Lytics in CRAO

What is the role of thrombolysis in central retinal artery occlusion?

Bottom line up top: Current evidence does not support routine intravenous thrombolysis for acute central retinal artery occlusion (CRAO).

Clinical scenario

A 71-year-old woman with hypertension and atrial fibrillation presents 2.5 hours after sudden vision loss in her left eye. She has profound monocular vision loss. CTA is negative, but bedside POCUS shows a retrobulbar spot sign, confirming acute CRAO. Because she is within the traditional 4.5-hour thrombolytic window, you consider IV thrombolysis.

What your gut says: CRAO is an "eye stroke." If thrombolytics improve outcomes in acute ischemic stroke, they should help restore vision in CRAO too.

What the evidence says

The rationale for lytics

  • CRAO is an acute ischemic injury of the retina, most often from embolic occlusion of the central retinal artery or one of its branches.

  • Because the retinal and cerebral circulations share a common vascular origin, thrombolysis has long been considered a possible treatment (Dumitrascu 2020; Mac Grory 2021).

Why the eye is not the brain

  • The retina has minimal collateral circulation, so ischemic injury is rapid and irreversible.

  • The small caliber of the retinal vessels and the varied causes of CRAO may reduce the effectiveness of systemic thrombolysis (Hayreh 2011).

Early evidence: observational

Early support came mainly from observational studies and patient-level meta-analyses. This led the 2021 AHA scientific statement to recommend considering thrombolysis in carefully selected patients within 4.5 hours, while acknowledging the absence of randomized evidence (Mac Grory 2021; Schrag 2015).

Recent evidence: randomized trials

Two high-quality RCTs have since challenged this practice. Randomization reduces the selection bias and confounding inherent in the earlier studies, so these trials are the strongest evidence to date.

  • THEIA: IV alteplase versus aspirin showed no improvement in visual recovery, with a trend toward more adverse events (Préterre 2025).

  • TenCRAOS: tenecteplase versus aspirin showed no significant difference in visual recovery, with one symptomatic intracranial hemorrhage in the thrombolysis group (Ryan 2026).

Together, these trials suggest the risks of thrombolysis outweigh any unproven benefit.

Clinical bottom line

Routine IV thrombolysis is not supported for acute non-arteritic CRAO. Instead, prioritize:

  • rapid diagnosis

  • ophthalmology and neurology consultation

  • a stroke evaluation (CRAO is a stroke equivalent)

  • secondary stroke prevention

CRAO remains a vascular emergency, but current evidence suggests thrombolytics do not improve visual outcomes and may cause harm (Préterre 2025; Ryan 2026).

Clinical pearls

  • CRAO is a stroke. The work-up (vascular imaging, cardiac monitoring, and stroke prevention) matters even when lytics are not given.

  • POCUS can support the diagnosis at the bedside: look for the retrobulbar spot sign.

References

  • Dumitrascu OM, Newman NJ, Biousse V. Thrombolysis for central retinal artery occlusion in 2020: time is vision! J Neuroophthalmol. 2020;40(3):333–345. PMID: 32739995. Full text

  • Hayreh SS. Ocular vascular occlusive disorders: natural history of visual outcome. Prog Retin Eye Res. 2011;30(5):359–394. PMID: 24769221. Full text

  • Mac Grory B, et al. Management of central retinal artery occlusion: a scientific statement from the American Heart Association. Stroke. 2021. PMID: 33677974

  • Préterre C, Gaultier A, Obadia M, et al. Intravenous alteplase versus oral aspirin for acute central retinal artery occlusion within 4.5 hours of severe vision loss (THEIA). Lancet Neurol. 2025. PMID: 41109232

  • Ryan SJ, Jørstad ØK, Skjelland M, et al. A randomized trial of tenecteplase in acute central retinal artery occlusion. N Engl J Med. 2026;394(5):442–450. PMID: 41604638

  • Schrag M, Youn T, Schindler J, Kirshner H, Greer D. Intravenous fibrinolytic therapy in central retinal artery occlusion: a patient-level meta-analysis. JAMA Neurol. 2015;72(10):1148–1154. PMID: 26258861

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