What are the possible differentials for painless, subacute loss of vision in one eye?

Differential Diagnosis for Painless, Subacute Monocular Vision Loss

The primary differentials for painless, subacute monocular vision loss are retinal artery occlusion (central or branch), retinal vein occlusion, optic neuritis, ischemic optic neuropathy (arteritic or non-arteritic), and retinal detachment, with the most critical immediate consideration being whether this represents a stroke equivalent requiring emergency evaluation. 1, 2

Vascular Etiologies (Stroke Equivalents - Require Emergency Evaluation)

Retinal Artery Occlusion (CRAO/BRAO)

• Central retinal artery occlusion presents with sudden, painless vision loss and is considered a stroke equivalent by the American Heart Association, requiring immediate stroke center evaluation 1, 2
• Up to 25% of CRAO patients have concurrent silent brain infarction on MRI, making this a neurological emergency 3, 2
• Branch retinal artery occlusion causes sectoral vision loss and similarly requires urgent stroke evaluation within 24 hours 2
• Fundoscopic findings include retinal whitening, cherry-red spot (in CRAO), retinal emboli, "boxcarring" of vessels, and cotton-wool spots 3
• Risk factors include cardiovascular disease, hypertension, diabetes, hyperlipidemia, and smoking 3

Transient Monocular Vision Loss (Amaurosis Fugax)

• Represents a retinal TIA with vision loss lasting seconds to minutes that resolves completely 1
• Stroke risk is highest within the first 7 days after onset and remains elevated for 30 days 1, 2
• Requires the same emergency stroke protocol as cerebral TIA 3, 1

Retinal Vein Occlusion (CRVO/BRVO)

• Presents with painless vision loss, often less acute than arterial occlusion 4
• Fundoscopy reveals multiple retinal hemorrhages, dilated tortuous veins, cotton-wool spots, and optic disc edema 5
• Associated with hypertension, diabetes, hyperlipidemia, and hypercoagulable states 5

Optic Nerve Etiologies

Giant Cell Arteritis (Arteritic Anterior Ischemic Optic Neuropathy)

• Must be considered in all patients over 50 years old with sudden vision loss 1, 2
• Associated symptoms include jaw claudication (most specific, LR 4.90), scalp tenderness, temporal tenderness, headaches, and constitutional symptoms 1, 6
• ESR >60 mm/h has high likelihood ratio for diagnosis 1
• Requires immediate empiric high-dose steroids without waiting for temporal artery biopsy to prevent vision loss in the contralateral eye 2, 6

Non-Arteritic Anterior Ischemic Optic Neuropathy (NAION)

• Painless vision loss with optic disc edema on examination 4
• Associated with vascular risk factors, small cup-to-disc ratio ("disc at risk"), and nocturnal hypotension 4
• No proven acute treatment, but requires cardiovascular risk factor management 4

Optic Neuritis

• Can be painless in approximately 8% of cases, though pain with eye movement is typical 3, 6
• Features include color desaturation, relative afferent pupillary defect, and central scotoma 6
• Associated with multiple sclerosis, neuromyelitis optica, or other demyelinating conditions 3
• MRI of orbits and brain with contrast shows optic nerve enhancement and may reveal demyelinating lesions 3

Retinal Structural Etiologies

Retinal Detachment

• Presents with curtain-like visual field defect, often preceded by photopsias (flashes) and floaters 6
• Requires urgent ophthalmologic evaluation and usually surgical intervention 6
• Ultrasonography useful if media opacity prevents direct visualization 3

Vitreous Hemorrhage

• Sudden painless vision loss with floaters 4
• Risk factors include diabetic retinopathy, retinal tears, posterior vitreous detachment 4
• Fundoscopy may be obscured; ultrasonography helps assess retinal status 3

Critical Diagnostic Approach

Immediate Triage Decision

• If vascular etiology (CRAO, BRAO, or TMVL) is confirmed or suspected, immediately refer to certified stroke center ED with note stating "Ocular TIA" or "Ocular Stroke" without performing additional testing 3, 2
• Do not delay referral for additional ophthalmologic workup if vascular cause is suspected 2

Essential History Elements

• Duration and pattern of vision loss (transient vs. persistent, sudden vs. gradual) 3
• Age over 50 years mandates GCA screening: jaw claudication, scalp tenderness, temporal tenderness, headaches, constitutional symptoms 3, 1
• Cardiovascular risk factors: hypertension, diabetes, hyperlipidemia, smoking, prior stroke/TIA 3
• Preceding symptoms: flashes, floaters, curtain-like defect 6
• Pain with eye movement (suggests optic neuritis) 6

Essential Examination Findings

• Visual acuity and relative afferent pupillary defect 3
• Fundoscopy through dilated pupil: look for retinal whitening, cherry-red spot, hemorrhages, emboli, disc edema, neovascularization 3
• Intraocular pressure (elevated in acute angle-closure glaucoma, which presents with pain) 3

Emergency Diagnostic Workup (for vascular etiologies)

• Brain MRI with diffusion-weighted imaging to identify concurrent stroke (present in up to 24% of retinal vascular events) 1, 2
• Vascular imaging (CTA or MRA) to assess carotid stenosis (found in up to 70% of symptomatic retinal vascular events) 1, 2
• ESR and CRP in patients over 50 years to evaluate for GCA 1, 2
• Cardiac monitoring and echocardiography to identify embolic sources 2

Common Pitfalls to Avoid

• Never assume reperfusion eliminates stroke risk - stroke risk remains highest in first 7 days even if vision improves 2
• Never delay GCA treatment for biopsy - empiric steroids should be started immediately in suspected cases 2, 6
• Never underestimate cardiovascular risk - new significant cardiovascular conditions are discovered in up to 70% of CRAO patients 2
• Never perform extensive ophthalmologic workup before stroke center referral if vascular etiology is suspected 3, 2
• Always check inflammatory markers in patients over 50 regardless of whether classic GCA symptoms are present 2