Central retinal artery occlusion: Difference between revisions
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*Abbreviation: CRAO | *Abbreviation: CRAO | ||
*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 | *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 | ||
*Restoration of blood flow within 100min may lead to complete recovery | *Restoration of blood flow within 100min may lead to complete recovery | ||
**Occlusion >240min leads to irreversible damage | **Occlusion >240min leads to irreversible damage | ||
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==Evaluation== | ==Evaluation== | ||
*APD | *APD | ||
*Etiology work-up | *Etiology work-up | ||
**ESR and CRP | **ESR and CRP | ||
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**Echo for embolus or atrial shunt | **Echo for embolus or atrial shunt | ||
**CBC, coags, ANA, syphilis | **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== | ==Management== | ||
Revision as of 04:17, 19 September 2016
Background
- Abbreviation: CRAO
- 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
- 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
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.