Sudden Painless Vision Loss in a 68-Year-Old with Vascular Risk Factors
A 68-year-old man presents the same morning with sudden, painless loss of the superior half of the vision in his left eye, noticed on waking. History includes hypertension, type 2 diabetes, and a 30 pack-year smoking history; he stopped his antihypertensives two weeks ago because of dizziness. Acuity is 20/40 OS and 20/20 OD. Confrontation fields show a dense inferior altitudinal defect OS. Anterior segment and IOP are normal. Dilated funduscopy of the left eye shows a pale, milky, opacified superior retina with a cherry-red spot at the macula and a boxcar appearance in the superotemporal arteriole. The right fundus shows moderate hypertensive changes.
1. What is the most likely diagnosis, what is the mechanism, and what immediate actions and referrals are indicated?
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Diagnosis: central retinal artery occlusion (CRAO), left eye, with the classic triad of sudden painless monocular loss, altitudinal/global field defect, and retinal whitening with a cherry-red spot. Boxcar segmentation confirms arteriolar stasis.
Mechanism: embolic or thrombotic occlusion of the central retinal artery, most often from a carotid or cardiac source in a patient with multiple vascular risk factors. The retina infarcts within roughly 90-100 minutes, so time is critical.
Immediate actions:
- Treat as an ocular stroke. Same-day stroke workup: the patient needs urgent evaluation for concomitant cerebral ischemia. CRAO carries a substantial risk of concurrent or subsequent stroke, so emergency department referral and stroke-team involvement are appropriate, not routine outpatient follow-up.
- Check blood pressure, glucose, and arrange ECG, carotid imaging, and echocardiography per the receiving team.
- Ocular maneuvers (ocular massage, anterior chamber paracentesis, IOP lowering) have limited and unproven benefit but are sometimes attempted if the patient is seen within hours; do not delay systemic referral for them.
Communication: Document the visual prognosis honestly (often poor, though some recover peripheral field), and emphasize that the priority is preventing a stroke.
2. How would you differentiate this from anterior ischemic optic neuropathy at the chair, and why does the distinction matter?
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Both cause sudden painless monocular loss, but the signs diverge:
| Feature | CRAO | AION |
|---|---|---|
| Disc | Normal or mildly pale; retina whitened | Swollen, hyperemic (or pale in arteritic) disc |
| Retinal appearance | Diffuse whitening, cherry-red spot, boxcar | Normal retina |
| Field | Altitudinal or global | Altitudinal (often inferior) |
| Laterality | Usually unilateral | Unilateral, but fellow eye at risk |
Why it matters:
- AION is an optic nerve problem; giant cell arteritis must be excluded urgently in older patients with systemic symptoms, jaw claudication, or elevated ESR/CRP, because the fellow eye can be lost within days and steroids are sight-saving.
- CRAO triggers a systemic embolic/stroke workup.
- The two have different follow-up pathways, so the fundus exam is the deciding test. In this case, retinal whitening with a cherry-red spot and a normal-appearing disc confirms CRAO.