cell arteritis. [2, 29]

Understanding these etiologies and classifications is fundamental when considering the crao differential diagnosis. For instance, in older patients, arteritic CRAO must be promptly ruled out due to the need for immediate steroid treatment, differentiating it from nonarteritic causes that require different management strategies.

Epidemiology and Risk Factors: Context for Differential Diagnosis

The incidence of CRAO in the United States is approximately 1 to 1.9 per 100,000 people, with bilateral involvement in less than 2% of cases. [3, 8] Age-standardized incidence rates vary geographically, with 2.53 per 100,000 person-years in Japan, 2.7 in Germany, and 1.8 in Korea. [30, 31] Incidence increases with age, reaching about 10 per 100,000 person-years in adults aged 80 and older. [32] Typically, CRAO occurs in individuals aged 60 to 70, although age at presentation can vary geographically. [33] It can also occur in children, often related to non-atherosclerotic causes such as trauma, emboli from calcified cardiac valves, and infections. [34] Men are slightly more affected than women. [35] Patients with CRAO have a reduced life expectancy compared to age-matched controls. [36, 37]

Risk factors for CRAO mirror those of other thromboembolic diseases, including hypertension, smoking, hyperlipidemia, diabetes, high BMI, dyslipidemia, atrial fibrillation, hypercoagulable states, cardiac disease, and male gender. [10, 25] Significant ipsilateral carotid artery stenosis is found in approximately 37% to 40% of CRAO patients. [38, 39, 40]

Epidemiological data and risk factor profiles are vital in the crao differential diagnosis. For instance, an older patient with new-onset vision loss and risk factors for giant cell arteritis (e.g., age >50, headache, jaw claudication) increases the suspicion for arteritic CRAO. Conversely, in a younger patient without arteritis risk factors but with a history of migraine or vasospasm, transient CRAO or other vasospastic retinal conditions might be considered in the differential.

Clinical Presentation: Recognizing CRAO and its Mimics

CRAO typically presents with sudden, painless, monocular vision loss and visual field defects occurring within seconds. Patients may report prior transient visual loss (amaurosis fugax) and a history of atherosclerotic disease. [50] Absence of light perception may suggest ophthalmic artery occlusion, optic nerve abnormalities, or short posterior ciliary artery occlusion, which should be considered in the crao differential diagnosis. [51]

Patients often exhibit severe monocular vision loss and an afferent pupillary defect (Marcus Gunn pupil). [52] Visual acuity can range from no light perception to finger counting. About 75% of patients present with vision of finger counting or worse. [29] However, some patients may have better visual acuity (better than 20/40), potentially due to collateral circulation, foveal sparing by a patent cilioretinal artery, peripheral retinal arterial occlusion, retrograde blood flow, paracentral acute middle maculopathy, individual variability, or incomplete CRAO. [53, 54] Early CRAO may show mild retinal whitening and inner nuclear layer hyperreflectivity on OCT before the classic fundus appearance is evident. [55] Intraocular pressure, anterior chamber, and extraocular movements are typically normal.

Fundoscopic examination is critical for diagnosing CRAO. A dilated exam should be performed in any patient with suggestive symptoms unless contraindicated. Initially, the fundus may appear normal, and the typical white retina and cherry-red spot might take hours to develop. However, OCT can reveal early inner retinal hyperreflectivity. [56] Key fundoscopic findings include diffuse retinal pallor with a cherry-red spot at the macula. [9] The retinal whitening is due to nerve fiber layer ischemia around the fovea, becoming opaque and swollen. The cherry-red spot results from preserved choroidal circulation visible through the thin fovea, contrasted against the surrounding white retina. Comparing the affected eye to the unaffected eye can enhance the appreciation of retinal whitening. However, a cherry-red spot may be absent in some CRAO cases. [57]

Other possible findings include narrowing or segmentation of blood flow in arterioles and venules (boxcarring or cattle-tracking) (see Image. Central Retinal Arterial Occlusion). Slow blood flow can be visualized during slit-lamp biomicroscopy with a 90D lens. Fluorescein angiography also demonstrates slow arteriolar filling. Retinal arteriolar caliber may be irregularly narrowed. Cilioretinal arteries, present in 15% to 25% of patients, can spare central vision in CRAO if patent (cilioretinal artery sparing) (see Image. Central Retinal Artery Occlusion with Cilioretinal Artery Sparing). Transient nonarteritic CRAO may show multiple cotton wool spots, resembling Purtscher retinopathy. [59]

Arteriolar emboli are visible in up to 40% of cases. [60] Conditions like commotio retinae, Tay-Sachs disease, and Niemann-Pick disease can present with a cherry-red spot but are differentiated by clinical context. [61, 62] Arteritic CRAO often presents with a pale, edematous disc indicative of arteritic anterior ischemic optic neuropathy alongside CRAO features. [63, 64, 65] Suspect arteritic CRAO in older patients with symptoms of giant cell arteritis (jaw claudication, polymyalgia rheumatica, scalp tenderness). Ipsilateral carotid artery disease may cause contralateral motor or sensory deficits. [66] Carotid pulse should be assessed.

In the crao differential diagnosis, clinical presentation is paramount. Sudden, painless vision loss is the hallmark of CRAO, but this symptom is shared with other conditions. The presence of a cherry-red spot, retinal whitening, and boxcarring of retinal vessels strengthens the likelihood of CRAO. However, atypical presentations, such as preserved visual acuity or absence of a cherry-red spot, and associated symptoms like pain, photophobia, or systemic features, necessitate a broader differential consideration.

Diagnostic Evaluation: Tools for Differential Diagnosis

CRAO is considered a retinal stroke, necessitating a workup similar to that for cerebral stroke or transient ischemic attacks. [12] Ophthalmic evaluation includes color fundus photography and macular OCT. Color fundus photos may show retinal whitening in the affected eye and the presence or absence of a cherry-red spot. OCT reveals inner retinal hyperreflectivity in acute CRAO (see Image. Optical Coherence Tomography of Macula in Central Retinal Artery Occlusion). Paracentral acute middle maculopathy may also be observed, characterized by inner nuclear layer hyperreflectivity. [67] Over time, inner retinal thinning becomes apparent. Fundus fluorescein angiography (FFA) is not mandatory for diagnosis but can show slow arteriolar dye progression (see Image. Fundus Fluorescein Angiogram in Central Retinal Artery Occlusion). Choroidal filling is typically normal in nonarteritic CRAO. Arteritic CRAO or ophthalmic artery occlusion may show choroidal hypoperfusion. In some CRAO cases, FFA may be normal. [58, 68]

Initial blood work should include point-of-care glucose, complete blood count, coagulation assays (PT, INR, PTT), ESR, and CRP to rule out giant cell arteritis. If inflammatory markers are elevated and giant cell arteritis is suspected, initiate high-dose IV steroids immediately. [69] Temporal artery biopsy should be planned within 2 weeks of starting steroids. [70, 71]

If symptom onset is within 4.5 hours, obtain a non-contrast CT head to exclude intracranial hemorrhage and assess thrombolytic therapy eligibility. [8] Additional tests based on individual risk factors include hemoglobin A1c, lipid profile, rheumatoid factor, antinuclear antibody, FTA-ABS, hypercoagulability labs, carotid artery imaging, electrocardiogram, echocardiogram, and Holter monitoring. [72] Carotid artery imaging (duplex ultrasound, CT, MRI, digital subtraction angiography) is crucial as carotid emboli are the most common source. If carotid imaging is normal, cardiac evaluation, including echocardiography, is indicated. Interprofessional collaboration among ophthalmologists, cardiologists, primary care physicians, and neurologists is essential.

Diagnostic evaluations are crucial in the crao differential diagnosis. OCT findings of inner retinal hyperreflectivity support CRAO, but similar findings can be seen in other retinal ischemic conditions. FFA can help confirm vascular occlusion but is not always definitive and might be normal in some CRAO cases or abnormal in other retinal vascular diseases. Blood tests, especially ESR and CRP, are critical for ruling out arteritic CRAO, a key step in differentiation. Systemic investigations like carotid and cardiac imaging are essential to identify embolic sources, informing the overall management but not directly aiding in differentiating CRAO from its immediate mimics.

Differential Diagnosis of Central Retinal Artery Occlusion: Key Distinctions

The differential diagnosis of CRAO includes several conditions that can present with acute vision loss and overlapping ophthalmoscopic findings. A systematic approach, considering clinical features, ancillary testing, and risk factors, is crucial for accurate differentiation. The primary conditions to consider in the differential diagnosis are:

1. Ophthalmic Artery Occlusion (OAO): OAO involves occlusion of the ophthalmic artery, affecting both retinal and choroidal circulation.

   • Distinguishing Features from CRAO: Profound vision loss, often to no light perception. Cherry-red spot may be absent or less prominent due to choroidal ischemia. Fundus may appear more diffusely pale, and retinal whitening may extend more posteriorly. FFA typically shows delayed or absent filling of both retinal and choroidal vessels. Associated symptoms might include orbital pain or tenderness, and signs of ischemia in other anterior segment structures. OAO is rarer than CRAO and suggests more proximal vascular occlusion.

2. Transient Ischemic Attack (TIA) or Amaurosis Fugax: While amaurosis fugax can be a precursor to CRAO, it is also a separate entity and must be differentiated from completed CRAO and other conditions.

   • Distinguishing Features from CRAO: Transient and often brief vision loss, lasting seconds to minutes, with complete visual recovery in between episodes. Fundus examination is typically normal between attacks. In CRAO, vision loss is persistent and profound. However, transient CRAO exists, making history critical. Recurrent, fleeting vision loss is more suggestive of amaurosis fugax or vasospasm rather than established CRAO.

3. Retinal Migraine: A vasospastic disorder causing transient monocular visual disturbances.

   • Distinguishing Features from CRAO: Episodes of vision loss are typically transient and may be associated with scintillations, scotomas, or other migrainous phenomena. Headache may or may not be present. Fundus examination is normal between attacks. Unlike CRAO, visual loss in retinal migraine is reversible and often has a distinct migrainous aura. However, vasospasm can be a rare cause of transient CRAO, making differentiation challenging in some cases.

4. Optic Neuritis: Inflammation of the optic nerve, often causing acute vision loss.

   • Distinguishing Features from CRAO: Vision loss in optic neuritis may develop over hours to days and is often associated with ocular pain, particularly with eye movements. Afferent pupillary defect is present, similar to CRAO. Fundus examination may show optic disc swelling (papillitis) or may be normal (retrobulbar optic neuritis). Cherry-red spot and retinal whitening are absent in optic neuritis. Visual field defects in optic neuritis are typically central scotomas or altitudinal defects, differing from the generalized visual field constriction in CRAO. MRI of the brain and optic nerves may be necessary to confirm optic neuritis and rule out other optic neuropathies.

5. Anterior Ischemic Optic Neuropathy (AION): Ischemic insult to the optic nerve head, causing sudden vision loss.

   • Distinguishing Features from CRAO: Vision loss in AION is also sudden but may be less severe than in CRAO, and progression can occur over hours to days. Afferent pupillary defect is present. Fundus examination in AION typically shows optic disc edema, often sectoral or diffuse, and sometimes flame-shaped hemorrhages. Cherry-red spot and retinal whitening are absent. AION can be arteritic (giant cell arteritis) or nonarteritic. Arteritic AION must be considered in the differential of arteritic CRAO, as both can be manifestations of giant cell arteritis. Nonarteritic AION is more common and associated with vascular risk factors similar to nonarteritic CRAO.

6. Retinal Detachment involving the macula: Separation of the neurosensory retina from the retinal pigment epithelium, leading to vision loss.

   • Distinguishing Features from CRAO: Vision loss in retinal detachment may be gradual or sudden if the macula is acutely involved. Patients may report floaters, flashes of light, and a curtain-like visual field defect preceding vision loss. Fundus examination reveals the detached retina, which appears elevated and undulating, often with a retinal tear or break visible. Cherry-red spot and retinal whitening are absent. Ultrasound B-scan of the eye can confirm retinal detachment if the fundus is obscured by media opacity.

7. Central Retinal Vein Occlusion (CRVO): Blockage of the central retinal vein, leading to venous congestion and retinal edema.

   • Distinguishing Features from CRAO: Vision loss in CRVO is typically less sudden and severe than in CRAO, often developing over hours to days. Fundus examination in CRVO shows dilated and tortuous retinal veins, retinal hemorrhages in all quadrants (“blood and thunder” fundus), and optic disc edema. Cotton wool spots and macular edema are common. Cherry-red spot and retinal whitening are absent in typical CRVO, although ischemic CRVO can present with retinal pallor due to capillary nonperfusion. FFA in CRVO shows delayed venous filling and capillary nonperfusion.

8. Paracentral Acute Middle Maculopathy (PAMM): A localized ischemic event affecting the middle layers of the retina.

   • Distinguishing Features from CRAO: PAMM typically presents with acute paracentral scotoma rather than generalized vision loss. Visual acuity may be relatively preserved. Fundus examination may be normal or show subtle gray-white lesions in the paracentral macula. OCT is crucial for diagnosis, revealing hyperreflectivity in the inner nuclear layer, corresponding to the PAMM lesion. PAMM can occur in association with CRAO or branch retinal artery occlusion, representing a milder form of retinal ischemia. It is considered part of the ischemic spectrum of retinal vascular occlusions. [55, 67]

9. Purtscher Retinopathy: Retinopathy associated with trauma, particularly chest compression injuries, or other systemic conditions.

   • Distinguishing Features from CRAO: Purtscher retinopathy typically presents with bilateral vision loss, although unilateral cases can occur. Fundus examination shows multiple cotton wool spots, retinal hemorrhages, and macular edema. Cherry-red spot and retinal whitening are absent. History of trauma or associated systemic conditions (e.g., pancreatitis, connective tissue diseases) is crucial. Cotton wool spots in transient nonarteritic CRAO can mimic Purtscher retinopathy, but the clinical context and associated fundus findings help differentiate. [59]

10. Lysosomal Storage Disorders (e.g., Tay-Sachs, Niemann-Pick): Genetic disorders that can present with a cherry-red spot in infancy or early childhood.

    • Distinguishing Features from CRAO: Lysosomal storage disorders typically present in infants or young children with progressive neurological and systemic symptoms. Cherry-red spot is bilateral and is a chronic finding, unlike the acute onset in CRAO. Other systemic and neurological findings, developmental delay, and family history are crucial differentiating factors. CRAO is exceptionally rare in this age group and clinical context. [61, 62]

11. Commotio Retinae (Berlin’s Edema): Retinal whitening following blunt trauma to the eye.

    • Distinguishing Features from CRAO: Commotio retinae occurs after blunt ocular trauma. Retinal whitening in commotio retinae is typically more diffuse and less intense than in CRAO, and a cherry-red spot may or may not be present. Vision loss is often less severe and may improve over time. History of ocular trauma is key. CRAO is not associated with direct ocular trauma. [61]

12. Drug-Induced Retinopathy: Certain medications can cause retinal changes that may mimic ischemic conditions.

    • Distinguishing Features from CRAO: A thorough medication history is essential. Drugs like interferon, talc (in intravenous drug abusers), and canthaxanthin can cause retinal changes that might be confused with ischemic retinopathy. Clinical presentation, fundus findings, and temporal relationship to drug exposure are crucial differentiating points. CRAO is typically not drug-induced, except in rare cases of cosmetic filler injections.

This detailed breakdown of the crao differential diagnosis highlights the importance of a comprehensive approach. A careful history, thorough clinical examination, appropriate ancillary testing (OCT, FFA, blood work, imaging), and consideration of risk factors are essential to distinguish CRAO from its mimics and ensure optimal patient management.

Management and Prognosis: Implications of Accurate Differential Diagnosis

While there is no universally accepted effective treatment for CRAO, prompt management focuses on restoring retinal perfusion and preventing further vascular events. Various therapies have been tried with limited success, including ocular massage, IOP-lowering agents, carbogen inhalation, hyperventilation, vasodilators, supplemental oxygen, and thrombolysis. For arteritic CRAO, high-dose intravenous methylprednisolone is the mainstay of treatment to address the underlying inflammation.

The visual prognosis for CRAO remains generally poor. Less than 10% to 20% of patients regain functional vision. [82, 89] Prognosis varies depending on the type of CRAO, with transient CRAO and CRAO with cilioretinal artery sparing having better visual outcomes. CRAO is considered a retinal stroke and is associated with an increased risk of subsequent stroke, cardiovascular events, and higher mortality rates. [90, 91, 92]

Accurate crao differential diagnosis is critical because management strategies and prognostic implications differ significantly across the conditions in the differential. For example, promptly identifying and treating arteritic CRAO with steroids can be vision-saving and prevent bilateral involvement, while misdiagnosing it as nonarteritic CRAO would delay crucial treatment. Distinguishing CRAO from conditions like optic neuritis or retinal detachment guides appropriate referral and management pathways. Furthermore, differentiating CRAO from transient conditions like amaurosis fugax or retinal migraine informs risk stratification and secondary prevention strategies for systemic vascular disease.

Deterrence, Patient Education, and Healthcare Team Coordination

Patients should be educated about CRAO symptoms, emphasizing the need for immediate medical attention for sudden vision loss. Regular vision checks and awareness of risk factors like hypertension, diabetes, and smoking are crucial. Patients should understand the potential for permanent vision loss and the importance of managing underlying vascular risk factors.

Effective healthcare team outcomes in CRAO management rely on prompt referral to ophthalmology, efficient diagnostic workup, and interprofessional collaboration. Ophthalmologists confirm the diagnosis and manage ocular complications. Cardiologists, neurologists, and primary care physicians investigate embolic sources and manage systemic vascular risk factors. Nurses and pharmacists play crucial roles in patient monitoring and medication management. Seamless communication and coordination among team members are essential to optimize patient care and potentially improve outcomes in this ophthalmic emergency.

Conclusion: Mastering CRAO Differential Diagnosis for Optimal Patient Care

Central retinal artery occlusion is a sight-threatening emergency requiring rapid and accurate diagnosis. A thorough understanding of the crao differential diagnosis is paramount for clinicians to distinguish CRAO from its mimics and ensure appropriate patient management. By considering clinical presentation, ophthalmoscopic findings, ancillary testing, and risk factors, clinicians can confidently navigate the differential diagnosis and provide timely, effective care, aiming to minimize vision loss and prevent systemic vascular complications associated with CRAO. Continued education and collaborative practice are essential to enhance outcomes for patients presenting with this challenging condition.

Review Questions

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Alt Text: Fundus photograph showing central retinal artery occlusion with whitened retina and segmented blood flow (boxcarring) around the fovea.

Alt Text: Fundus photograph illustrating central retinal artery occlusion with cilioretinal artery sparing, demonstrating maintained central vision area but reduced peripheral visual field.

Alt Text: Optical coherence tomography (OCT) scan of the macula in central retinal artery occlusion, revealing hyperreflectivity of the inner retinal layers in the acute phase of the occlusion.

Alt Text: Fundus fluorescein angiography (FFA) images in central retinal artery occlusion, showing slow progression of dye filling in the retinal arteries captured at 35 and 37 seconds post-injection.

References

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Disclosure: Koushik Tripathy declares no relevant financial relationships with ineligible companies.

Disclosure: Shalin Shah declares no relevant financial relationships with ineligible companies.

Disclosure: James Waymack declares no relevant financial relationships with ineligible companies.