Central Retinal Artery Occlusion (CRAO): Clinical Presentation, Diagnostic Evaluation, and Outcome – A Case Report

Abstract

Central retinal artery occlusion (CRAO) is an ophthalmic emergency characterized by sudden, painless, and severe vision loss due to acute interruption of retinal arterial blood flow. It is often associated with embolic or thrombotic events and shares risk factors with systemic vascular diseases such as hypertension, diabetes mellitus, and atherosclerosis. The retina is highly sensitive to ischemia, and irreversible damage can occur within a short time window. Diagnosis is primarily clinical, supported by fundoscopic findings and imaging modalities such as optical coherence tomography (OCT) and fluorescein angiography. Despite various treatment attempts, visual prognosis remains poor in most patients. This case report highlights the clinical presentation, diagnostic approach, management, and outcome of CRAO in a middle-aged patient.

Introduction

Central retinal artery occlusion represents the ocular equivalent of an ischemic stroke and requires immediate recognition and intervention. The central retinal artery, a branch of the ophthalmic artery, supplies the inner retinal layers. Any obstruction in this artery results in rapid retinal ischemia and subsequent vision loss.

CRAO most commonly occurs due to emboli originating from atherosclerotic plaques in the carotid arteries or cardiac sources such as atrial fibrillation. Less frequently, it may result from thrombosis, vasculitis, or hypercoagulable states. The condition predominantly affects older adults with underlying vascular risk factors.

Clinically, CRAO presents as sudden, painless, unilateral vision loss, often described as a curtain descending over the visual field. Prompt diagnosis is critical, although the therapeutic window for meaningful visual recovery is extremely narrow.

Case Report

Patient History

A 60-year-old male presented to the emergency department with sudden onset of vision loss in the left eye for approximately 3 hours. The loss of vision was painless and complete, with no preceding trauma, redness, or discharge.

The patient had a known history of hypertension, type 2 diabetes mellitus, and hyperlipidemia for over 10 years. He was a chronic smoker with poor adherence to medications. There was no prior history of ocular disease or similar episodes.

Clinical Examination

On examination, the patient was hemodynamically stable.

Ophthalmic findings included:

• Visual acuity: Hand movements in the left eye; normal in the right eye
• Relative afferent pupillary defect (RAPD) in the affected eye

Fundus examination revealed:

• Diffuse retinal whitening
• A prominent cherry-red spot at the macula
• Attenuated and narrowed retinal arteries

Anterior segment examination was normal, and intraocular pressure was within normal limits.

Clinical Evaluation

Differential Diagnosis

The differential diagnoses considered included:

• Central retinal artery occlusion
• Central retinal vein occlusion
• Retinal detachment
• Optic neuritis
• Anterior ischemic optic neuropathy

The classic fundoscopic findings and sudden painless vision loss strongly indicated CRAO.

Investigations

Laboratory Findings

• Elevated fasting blood glucose levels
• Increased serum cholesterol and triglycerides
• Normal complete blood count except mild leukocytosis

Ophthalmic Imaging

• Optical Coherence Tomography (OCT): Hyperreflectivity and thickening of inner retinal layers
• Fundus Fluorescein Angiography: Delayed arterial filling and reduced retinal perfusion

Systemic Evaluation

• Carotid Doppler ultrasound: Atherosclerotic plaque in the internal carotid artery

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• Electrocardiogram (ECG): No arrhythmia detected
• Echocardiography: No significant cardiac source of emboli

Diagnosis

Based on clinical presentation and supporting investigations, the diagnosis was confirmed as:
Acute Central Retinal Artery Occlusion

Management and Outcome

Initial Management

Immediate treatment was initiated in an attempt to restore retinal perfusion:

• Ocular massage to dislodge embolus
• Reduction of intraocular pressure using topical beta-blockers and systemic agents
• Administration of carbon dioxide via rebreathing technique to induce vasodilation

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Medical Management

• Antiplatelet therapy initiated
• Statins prescribed for lipid control
• Optimization of blood pressure and glycemic status

Follow-Up

At 1 week:

• No significant improvement in vision

At 1 month:

• Persistent severe visual impairment
• Fundus showed resolving edema

At 3 months:

• Optic disc pallor indicating optic atrophy
• Permanent loss of central vision

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Outcome

The patient experienced:

• Irreversible vision loss in the affected eye
• Stabilization of systemic risk factors with medical therapy
• No recurrence or involvement of the contralateral eye

Discussion

Central retinal artery occlusion is a devastating ocular condition with limited treatment options and poor visual prognosis. The retina has one of the highest metabolic demands in the body, making it extremely vulnerable to ischemia. Experimental studies suggest that irreversible damage can occur within 90–120 minutes of occlusion.

The most common etiology is embolic occlusion from carotid artery atherosclerosis or cardiac sources. Risk factors such as hypertension, diabetes, smoking, and hyperlipidemia significantly increase the likelihood of occurrence.

The hallmark clinical feature is sudden, painless, unilateral vision loss. Fundoscopic examination typically reveals retinal whitening due to ischemia and a cherry-red spot at the fovea, where the underlying choroidal circulation remains intact.

Diagnosis is largely clinical but is supported by imaging modalities. OCT findings reflect ischemic damage to inner retinal layers, while fluorescein angiography demonstrates delayed or absent arterial filling.

Management remains controversial and largely ineffective in restoring vision. Conventional approaches such as ocular massage, reduction of intraocular pressure, and vasodilation techniques are often attempted but lack strong evidence. Recent studies have explored thrombolytic therapy; however, its use remains limited due to potential risks and lack of consensus.

Importantly, CRAO is considered a manifestation of systemic vascular disease and is associated with an increased risk of stroke and cardiovascular events. Therefore, comprehensive systemic evaluation is essential.

Complications include:

• Permanent vision loss
• Optic atrophy
• Neovascularization (rare)
• Increased risk of cerebrovascular events

Preventive strategies focus on aggressive management of cardiovascular risk factors and lifestyle modifications such as smoking cessation.

Conclusion

Central retinal artery occlusion is a true ophthalmic emergency that requires rapid diagnosis and immediate intervention. Despite timely management, visual outcomes are often poor due to the rapid onset of irreversible retinal ischemia. This case highlights the importance of early recognition, prompt referral, and systemic evaluation to reduce the risk of further vascular events. Clinicians should maintain a high index of suspicion in patients presenting with sudden painless vision loss, particularly those with underlying vascular risk factors.

References

1. Hayreh SS, Zimmerman MB, Kimura A, Sanon A. Central retinal artery occlusion. https://pubmed.ncbi.nlm.nih.gov/16678504/
2. Varma DD, Cugati S, Lee AW, Chen CS. A review of central retinal artery occlusion: clinical presentation and management. https://pubmed.ncbi.nlm.nih.gov/24068003/
3. Schrag M, Youn T, Schindler J, et al. Intravenous fibrinolytic therapy in central retinal artery occlusion. https://pubmed.ncbi.nlm.nih.gov/26642484/
4. Mac Grory B, Schrag M, Biousse V, et al. Management of central retinal artery occlusion: A scientific statement. https://pubmed.ncbi.nlm.nih.gov/33626989/
5. Biousse V, Nahab F, Newman NJ. Management of acute retinal ischemia. https://pubmed.ncbi.nlm.nih.gov/21282583/
6. Fraser SG, Adams W. Interventions for acute non-arteritic central retinal artery occlusion. https://pubmed.ncbi.nlm.nih.gov/24395564/

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