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Central retinal artery occlusion
From WikEM
Contents
Background
- Abbreviation: CRAO
- The first branch of internal carotid artery is the ophthalmic artery
- More common in the elderly with carotid artery disease
- Restoration of blood flow within 100min may lead to complete recovery
- Occlusion >240min leads to irreversible damage
- 5-10% of CRAO is associated with giant cell arteritis[1]
Etiology
- Embolism
- Thrombosis
- Temporal Arteritis
- Vasculitis
- Sickle Cell Disease
- Trauma
- Vasospasm (migraine)
- Glaucoma
- Low retinal blood flow (carotid stenosis or hypotension)
Clinical Features
- Sudden, painless, monocular vision loss
- Often preceded by episodes of amaurosis fugax
Differential Diagnosis
Acute Vision Loss (Noninflamed)
- Arteritic anterior ischemic optic neuropathy
- Amaurosis fugax
- Central retinal artery occlusion (CRAO)†
- Central retinal vein occlusion (CRVO)†
- High altitude retinopathy
- Open-angle glaucoma
- Optic neuritis
- Posterior Reversible Encephalopathy Syndrome (PRES)
- Retinal detachment†
- Temporal arteritis†
- Traumatic optic neuropathy
- Vitreous hemorrhage
- Stroke†
†Emergent Diagnosis
Evaluation
- APD
- Etiology work-up
- ESR and CRP
- Carotid US
- ECG
- Echo for embolus or atrial shunt
- CBC, coags, ANA, syphilis
Fundoscopy
- Pale retina, cherry red macula
- Boxcar segmentation of blood column
- Cherry red spot
- Macula is thinnest portion of retina
- Intact underlying choroidal circulation remains visible through this section
- Macular area maintains normal color (red) versus surrounding ischemic, pale retina due to differing blood supplies
Management
- Consult ophtho with goals for reducing itraocular pressure, dislodging the embolus or increasing arterial flow
- Start high dose systemic corticosteroids if high ESR/CRP (especially high CRP) and sudden vision loss
- Median starting PO prednisone 80mg/day, with 40% of patients on > 100mg/day
- Treat until BOTH ESR and CRP stabilize (~2-3 wks)[2]
No evidence supporting or refuting the following treatments: [3]
- Ocular massage
- Intermittent direct digital pressure applied through closed eyelid x 10-15 sec with rapid release to create pressure gradient to dislodge embolism
- Timolol ophthalmic 0.5% to decrease intraocular pressure
- Alternative acetazolamide 500mg IV or PO[4]
- Increase PCO2 leading to retinal artery vasodilation/increased retinal blood flow
- Rebreathe into paper bag x10 min q hr
- Inhale 95% O2 and 5% CO2 (Carbogen)[5]
- Anterior chamber paracentesis
- Causes acute drop in IOP to dislodge embolism
- Intraarterial fibrinolysis or low dose systemic thrombolytics[6][7]
- Acetazolamide, 500mg IV or PO
- Mannitol
Disposition
- Discharge with ophtho follow up in 1-4wk
See Also
References
- ↑ Miller N, Newman N. Walsh & Hoyt’s Clinical Neuro-ophthalmology. 5th Edition. Baltimore: Williams and Wilkins 1998. pp. 3758-9.
- ↑ Hayreh SS. Anterior Ischemic Optic Neuropathy. [Internet]. 2013 Available from: http://www.medicine.uiowa.edu/eye/AION-part2/.
- ↑ Rudkin A et al. Clinical characteristics and outcome of current standard management of central retinal artery occlusion. Clin Experiment Ophthalmol 2010; 38:496-501
- ↑ Gerstenblith BI, Fecarotta CM. The Wills Eye Manual. Lippincott 2012.
- ↑ Atebara N. Efficacy of anterior chamber paracentesis and carbogen in treating nonarteritic central retinal artery occlusion. Ophthalmology 1995; 102:2029-2038
- ↑ Schumacher M, et al: Central retinal artery occlusion: Local intraarterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology 2010; 117:1367-1375
- ↑ Chen C et al: Efficacy of intravenous tissue-type plasminogen activator in central retinal artery occlusion: Report from a randomized, controlled trial. Stroke 2011; 42:2229-2234.
Authors
Daniel Ostermayer, Kevin Lu, Ross Donaldson, Jordan Swartz, Tiffany Joe, Neil Young, Claire
