Central retinal artery occlusion: Difference between revisions

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== Background ==
==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
[[File:Schematic diagram of the human eye en.png|thumb|Eye anatomy.]]
*Cherry red spot (fundoscopy)
*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<ref>Miller N, Newman N. Walsh & Hoyt’s Clinical Neuro-ophthalmology. 5th Edition. Baltimore: Williams and Wilkins 1998. pp. 3758-9.</ref>
 
===Etiology===
*[[thromboembolism|Embolism]]
*Thrombosis
*[[Temporal Arteritis]]
*[[Vasculitis]]
*[[Sickle Cell Disease]]
*[[Blunt orbital trauma|Trauma]]
*Vasospasm ([[migraine]])
*[[Acute_Angle-Closure_Glaucoma|Glaucoma]]
*Low retinal blood flow ([[carotid stenosis]] or [[hypotension]])
 
==Clinical Features==
*Sudden, [[Acute vision loss (noninflamed)|painless, monocular vision loss]]
**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  
**Macula is thinnest portion of retina  
**Intact underlying choroidal circulation remains visible through this section  
**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
***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 &gt;240min leads to irreversible damage


==Etiology==
==Differential Diagnosis==
#Embolism
{{Acute vision loss noninflamed DDX}}
#Thrombosis
#[[Temporal Arteritis]]
#Vasculitis
#[[Sickle Cell Disease]]
#Trauma
#Vasospasm (migraine)
#[[Acute_Angle-Closure_Glaucoma|Glaucoma]]
#Low retinal blood flow (carotid stenosis or hypotension)


== Clinical Features  ==
==Evaluation==
#Sudden, painless, monocular vision loss
*Etiology work-up
##Often preceded by episodes of amaurosis fugax
**ESR and CRP
**Carotid [[ultrasound|US]]
**[[ECG]]
**[[Echocardiography]] for embolus or atrial shunt
**CBC, coags, ANA, syphilis


== Diagnosis  ==
==Management==
#APD
*Consult ophtho with goals for reducing [[intraocular pressure]], dislodging  the embolus or increasing arterial flow
#Fundoscopy
##Pale retina, cherry red macula
##Boxcar segmentation of blood column


== DDx  ==
*Start high dose systemic [[corticosteroids]] if high ESR/CRP (especially high CRP) and sudden vision loss
#Amaurosis fugax
**Median starting PO [[prednisone]] 80mg/day, with 40% of patients on > 100mg/day
#CRVO
**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>
#[[Temporal Arteritis]]  
#[[Acute_Angle-Closure_Glaucoma|Acute glaucoma]]
 
== Treatment  ==
;Consult ophtho with goals for reducing itraocular pressure, dislodging  the embolus or increasing arterial flow


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  
*Ocular massage  
#*Intermittent direct digital pressure applied through closed eyelid x 10-15 sec w/ rapid release to create pressure gradient to dislodge embolism  
**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
*[[Timolol]] ophthalmic 0.5% to decrease intraocular pressure
#Increase PCO2 leading to retinal artery vasodilation/increased retinal blood flow   
**Alternative [[acetazolamide]] 500mg IV or PO<ref>Gerstenblith BI, Fecarotta CM. The Wills Eye Manual. Lippincott 2012.</ref>
#*Rebreathe into paper bag x10 min q hr  
*Increase PCO2 leading to retinal artery vasodilation/increased retinal blood flow   
#*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>
**Rebreathe into paper bag x10 min q hr  
#Anterior chamber paracentesis  
**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>
#*Causes acute drop in IOP to dislodge embolism  
*Anterior chamber paracentesis  
#Intraarterial fibrinolysis or low dose systemic thrombolytics<ref>Schumacher M, et al: Central retinal artery occlusion: Local intraarterial fibrinolysis versus conservative treatment, a multicenter
**Causes acute drop in IOP to dislodge embolism  
randomized trial. Ophthalmology 2010; 117:1367-1375</ref><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>
*Intraarterial fibrinolysis or low dose systemic [[thrombolytics]]<ref>Schumacher M, et al: Central retinal artery occlusion: Local intraarterial fibrinolysis versus conservative treatment, a multicenter
#Acetazolamide, 500 mg IV or PO  
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>
#Mannitol
*[[Acetazolamide]], 500mg IV or PO  
 
*[[Mannitol]]
== Disposition ==
 
*D/c w/ ophtho f/u in 1-4wk
 
== See Also  ==


*[[Acute Vision Loss (Noninflamed)]]
==Disposition==
*Immediate ophthalmology consult


== Source  ==
==See Also==


*Tintinalli
*[[Acute vision loss (noninflamed)]]
*UpToDate
*Rosen's


<br>  
==References==
<references/>  


[[Category:Ophtho]]
[[Category:Ophthalmology]]
[[Category:Vascular]]

Latest revision as of 20:57, 16 December 2020

Background

Eye anatomy.
  • 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

Clinical Features

Fundoscopy

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

Acute Vision Loss (Noninflamed)

†Emergent Diagnosis

Evaluation

  • Etiology work-up

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
  • 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

  1. ↑ Miller N, Newman N. Walsh & Hoyt’s Clinical Neuro-ophthalmology. 5th Edition. Baltimore: Williams and Wilkins 1998. pp. 3758-9.
  2. ↑ Hayreh SS. Anterior Ischemic Optic Neuropathy. [Internet]. 2013 Available from: http://www.medicine.uiowa.edu/eye/AION-part2/.
  3. ↑ Rudkin A et al. Clinical characteristics and outcome of current standard management of central retinal artery occlusion. Clin Experiment Ophthalmol 2010; 38:496-501
  4. ↑ Gerstenblith BI, Fecarotta CM. The Wills Eye Manual. Lippincott 2012.
  5. ↑ Atebara N. Efficacy of anterior chamber paracentesis and carbogen in treating nonarteritic central retinal artery occlusion. Ophthalmology 1995; 102:2029-2038
  6. ↑ Schumacher M, et al: Central retinal artery occlusion: Local intraarterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology 2010; 117:1367-1375
  7. ↑ 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.
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