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
*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===
===Etiology===
#Retinal Embolism (20%)
*[[thromboembolism|Embolism]]
#Atherosclerotic changes
*Thrombosis
#Angiospasm
*[[Temporal Arteritis]]
#Inflammatory Endarteritis
*[[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
**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


===Epidemiology===
==Differential Diagnosis==
#Bilateral 1-2%
{{Acute vision loss noninflamed DDX}}
#M>F


==Symptoms==
==Evaluation==
Painless, monocular loss of vision
*Etiology work-up
**ESR and CRP
**Carotid [[ultrasound|US]]
**[[ECG]]
**[[Echocardiography]] for embolus or atrial shunt
**CBC, coags, ANA, syphilis


==DDx==
==Management==
#Amaurosis fugax (painless, fleeting; nl exam)
*Consult ophtho with goals for reducing [[intraocular pressure]], dislodging  the embolus or increasing arterial flow
#CRVO (painless, over hours; blood and thunder)
#Temporal Arteritis
#Acute glaucoma (blurry vision, eye pain)


==Exam==
*Start high dose systemic [[corticosteroids]] if high ESR/CRP (especially high CRP) and sudden vision loss
#Pale retina with edema
**Median starting PO [[prednisone]] 80mg/day, with 40% of patients on > 100mg/day
#Cherry red spot at the macula
**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>
#APD
#Boxcar segmentation of blood column


==Workup==
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>
#Fundoscopic exam
*Ocular massage
#CBC, ESR, EKG
**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>
*[[Acetazolamide]], 500mg IV or PO
*[[Mannitol]]


==Treatment==
==Disposition==
# Ocular massage
*Immediate ophthalmology consult
# Anterior chamber paracentesis
# Intraarterial fibrinolysis
# Acetazolamide
# Mannitol
# Timolol
# Steroids
# Hyperbarics (most effective if within 2-12h of presentation)


==Dispo==
==See Also==
Admit: comorbid disease


D/C: f/u with ophtho in 1-4 weeks
*[[Acute vision loss (noninflamed)]]


==Source==
==References==
H-N
<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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