Central retinal artery occlusion
Background
The first branch of internal carotid artery is the ophthalmic artery. Visual loss from CRAO is usually painless and is more common in the elderly with carotid artery disease
- Cherry red spot (fundoscopy)
- 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
- 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)
- Painful
- Arteritic anterior ischemic optic neuropathy
- Optic neuritis
- Temporal arteritis†
- Painless
- Amaurosis fugax
- Central retinal artery occlusion (CRAO)†
- Central retinal vein occlusion (CRVO)†
- High altitude retinopathy
- Open-angle glaucoma
- Posterior reversible encephalopathy syndrome (PRES)
- Retinal detachment†
- Stroke†
- Vitreous hemorrhage
- Traumatic optic neuropathy (although may have pain from the trauma)
†Emergent Diagnosis
Diagnosis
- APD
- Fundoscopy
- Pale retina, cherry red macula
- Boxcar segmentation of blood column
- Etiology work-up
- ESR and CRP
- Carotid US
- ECG
- Echo for embolus or atrial shunt
- CBC, coags, ANA, syphilis
- Amaurosis fugax
- Acute glaucoma
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 80 mg/day, with 40% of patients on > 100 mg/day
- Maintain Tx 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 IOP
- Alternative acetazolamide 500 mg 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, 500 mg IV or PO
- Mannitol
Disposition
- D/c with ophtho f/u 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.
