What is the differential diagnosis and management for sudden loss of vision in one eye?

Differential Diagnosis of Sudden Monocular Vision Loss

Sudden, painless loss of vision in one eye is a stroke equivalent requiring immediate emergency department evaluation at a certified stroke center without delay. 1, 2

Critical Time-Sensitive Vascular Etiologies (Highest Priority)

Central Retinal Artery Occlusion (CRAO)

• Presents with sudden, painless monocular vision loss with visual acuity of "count fingers" or worse in >80% of cases 1
• Funduscopic findings include diffuse retinal whitening (edema), cherry red spot at the fovea, and attenuated retinal arteries 1
• Relative afferent pupillary defect is typically present 1
• Up to 25% have concurrent silent brain infarction on MRI, making this a true stroke equivalent 2
• Natural history shows only 17.7% achieve functional visual recovery without intervention 1

Branch Retinal Artery Occlusion (BRAO)

• Similar presentation to CRAO but with sectoral rather than complete vision loss 1
• Requires urgent stroke evaluation within 24 hours even if vision improves 2
• High risk of concurrent cerebrovascular events 2

Transient Monocular Vision Loss (TMVL/Amaurosis Fugax)

• Sudden, painless vision loss clearing within seconds to minutes, representing a retinal TIA 3
• Stroke risk is maximum within the first few days after onset, with highest risk in first 7 days 3, 2
• Most commonly caused by atherothromboembolism from the internal carotid artery origin 4
• Funduscopic examination is typically normal between episodes 1
• Description of "blackened vision" suggests higher cardiovascular risk than "blurred vision" 4

Giant Cell Arteritis (GCA) - Arteritic CRAO

• Must be considered in all patients >50 years old with sudden vision loss 3, 2
• Jaw claudication is the most specific symptom (likelihood ratio 4.90) 3
• ESR >60 mm/h has high likelihood ratio for GCA 3
• Can cause combined CRAO, anterior ischemic optic neuropathy (AION), and choroidal ischemia 1
• Empiric high-dose steroids should not be delayed for temporal artery biopsy if clinical suspicion is high 2

Other Vascular Etiologies

Central Retinal Vein Occlusion (CRVO)

• Presents with sudden painless vision loss but typically less severe than CRAO 5
• Funduscopy shows multiple retinal hemorrhages, dilated tortuous veins, cotton-wool spots, and optic disc edema 5
• Associated with hypertension, diabetes, and hypercoagulable states 6

Ischemic Optic Neuropathy (ION)

• Sudden painless vision loss with optic disc swelling 5
• Arteritic form (from GCA) requires immediate steroid treatment 1
• Non-arteritic form associated with cardiovascular risk factors 5

Posterior Circulation Stroke

• Can cause monocular or binocular vision loss depending on location 5
• Associated with other neurological deficits in most cases 5

Non-Vascular Etiologies (Lower Acuity)

Vitreous Hemorrhage

• Sudden vision loss with floaters and "red haze" 5
• Funduscopy shows blood obscuring retinal details 5
• Common causes include diabetic retinopathy, retinal tear, or trauma 5

Retinal Detachment

• Progressive visual field loss described as "curtain coming down" 5
• Flashes and floaters typically precede vision loss 5
• Requires urgent (but not emergent) ophthalmologic intervention 5

Optic Neuritis

• Can rarely present with transient vision loss mimicking amaurosis fugax 7
• Typically associated with retro-orbital pain worsened by eye movement 7
• MRI may show optic nerve enhancement and periventricular white matter lesions 7
• Responds to high-dose parenteral steroids 7

Immediate Management Algorithm

Step 1: Establish Vascular vs. Non-Vascular Etiology

• If history suggests vascular cause (sudden, painless, CRAO/BRAO/TMVL pattern): Send immediately to ED at certified stroke center with note stating "Ocular TIA" or "Ocular Stroke" 1, 2
• Call ahead to warn stroke team that "a stroke patient is on the way" 1
• Do not delay referral to perform additional testing 2

Step 2: Age-Based Risk Stratification

• All patients >50 years: Check ESR and CRP immediately to evaluate for GCA 3, 2
• If GCA suspected clinically, start empiric high-dose steroids before biopsy 2

Step 3: Emergency Department Workup (Within 23-Hour Observation)

• Brain MRI with diffusion-weighted imaging to detect concurrent stroke (found in up to 24% of cases) 2
• Vascular imaging (MRA or CTA) of carotids and vertebrobasilar system (significant stenosis found in up to 70% of symptomatic cases) 3, 2
• Cardiac monitoring for arrhythmias 2
• Echocardiography to evaluate for cardioembolic sources 2, 8
• Start antiplatelet therapy immediately unless contraindicated 2

Step 4: Hospitalization Criteria

• Admit if presenting within 72 hours AND any of the following: 2
  • Abnormal brain DWI-MRI showing acute infarction
  • Large artery atherosclerosis (>50% stenosis)
  • Abnormal cardiac evaluation (atrial fibrillation, valvular disease, PFO with atrial septal aneurysm)
  • Recurrent episodes
  • Inability to provide expedited outpatient follow-up

Critical Pitfalls to Avoid

• Never assume that vision recovery eliminates stroke risk—the 7-day stroke risk remains elevated even with complete visual recovery 2
• Never delay stroke center referral to obtain ophthalmology consultation first—eye care providers should refer immediately after confirming vascular etiology 1, 2
• Never miss GCA in elderly patients—always check inflammatory markers in patients >50 years 2
• Never underestimate cardiovascular risk—new significant cardiovascular conditions are discovered in up to 70% of CRAO patients 2
• Never forget that paradoxical embolism through PFO can cause CRAO, especially in younger patients without traditional risk factors 8

Secondary Prevention (After Acute Phase)

• High-intensity statin therapy for hyperlipidemia 2
• Blood pressure control targeting <130/80 mmHg 2
• Antiplatelet therapy (aspirin or clopidogrel) 2
• Smoking cessation 6
• Neurology follow-up within 2 weeks 2
• Ophthalmology follow-up within 1-2 weeks to monitor for neovascular complications 6