Central retinal artery occlusion: Difference between revisions
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==Background== | ==Background== | ||
[[File:Schematic diagram of the human eye en.png|thumb|Eye anatomy.]] | |||
*Abbreviation: CRAO | *Abbreviation: CRAO | ||
*The first branch of internal carotid artery is the ophthalmic artery | *The first branch of internal carotid artery is the ophthalmic artery | ||
*More common in the elderly with carotid artery disease | *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 | **Occlusion >240min leads to irreversible damage | ||
*5-10% of CRAO is associated with giant cell arteritis<ref>Miller N, Newman N. Walsh & Hoyt’s Clinical Neuro-ophthalmology. 5th Edition. Baltimore: Williams and Wilkins 1998. pp. 3758-9.</ref> | *5-10% of CRAO is associated with giant cell arteritis<ref>Miller N, Newman N. Walsh & Hoyt’s Clinical Neuro-ophthalmology. 5th Edition. Baltimore: Williams and Wilkins 1998. pp. 3758-9.</ref> | ||
===Etiology=== | ===Etiology=== | ||
*Embolism | *[[thromboembolism|Embolism]] | ||
*Thrombosis | *Thrombosis | ||
*[[Temporal Arteritis]] | *[[Temporal Arteritis]] | ||
*Vasculitis | *[[Vasculitis]] | ||
*[[Sickle Cell Disease]] | *[[Sickle Cell Disease]] | ||
*[[Blunt orbital trauma|Trauma]] | *[[Blunt orbital trauma|Trauma]] | ||
*Vasospasm (migraine) | *Vasospasm ([[migraine]]) | ||
*[[Acute_Angle-Closure_Glaucoma|Glaucoma]] | *[[Acute_Angle-Closure_Glaucoma|Glaucoma]] | ||
*Low retinal blood flow ([[carotid stenosis]] or hypotension) | *Low retinal blood flow ([[carotid stenosis]] or [[hypotension]]) | ||
==Clinical Features== | ==Clinical Features== | ||
*Sudden, [[Acute vision loss (noninflamed)|painless, monocular vision loss]] | *Sudden, [[Acute vision loss (noninflamed)|painless, monocular vision loss]] | ||
**Often preceded by episodes of amaurosis fugax | **Often preceded by episodes of [[amaurosis fugax]] | ||
*APD | |||
===[[Fundoscopy]]=== | |||
[[File:CRAO.png|thumb|Typical central retinal artery occlusion with cherry-red spot, retinal edema and narrowing of the vessels.]] | |||
*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 | |||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
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==Evaluation== | ==Evaluation== | ||
*Etiology work-up | *Etiology work-up | ||
**ESR and CRP | **ESR and CRP | ||
**Carotid US | **Carotid [[ultrasound|US]] | ||
**ECG | **[[ECG]] | ||
** | **[[Echocardiography]] for embolus or atrial shunt | ||
**CBC, coags, ANA, syphilis | **CBC, coags, ANA, syphilis | ||
==Management== | ==Management== | ||
*Consult ophtho with goals for reducing [[intraocular 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 | **Median starting PO [[prednisone]] 80mg/day, with 40% of patients on > 100mg/day | ||
*Treat until BOTH ESR and CRP stabilize (~2-3 wks)<ref>Hayreh SS. Anterior Ischemic Optic Neuropathy. [Internet]. 2013 Available from: http://www.medicine.uiowa.edu/eye/AION-part2/.</ref> | **Treat until BOTH ESR and CRP stabilize (~2-3 wks)<ref>Hayreh SS. Anterior Ischemic Optic Neuropathy. [Internet]. 2013 Available from: http://www.medicine.uiowa.edu/eye/AION-part2/.</ref> | ||
No evidence supporting or refuting the following treatments: <ref>Rudkin A et al. Clinical characteristics and outcome of current standard management of central retinal artery occlusion. Clin Experiment Ophthalmol 2010; 38:496-501</ref> | No evidence supporting or refuting the following treatments: <ref>Rudkin A et al. Clinical characteristics and outcome of current standard management of central retinal artery occlusion. Clin Experiment Ophthalmol 2010; 38:496-501</ref> | ||
*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<ref>Gerstenblith BI, Fecarotta CM. The Wills Eye Manual. Lippincott 2012.</ref> | |||
*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)<ref>Atebara N. Efficacy of anterior chamber paracentesis and carbogen in treating nonarteritic central retinal artery occlusion. Ophthalmology 1995; 102:2029-2038</ref> | |||
*Anterior chamber paracentesis | |||
**Causes acute drop in IOP to dislodge embolism | |||
*Intraarterial fibrinolysis or low dose systemic [[thrombolytics]]<ref>Schumacher M, et al: Central retinal artery occlusion: Local intraarterial fibrinolysis versus conservative treatment, a multicenter | |||
randomized trial. Ophthalmology 2010; 117:1367-1375</ref><ref>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.</ref> | randomized trial. Ophthalmology 2010; 117:1367-1375</ref><ref>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.</ref> | ||
*[[Acetazolamide]], 500mg IV or PO | |||
*[[Mannitol]] | |||
==Disposition== | ==Disposition== | ||
*Immediate ophthalmology consult | |||
* | |||
==See Also== | ==See Also== | ||
*[[Acute | *[[Acute vision loss (noninflamed)]] | ||
==References== | ==References== | ||
Latest revision as of 20:57, 16 December 2020
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
- APD
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
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
- Etiology work-up
- ESR and CRP
- Carotid US
- ECG
- Echocardiography for embolus or atrial shunt
- CBC, coags, ANA, syphilis
Management
- Consult ophtho with goals for reducing intraocular 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
- Immediate ophthalmology consult
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.